A vague complaint of debility, fatigue, or exhaustion attributable to weakness of various muscles. The weakness can be characterized as subacute or chronic, often progressive, and is a manifestation of many muscle and neuromuscular diseases. (From Wyngaarden et al., Cecil Textbook of Medicine, 19th ed, p2251)
Contractile tissue that produces movement in animals.
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
A group of inherited congenital myopathic conditions characterized clinically by weakness, hypotonia, and prominent hypoplasia of proximal muscles including the face. Muscle biopsy reveals large numbers of rod-shaped structures beneath the muscle fiber plasma membrane. This disorder is genetically heterogeneous and may occasionally present in adults. (Adams et al., Principles of Neurology, 6th ed, p1453)
Large, multinucleate single cells, either cylindrical or prismatic in shape, that form the basic unit of SKELETAL MUSCLE. They consist of MYOFIBRILS enclosed within and attached to the SARCOLEMMA. They are derived from the fusion of skeletal myoblasts (MYOBLASTS, SKELETAL) into a syncytium, followed by differentiation.
Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.
These include the muscles of the DIAPHRAGM and the INTERCOSTAL MUSCLES.
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)
A general term encompassing lower MOTOR NEURON DISEASE; PERIPHERAL NERVOUS SYSTEM DISEASES; and certain MUSCULAR DISEASES. Manifestations include MUSCLE WEAKNESS; FASCICULATION; muscle ATROPHY; SPASM; MYOKYMIA; MUSCLE HYPERTONIA, myalgias, and MUSCLE HYPOTONIA.
The nonstriated involuntary muscle tissue of blood vessels.
Developmental events leading to the formation of adult muscular system, which includes differentiation of the various types of muscle cell precursors, migration of myoblasts, activation of myogenesis and development of muscle anchorage.
A state arrived at through prolonged and strong contraction of a muscle. Studies in athletes during prolonged submaximal exercise have shown that muscle fatigue increases in almost direct proportion to the rate of muscle glycogen depletion. Muscle fatigue in short-term maximal exercise is associated with oxygen lack and an increased level of blood and muscle lactic acid, and an accompanying increase in hydrogen-ion concentration in the exercised muscle.
Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation.
Diseases characterized by inflammation involving multiple muscles. This may occur as an acute or chronic condition associated with medication toxicity (DRUG TOXICITY); CONNECTIVE TISSUE DISEASES; infections; malignant NEOPLASMS; and other disorders. The term polymyositis is frequently used to refer to a specific clinical entity characterized by subacute or slowly progressing symmetrical weakness primarily affecting the proximal limb and trunk muscles. The illness may occur at any age, but is most frequent in the fourth to sixth decade of life. Weakness of pharyngeal and laryngeal muscles, interstitial lung disease, and inflammation of the myocardium may also occur. Muscle biopsy reveals widespread destruction of segments of muscle fibers and an inflammatory cellular response. (Adams et al., Principles of Neurology, 6th ed, pp1404-9)
Inflammation of a muscle or muscle tissue.
Skeletal muscle fibers characterized by their expression of the Type I MYOSIN HEAVY CHAIN isoforms which have low ATPase activity and effect several other functional properties - shortening velocity, power output, rate of tension redevelopment.
Skeletal muscle fibers characterized by their expression of the Type II MYOSIN HEAVY CHAIN isoforms which have high ATPase activity and effect several other functional properties - shortening velocity, power output, rate of tension redevelopment. Several fast types have been identified.
The musculofibrous partition that separates the THORACIC CAVITY from the ABDOMINAL CAVITY. Contraction of the diaphragm increases the volume of the thoracic cavity aiding INHALATION.
The amount of force generated by MUSCLE CONTRACTION. Muscle strength can be measured during isometric, isotonic, or isokinetic contraction, either manually or using a device such as a MUSCLE STRENGTH DYNAMOMETER.
The quadriceps femoris. A collective name of the four-headed skeletal muscle of the thigh, comprised of the rectus femoris, vastus intermedius, vastus lateralis, and vastus medialis.
Recording of the changes in electric potential of muscle by means of surface or needle electrodes.
Mitochondria of skeletal and smooth muscle. It does not include myocardial mitochondria for which MITOCHONDRIA, HEART is available.
A subacute or chronic inflammatory disease of muscle and skin, marked by proximal muscle weakness and a characteristic skin rash. The illness occurs with approximately equal frequency in children and adults. The skin lesions usually take the form of a purplish rash (or less often an exfoliative dermatitis) involving the nose, cheeks, forehead, upper trunk, and arms. The disease is associated with a complement mediated intramuscular microangiopathy, leading to loss of capillaries, muscle ischemia, muscle-fiber necrosis, and perifascicular atrophy. The childhood form of this disease tends to evolve into a systemic vasculitis. Dermatomyositis may occur in association with malignant neoplasms. (From Adams et al., Principles of Neurology, 6th ed, pp1405-6)
An autosomal dominant familial disorder characterized by recurrent episodes of skeletal muscle weakness associated with falls in serum potassium levels. The condition usually presents in the first or second decade of life with attacks of trunk and leg paresis during sleep or shortly after awakening. Symptoms may persist for hours to days and generally are precipitated by exercise or a meal high in carbohydrates. (Adams et al., Principles of Neurology, 6th ed, p1483)
The resection or removal of the innervation of a muscle or muscle tissue.
Muscular contractions characterized by increase in tension without change in length.
A heterogeneous group of diseases characterized by the early onset of hypotonia, developmental delay of motor skills, non-progressive weakness. Each of these disorders is associated with a specific histologic muscle fiber abnormality.
A heterogeneous group of inherited MYOPATHIES, characterized by wasting and weakness of the SKELETAL MUSCLE. They are categorized by the sites of MUSCLE WEAKNESS; AGE OF ONSET; and INHERITANCE PATTERNS.
A disorder of neuromuscular transmission characterized by weakness of cranial and skeletal muscles. Autoantibodies directed against acetylcholine receptors damage the motor endplate portion of the NEUROMUSCULAR JUNCTION, impairing the transmission of impulses to skeletal muscles. Clinical manifestations may include diplopia, ptosis, and weakness of facial, bulbar, respiratory, and proximal limb muscles. The disease may remain limited to the ocular muscles. THYMOMA is commonly associated with this condition. (Adams et al., Principles of Neurology, 6th ed, p1459)
A heterogeneous group of disorders characterized by a congenital defect in neuromuscular transmission at the NEUROMUSCULAR JUNCTION. This includes presynaptic, synaptic, and postsynaptic disorders (that are not of autoimmune origin). The majority of these diseases are caused by mutations of various subunits of the nicotinic acetylcholine receptor (RECEPTORS, NICOTINIC) on the postsynaptic surface of the junction. (From Arch Neurol 1999 Feb;56(2):163-7)
Non-striated, elongated, spindle-shaped cells found lining the digestive tract, uterus, and blood vessels. They are derived from specialized myoblasts (MYOBLASTS, SMOOTH MUSCLE).
Progressive myopathies characterized by the presence of inclusion bodies on muscle biopsy. Sporadic and hereditary forms have been described. The sporadic form is an acquired, adult-onset inflammatory vacuolar myopathy affecting proximal and distal muscles. Familial forms usually begin in childhood and lack inflammatory changes. Both forms feature intracytoplasmic and intranuclear inclusions in muscle tissue. (Adams et al., Principles of Neurology, 6th ed, pp1409-10)
The muscles that move the eye. Included in this group are the medial rectus, lateral rectus, superior rectus, inferior rectus, inferior oblique, superior oblique, musculus orbitalis, and levator palpebrae superioris.
The neck muscles consist of the platysma, splenius cervicis, sternocleidomastoid(eus), longus colli, the anterior, medius, and posterior scalenes, digastric(us), stylohyoid(eus), mylohyoid(eus), geniohyoid(eus), sternohyoid(eus), omohyoid(eus), sternothyroid(eus), and thyrohyoid(eus).
A diminution of the skeletal muscle tone marked by a diminished resistance to passive stretching.
Complete or severe weakness of the muscles of respiration. This condition may be associated with MOTOR NEURON DISEASES; PERIPHERAL NERVE DISEASES; NEUROMUSCULAR JUNCTION DISEASES; SPINAL CORD DISEASES; injury to the PHRENIC NERVE; and other disorders.
An X-linked recessive muscle disease caused by an inability to synthesize DYSTROPHIN, which is involved with maintaining the integrity of the sarcolemma. Muscle fibers undergo a process that features degeneration and regeneration. Clinical manifestations include proximal weakness in the first few years of life, pseudohypertrophy, cardiomyopathy (see MYOCARDIAL DISEASES), and an increased incidence of impaired mentation. Becker muscular dystrophy is a closely related condition featuring a later onset of disease (usually adolescence) and a slowly progressive course. (Adams et al., Principles of Neurology, 6th ed, p1415)
One of two types of muscle in the body, characterized by the array of bands observed under microscope. Striated muscles can be divided into two subtypes: the CARDIAC MUSCLE and the SKELETAL MUSCLE.
A device that measures MUSCLE STRENGTH during muscle contraction, such as gripping, pushing, and pulling. It is used to evaluate the health status of muscle in sports medicine or physical therapy.
A heterogenous group of inherited muscular dystrophy that can be autosomal dominant or autosomal recessive. There are many forms (called LGMDs) involving genes encoding muscle membrane proteins such as the sarcoglycan (SARCOGLYCANS) complex that interacts with DYSTROPHIN. The disease is characterized by progressing wasting and weakness of the proximal muscles of arms and legs around the HIPS and SHOULDERS (the pelvic and shoulder girdles).
Skeletal muscle structures that function as the MECHANORECEPTORS responsible for the stretch or myotactic reflex (REFLEX, STRETCH). They are composed of a bundle of encapsulated SKELETAL MUSCLE FIBERS, i.e., the intrafusal fibers (nuclear bag 1 fibers, nuclear bag 2 fibers, and nuclear chain fibers) innervated by SENSORY NEURONS.
That phase of a muscle twitch during which a muscle returns to a resting position.
The synapse between a neuron and a muscle.
Conical muscular projections from the walls of the cardiac ventricles, attached to the cusps of the atrioventricular valves by the chordae tendineae.
Necrosis or disintegration of skeletal muscle often followed by myoglobinuria.
The larger subunits of MYOSINS. The heavy chains have a molecular weight of about 230 kDa and each heavy chain is usually associated with a dissimilar pair of MYOSIN LIGHT CHAINS. The heavy chains possess actin-binding and ATPase activity.
Paralysis of one or more of the ocular muscles due to disorders of the eye muscles, neuromuscular junction, supporting soft tissue, tendons, or innervation to the muscles.
A heterogeneous group of genetic disorders characterized by progressive MUSCULAR ATROPHY and MUSCLE WEAKNESS beginning in the hands, the legs, or the feet. Most are adult-onset autosomal dominant forms. Others are autosomal recessive.
An autoimmune disease characterized by weakness and fatigability of proximal muscles, particularly of the pelvic girdle, lower extremities, trunk, and shoulder girdle. There is relative sparing of extraocular and bulbar muscles. CARCINOMA, SMALL CELL of the lung is a frequently associated condition, although other malignancies and autoimmune diseases may be associated. Muscular weakness results from impaired impulse transmission at the NEUROMUSCULAR JUNCTION. Presynaptic calcium channel dysfunction leads to a reduced amount of acetylcholine being released in response to stimulation of the nerve. (From Adams et al., Principles of Neurology, 6th ed, pp 1471)
Abnormally low potassium concentration in the blood. It may result from potassium loss by renal secretion or by the gastrointestinal route, as by vomiting or diarrhea. It may be manifested clinically by neuromuscular disorders ranging from weakness to paralysis, by electrocardiographic abnormalities (depression of the T wave and elevation of the U wave), by renal disease, and by gastrointestinal disorders. (Dorland, 27th ed)
Muscular Dystrophy, Animal: A group of genetic disorders causing progressive skeletal muscle weakness and degeneration, characterized by the lack of or defective dystrophin protein, which can also affect other organ systems such as heart and brain, occurring in various forms with different degrees of severity and age of onset, like Duchenne, Becker, Myotonic, Limb-Girdle, and Facioscapulohumeral types, among others.
A strain of mice arising from a spontaneous MUTATION (mdx) in inbred C57BL mice. This mutation is X chromosome-linked and produces viable homozygous animals that lack the muscle protein DYSTROPHIN, have high serum levels of muscle ENZYMES, and possess histological lesions similar to human MUSCULAR DYSTROPHY. The histological features, linkage, and map position of mdx make these mice a worthy animal model of DUCHENNE MUSCULAR DYSTROPHY.
Neuromuscular disorder characterized by PROGRESSIVE MUSCULAR ATROPHY; MYOTONIA, and various multisystem atrophies. Mild INTELLECTUAL DISABILITY may also occur. Abnormal TRINUCLEOTIDE REPEAT EXPANSION in the 3' UNTRANSLATED REGIONS of DMPK PROTEIN gene is associated with Myotonic Dystrophy 1. DNA REPEAT EXPANSION of zinc finger protein-9 gene intron is associated with Myotonic Dystrophy 2.
The long cylindrical contractile organelles of STRIATED MUSCLE cells composed of ACTIN FILAMENTS; MYOSIN filaments; and other proteins organized in arrays of repeating units called SARCOMERES .
Muscles forming the ABDOMINAL WALL including RECTUS ABDOMINIS, external and internal oblique muscles, transversus abdominis, and quadratus abdominis. (from Stedman, 25th ed)
Muscles of facial expression or mimetic muscles that include the numerous muscles supplied by the facial nerve that are attached to and move the skin of the face. (From Stedman, 25th ed)
A hereditary motor and sensory neuropathy transmitted most often as an autosomal dominant trait and characterized by progressive distal wasting and loss of reflexes in the muscles of the legs (and occasionally involving the arms). Onset is usually in the second to fourth decade of life. This condition has been divided into two subtypes, hereditary motor and sensory neuropathy (HMSN) types I and II. HMSN I is associated with abnormal nerve conduction velocities and nerve hypertrophy, features not seen in HMSN II. (Adams et al., Principles of Neurology, 6th ed, p1343)
Mature contractile cells, commonly known as myocytes, that form one of three kinds of muscle. The three types of muscle cells are skeletal (MUSCLE FIBERS, SKELETAL), cardiac (MYOCYTES, CARDIAC), and smooth (MYOCYTES, SMOOTH MUSCLE). They are derived from embryonic (precursor) muscle cells called MYOBLASTS.
Cell surface proteins that bind acetylcholine with high affinity and trigger intracellular changes influencing the behavior of cells. Cholinergic receptors are divided into two major classes, muscarinic and nicotinic, based originally on their affinity for nicotine and muscarine. Each group is further subdivided based on pharmacology, location, mode of action, and/or molecular biology.
An organophosphate insecticide that inhibits monoamine oxidase and acetylcholinesterase. It has been shown to be genotoxic.
A masticatory muscle whose action is closing the jaws.
An autosomal recessively inherited glycogen storage disease caused by GLUCAN 1,4-ALPHA-GLUCOSIDASE deficiency. Large amounts of GLYCOGEN accumulate in the LYSOSOMES of skeletal muscle (MUSCLE, SKELETAL); HEART; LIVER; SPINAL CORD; and BRAIN. Three forms have been described: infantile, childhood, and adult. The infantile form is fatal in infancy and presents with hypotonia and a hypertrophic cardiomyopathy (CARDIOMYOPATHY, HYPERTROPHIC). The childhood form usually presents in the second year of life with proximal weakness and respiratory symptoms. The adult form consists of a slowly progressive proximal myopathy. (From Muscle Nerve 1995;3:S61-9; Menkes, Textbook of Child Neurology, 5th ed, pp73-4)
A transferase that catalyzes formation of PHOSPHOCREATINE from ATP + CREATINE. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic ISOENZYMES have been identified in human tissues: the MM type from SKELETAL MUSCLE, the MB type from myocardial tissue and the BB type from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins.
Muscles arising in the zygomatic arch that close the jaw. Their nerve supply is masseteric from the mandibular division of the trigeminal nerve. (From Stedman, 25th ed)
Prolonged failure of muscle relaxation after contraction. This may occur after voluntary contractions, muscle percussion, or electrical stimulation of the muscle. Myotonia is a characteristic feature of MYOTONIC DISORDERS.
Respiratory muscles that arise from the lower border of one rib and insert into the upper border of the adjoining rib, and contract during inspiration or respiration. (From Stedman, 25th ed)
A heterogenous group of inherited disorders characterized by recurring attacks of rapidly progressive flaccid paralysis or myotonia. These conditions have in common a mutation of the gene encoding the alpha subunit of the sodium channel in skeletal muscle. They are frequently associated with fluctuations in serum potassium levels. Periodic paralysis may also occur as a non-familial process secondary to THYROTOXICOSIS and other conditions. (From Adams et al., Principles of Neurology, 6th ed, p1481)
The properties, processes, and behavior of biological systems under the action of mechanical forces.
A syndrome characterized by new neuromuscular symptoms that occur at least 15 years after clinical stability has been attained in patients with a prior history of symptomatic poliomyelitis. Clinical features include new muscular weakness and atrophy of the limbs, bulbar innervated musculature, and muscles of respiration, combined with excessive fatigue, joint pain, and reduced stamina. The process is marked by slow progression and periods of stabilization. (From Ann NY Acad Sci 1995 May 25;753:68-80)
The maximum volume of air that can be inspired after reaching the end of a normal, quiet expiration. It is the sum of the TIDAL VOLUME and the INSPIRATORY RESERVE VOLUME. Common abbreviation is IC.
Elements of limited time intervals, contributing to particular results or situations.
A muscle protein localized in surface membranes which is the product of the Duchenne/Becker muscular dystrophy gene. Individuals with Duchenne muscular dystrophy usually lack dystrophin completely while those with Becker muscular dystrophy have dystrophin of an altered size. It shares features with other cytoskeletal proteins such as SPECTRIN and alpha-actinin but the precise function of dystrophin is not clear. One possible role might be to preserve the integrity and alignment of the plasma membrane to the myofibrils during muscle contraction and relaxation. MW 400 kDa.
Neurons which activate MUSCLE CELLS.
A group of disorders marked by progressive degeneration of motor neurons in the spinal cord resulting in weakness and muscular atrophy, usually without evidence of injury to the corticospinal tracts. Diseases in this category include Werdnig-Hoffmann disease and later onset SPINAL MUSCULAR ATROPHIES OF CHILDHOOD, most of which are hereditary. (Adams et al., Principles of Neurology, 6th ed, p1089)
Diseases characterized by a selective degeneration of the motor neurons of the spinal cord, brainstem, or motor cortex. Clinical subtypes are distinguished by the major site of degeneration. In AMYOTROPHIC LATERAL SCLEROSIS there is involvement of upper, lower, and brainstem motor neurons. In progressive muscular atrophy and related syndromes (see MUSCULAR ATROPHY, SPINAL) the motor neurons in the spinal cord are primarily affected. With progressive bulbar palsy (BULBAR PALSY, PROGRESSIVE), the initial degeneration occurs in the brainstem. In primary lateral sclerosis, the cortical neurons are affected in isolation. (Adams et al., Principles of Neurology, 6th ed, p1089)
The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.
The repeating contractile units of the MYOFIBRIL, delimited by Z bands along its length.
Elongated, spindle-shaped, quiescent myoblasts lying in close contact with adult skeletal muscle. They are thought to play a role in muscle repair and regeneration.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
A general term most often used to describe severe or complete loss of muscle strength due to motor system disease from the level of the cerebral cortex to the muscle fiber. This term may also occasionally refer to a loss of sensory function. (From Adams et al., Principles of Neurology, 6th ed, p45)
Embryonic (precursor) cells of the myogenic lineage that develop from the MESODERM. They undergo proliferation, migrate to their various sites, and then differentiate into the appropriate form of myocytes (MYOCYTES, SKELETAL; MYOCYTES, CARDIAC; MYOCYTES, SMOOTH MUSCLE).
An autosomal dominant familial disorder which presents in infancy or childhood and is characterized by episodes of weakness associated with hyperkalemia. During attacks, muscles of the lower extremities are initially affected, followed by the lower trunk and arms. Episodes last from 15-60 minutes and typically occur after a period of rest following exercise. A defect in skeletal muscle sodium channels has been identified as the cause of this condition. Normokalemic periodic paralysis is a closely related disorder marked by a lack of alterations in potassium levels during attacks of weakness. (Adams et al., Principles of Neurology, 6th ed, p1481)
Use of electric potential or currents to elicit biological responses.
The rotational force about an axis that is equal to the product of a force times the distance from the axis where the force is applied.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Diseases characterized by MYOTONIA, which may be inherited or acquired. Myotonia may be restricted to certain muscles (e.g., intrinsic hand muscles) or occur as a generalized condition.
The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.
Therapeutic exercises aimed to deepen inspiration or expiration or even to alter the rate and rhythm of respiration.
The pectoralis major and pectoralis minor muscles that make up the upper and fore part of the chest in front of the AXILLA.
Failure to adequately provide oxygen to cells of the body and to remove excess carbon dioxide from them. (Stedman, 25th ed)
A motor neuron disease marked by progressive weakness of the muscles innervated by cranial nerves of the lower brain stem. Clinical manifestations include dysarthria, dysphagia, facial weakness, tongue weakness, and fasciculations of the tongue and facial muscles. The adult form of the disease is marked initially by bulbar weakness which progresses to involve motor neurons throughout the neuroaxis. Eventually this condition may become indistinguishable from AMYOTROPHIC LATERAL SCLEROSIS. Fazio-Londe syndrome is an inherited form of this illness which occurs in children and young adults. (Adams et al., Principles of Neurology, 6th ed, p1091; Brain 1992 Dec;115(Pt 6):1889-1900)
An autosomal dominant hereditary disease that presents in late in life and is characterized by DYSPHAGIA and progressive ptosis of the eyelids. Mutations in the gene for POLY(A)-BINDING PROTEIN II have been associated with oculopharyngeal muscular dystrophy.
A characteristic symptom complex.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
A syndrome associated with inflammation of the BRACHIAL PLEXUS. Clinical features include severe pain in the shoulder region which may be accompanied by MUSCLE WEAKNESS and loss of sensation in the upper extremity. This condition may be associated with VIRUS DISEASES; IMMUNIZATION; SURGERY; heroin use (see HEROIN DEPENDENCE); and other conditions. The term brachial neuralgia generally refers to pain associated with brachial plexus injury. (From Adams et al., Principles of Neurology, 6th ed, pp1355-6)
An autosomal dominant degenerative muscle disease characterized by slowly progressive weakness of the muscles of the face, upper-arm, and shoulder girdle. The onset of symptoms usually occurs in the first or second decade of life. Affected individuals usually present with impairment of upper extremity elevation. This tends to be followed by facial weakness, primarily involving the orbicularis oris and orbicularis oculi muscles. (Neuromuscul Disord 1997;7(1):55-62; Adams et al., Principles of Neurology, 6th ed, p1420)
Inhaling liquid or solids, such as stomach contents, into the RESPIRATORY TRACT. When this causes severe lung damage, it is called ASPIRATION PNEUMONIA.
A form of muscle hypertonia associated with upper MOTOR NEURON DISEASE. Resistance to passive stretch of a spastic muscle results in minimal initial resistance (a "free interval") followed by an incremental increase in muscle tone. Tone increases in proportion to the velocity of stretch. Spasticity is usually accompanied by HYPERREFLEXIA and variable degrees of MUSCLE WEAKNESS. (From Adams et al., Principles of Neurology, 6th ed, p54)
Conditions characterized by impaired transmission of impulses at the NEUROMUSCULAR JUNCTION. This may result from disorders that affect receptor function, pre- or postsynaptic membrane function, or ACETYLCHOLINESTERASE activity. The majority of diseases in this category are associated with autoimmune, toxic, or inherited conditions.
An abnormal response to a stimulus applied to the sensory components of the nervous system. This may take the form of increased, decreased, or absent reflexes.
The portion of the leg in humans and other animals found between the HIP and KNEE.
An intermediate filament protein found predominantly in smooth, skeletal, and cardiac muscle cells. Localized at the Z line. MW 50,000 to 55,000 is species dependent.
A voltage-gated sodium channel subtype that mediates the sodium ion PERMEABILITY of SKELETAL MYOCYTES. Defects in the SCN4A gene, which codes for the alpha subunit of this sodium channel, are associated with several MYOTONIC DISORDERS.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Bis(nitrato-O)dioxouranium. A compound used in photography and the porcelain industry. It causes severe renal insufficiency and renal tubular necrosis in mammals and is an effective lymphocyte mitogen.
A group of muscle diseases associated with abnormal mitochondria function.
Filamentous proteins that are the main constituent of the thin filaments of muscle fibers. The filaments (known also as filamentous or F-actin) can be dissociated into their globular subunits; each subunit is composed of a single polypeptide 375 amino acids long. This is known as globular or G-actin. In conjunction with MYOSINS, actin is responsible for the contraction and relaxation of muscle.
Neoplasms composed of connective tissue, including elastic, mucous, reticular, osseous, and cartilaginous tissue. The concept does not refer to neoplasms located in connective tissue.
A protein found in the thin filaments of muscle fibers. It inhibits contraction of the muscle unless its position is modified by TROPONIN.
Diseases of multiple peripheral nerves simultaneously. Polyneuropathies usually are characterized by symmetrical, bilateral distal motor and sensory impairment with a graded increase in severity distally. The pathological processes affecting peripheral nerves include degeneration of the axon, myelin or both. The various forms of polyneuropathy are categorized by the type of nerve affected (e.g., sensory, motor, or autonomic), by the distribution of nerve injury (e.g., distal vs. proximal), by nerve component primarily affected (e.g., demyelinating vs. axonal), by etiology, or by pattern of inheritance.
A powerful flexor of the thigh at the hip joint (psoas major) and a weak flexor of the trunk and lumbar spinal column (psoas minor). Psoas is derived from the Greek "psoa", the plural meaning "muscles of the loin". It is a common site of infection manifesting as abscess (PSOAS ABSCESS). The psoas muscles and their fibers are also used frequently in experiments in muscle physiology.
An acute inflammatory autoimmune neuritis caused by T cell- mediated cellular immune response directed towards peripheral myelin. Demyelination occurs in peripheral nerves and nerve roots. The process is often preceded by a viral or bacterial infection, surgery, immunization, lymphoma, or exposure to toxins. Common clinical manifestations include progressive weakness, loss of sensation, and loss of deep tendon reflexes. Weakness of respiratory muscles and autonomic dysfunction may occur. (From Adams et al., Principles of Neurology, 6th ed, pp1312-1314)
An inherited congenital myopathic condition characterized by weakness and hypotonia in infancy and delayed motor development. Muscle biopsy reveals a condensation of myofibrils and myofibrillar material in the central portion of each muscle fiber. (Adams et al., Principles of Neurology, 6th ed, p1452)
Clinical sign or symptom manifested as debility, or lack or loss of strength and energy.
Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)
An opioid analgesic that is used as an adjunct in anesthesia, in balanced anesthesia, and as a primary anesthetic agent.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
A group of slowly progressive inherited disorders affecting motor and sensory peripheral nerves. Subtypes include HMSNs I-VII. HMSN I and II both refer to CHARCOT-MARIE-TOOTH DISEASE. HMSN III refers to hypertrophic neuropathy of infancy. HMSN IV refers to REFSUM DISEASE. HMSN V refers to a condition marked by a hereditary motor and sensory neuropathy associated with spastic paraplegia (see SPASTIC PARAPLEGIA, HEREDITARY). HMSN VI refers to HMSN associated with an inherited optic atrophy (OPTIC ATROPHIES, HEREDITARY), and HMSN VII refers to HMSN associated with retinitis pigmentosa. (From Adams et al., Principles of Neurology, 6th ed, p1343)
Manner or style of walking.
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)
A masticatory muscle whose action is closing the jaws; its posterior portion retracts the mandible.
The muscles of the PHARYNX are voluntary muscles arranged in two layers. The external circular layer consists of three constrictors (superior, middle, and inferior). The internal longitudinal layer consists of the palatopharyngeus, the salpingopharyngeus, and the stylopharyngeus. During swallowing, the outer layer constricts the pharyngeal wall and the inner layer elevates pharynx and LARYNX.
Physical activity which is usually regular and done with the intention of improving or maintaining PHYSICAL FITNESS or HEALTH. Contrast with PHYSICAL EXERTION which is concerned largely with the physiologic and metabolic response to energy expenditure.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
A cholinesterase inhibitor with a slightly longer duration of action than NEOSTIGMINE. It is used in the treatment of myasthenia gravis and to reverse the actions of muscle relaxants.
The volume of air that is exhaled by a maximal expiration following a maximal inspiration.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Inherited myotonic disorders with early childhood onset MYOTONIA. Muscular hypertrophy is common and myotonia may impair ambulation and other movements. It is classified as Thomsen (autosomal dominant) or Becker (autosomal recessive) generalized myotonia mainly based on the inheritance pattern. Becker type is also clinically more severe. An autosomal dominant variant with milder symptoms and later onset is known as myotonia levior. Mutations in the voltage-dependent skeletal muscle chloride channel are associated with the disorders.
A rapid-onset, short-acting cholinesterase inhibitor used in cardiac arrhythmias and in the diagnosis of myasthenia gravis. It has also been used as an antidote to curare principles.
The time span between the beginning of physical activity by an individual and the termination because of exhaustion.
Disorders of the special senses (i.e., VISION; HEARING; TASTE; and SMELL) or somatosensory system (i.e., afferent components of the PERIPHERAL NERVOUS SYSTEM).
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Severe or complete loss of motor function in all four limbs which may result from BRAIN DISEASES; SPINAL CORD DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; or rarely MUSCULAR DISEASES. The locked-in syndrome is characterized by quadriplegia in combination with cranial muscle paralysis. Consciousness is spared and the only retained voluntary motor activity may be limited eye movements. This condition is usually caused by a lesion in the upper BRAIN STEM which injures the descending cortico-spinal and cortico-bulbar tracts.
A type of strength-building exercise program that requires the body muscle to exert a force against some form of resistance, such as weight, stretch bands, water, or immovable objects. Resistance exercise is a combination of static and dynamic contractions involving shortening and lengthening of skeletal muscles.
A family of transmembrane dystrophin-associated proteins that play a role in the membrane association of the DYSTROPHIN-ASSOCIATED PROTEIN COMPLEX.
Diseases of the cervical (and first thoracic) roots, nerve trunks, cords, and peripheral nerve components of the BRACHIAL PLEXUS. Clinical manifestations include regional pain, PARESTHESIA; MUSCLE WEAKNESS, and decreased sensation (HYPESTHESIA) in the upper extremity. These disorders may be associated with trauma (including BIRTH INJURIES); THORACIC OUTLET SYNDROME; NEOPLASMS; NEURITIS; RADIOTHERAPY; and other conditions. (From Adams et al., Principles of Neurology, 6th ed, pp1351-2)
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
A non-fibrillar collagen that forms a network of MICROFIBRILS within the EXTRACELLULAR MATRIX of CONNECTIVE TISSUE. The alpha subunits of collagen type VI assemble into antiparallel, overlapping dimers which then align to form tetramers.
Prolonged shortening of the muscle or other soft tissue around a joint, preventing movement of the joint.
The specialized postsynaptic region of a muscle cell. The motor endplate is immediately across the synaptic cleft from the presynaptic axon terminal. Among its anatomical specializations are junctional folds which harbor a high density of cholinergic receptors.
Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves.
Measurement of the various processes involved in the act of respiration: inspiration, expiration, oxygen and carbon dioxide exchange, lung volume and compliance, etc.
The farthest or outermost projections of the body, such as the HAND and FOOT.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Drugs that inhibit cholinesterases. The neurotransmitter ACETYLCHOLINE is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system.
The physical activity of a human or an animal as a behavioral phenomenon.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
The mechanical laws of fluid dynamics as they apply to urine transport.
In patients with neoplastic diseases a wide variety of clinical pictures which are indirect and usually remote effects produced by tumor cell metabolites or other products.
The exercise capacity of an individual as measured by endurance (maximal exercise duration and/or maximal attained work load) during an EXERCISE TEST.
The projecting part on each side of the body, formed by the side of the pelvis and the top portion of the femur.
The age, developmental stage, or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual.
Difficult or labored breathing.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)
A pteridinetriamine compound that inhibits SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS.
A reduction in the amount of air entering the pulmonary alveoli.
An autosomal recessive disorder of fatty acid oxidation, and branched chain amino acids (AMINO ACIDS, BRANCHED-CHAIN); LYSINE; and CHOLINE catabolism, that is due to defects in either subunit of ELECTRON TRANSFER FLAVOPROTEIN or its dehydrogenase, electron transfer flavoprotein-ubiquinone oxidoreductase (EC 1.5.5.1).
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Drugs that interrupt transmission of nerve impulses at the skeletal neuromuscular junction. They can be of two types, competitive, stabilizing blockers (NEUROMUSCULAR NONDEPOLARIZING AGENTS) or noncompetitive, depolarizing agents (NEUROMUSCULAR DEPOLARIZING AGENTS). Both prevent acetylcholine from triggering the muscle contraction and they are used as anesthesia adjuvants, as relaxants during electroshock, in convulsive states, etc.
Any autoimmune animal disease model used in the study of MYASTHENIA GRAVIS. Injection with purified neuromuscular junction acetylcholine receptor (AChR) (see RECEPTORS, CHOLINERGIC) components results in a myasthenic syndrome that has acute and chronic phases. The motor endplate pathology, loss of acetylcholine receptors, presence of circulating anti-AChR antibodies, and electrophysiologic changes make this condition virtually identical to human myasthenia gravis. Passive transfer of AChR antibodies or lymphocytes from afflicted animals to normals induces passive transfer experimental autoimmune myasthenia gravis. (From Joynt, Clinical Neurology, 1997, Ch 54, p3)
Measurement of the amount of air that the lungs may contain at various points in the respiratory cycle.
A type of stress exerted uniformly in all directions. Its measure is the force exerted per unit area. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
Glycogen is a multibranched polysaccharide of glucose serving as the primary form of energy storage in animals, fungi, and bacteria, stored mainly in liver and muscle tissues. (Two sentences combined as per your request)
A network of tubules and sacs in the cytoplasm of SKELETAL MUSCLE FIBERS that assist with muscle contraction and relaxation by releasing and storing calcium ions.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The inferior part of the lower extremity between the KNEE and the ANKLE.
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.
A general term referring to a mild to moderate degree of muscular weakness, occasionally used as a synonym for PARALYSIS (severe or complete loss of motor function). In the older literature, paresis often referred specifically to paretic neurosyphilis (see NEUROSYPHILIS). "General paresis" and "general paralysis" may still carry that connotation. Bilateral lower extremity paresis is referred to as PARAPARESIS.
A constituent of STRIATED MUSCLE and LIVER. It is an amino acid derivative and an essential cofactor for fatty acid metabolism.
A group of recessively inherited diseases that feature progressive muscular atrophy and hypotonia. They are classified as type I (Werdnig-Hoffman disease), type II (intermediate form), and type III (Kugelberg-Welander disease). Type I is fatal in infancy, type II has a late infantile onset and is associated with survival into the second or third decade. Type III has its onset in childhood, and is slowly progressive. (J Med Genet 1996 Apr:33(4):281-3)
The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli.
Pathological processes involving the PHARYNX.
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
A sustained and usually painful contraction of muscle fibers. This may occur as an isolated phenomenon or as a manifestation of an underlying disease process (e.g., UREMIA; HYPOTHYROIDISM; MOTOR NEURON DISEASE; etc.). (From Adams et al., Principles of Neurology, 6th ed, p1398)
The act of breathing with the LUNGS, consisting of INHALATION, or the taking into the lungs of the ambient air, and of EXHALATION, or the expelling of the modified air which contains more CARBON DIOXIDE than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= OXYGEN CONSUMPTION) or cell respiration (= CELL RESPIRATION).
A condition of an abnormally low level of PHOSPHATES in the blood.
A growth differentiation factor that is a potent inhibitor of SKELETAL MUSCLE growth. It may play a role in the regulation of MYOGENESIS and in muscle maintenance during adulthood.
Disorder caused by an interruption of the mineralization of organic bone matrix leading to bone softening, bone pain, and weakness. It is the adult form of rickets resulting from disruption of VITAMIN D; PHOSPHORUS; or CALCIUM homeostasis.
A tetrameric calcium release channel in the SARCOPLASMIC RETICULUM membrane of SMOOTH MUSCLE CELLS, acting oppositely to SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES. It is important in skeletal and cardiac excitation-contraction coupling and studied by using RYANODINE. Abnormalities are implicated in CARDIAC ARRHYTHMIAS and MUSCULAR DISEASES.
Any method of artificial breathing that employs mechanical or non-mechanical means to force the air into and out of the lungs. Artificial respiration or ventilation is used in individuals who have stopped breathing or have RESPIRATORY INSUFFICIENCY to increase their intake of oxygen (O2) and excretion of carbon dioxide (CO2).
The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.
A regimen or plan of physical activities designed and prescribed for specific therapeutic goals. Its purpose is to restore normal musculoskeletal function or to reduce pain caused by diseases or injuries.
The position or attitude of the body.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Apparatus used to support, align, prevent, or correct deformities or to improve the function of movable parts of the body.
Expenditure of energy during PHYSICAL ACTIVITY. Intensity of exertion may be measured by rate of OXYGEN CONSUMPTION; HEAT produced, or HEART RATE. Perceived exertion, a psychological measure of exertion, is included.
The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium.
Enzymes that catalyze the exohydrolysis of 1,4-alpha-glucosidic linkages with release of alpha-glucose. Deficiency of alpha-1,4-glucosidase may cause GLYCOGEN STORAGE DISEASE TYPE II.
Assessment of sensory and motor responses and reflexes that is used to determine impairment of the nervous system.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
A SMN complex protein that is essential for the function of the SMN protein complex. In humans the protein is encoded by a single gene found near the inversion telomere of a large inverted region of CHROMOSOME 5. Mutations in the gene coding for survival of motor neuron 1 protein may result in SPINAL MUSCULAR ATROPHIES OF CHILDHOOD.
An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.

Autosomal dominant myopathy with proximal weakness and early respiratory muscle involvement maps to chromosome 2q. (1/934)

Two Swedish families with autosomal dominant myopathy, who also had proximal weakness, early respiratory failure, and characteristic cytoplasmic bodies in the affected muscle biopsies, were screened for linkage by means of the human genome screening set (Cooperative Human Linkage Center Human Screening Set/Weber version 6). Most chromosome regions were completely excluded by linkage analysis (LOD score <-2). Linkage to the chromosomal region 2q24-q31 was established. A maximum combined two-point LOD score of 4.87 at a recombination fraction of 0 was obtained with marker D2S1245. Haplotype analysis indicated that the gene responsible for the disease is likely to be located in the 17-cM region between markers D2S2384 and D2S364. The affected individuals from these two families share an identical haplotype, which suggests a common origin.  (+info)

Mice with IFN-gamma receptor deficiency are less susceptible to experimental autoimmune myasthenia gravis. (2/934)

IFN-gamma can either adversely or beneficially affect certain experimental autoimmune diseases. To study the role of IFN-gamma in the autoantibody-mediated experimental autoimmune myasthenia gravis (EAMG), an animal model of myasthenia gravis in humans, IFN-gammaR-deficient (IFN-gammaR-/-) mutant C57BL/6 mice and congenic wild-type mice were immunized with Torpedo acetylcholine receptor (AChR) plus CFA. IFN-gammaR-/- mice exhibited significantly lower incidence and severity of muscle weakness, lower anti-AChR IgG Ab levels, and lower Ab affinity to AChR compared with wild-type mice. Passive transfer of serum from IFN-gammaR-/- mice induced less muscular weakness compared with serum from wild-type mice. In contrast, numbers of lymph node cells secreting IFN-gamma and of those expressing IFN-gamma mRNA were strongly augmented in the IFN-gammaR-/- mice, reflecting a failure of negative feedback circuits. Cytokine studies by in situ hybridization revealed lower levels of lymphoid cells expressing AChR-reactive IL-1beta and TNF-alpha mRNA in AChR + CFA-immunized IFN-gammaR-/- mice compared with wild-type mice. No differences were found for AChR-reactive cells expressing IL-4, IL-10, or TGF-beta mRNA. These results indicate that IFN-gamma promotes systemic humoral responses in EAMG by up-regulating the production and the affinity of anti-AChR autoantibodies, thereby contributing to susceptibility to EAMG in C57BL/6-type mice.  (+info)

Contribution of lung function to exercise capacity in patients with chronic heart failure. (3/934)

BACKGROUND: The importance of exercise capacity as an indicator of prognosis in patients with heart disease is well recognized. However, factors contributing to exercise limitation in such patients have not been fully characterized and in particular, the role of lung function in determining exercise capacity has not been extensively investigated. OBJECTIVE: To examine the extent to which pulmonary function and respiratory muscle strength indices predict exercise performance in patients with moderate to severe heart failure. METHODS: Fifty stable heart failure patients underwent a maximal symptom-limited cardiopulmonary exercise test on a treadmill to determine maximum oxygen consumption (VO2max), pulmonary function tests and maximum inspiratory (PImax) and expiratory (PEmax) pressure measurement. RESULTS: In univariate analysis, VO2max correlated with forced vital capacity (r = 0.35, p = 0.01), forced expiratory volume in 1 s (r = 0.45, p = 0.001), FEV1/FVC ratio (r = 0.37, p = 0.009), maximal midexpiratory flow rate (FEF25-75, r = 0. 47, p < 0.001), and PImax (r = 0.46, p = 0.001), but not with total lung capacity, diffusion capacity or PEmax. In stepwise linear regression analysis, FEF25-75 and PImax were shown to be independently related to VO2max, with a combined r and r2 value of 0. 56 and 0.32, respectively. CONCLUSIONS: Lung function indices overall accounted for only approximately 30% of the variance in maximum exercise capacity observed in heart failure patients. The mechanism(s) by which these variables could set exercise limitation in heart failure awaits further investigation.  (+info)

Dominant hereditary inclusion-body myopathy gene (IBM3) maps to chromosome region 17p13.1. (4/934)

We recently described an autosomal dominant inclusion-body myopathy characterized by congenital joint contractures, external ophthalmoplegia, and predominantly proximal muscle weakness. A whole-genome scan, performed with 161 polymorphic markers and with DNA from 40 members of one family, indicated strong linkage for markers on chromosome 17p. After analyses with additional markers in the region and with DNA from eight additional family members, a maximum LOD score (Zmax) was detected for marker D17S1303 (Zmax=7.38; recombination fraction (theta)=0). Haplotype analyses showed that the locus (Genome Database locus name: IBM3) is flanked distally by marker D17S945 and proximally by marker D17S969. The positions of cytogenetically localized flanking markers suggest that the location of the IBM3 gene is in chromosome region 17p13.1. Radiation hybrid mapping showed that IBM3 is located in a 2-Mb chromosomal region and that the myosin heavy-chain (MHC) gene cluster, consisting of at least six genes, co-localizes to the same region. This localization raises the possibility that one of the MHC genes clustered in this region may be involved in this disorder.  (+info)

Myasthenic syndrome of snake envenomation: a clinical and neurophysiological study. (5/934)

In this prospective study, 65 consecutive patients with neurological manifestations after snake envenomation, were examined in order to describe the natural history of the reversible nature of muscle weakness. Snake envenoming led to a completely reversible muscle paralysis involving the external ocular muscles with sparing of the pupils, muscles of mastication, facial muscles, palatal muscles, neck and proximal limb muscles. The deep tendon reflexes were preserved with no sensory abnormalities. The muscular weakness usually set in within an hour of envenomation and lasted up to 10 days, with fatigability lasting for 12 days. Respiratory muscle paralysis led to ventilatory failure needing ventilation in severely envenomed patients. Motor and sensory nerve conduction were normal with normal resting compound motor action potentials on electromyography. Repetitive nerve stimulation gave rise to a decremental response during high frequency stimulation. The edrophonium test gave negative results. These manifestations are due to abnormalities of neuromuscular transmission and are not typical of myasthenia gravis. As the exact pathophysiology of venom-related neurotoxicity is not known, it is suggested that the neurological manifestations of snake envenoming be designated a myasthenic syndrome. Further studies to isolate the neurotoxin and its mechanism and exact site of blocking at the neuromuscular junction would pave the way for the development of a novel long-acting neuromuscular blocking agent.  (+info)

MR imaging of Dejerine-Sottas disease. (6/934)

We report the MR findings in two patients with clinically and histologically proved Dejerine-Sottas disease. One patient had spinal involvement with multiple thickened and clumped nerve roots of the cauda equina; the second had multiple enlarged and enhancing cranial nerves. Although these findings are not specific for Dejerine-Sottas disease, they are suggestive of the diagnosis, which is further corroborated with history and confirmed with sural nerve biopsy and laboratory studies.  (+info)

Bethlem myopathy: a slowly progressive congenital muscular dystrophy with contractures. (7/934)

Bethlem myopathy is an early-onset benign autosomal dominant myopathy with contractures caused by mutations in collagen type VI genes. It has been reported that onset occurs in early childhood. We investigated the natural course of Bethlem myopathy in five previously published kindreds and two novel pedigrees, with particular attention to the mode of onset in 23 children and the progression of weakness in 36 adult patients. Our analysis shows that nearly all children exhibit weakness or contractures during the first 2 years of life. Early features include diminished foetal movements, neonatal hypotonia and congenital contractures which are of a dynamic nature during childhood. The course of Bethlem myopathy in adult patients is less benign than previously thought. Due to slow but ongoing progression, more than two-thirds of patients over 50 years of age use a wheelchair.  (+info)

Mechanisms of nasal tolerance induction in experimental autoimmune myasthenia gravis: identification of regulatory cells. (8/934)

Autoantigen administration via nasal mucosal tissue can induce systemic tolerance more effectively than oral administration in a number of experimental autoimmune diseases, including Ab-mediated experimental autoimmune myasthenia gravis, a murine model of myasthenia gravis. The mechanisms underlying nasal tolerance induction are not clear. In this study, we show that nasal administration of acetylcholine receptor (AChR) in C57BL/6 mice, before immunizations with AChR in adjuvant, results in delayed onset and reduced muscle weakness compared with control mice. The delayed onset and reduced muscle weakness were associated with decreased AChR-specific lymphocyte proliferation and decreased levels of anti-AChR Abs of the IgG2a and IgG2b isotypes in serum. The clinical and immunological changes in the AChR-pretreated C57BL/6 wild-type (wt) mice were comparable with those observed in AChR-pretreated CD8-/- mice, indicating that CD8+ T cells were not required for the generation of nasal tolerance. AChR-pretreated wt and CD8-/- mice showed augmented TGF-beta and reduced IFN-gamma responses, whereas levels of IL-4 were unaltered. Splenocytes from AChR-pretreated wt and CD8-/- mice, but not from CD4-/- mice, suppressed AChR-specific lymphocyte proliferation. This suppression could be blocked by Abs against TGF-beta. Thus, our results demonstrate that the suppression induced in the present model is independent of CD8+ T cells and suggest the involvement of Ag-specific CD4+ Th3 cells producing TGF-beta.  (+info)

Muscle weakness is a condition in which muscles cannot develop the expected level of physical force or power. This results in reduced muscle function and can be caused by various factors, including nerve damage, muscle diseases, or hormonal imbalances. Muscle weakness may manifest as difficulty lifting objects, maintaining posture, or performing daily activities. It is essential to consult a healthcare professional for proper diagnosis and treatment of muscle weakness.

A muscle is a soft tissue in our body that contracts to produce force and motion. It is composed mainly of specialized cells called muscle fibers, which are bound together by connective tissue. There are three types of muscles: skeletal (voluntary), smooth (involuntary), and cardiac. Skeletal muscles attach to bones and help in movement, while smooth muscles are found within the walls of organs and blood vessels, helping with functions like digestion and circulation. Cardiac muscle is the specific type that makes up the heart, allowing it to pump blood throughout the body.

Skeletal muscle, also known as striated or voluntary muscle, is a type of muscle that is attached to bones by tendons or aponeuroses and functions to produce movements and support the posture of the body. It is composed of long, multinucleated fibers that are arranged in parallel bundles and are characterized by alternating light and dark bands, giving them a striped appearance under a microscope. Skeletal muscle is under voluntary control, meaning that it is consciously activated through signals from the nervous system. It is responsible for activities such as walking, running, jumping, and lifting objects.

Muscle proteins are a type of protein that are found in muscle tissue and are responsible for providing structure, strength, and functionality to muscles. The two major types of muscle proteins are:

1. Contractile proteins: These include actin and myosin, which are responsible for the contraction and relaxation of muscles. They work together to cause muscle movement by sliding along each other and shortening the muscle fibers.
2. Structural proteins: These include titin, nebulin, and desmin, which provide structural support and stability to muscle fibers. Titin is the largest protein in the human body and acts as a molecular spring that helps maintain the integrity of the sarcomere (the basic unit of muscle contraction). Nebulin helps regulate the length of the sarcomere, while desmin forms a network of filaments that connects adjacent muscle fibers together.

Overall, muscle proteins play a critical role in maintaining muscle health and function, and their dysregulation can lead to various muscle-related disorders such as muscular dystrophy, myopathies, and sarcopenia.

Nemaline myopathy is a genetic muscle disorder characterized by the presence of rod-like structures called nemalines in the muscle fibers. These rods, which are composed of accumulated protein, can be observed under a microscope in biopsied muscle tissue. The condition is typically present at birth or appears in early childhood and is often associated with muscle weakness, hypotonia (low muscle tone), and delayed motor development.

There are several types of nemaline myopathy, which vary in severity and age of onset. Some individuals with the disorder may have only mild symptoms and be able to lead relatively normal lives, while others may experience significant disability and require assistance with daily activities. The condition can also affect the heart and respiratory muscles, leading to serious complications.

Nemaline myopathy is caused by mutations in one of several genes that are involved in the formation and maintenance of muscle fibers. These genetic defects lead to abnormalities in the structure and function of the muscle fibers, resulting in the characteristic symptoms of the disorder. There is currently no cure for nemaline myopathy, but treatment is focused on managing the symptoms and improving quality of life. This may include physical therapy, assistive devices, and respiratory support, as well as medications to help manage muscle spasticity and other complications.

Skeletal muscle fibers, also known as striated muscle fibers, are the type of muscle cells that make up skeletal muscles, which are responsible for voluntary movements of the body. These muscle fibers are long, cylindrical, and multinucleated, meaning they contain multiple nuclei. They are surrounded by a connective tissue layer called the endomysium, and many fibers are bundled together into fascicles, which are then surrounded by another layer of connective tissue called the perimysium.

Skeletal muscle fibers are composed of myofibrils, which are long, thread-like structures that run the length of the fiber. Myofibrils contain repeating units called sarcomeres, which are responsible for the striated appearance of skeletal muscle fibers. Sarcomeres are composed of thick and thin filaments, which slide past each other during muscle contraction to shorten the sarcomere and generate force.

Skeletal muscle fibers can be further classified into two main types based on their contractile properties: slow-twitch (type I) and fast-twitch (type II). Slow-twitch fibers have a high endurance capacity and are used for sustained, low-intensity activities such as maintaining posture. Fast-twitch fibers, on the other hand, have a higher contractile speed and force generation capacity but fatigue more quickly and are used for powerful, explosive movements.

Muscular diseases, also known as myopathies, refer to a group of conditions that affect the functionality and health of muscle tissue. These diseases can be inherited or acquired and may result from inflammation, infection, injury, or degenerative processes. They can cause symptoms such as weakness, stiffness, cramping, spasms, wasting, and loss of muscle function.

Examples of muscular diseases include:

1. Duchenne Muscular Dystrophy (DMD): A genetic disorder that results in progressive muscle weakness and degeneration due to a lack of dystrophin protein.
2. Myasthenia Gravis: An autoimmune disease that causes muscle weakness and fatigue, typically affecting the eyes and face, throat, and limbs.
3. Inclusion Body Myositis (IBM): A progressive muscle disorder characterized by muscle inflammation and wasting, typically affecting older adults.
4. Polymyositis: An inflammatory myopathy that causes muscle weakness and inflammation throughout the body.
5. Metabolic Myopathies: A group of inherited disorders that affect muscle metabolism, leading to exercise intolerance, muscle weakness, and other symptoms.
6. Muscular Dystonias: Involuntary muscle contractions and spasms that can cause abnormal postures or movements.

It is important to note that muscular diseases can have a significant impact on an individual's quality of life, mobility, and overall health. Proper diagnosis and treatment are crucial for managing symptoms and improving outcomes.

Respiratory muscles are a group of muscles involved in the process of breathing. They include the diaphragm, intercostal muscles (located between the ribs), scalene muscles (located in the neck), and abdominal muscles. These muscles work together to allow the chest cavity to expand or contract, which draws air into or pushes it out of the lungs. The diaphragm is the primary muscle responsible for breathing, contracting to increase the volume of the chest cavity and draw air into the lungs during inhalation. The intercostal muscles help to further expand the ribcage, while the abdominal muscles assist in exhaling by compressing the abdomen and pushing up on the diaphragm.

Muscle contraction is the physiological process in which muscle fibers shorten and generate force, leading to movement or stability of a body part. This process involves the sliding filament theory where thick and thin filaments within the sarcomeres (the functional units of muscles) slide past each other, facilitated by the interaction between myosin heads and actin filaments. The energy required for this action is provided by the hydrolysis of adenosine triphosphate (ATP). Muscle contractions can be voluntary or involuntary, and they play a crucial role in various bodily functions such as locomotion, circulation, respiration, and posture maintenance.

Smooth muscle, also known as involuntary muscle, is a type of muscle that is controlled by the autonomic nervous system and functions without conscious effort. These muscles are found in the walls of hollow organs such as the stomach, intestines, bladder, and blood vessels, as well as in the eyes, skin, and other areas of the body.

Smooth muscle fibers are shorter and narrower than skeletal muscle fibers and do not have striations or sarcomeres, which give skeletal muscle its striped appearance. Smooth muscle is controlled by the autonomic nervous system through the release of neurotransmitters such as acetylcholine and norepinephrine, which bind to receptors on the smooth muscle cells and cause them to contract or relax.

Smooth muscle plays an important role in many physiological processes, including digestion, circulation, respiration, and elimination. It can also contribute to various medical conditions, such as hypertension, gastrointestinal disorders, and genitourinary dysfunction, when it becomes overactive or underactive.

Neuromuscular diseases are a group of disorders that involve the peripheral nervous system, which includes the nerves and muscles outside of the brain and spinal cord. These conditions can affect both children and adults, and they can be inherited or acquired. Neuromuscular diseases can cause a wide range of symptoms, including muscle weakness, numbness, tingling, pain, cramping, and twitching. Some common examples of neuromuscular diseases include muscular dystrophy, amyotrophic lateral sclerosis (ALS), peripheral neuropathy, and myasthenia gravis. The specific symptoms and severity of these conditions can vary widely depending on the underlying cause and the specific muscles and nerves that are affected. Treatment for neuromuscular diseases may include medications, physical therapy, assistive devices, or surgery, depending on the individual case.

A smooth muscle within the vascular system refers to the involuntary, innervated muscle that is found in the walls of blood vessels. These muscles are responsible for controlling the diameter of the blood vessels, which in turn regulates blood flow and blood pressure. They are called "smooth" muscles because their individual muscle cells do not have the striations, or cross-striped patterns, that are observed in skeletal and cardiac muscle cells. Smooth muscle in the vascular system is controlled by the autonomic nervous system and by hormones, and can contract or relax slowly over a period of time.

Muscle development, also known as muscle hypertrophy, refers to the increase in size and mass of the muscles through a process called myofiber growth. This is primarily achieved through resistance or strength training exercises that cause micro-tears in the muscle fibers, leading to an inflammatory response and the release of hormones that promote muscle growth. As the muscles repair themselves, they become larger and stronger than before. Proper nutrition, including adequate protein intake, and rest are also essential components of muscle development.

It is important to note that while muscle development can lead to an increase in strength and muscular endurance, it does not necessarily result in improved athletic performance or overall fitness. A well-rounded exercise program that includes cardiovascular activity, flexibility training, and resistance exercises is recommended for optimal health and fitness outcomes.

Muscle fatigue is a condition characterized by a reduction in the ability of a muscle to generate force or power, typically after prolonged or strenuous exercise. It is often accompanied by sensations of tiredness, weakness, and discomfort in the affected muscle(s). The underlying mechanisms of muscle fatigue are complex and involve both peripheral factors (such as changes in muscle metabolism, ion handling, and neuromuscular transmission) and central factors (such as changes in the nervous system's ability to activate muscles). Muscle fatigue can also occur as a result of various medical conditions or medications that impair muscle function.

Muscular atrophy is a condition characterized by a decrease in the size and mass of muscles due to lack of use, disease, or injury. This occurs when there is a disruption in the balance between muscle protein synthesis and degradation, leading to a net loss of muscle proteins. There are two main types of muscular atrophy:

1. Disuse atrophy: This type of atrophy occurs when muscles are not used or are immobilized for an extended period, such as after an injury, surgery, or prolonged bed rest. In this case, the nerves that control the muscles may still be functioning properly, but the muscles themselves waste away due to lack of use.
2. Neurogenic atrophy: This type of atrophy is caused by damage to the nerves that supply the muscles, leading to muscle weakness and wasting. Conditions such as amyotrophic lateral sclerosis (ALS), spinal cord injuries, and peripheral neuropathies can cause neurogenic atrophy.

In both cases, the affected muscles may become weak, shrink in size, and lose their tone and mass. Treatment for muscular atrophy depends on the underlying cause and may include physical therapy, exercise, and medication to manage symptoms and improve muscle strength and function.

Polymyositis is defined as a rare inflammatory disorder that causes muscle weakness and inflammation (swelling) of the muscles. It primarily affects the skeletal muscles, which are the muscles responsible for voluntary movements such as walking, talking, and swallowing. The onset of polymyositis can occur at any age but is most commonly seen in adults between 31 to 60 years old, with women being slightly more affected than men.

The exact cause of polymyositis remains unknown; however, it is believed to be an autoimmune disorder, where the body's immune system mistakenly attacks its own muscle tissue. Certain factors such as genetics, viral infections, and exposure to certain drugs may contribute to the development of this condition.

Polymyositis can cause various symptoms, including:
- Progressive muscle weakness and wasting, particularly affecting the proximal muscles (those closest to the trunk of the body) such as the hips, thighs, shoulders, and upper arms.
- Difficulty climbing stairs, lifting objects, or rising from a seated position.
- Fatigue and stiffness, especially after periods of inactivity.
- Joint pain and swelling.
- Difficulty swallowing or speaking.
- Shortness of breath due to weakened respiratory muscles.

Diagnosis of polymyositis typically involves a combination of medical history, physical examination, laboratory tests, electromyography (EMG), and muscle biopsy. Treatment usually includes medications such as corticosteroids and immunosuppressants to reduce inflammation and control the immune response. Physical therapy may also be recommended to help maintain muscle strength and flexibility.

If left untreated, polymyositis can lead to significant disability and complications, including respiratory failure, malnutrition, and cardiovascular disease. Early diagnosis and treatment are crucial for improving outcomes and preventing long-term complications.

Myositis is a medical term that refers to inflammation of the muscle tissue. This condition can cause various symptoms, including muscle weakness, pain, swelling, and stiffness. There are several types of myositis, such as polymyositis, dermatomyositis, and inclusion body myositis, which have different causes and characteristics.

Polymyositis is a type of myositis that affects multiple muscle groups, particularly those close to the trunk of the body. Dermatomyositis is characterized by muscle inflammation as well as a skin rash. Inclusion body myositis is a less common form of myositis that typically affects older adults and can cause both muscle weakness and wasting.

The causes of myositis vary depending on the type, but they can include autoimmune disorders, infections, medications, and other medical conditions. Treatment for myositis may involve medication to reduce inflammation, physical therapy to maintain muscle strength and flexibility, and lifestyle changes to manage symptoms and prevent complications.

Slow-twitch muscle fibers, also known as type I muscle fibers, are specialized skeletal muscle cells that contract relatively slowly and generate less force than fast-twitch fibers. However, they can maintain contraction for longer periods of time and have a higher resistance to fatigue. These fibers primarily use oxygen and aerobic metabolism to produce energy, making them highly efficient during prolonged, lower-intensity activities such as long-distance running or cycling. Slow-twitch muscle fibers also have an abundant blood supply, which allows for efficient delivery of oxygen and removal of waste products.

Fast-twitch muscle fibers, also known as type II fibers, are a type of skeletal muscle fiber that are characterized by their rapid contraction and relaxation rates. These fibers have a larger diameter and contain a higher concentration of glycogen, which serves as a quick source of energy for muscle contractions. Fast-twitch fibers are further divided into two subcategories: type IIa and type IIb (or type IIx). Type IIa fibers have a moderate amount of mitochondria and can utilize both aerobic and anaerobic metabolic pathways, making them fatigue-resistant. Type IIb fibers, on the other hand, have fewer mitochondria and primarily use anaerobic metabolism, leading to faster fatigue. Fast-twitch fibers are typically used in activities that require quick, powerful movements such as sprinting or weightlifting.

A diaphragm is a thin, dome-shaped muscle that separates the chest cavity from the abdominal cavity. It plays a vital role in the process of breathing as it contracts and flattens to draw air into the lungs (inhalation) and relaxes and returns to its domed shape to expel air out of the lungs (exhalation).

In addition, a diaphragm is also a type of barrier method of birth control. It is a flexible dome-shaped device made of silicone that fits over the cervix inside the vagina. When used correctly and consistently, it prevents sperm from entering the uterus and fertilizing an egg, thereby preventing pregnancy.

Muscle strength, in a medical context, refers to the amount of force a muscle or group of muscles can produce during contraction. It is the maximum amount of force that a muscle can generate through its full range of motion and is often measured in units of force such as pounds or newtons. Muscle strength is an important component of physical function and mobility, and it can be assessed through various tests, including manual muscle testing, dynamometry, and isokinetic testing. Factors that can affect muscle strength include age, sex, body composition, injury, disease, and physical activity level.

The Quadriceps muscle, also known as the Quadriceps Femoris, is a large muscle group located in the front of the thigh. It consists of four individual muscles - the Rectus Femoris, Vastus Lateralis, Vastus Intermedius, and Vastus Medialis. These muscles work together to extend the leg at the knee joint and flex the thigh at the hip joint. The Quadriceps muscle is crucial for activities such as walking, running, jumping, and kicking.

Electromyography (EMG) is a medical diagnostic procedure that measures the electrical activity of skeletal muscles during contraction and at rest. It involves inserting a thin needle electrode into the muscle to record the electrical signals generated by the muscle fibers. These signals are then displayed on an oscilloscope and may be heard through a speaker.

EMG can help diagnose various neuromuscular disorders, such as muscle weakness, numbness, or pain, and can distinguish between muscle and nerve disorders. It is often used in conjunction with other diagnostic tests, such as nerve conduction studies, to provide a comprehensive evaluation of the nervous system.

EMG is typically performed by a neurologist or a physiatrist, and the procedure may cause some discomfort or pain, although this is usually minimal. The results of an EMG can help guide treatment decisions and monitor the progression of neuromuscular conditions over time.

Mitochondria in muscle, also known as the "powerhouses" of the cell, are organelles that play a crucial role in generating energy for muscle cells through a process called cellular respiration. They convert the chemical energy found in glucose and oxygen into ATP (adenosine triphosphate), which is the main source of energy used by cells.

Muscle cells contain a high number of mitochondria due to their high energy demands for muscle contraction and relaxation. The number and size of mitochondria in muscle fibers can vary depending on the type of muscle fiber, with slow-twitch, aerobic fibers having more numerous and larger mitochondria than fast-twitch, anaerobic fibers.

Mitochondrial dysfunction has been linked to various muscle disorders, including mitochondrial myopathies, which are characterized by muscle weakness, exercise intolerance, and other symptoms related to impaired energy production in the muscle cells.

Dermatomyositis is a medical condition characterized by inflammation and weakness in the muscles and skin. It is a type of inflammatory myopathy, which means that it causes muscle inflammation and damage. Dermatomyositis is often associated with a distinctive rash that affects the skin around the eyes, nose, mouth, fingers, and toes.

The symptoms of dermatomyositis can include:

* Progressive muscle weakness, particularly in the hips, thighs, shoulders, and neck
* Fatigue
* Difficulty swallowing or speaking
* Skin rash, which may be pink or purple and is often accompanied by itching
* Muscle pain and tenderness
* Joint pain and swelling
* Raynaud's phenomenon, a condition that affects blood flow to the fingers and toes

The exact cause of dermatomyositis is not known, but it is believed to be related to an autoimmune response in which the body's immune system mistakenly attacks healthy tissue. Treatment for dermatomyositis typically involves medications to reduce inflammation and suppress the immune system, as well as physical therapy to help maintain muscle strength and function.

Hypokalemic Periodic Paralysis (HPP) is a group of rare inherited disorders characterized by episodes of muscle weakness or paralysis, often associated with low potassium levels in the blood (hypokalemia). During an attack, muscles may become weak or fully paralyzed, typically affecting the legs and arms. The episodes can last from several hours to days. HPP is caused by genetic mutations that affect ion channels in muscle cells, leading to an imbalance of electrolytes and impaired muscle function. There are two main types: primary (or classic) HPP and secondary HPP. Primary HPP is further divided into thyrotoxic HPP and normokalemic HPP. Secondary HPP can be caused by various factors, such as medications or underlying medical conditions that cause hypokalemia.

Muscle denervation is a medical term that refers to the loss of nerve supply to a muscle or group of muscles. This can occur due to various reasons, such as injury to the nerves, nerve compression, or certain medical conditions like neuromuscular disorders. When the nerve supply to the muscle is interrupted, it can lead to muscle weakness, atrophy (wasting), and ultimately, paralysis.

In denervation, the communication between the nervous system and the muscle is disrupted, which means that the muscle no longer receives signals from the brain to contract and move. Over time, this can result in significant muscle wasting and disability, depending on the severity and extent of the denervation.

Denervation may be treated with various therapies, including physical therapy, medication, or surgical intervention, such as nerve grafting or muscle transfers, to restore function and prevent further muscle wasting. The specific treatment approach will depend on the underlying cause and severity of the denervation.

Isometric contraction is a type of muscle activation where the muscle contracts without any change in the length of the muscle or movement at the joint. This occurs when the force generated by the muscle matches the external force opposing it, resulting in a balanced state with no visible movement. It is commonly experienced during activities such as holding a heavy object in static position or trying to push against an immovable object. Isometric contractions are important in maintaining posture and providing stability to joints.

Congenital structural myopathies are a group of inherited genetic disorders that affect the structure and function of skeletal muscles. These conditions are present at birth or develop in early infancy and are caused by genetic mutations that lead to abnormalities in the muscle contractile apparatus, including the sarcomere, muscle filaments, and muscle membrane.

The structural abnormalities can affect the muscle fibers' ability to generate force, leading to muscle weakness, hypotonia (low muscle tone), and other symptoms. The severity of the condition can vary widely, from mild to severe, depending on the specific type of myopathy and the extent of muscle involvement.

Examples of congenital structural myopathies include:

1. Congenital fiber-type disproportion (CFTD): a condition characterized by small, atrophic type 1 muscle fibers and normal or enlarged type 2 fibers.
2. Central core disease (CCD): a condition caused by mutations in the ryanodine receptor gene, which leads to the formation of abnormal structures called cores within the muscle fibers.
3. Nemaline myopathy: a condition characterized by the presence of rod-shaped structures called nemalines in the muscle fibers.
4. Myotubular myopathy: a condition caused by mutations in the myotubularin gene, which leads to abnormalities in the muscle fiber nuclei and weakened muscle function.
5. Congenital muscular dystrophy (CMD): a group of conditions characterized by muscle weakness, hypotonia, and joint contractures, often associated with structural abnormalities in the muscle membrane or extracellular matrix.

Diagnosis of congenital structural myopathies typically involves a combination of clinical evaluation, genetic testing, and muscle biopsy. Treatment is generally supportive and may include physical therapy, orthotics, and assistive devices to help manage symptoms and improve function. In some cases, medications or surgical interventions may be necessary to address specific complications.

Muscular dystrophies are a group of genetic disorders that primarily affect skeletal muscles, causing progressive weakness and degeneration. They are characterized by the lack or deficiency of a protein called dystrophin, which is essential for maintaining the integrity of muscle fibers. The most common form is Duchenne muscular dystrophy (DMD), but there are many other types with varying symptoms and severity. Over time, muscle wasting and weakness can lead to disability and shortened lifespan, depending on the type and progression of the disease. Treatment typically focuses on managing symptoms, maintaining mobility, and supporting quality of life.

Myasthenia Gravis is a long-term autoimmune neuromuscular disorder that leads to muscle weakness. It occurs when communication between nerves and muscles is disrupted at the nerve endings, resulting in fewer impulses being transmitted to activate the muscles. This results in muscle weakness and rapid fatigue. The condition can affect any voluntary muscle, but it most commonly affects muscles of the eyes, face, throat, and limbs. Symptoms may include drooping eyelids (ptosis), double vision (diplopia), difficulty swallowing, slurred speech, and weakness in the arms and legs. The severity of symptoms can vary greatly from person to person, ranging from mild to life-threatening.

The disorder is caused by an abnormal immune system response that produces antibodies against the acetylcholine receptors in the postsynaptic membrane of the neuromuscular junction. These antibodies block or destroy the receptors, which leads to a decrease in the number of available receptors for nerve impulses to activate the muscle fibers.

Myasthenia Gravis can be treated with medications that improve communication between nerves and muscles, such as cholinesterase inhibitors, immunosuppressants, and plasmapheresis or intravenous immunoglobulin (IVIG) to remove the harmful antibodies from the blood. With proper treatment, many people with Myasthenia Gravis can lead normal or nearly normal lives.

Congenital Myasthenic Syndromes (CMS) are a heterogeneous group of inherited neuromuscular disorders characterized by muscle weakness and fatigability. They are caused by genetic defects that affect the function of the neuromuscular junction, which is the site where nerve impulses are transmitted to muscles.

Unlike acquired myasthenia gravis, CMS are present at birth or develop in early childhood. The muscle weakness can vary from mild to severe and can affect any part of the body, including the eyes, face, neck, limbs, and respiratory muscles. The severity and distribution of symptoms can differ widely among individuals with CMS, depending on the specific genetic defect involved.

CMS are caused by mutations in genes that encode proteins involved in the formation, maintenance, or function of the neuromuscular junction. These proteins include receptors for neurotransmitters, enzymes involved in neurotransmitter metabolism, and structural components of the synaptic cleft.

The diagnosis of CMS is based on clinical features, electrophysiological studies, and genetic testing. Treatment options depend on the specific type of CMS and may include medications that improve neuromuscular transmission, such as cholinesterase inhibitors, or therapies that modulate the immune system, such as plasma exchange or intravenous immunoglobulin. In some cases, supportive care, such as respiratory assistance or physical therapy, may be necessary to manage symptoms and prevent complications.

Smooth muscle myocytes are specialized cells that make up the contractile portion of non-striated, or smooth, muscles. These muscles are found in various organs and structures throughout the body, including the walls of blood vessels, the digestive system, the respiratory system, and the reproductive system.

Smooth muscle myocytes are smaller than their striated counterparts (skeletal and cardiac muscle cells) and have a single nucleus. They lack the distinctive banding pattern seen in striated muscles and instead have a uniform appearance of actin and myosin filaments. Smooth muscle myocytes are controlled by the autonomic nervous system, which allows them to contract and relax involuntarily.

These cells play an essential role in many physiological processes, such as regulating blood flow, moving food through the digestive tract, and facilitating childbirth. They can also contribute to various pathological conditions, including hypertension, atherosclerosis, and gastrointestinal disorders.

Inclusion body myositis (IBM) is a rare inflammatory muscle disease characterized by progressive weakness and wasting (atrophy) of skeletal muscles. The term "inclusion body" refers to the presence of abnormal protein accumulations within muscle fibers, which are observed under a microscope during muscle biopsy. These inclusions are primarily composed of aggregated forms of amyloid-β and tau proteins, similar to those found in neurodegenerative disorders like Alzheimer's disease.

IBM typically affects individuals over 50 years old, and it is more common in men than women. The disease usually starts with weakness in the wrist and finger flexors, making it difficult to perform tasks such as gripping, buttoning shirts, or lifting objects. Over time, the weakness spreads to other muscle groups, including the thigh muscles (quadriceps), resulting in difficulty climbing stairs or rising from a seated position.

The exact cause of inclusion body myositis remains unclear; however, both immune-mediated and degenerative mechanisms are believed to contribute to its pathogenesis. Currently, there is no cure for IBM, and treatment options are primarily aimed at managing symptoms and improving quality of life. Immunosuppressive medications may be used to target the inflammatory component of the disease; however, their efficacy varies among patients. Physical therapy and exercise programs can help maintain muscle strength and function as much as possible.

The oculomotor muscles are a group of extraocular muscles that control the movements of the eye. They include:

1. Superior rectus: This muscle is responsible for elevating the eye and helping with inward rotation (intorsion) when looking downwards.
2. Inferior rectus: It depresses the eye and helps with outward rotation (extorsion) when looking upwards.
3. Medial rectus: This muscle adducts, or moves, the eye towards the midline of the face.
4. Inferior oblique: The inferior oblique muscle intorts and elevates the eye.
5. Superior oblique: It extorts and depresses the eye.

These muscles work together to allow for smooth and precise movements of the eyes, enabling tasks such as tracking moving objects, reading, and maintaining visual fixation on a single point in space.

Neck muscles, also known as cervical muscles, are a group of muscles that provide movement, support, and stability to the neck region. They are responsible for various functions such as flexion, extension, rotation, and lateral bending of the head and neck. The main neck muscles include:

1. Sternocleidomastoid: This muscle is located on either side of the neck and is responsible for rotating and flexing the head. It also helps in tilting the head to the same side.

2. Trapezius: This large, flat muscle covers the back of the neck, shoulders, and upper back. It is involved in movements like shrugging the shoulders, rotating and extending the head, and stabilizing the scapula (shoulder blade).

3. Scalenes: These three pairs of muscles are located on the side of the neck and assist in flexing, rotating, and laterally bending the neck. They also help with breathing by elevating the first two ribs during inspiration.

4. Suboccipitals: These four small muscles are located at the base of the skull and are responsible for fine movements of the head, such as tilting and rotating.

5. Longus Colli and Longus Capitis: These muscles are deep neck flexors that help with flexing the head and neck forward.

6. Splenius Capitis and Splenius Cervicis: These muscles are located at the back of the neck and assist in extending, rotating, and laterally bending the head and neck.

7. Levator Scapulae: This muscle is located at the side and back of the neck, connecting the cervical vertebrae to the scapula. It helps with rotation, extension, and elevation of the head and scapula.

Muscle hypotonia, also known as decreased muscle tone, refers to a condition where the muscles appear to be flaccid or lacking in tension and stiffness. This results in reduced resistance to passive movements, making the limbs feel "floppy" or "like a rag doll." It can affect any muscle group in the body and can be caused by various medical conditions, including neurological disorders, genetic diseases, and injuries to the nervous system. Hypotonia should not be confused with muscle weakness, which refers to the inability to generate normal muscle strength.

Respiratory paralysis is a condition characterized by the inability to breathe effectively due to the failure or weakness of the muscles involved in respiration. This can include the diaphragm, intercostal muscles, and other accessory muscles.

In medical terms, it's often associated with conditions that affect the neuromuscular junction, such as botulism, myasthenia gravis, or spinal cord injuries. It can also occur as a complication of general anesthesia, sedative drugs, or certain types of poisoning.

Respiratory paralysis is a serious condition that requires immediate medical attention, as it can lead to lack of oxygen (hypoxia) and buildup of carbon dioxide (hypercapnia) in the body, which can be life-threatening if not treated promptly.

Duchenne Muscular Dystrophy (DMD) is a genetic disorder characterized by progressive muscle weakness and degeneration. It is caused by the absence of dystrophin, a protein that helps keep muscle cells intact. Without dystrophin, the muscle cells break down and are replaced with scar tissue, leading to loss of muscle function over time.

DMD primarily affects boys, as it is inherited in an X-linked recessive pattern, meaning that females who carry one affected X chromosome typically do not show symptoms but can pass the gene on to their offspring. Symptoms usually begin in early childhood and include difficulty with motor skills such as walking, running, and climbing stairs. Over time, the muscle weakness progresses and can lead to loss of ambulation, respiratory and cardiac complications, and ultimately, premature death.

Currently, there is no cure for DMD, but various treatments such as corticosteroids, physical therapy, and assisted ventilation can help manage symptoms and improve quality of life. Gene therapy approaches are also being investigated as potential treatments for this disorder.

Striated muscle, also known as skeletal or voluntary muscle, is a type of muscle tissue that is characterized by the presence of distinct light and dark bands, or striations, when viewed under a microscope. These striations correspond to the arrangement of sarcomeres, which are the functional units of muscle fibers.

Striated muscle is under voluntary control, meaning that it is consciously activated by signals from the nervous system. It is attached to bones via tendons and is responsible for producing movements of the body. Striated muscle fibers are multinucleated, meaning that they contain many nuclei, and are composed of numerous myofibrils, which are rope-like structures that run the length of the fiber.

The myofibrils are composed of thick and thin filaments that slide past each other to cause muscle contraction. The thick filaments are made up of the protein myosin, while the thin filaments are composed of actin, tropomyosin, and troponin. When a nerve impulse arrives at the muscle fiber, it triggers the release of calcium ions from the sarcoplasmic reticulum, which bind to troponin and cause a conformational change that exposes the binding sites on actin for myosin. The myosin heads then bind to the actin filaments and pull them towards the center of the sarcomere, causing the muscle fiber to shorten and contract.

A muscle strength dynamometer is a medical device used to measure the force or strength of a muscle or group of muscles. It typically consists of a handheld handle connected to a spring scale or digital force gauge, which measures the amount of force applied by the individual being tested. The person being tested pushes or pulls against the handle with as much force as possible, and the dynamometer provides an objective measurement of their muscle strength in units such as pounds or kilograms.

Muscle strength dynamometers are commonly used in clinical settings to assess muscle weakness or dysfunction, monitor changes in muscle strength over time, and evaluate the effectiveness of rehabilitation interventions. They can be used to test various muscle groups, including the handgrip, quadriceps, hamstrings, biceps, triceps, and shoulder muscles.

When using a muscle strength dynamometer, it is important to follow standardized testing protocols to ensure accurate and reliable measurements. This may include positioning the individual in a specific way, providing standardized instructions, and averaging multiple trials to obtain an accurate measure of their muscle strength.

Limb-girdle muscular dystrophy (LGMD) is a group of rare inherited disorders that cause progressive weakness and wasting of the muscles in the arms and legs, particularly those around the shoulders and hips (the limb-girdle region). The condition affects both males and females and presents at different ages, depending on the specific type of LGMD.

LGMD is caused by mutations in various genes that play a role in maintaining muscle integrity and function. These genetic defects lead to a deficiency or dysfunction of certain proteins necessary for muscle health, ultimately resulting in muscle degeneration and weakness. There are more than 30 different subtypes of LGMD, each with its own set of causative genes and inheritance patterns (autosomal dominant or autosomal recessive).

Symptoms of limb-girdle muscular dystrophy may include:

1. Progressive muscle weakness and wasting in the arms, legs, shoulders, and hips
2. Difficulty with activities such as climbing stairs, lifting objects, or getting up from a seated position
3. Enlarged calf muscles (pseudohypertrophy) due to muscle degeneration and fat replacement
4. Muscle contractures, joint stiffness, and limited range of motion
5. Difficulty walking, using wheelchair assistance in advanced stages
6. Respiratory complications due to weakened chest muscles in some cases

Diagnosis of LGMD typically involves a combination of clinical evaluation, family history, muscle biopsy, genetic testing, and blood tests for creatine kinase (CK) levels, which are often elevated in muscular dystrophies. Treatment is primarily supportive and focuses on maintaining mobility, preventing complications, and preserving quality of life through physical therapy, assistive devices, and orthopedic interventions as needed. No cure currently exists for limb-girdle muscular dystrophy, but ongoing research aims to develop targeted therapies based on the underlying genetic defects.

Muscle spindles are specialized sensory organs found within the muscle belly, which primarily function as proprioceptors, providing information about the length and rate of change in muscle length. They consist of small, encapsulated bundles of intrafusal muscle fibers that are interspersed among the extrafusal muscle fibers (the ones responsible for force generation).

Muscle spindles have two types of sensory receptors called primary and secondary endings. Primary endings are located near the equatorial region of the intrafusal fiber, while secondary endings are situated more distally. These endings detect changes in muscle length and transmit this information to the central nervous system (CNS) through afferent nerve fibers.

The activation of muscle spindles plays a crucial role in reflexive responses, such as the stretch reflex (myotatic reflex), which helps maintain muscle tone and joint stability. Additionally, they contribute to our sense of body position and movement awareness, known as kinesthesia.

Muscle relaxation, in a medical context, refers to the process of reducing tension and promoting relaxation in the skeletal muscles. This can be achieved through various techniques, including progressive muscle relaxation (PMR), where individuals consciously tense and then release specific muscle groups in a systematic manner.

PMR has been shown to help reduce anxiety, stress, and muscle tightness, and improve overall well-being. It is often used as a complementary therapy in conjunction with other treatments for conditions such as chronic pain, headaches, and insomnia.

Additionally, muscle relaxation can also be facilitated through pharmacological interventions, such as the use of muscle relaxant medications. These drugs work by inhibiting the transmission of signals between nerves and muscles, leading to a reduction in muscle tone and spasticity. They are commonly used to treat conditions such as multiple sclerosis, cerebral palsy, and spinal cord injuries.

The neuromuscular junction (NMJ) is the specialized synapse or chemical communication point, where the motor neuron's nerve terminal (presynaptic element) meets the muscle fiber's motor end plate (postsynaptic element). This junction plays a crucial role in controlling muscle contraction and relaxation.

At the NMJ, the neurotransmitter acetylcholine is released from the presynaptic nerve terminal into the synaptic cleft, following an action potential. Acetylcholine then binds to nicotinic acetylcholine receptors on the postsynaptic membrane of the muscle fiber, leading to the generation of an end-plate potential. If sufficient end-plate potentials are generated and summate, they will trigger an action potential in the muscle fiber, ultimately causing muscle contraction.

Dysfunction at the neuromuscular junction can result in various neuromuscular disorders, such as myasthenia gravis, where autoantibodies attack acetylcholine receptors, leading to muscle weakness and fatigue.

Papillary muscles are specialized muscle structures located in the heart, specifically in the ventricles (the lower chambers of the heart). They are attached to the tricuspid and mitral valves' leaflets via tendinous cords, also known as chordae tendineae. The main function of papillary muscles is to prevent the backflow of blood during contraction by providing tension to the valve leaflets through these tendinous cords.

There are two sets of papillary muscles in the heart:

1. Anterior and posterior papillary muscles in the left ventricle, which are attached to the mitral (bicuspid) valve.
2. Three smaller papillary muscles in the right ventricle, which are attached to the tricuspid valve.

These muscle structures play a crucial role in maintaining proper blood flow through the heart and ensuring efficient cardiac function.

Rhabdomyolysis is a medical condition characterized by the breakdown and degeneration of skeletal muscle fibers, leading to the release of their intracellular contents into the bloodstream. This can result in various complications, including electrolyte imbalances, kidney injury or failure, and potentially life-threatening conditions if not promptly diagnosed and treated.

The process of rhabdomyolysis typically involves three key components:

1. Muscle injury: Direct trauma, excessive exertion, prolonged immobilization, infections, metabolic disorders, toxins, or medications can cause muscle damage, leading to the release of intracellular components into the bloodstream.
2. Release of muscle contents: When muscle fibers break down, they release various substances, such as myoglobin, creatine kinase (CK), lactate dehydrogenase (LDH), aldolase, and potassium ions. Myoglobin is a protein that can cause kidney damage when present in high concentrations in the bloodstream, particularly when it is filtered through the kidneys and deposits in the renal tubules.
3. Systemic effects: The release of muscle contents into the bloodstream can lead to various systemic complications, such as electrolyte imbalances (particularly hyperkalemia), acidosis, hypocalcemia, and kidney injury or failure due to myoglobin-induced tubular damage.

Symptoms of rhabdomyolysis can vary widely depending on the severity and extent of muscle damage but may include muscle pain, weakness, swelling, stiffness, dark urine, and tea-colored or cola-colored urine due to myoglobinuria. In severe cases, patients may experience symptoms related to kidney failure, such as nausea, vomiting, fatigue, and decreased urine output.

Diagnosis of rhabdomyolysis typically involves measuring blood levels of muscle enzymes (such as CK and LDH) and evaluating renal function through blood tests and urinalysis. Treatment generally focuses on addressing the underlying cause of muscle damage, maintaining fluid balance, correcting electrolyte imbalances, and preventing or managing kidney injury.

Myosin Heavy Chains are the large, essential components of myosin molecules, which are responsible for the molecular motility in muscle cells. These heavy chains have a molecular weight of approximately 200 kDa and form the motor domain of myosin, which binds to actin filaments and hydrolyzes ATP to generate force and movement during muscle contraction. There are several different types of myosin heavy chains, each with specific roles in various tissues and cellular functions. In skeletal and cardiac muscles, for example, myosin heavy chains have distinct isoforms that contribute to the contractile properties of these tissues.

Ophthalmoplegia is a medical term that refers to the paralysis or weakness of the eye muscles, which can result in double vision (diplopia) or difficulty moving the eyes. It can be caused by various conditions, including nerve damage, muscle disorders, or neurological diseases such as myasthenia gravis or multiple sclerosis. Ophthalmoplegia can affect one or more eye muscles and can be partial or complete. Depending on the underlying cause, ophthalmoplegia may be treatable with medications, surgery, or other interventions.

Distal myopathies are a group of rare genetic muscle disorders that primarily affect the muscles of the hands, feet, and lower legs. These myopathies are characterized by progressive weakness and wasting (atrophy) of the distal muscles, which are located further from the center of the body. The onset of symptoms can vary widely, ranging from early childhood to late adulthood.

There are several different types of distal myopathies, each caused by mutations in specific genes that affect muscle function. Some common forms include:

1. Nonaka Distal Myopathy: This form is caused by mutations in the GNE gene and typically presents in the third or fourth decade of life with weakness and wasting of the ankle dorsiflexors, foot extensors, and wrist and finger extensors.

2. Miyoshi Distal Myopathy: This form is caused by mutations in the DYSF gene and affects the calf muscles initially, followed by weakness in other distal muscles over time.

3. Welander Distal Myopathy: This form is caused by mutations in the TIA1 gene and typically presents in adulthood with weakness and wasting of the hand and forearm muscles.

4. Laing Distal Myopathy: This form is caused by mutations in the CAV3 gene and affects the anterior compartment of the lower leg, resulting in foot drop and weakness of the ankle dorsiflexors.

5. Gowers Distal Myopathy: This form is caused by mutations in the HNRNPDL gene and typically presents in adulthood with weakness and wasting of the hand and forearm muscles, as well as foot drop.

There is no cure for distal myopathies, but treatment can help manage symptoms and improve quality of life. Physical therapy, bracing, and orthotics may be used to support weakened muscles and maintain mobility. In some cases, medications such as corticosteroids or immunosuppressants may be prescribed to reduce muscle inflammation and slow disease progression.

Lambert-Eaton Myasthenic Syndrome (LEMS) is a rare autoimmune disorder characterized by muscle weakness and fatigability. It is caused by the presence of antibodies against voltage-gated calcium channels (VGCC) in the neuromuscular junction, which disrupts the normal transmission of signals between nerves and muscles.

The symptoms of LEMS include proximal muscle weakness, which may affect the legs more than the arms, and autonomic dysfunction such as dry mouth and constipation. The weakness tends to improve with exercise but worsens after periods of rest. In some cases, LEMS can be associated with cancer, particularly small cell lung cancer.

Diagnosis of LEMS typically involves a combination of clinical evaluation, electromyography (EMG) studies, and blood tests to detect VGCC antibodies. Treatment may include medications such as pyridostigmine, which improves neuromuscular transmission, or intravenous immunoglobulin and plasma exchange, which help to reduce the immune response. In cases where LEMS is associated with cancer, treatment of the underlying malignancy can also improve muscle strength and function.

Hypokalemia is a medical condition characterized by abnormally low potassium levels in the blood, specifically when the concentration falls below 3.5 milliequivalents per liter (mEq/L). Potassium is an essential electrolyte that helps regulate heart function, nerve signals, and muscle contractions.

Hypokalemia can result from various factors, including inadequate potassium intake, increased potassium loss through the urine or gastrointestinal tract, or shifts of potassium between body compartments. Common causes include diuretic use, vomiting, diarrhea, certain medications, kidney diseases, and hormonal imbalances.

Mild hypokalemia may not cause noticeable symptoms but can still affect the proper functioning of muscles and nerves. More severe cases can lead to muscle weakness, fatigue, cramps, paralysis, heart rhythm abnormalities, and in rare instances, respiratory failure or cardiac arrest. Treatment typically involves addressing the underlying cause and replenishing potassium levels through oral or intravenous (IV) supplementation, depending on the severity of the condition.

I'm sorry for any confusion, but "Muscular Dystrophy, Animal" is not a standard medical term. Muscular Dystrophy is a group of genetic disorders that cause progressive weakness and loss of muscle mass. They are primarily human diseases and there are no known animal models of muscular dystrophy that directly correspond to any type of muscular dystrophy in humans.

However, scientists often use animals (like mice, dogs, and cats) as models for human diseases, including various types of muscular dystrophies. These animal models are used to study the disease process and to test potential treatments. For example, the mdx mouse is a well-known model of Duchenne Muscular Dystrophy (DMD), which is caused by a mutation in the dystrophin gene. This mouse lacks the muscle protein dystrophin, similar to humans with DMD, and shows many of the same symptoms, making it a valuable tool for research.

'Mice, Inbred mdx' is a genetic strain of laboratory mice that are widely used as a model to study Duchenne muscular dystrophy (DMD), a severe and progressive muscle-wasting disorder in humans. The 'mdx' designation refers to the specific genetic mutation present in these mice, which is a point mutation in the gene encoding for dystrophin, a crucial protein involved in maintaining the structural integrity of muscle fibers.

Inbred mdx mice carry a spontaneous mutation in exon 23 of the dystrophin gene, resulting in the production of a truncated and nonfunctional form of the protein. This leads to a phenotype that closely resembles DMD in humans, including muscle weakness, degeneration, and fibrosis. The inbred nature of these mice ensures consistent genetic backgrounds and disease manifestations, making them valuable tools for studying the pathophysiology of DMD and testing potential therapies.

It is important to note that while the inbred mdx mouse model has been instrumental in advancing our understanding of DMD, it does not fully recapitulate all aspects of the human disease. Therefore, findings from these mice should be carefully interpreted and validated in more complex models or human studies before translating them into clinical applications.

Myotonic dystrophy is a genetic disorder characterized by progressive muscle weakness, myotonia (delayed relaxation of muscles after contraction), and other symptoms. It is caused by an expansion of repetitive DNA sequences in the DMPK gene on chromosome 19 (type 1) or the ZNF9 gene on chromosome 3 (type 2). These expansions result in abnormal protein production and accumulation, which disrupt muscle function and can also affect other organs such as the heart, eyes, and endocrine system. Myotonic dystrophy is a progressive disease, meaning that symptoms tend to worsen over time. It is typically divided into two types: myotonic dystrophy type 1 (DM1), which is more common and severe, and myotonic dystrophy type 2 (DM2), which tends to be milder with a later onset of symptoms.

Myofibrils are the basic contractile units of muscle fibers, composed of highly organized arrays of thick and thin filaments. They are responsible for generating the force necessary for muscle contraction. The thick filaments are primarily made up of the protein myosin, while the thin filaments are mainly composed of actin. Myofibrils are surrounded by a membrane called the sarcolemma and are organized into repeating sections called sarcomeres, which are the functional units of muscle contraction.

The abdominal muscles, also known as the abdominals or abs, are a group of muscles in the anterior (front) wall of the abdominopelvic cavity. They play a crucial role in maintaining posture, supporting the trunk, and facilitating movement of the torso. The main abdominal muscles include:

1. Rectus Abdominis: These are the pair of long, flat muscles that run vertically along the middle of the anterior abdominal wall. They are often referred to as the "six-pack" muscles due to their visible, segmented appearance in well-trained individuals. The primary function of the rectus abdominis is to flex the spine, allowing for actions such as sitting up from a lying down position or performing a crunch exercise.

2. External Obliques: These are the largest and most superficial of the oblique muscles, located on the lateral (side) aspects of the abdominal wall. They run diagonally downward and forward from the lower ribs to the iliac crest (the upper part of the pelvis) and the pubic tubercle (a bony prominence at the front of the pelvis). The external obliques help rotate and flex the trunk, as well as assist in side-bending and exhalation.

3. Internal Obliques: These muscles lie deep to the external obliques and run diagonally downward and backward from the lower ribs to the iliac crest, pubic tubercle, and linea alba (the strong band of connective tissue that runs vertically along the midline of the abdomen). The internal obliques help rotate and flex the trunk, as well as assist in forced exhalation and increasing intra-abdominal pressure during actions such as coughing or lifting heavy objects.

4. Transversus Abdominis: This is the deepest of the abdominal muscles, located inner to both the internal obliques and the rectus sheath (a strong, fibrous covering that surrounds the rectus abdominis). The transversus abdominis runs horizontally around the abdomen, attaching to the lower six ribs, the thoracolumbar fascia (a broad sheet of connective tissue spanning from the lower back to the pelvis), and the pubic crest (the front part of the pelvic bone). The transversus abdominis helps maintain core stability by compressing the abdominal contents and increasing intra-abdominal pressure.

Together, these muscles form the muscular "corset" of the abdomen, providing support, stability, and flexibility to the trunk. They also play a crucial role in respiration, posture, and various movements such as bending, twisting, and lifting.

Facial muscles, also known as facial nerves or cranial nerve VII, are a group of muscles responsible for various expressions and movements of the face. These muscles include:

1. Orbicularis oculi: muscle that closes the eyelid and raises the upper eyelid
2. Corrugator supercilii: muscle that pulls the eyebrows down and inward, forming wrinkles on the forehead
3. Frontalis: muscle that raises the eyebrows and forms horizontal wrinkles on the forehead
4. Procerus: muscle that pulls the medial ends of the eyebrows downward, forming vertical wrinkles between the eyebrows
5. Nasalis: muscle that compresses or dilates the nostrils
6. Depressor septi: muscle that pulls down the tip of the nose
7. Levator labii superioris alaeque nasi: muscle that raises the upper lip and flares the nostrils
8. Levator labii superioris: muscle that raises the upper lip
9. Zygomaticus major: muscle that raises the corner of the mouth, producing a smile
10. Zygomaticus minor: muscle that raises the nasolabial fold and corner of the mouth
11. Risorius: muscle that pulls the angle of the mouth laterally, producing a smile
12. Depressor anguli oris: muscle that pulls down the angle of the mouth
13. Mentalis: muscle that raises the lower lip and forms wrinkles on the chin
14. Buccinator: muscle that retracts the cheek and helps with chewing
15. Platysma: muscle that depresses the corner of the mouth and wrinkles the skin of the neck.

These muscles are innervated by the facial nerve, which arises from the brainstem and exits the skull through the stylomastoid foramen. Damage to the facial nerve can result in facial paralysis or weakness on one or both sides of the face.

Charcot-Marie-Tooth disease (CMT) is a group of inherited disorders that cause nerve damage, primarily affecting the peripheral nerves. These are the nerves that transmit signals between the brain and spinal cord to the rest of the body. CMT affects both motor and sensory nerves, leading to muscle weakness and atrophy, as well as numbness or tingling in the hands and feet.

The disease is named after the three physicians who first described it: Jean-Martin Charcot, Pierre Marie, and Howard Henry Tooth. CMT is characterized by its progressive nature, meaning symptoms typically worsen over time, although the rate of progression can vary significantly among individuals.

There are several types of CMT, classified based on their genetic causes and patterns of inheritance. The two most common forms are CMT1 and CMT2:

1. CMT1: This form is caused by mutations in the genes responsible for the myelin sheath, which insulates peripheral nerves and allows for efficient signal transmission. As a result, demyelination occurs, slowing down nerve impulses and causing muscle weakness, particularly in the lower limbs. Symptoms usually begin in childhood or adolescence and include foot drop, high arches, and hammertoes.
2. CMT2: This form is caused by mutations in the genes responsible for the axons, the nerve fibers that transmit signals within peripheral nerves. As a result, axonal degeneration occurs, leading to muscle weakness and atrophy. Symptoms usually begin in early adulthood and progress more slowly than CMT1. They primarily affect the lower limbs but can also involve the hands and arms.

Diagnosis of CMT typically involves a combination of clinical evaluation, family history, nerve conduction studies, and genetic testing. While there is no cure for CMT, treatment focuses on managing symptoms and maintaining mobility and function through physical therapy, bracing, orthopedic surgery, and pain management.

Muscle cells, also known as muscle fibers, are specialized cells that have the ability to contract and generate force, allowing for movement of the body and various internal organ functions. There are three main types of muscle tissue: skeletal, cardiac, and smooth.

Skeletal muscle cells are voluntary striated muscles attached to bones, enabling body movements and posture. They are multinucleated, with numerous nuclei located at the periphery of the cell. These cells are often called muscle fibers and can be quite large, extending the entire length of the muscle.

Cardiac muscle cells form the contractile tissue of the heart. They are also striated but have a single nucleus per cell and are interconnected by specialized junctions called intercalated discs, which help coordinate contraction throughout the heart.

Smooth muscle cells are found in various internal organs such as the digestive, respiratory, and urinary tracts, blood vessels, and the reproductive system. They are involuntary, non-striated muscles that control the internal organ functions. Smooth muscle cells have a single nucleus per cell and can either be spindle-shaped or stellate (star-shaped).

In summary, muscle cells are specialized contractile cells responsible for movement and various internal organ functions in the human body. They can be categorized into three types: skeletal, cardiac, and smooth, based on their structure, location, and function.

Cholinergic receptors are a type of receptor in the body that are activated by the neurotransmitter acetylcholine. Acetylcholine is a chemical that nerve cells use to communicate with each other and with muscles. There are two main types of cholinergic receptors: muscarinic and nicotinic.

Muscarinic receptors are found in the heart, smooth muscle, glands, and the central nervous system. They are activated by muscarine, a type of alkaloid found in certain mushrooms. When muscarinic receptors are activated, they can cause changes in heart rate, blood pressure, and other bodily functions.

Nicotinic receptors are found in the nervous system and at the junction between nerves and muscles (the neuromuscular junction). They are activated by nicotine, a type of alkaloid found in tobacco plants. When nicotinic receptors are activated, they can cause the release of neurotransmitters and the contraction of muscles.

Cholinergic receptors play an important role in many physiological processes, including learning, memory, and movement. They are also targets for drugs used to treat a variety of medical conditions, such as Alzheimer's disease, Parkinson's disease, and myasthenia gravis (a disorder that causes muscle weakness).

Monocrotophos is not typically defined in medical terms, but it is a pesticide that can have medical implications. It's a type of organophosphate insecticide that works by inhibiting the enzyme acetylcholinesterase, leading to an overaccumulation of the neurotransmitter acetylcholine and resulting in symptoms such as muscle twitching, nausea, vomiting, diarrhea, sweating, and, at high exposures, seizures and respiratory failure. Chronic exposure can lead to neurological problems and an increased risk of certain cancers.

The masseter muscle is a strong chewing muscle in the jaw. It is a broad, thick, quadrilateral muscle that extends from the zygomatic arch (cheekbone) to the lower jaw (mandible). The masseter muscle has two distinct parts: the superficial part and the deep part.

The superficial part of the masseter muscle originates from the lower border of the zygomatic process of the maxilla and the anterior two-thirds of the inferior border of the zygomatic arch. The fibers of this part run almost vertically downward to insert on the lateral surface of the ramus of the mandible and the coronoid process.

The deep part of the masseter muscle originates from the deep surface of the zygomatic arch and inserts on the medial surface of the ramus of the mandible, blending with the temporalis tendon.

The primary function of the masseter muscle is to elevate the mandible, helping to close the mouth and clench the teeth together during mastication (chewing). It also plays a role in stabilizing the jaw during biting and speaking. The masseter muscle is one of the most powerful muscles in the human body relative to its size.

Glycogen Storage Disease Type II, also known as Pompe Disease, is a genetic disorder caused by a deficiency of the enzyme acid alpha-glucosidase (GAA). This enzyme is responsible for breaking down glycogen, a complex sugar that serves as energy storage, within lysosomes. When GAA is deficient, glycogen accumulates in various tissues, particularly in muscle cells, leading to their dysfunction and damage.

The severity of Pompe Disease can vary significantly, depending on the amount of functional enzyme activity remaining. The classic infantile-onset form presents within the first few months of life with severe muscle weakness, hypotonia, feeding difficulties, and respiratory insufficiency. This form is often fatal by 1-2 years of age if left untreated.

A later-onset form, which can present in childhood, adolescence, or adulthood, has a more variable clinical course. Affected individuals may experience progressive muscle weakness, respiratory insufficiency, and cardiomyopathy, although the severity and rate of progression are generally less pronounced than in the infantile-onset form.

Enzyme replacement therapy with recombinant human GAA is available for the treatment of Pompe Disease and has been shown to improve survival and motor function in affected individuals.

Creatine kinase (CK) is a muscle enzyme that is normally present in small amounts in the blood. It is primarily found in tissues that require a lot of energy, such as the heart, brain, and skeletal muscles. When these tissues are damaged or injured, CK is released into the bloodstream, causing the levels to rise.

Creatine kinase exists in several forms, known as isoenzymes, which can be measured in the blood to help identify the location of tissue damage. The three main isoenzymes are:

1. CK-MM: Found primarily in skeletal muscle
2. CK-MB: Found primarily in heart muscle
3. CK-BB: Found primarily in the brain

Elevated levels of creatine kinase, particularly CK-MB, can indicate damage to the heart muscle, such as occurs with a heart attack. Similarly, elevated levels of CK-BB may suggest brain injury or disease. Overall, measuring creatine kinase levels is a useful diagnostic tool for assessing tissue damage and determining the severity of injuries or illnesses.

Masticatory muscles are a group of skeletal muscles responsible for the mastication (chewing) process in humans and other animals. They include:

1. Masseter muscle: This is the primary muscle for chewing and is located on the sides of the face, running from the lower jawbone (mandible) to the cheekbone (zygomatic arch). It helps close the mouth and elevate the mandible during chewing.

2. Temporalis muscle: This muscle is situated in the temporal region of the skull, covering the temple area. It assists in closing the jaw, retracting the mandible, and moving it sideways during chewing.

3. Medial pterygoid muscle: Located deep within the cheek, near the angle of the lower jaw, this muscle helps move the mandible forward and grind food during chewing. It also contributes to closing the mouth.

4. Lateral pterygoid muscle: Found inside the ramus (the vertical part) of the mandible, this muscle has two heads - superior and inferior. The superior head helps open the mouth by pulling the temporomandibular joint (TMJ) downwards, while the inferior head assists in moving the mandible sideways during chewing.

These muscles work together to enable efficient chewing and food breakdown, preparing it for swallowing and digestion.

Myotonia is a condition characterized by the delayed relaxation of a muscle after voluntary contraction or electrical stimulation, resulting in stiffness or difficulty with relaxing the muscles. It's often associated with certain neuromuscular disorders such as myotonic dystrophy and myotonia congenita. The prolonged muscle contraction can cause stiffness, especially after periods of rest, and may improve with repeated contractions (warm-up phenomenon).

The intercostal muscles are a group of muscles located between the ribs (intercostal spaces) in the thoracic region of the body. They play a crucial role in the process of breathing by assisting in the expansion and contraction of the chest wall during inspiration and expiration.

There are two sets of intercostal muscles: the external intercostals and the internal intercostals. The external intercostals run from the lower edge of one rib to the upper edge of the next lower rib, forming a layer that extends from the tubercles of the ribs down to the costochondral junctions (where the rib meets the cartilage). These muscles help elevate the ribcage during inspiration.

The internal intercostals are deeper and run in the opposite direction, originating at the lower edge of a rib and inserting into the upper edge of the next higher rib. They assist in lowering the ribcage during expiration.

Additionally, there is a third layer called the innermost intercostal muscles, which are even deeper than the internal intercostals and have similar functions. The intercostal membranes connect the ends of the ribs and complete the muscle layers between the ribs. Together, these muscles help maintain the structural integrity of the chest wall and contribute to respiratory function.

Familial periodic paralysis is a group of rare genetic disorders characterized by episodes of muscle weakness or paralysis that recur over time. There are several types of familial periodic paralysis, including hypokalemic periodic paralysis, hyperkalemic periodic paralysis, and normokalemic periodic paralysis, each with its own specific genetic cause and pattern of symptoms.

In general, these disorders are caused by mutations in genes that regulate ion channels in muscle cells, leading to abnormalities in the flow of ions such as potassium in and out of the cells. This can result in changes in muscle excitability and contractility, causing episodes of weakness or paralysis.

The episodes of paralysis in familial periodic paralysis can vary in frequency, duration, and severity. They may be triggered by factors such as rest after exercise, cold or hot temperatures, emotional stress, alcohol consumption, or certain medications. During an episode, the affected muscles may become weak or completely paralyzed, often affecting the limbs but sometimes also involving the muscles of the face, throat, and trunk.

Familial periodic paralysis is typically inherited in an autosomal dominant pattern, meaning that a child has a 50% chance of inheriting the disorder if one parent is affected. However, some cases may arise from new mutations in the affected gene and occur in people with no family history of the disorder.

Treatment for familial periodic paralysis typically involves avoiding triggers and managing symptoms during episodes. In some cases, medications such as potassium-binding agents or diuretics may be used to help prevent or reduce the severity of episodes. Lifestyle modifications, such as a low-carbohydrate or high-sodium diet, may also be recommended in some cases.

Biomechanics is the application of mechanical laws to living structures and systems, particularly in the field of medicine and healthcare. A biomechanical phenomenon refers to a observable event or occurrence that involves the interaction of biological tissues or systems with mechanical forces. These phenomena can be studied at various levels, from the molecular and cellular level to the tissue, organ, and whole-body level.

Examples of biomechanical phenomena include:

1. The way that bones and muscles work together to produce movement (known as joint kinematics).
2. The mechanical behavior of biological tissues such as bone, cartilage, tendons, and ligaments under various loads and stresses.
3. The response of cells and tissues to mechanical stimuli, such as the way that bone tissue adapts to changes in loading conditions (known as Wolff's law).
4. The biomechanics of injury and disease processes, such as the mechanisms of joint injury or the development of osteoarthritis.
5. The use of mechanical devices and interventions to treat medical conditions, such as orthopedic implants or assistive devices for mobility impairments.

Understanding biomechanical phenomena is essential for developing effective treatments and prevention strategies for a wide range of medical conditions, from musculoskeletal injuries to neurological disorders.

Post-poliomyelitis syndrome (PPS) is a condition that affects polio survivors years after recovery from the initial acute poliomyelitis infection. The symptoms of PPS include new onset weakness, fatigue, and pain in the muscles that were previously affected by the poliovirus. These symptoms can occur gradually or suddenly, and they may be worsened by exercise or other physical stressors.

PPS is thought to be caused by ongoing degeneration of the enlarged motor neurons that survived the initial polio infection. It is estimated that up to 50% of polio survivors may experience symptoms of PPS. While there is no cure for PPS, treatment typically focuses on managing symptoms and maintaining function through physical therapy, assistive devices, and pain management strategies.

Inspiratory Capacity (IC) is the maximum volume of air that can be breathed in after a normal expiration. It is the sum of the tidal volume (the amount of air displaced between normal inspiration and expiration during quiet breathing) and the inspiratory reserve volume (the additional amount of air that can be inspired over and above the tidal volume). IC is an important parameter used in pulmonary function testing to assess lung volumes and capacities in patients with respiratory disorders.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Dystrophin is a protein that provides structural stability to muscle fibers. It is an essential component of the dystrophin-glycoprotein complex, which helps maintain the integrity of the sarcolemma (the membrane surrounding muscle cells) during muscle contraction and relaxation. Dystrophin plays a crucial role in connecting the cytoskeleton of the muscle fiber to the extracellular matrix, allowing for force transmission and protecting the muscle cell from damage.

Mutations in the DMD gene, which encodes dystrophin, can lead to various forms of muscular dystrophy, including Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD). In DMD, a severe form of the disease, genetic alterations typically result in little or no production of functional dystrophin, causing progressive muscle weakness, wasting, and degeneration. In BMD, a milder form of the disorder, partially functional dystrophin is produced, leading to less severe symptoms and later onset of the disease.

Motor neurons are specialized nerve cells in the brain and spinal cord that play a crucial role in controlling voluntary muscle movements. They transmit electrical signals from the brain to the muscles, enabling us to perform actions such as walking, talking, and swallowing. There are two types of motor neurons: upper motor neurons, which originate in the brain's motor cortex and travel down to the brainstem and spinal cord; and lower motor neurons, which extend from the brainstem and spinal cord to the muscles. Damage or degeneration of these motor neurons can lead to various neurological disorders, such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA).

Spinal muscular atrophy (SMA) is a genetic disorder that affects the motor neurons in the spinal cord, leading to muscle weakness and atrophy. It is caused by a mutation in the survival motor neuron 1 (SMN1) gene, which results in a deficiency of SMN protein necessary for the survival of motor neurons.

There are several types of SMA, classified based on the age of onset and severity of symptoms. The most common type is type 1, also known as Werdnig-Hoffmann disease, which presents in infancy and is characterized by severe muscle weakness, hypotonia, and feeding difficulties. Other types include type 2 (intermediate SMA), type 3 (Kugelberg-Welander disease), and type 4 (adult-onset SMA).

The symptoms of SMA may include muscle wasting, fasciculations, weakness, hypotonia, respiratory difficulties, and mobility impairment. The diagnosis of SMA typically involves genetic testing to confirm the presence of a mutation in the SMN1 gene. Treatment options for SMA may include medications, physical therapy, assistive devices, and respiratory support.

Motor Neuron Disease (MND) is a progressive neurodegenerative disorder that affects the motor neurons, which are nerve cells in the brain and spinal cord responsible for controlling voluntary muscles involved in movement, speaking, breathing, and swallowing. As the motor neurons degenerate and die, they stop sending signals to the muscles, causing them to weaken, waste away (atrophy), and eventually lead to paralysis.

There are several types of MND, including:

1. Amyotrophic Lateral Sclerosis (ALS): Also known as Lou Gehrig's disease, this is the most common form of MND. It affects both upper and lower motor neurons, causing muscle weakness, stiffness, twitching, and atrophy throughout the body.
2. Progressive Bulbar Palsy (PBP): This type primarily affects the bulbar muscles in the brainstem, which control speech, swallowing, and chewing. Patients with PBP experience difficulties with speaking, slurred speech, and problems swallowing and may also have weak facial muscles and limb weakness.
3. Primary Lateral Sclerosis (PLS): This form of MND affects only the upper motor neurons, causing muscle stiffness, spasticity, and weakness, primarily in the legs. PLS progresses more slowly than ALS, and patients usually maintain their ability to speak and swallow for a longer period.
4. Progressive Muscular Atrophy (PMA): This type of MND affects only the lower motor neurons, causing muscle wasting, weakness, and fasciculations (muscle twitches). PMA progresses more slowly than ALS but can still be severely disabling over time.
5. Spinal Muscular Atrophy (SMA): This is a genetic form of MND that typically presents in infancy or childhood, although adult-onset forms exist. SMA affects the lower motor neurons in the spinal cord, causing muscle weakness and atrophy, primarily in the legs and trunk.

The exact cause of Motor Neuron Disease is not fully understood, but it is believed to involve a combination of genetic, environmental, and lifestyle factors. There is currently no cure for MND, and treatment focuses on managing symptoms, maintaining quality of life, and slowing disease progression through various therapies and medications.

I must clarify that the term "pedigree" is not typically used in medical definitions. Instead, it is often employed in genetics and breeding, where it refers to the recorded ancestry of an individual or a family, tracing the inheritance of specific traits or diseases. In human genetics, a pedigree can help illustrate the pattern of genetic inheritance in families over multiple generations. However, it is not a medical term with a specific clinical definition.

A sarcomere is the basic contractile unit in a muscle fiber, and it's responsible for generating the force necessary for muscle contraction. It is composed of several proteins, including actin and myosin, which slide past each other to shorten the sarcomere during contraction. The sarcomere extends from one Z-line to the next in a muscle fiber, and it is delimited by the Z-discs where actin filaments are anchored. Sarcomeres play a crucial role in the functioning of skeletal, cardiac, and smooth muscles.

Satellite cells in skeletal muscle are undifferentiated stem cells that are crucial for postnatal growth, maintenance, and repair of skeletal muscle. They are located between the basal lamina and plasma membrane of myofibers. In response to muscle damage or injury, satellite cells become activated, proliferate, differentiate into myoblasts, fuse with existing muscle fibers, and contribute to muscle regeneration. Satellite cells also play a role in maintaining muscle homeostasis by fusing with mature muscle fibers to replace damaged proteins and organelles. They are essential for the adaptation of skeletal muscle to various stimuli such as exercise or mechanical load.

A phenotype is the physical or biochemical expression of an organism's genes, or the observable traits and characteristics resulting from the interaction of its genetic constitution (genotype) with environmental factors. These characteristics can include appearance, development, behavior, and resistance to disease, among others. Phenotypes can vary widely, even among individuals with identical genotypes, due to differences in environmental influences, gene expression, and genetic interactions.

Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:

Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.

Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.

Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.

Paralysis is a loss of muscle function in part or all of your body. It can be localized, affecting only one specific area, or generalized, impacting multiple areas or even the entire body. Paralysis often occurs when something goes wrong with the way messages pass between your brain and muscles. In most cases, paralysis is caused by damage to the nervous system, especially the spinal cord. Other causes include stroke, trauma, infections, and various neurological disorders.

It's important to note that paralysis doesn't always mean a total loss of movement or feeling. Sometimes, it may just cause weakness or numbness in the affected area. The severity and extent of paralysis depend on the underlying cause and the location of the damage in the nervous system.

Myoblasts are types of cells that are responsible for the development and growth of muscle tissue in the body. They are undifferentiated cells, meaning they have not yet developed into their final form or function. Myoblasts fuse together to form myotubes, which then develop into muscle fibers, also known as myofibers. This process is called myogenesis and it plays a crucial role in the growth, repair, and maintenance of skeletal muscle tissue throughout an individual's life.

Myoblasts can be derived from various sources, including embryonic stem cells, induced pluripotent stem cells, or satellite cells, which are adult stem cells found within mature muscle tissue. Satellite cells are typically quiescent but can be activated in response to muscle damage or injury, proliferate and differentiate into myoblasts, and fuse together to repair and replace damaged muscle fibers.

Dysregulation of myogenesis and impaired myoblast function have been implicated in various muscle-related disorders, including muscular dystrophies, sarcopenia, and cachexia. Therefore, understanding the biology of myoblasts and their role in muscle development and regeneration is an important area of research with potential therapeutic implications for muscle-related diseases.

Hyperkalemic periodic paralysis (HypPK) is a rare genetic disorder characterized by episodes of muscle weakness or paralysis due to an abnormality in the ion channels that regulate the movement of potassium into and out of muscle fibers. This results in an excessive accumulation of potassium in the blood (hyperkalemia) during attacks, which can interfere with the ability of nerve cells to communicate with muscles and cause temporary muscle weakness or paralysis.

HypPK is caused by mutations in the SCN4A gene, which encodes a sodium channel protein found in skeletal muscle. These genetic changes disrupt the normal functioning of the ion channels, leading to an imbalance in the flow of ions across the muscle cell membrane and affecting muscle excitability.

Episodes of paralysis in HypPK typically begin in childhood or adolescence and can last from several hours to days. Triggers for attacks may include rest following exercise, cold or hot weather, stress, alcohol consumption, infection, or certain medications. Between episodes, individuals with HypPK usually have normal muscle strength and function.

Management of HypPK includes avoiding triggers, maintaining a low-potassium diet, and using medications to prevent or treat attacks. Medications such as thiazide diuretics, acetazolamide, or dichlorphenamide can help lower potassium levels in the blood and reduce the frequency and severity of episodes. In some cases, intravenous glucose and insulin may be used to drive potassium into cells during an attack, thereby reducing its concentration in the blood and alleviating symptoms.

Electric stimulation, also known as electrical nerve stimulation or neuromuscular electrical stimulation, is a therapeutic treatment that uses low-voltage electrical currents to stimulate nerves and muscles. It is often used to help manage pain, promote healing, and improve muscle strength and mobility. The electrical impulses can be delivered through electrodes placed on the skin or directly implanted into the body.

In a medical context, electric stimulation may be used for various purposes such as:

1. Pain management: Electric stimulation can help to block pain signals from reaching the brain and promote the release of endorphins, which are natural painkillers produced by the body.
2. Muscle rehabilitation: Electric stimulation can help to strengthen muscles that have become weak due to injury, illness, or surgery. It can also help to prevent muscle atrophy and improve range of motion.
3. Wound healing: Electric stimulation can promote tissue growth and help to speed up the healing process in wounds, ulcers, and other types of injuries.
4. Urinary incontinence: Electric stimulation can be used to strengthen the muscles that control urination and reduce symptoms of urinary incontinence.
5. Migraine prevention: Electric stimulation can be used as a preventive treatment for migraines by applying electrical impulses to specific nerves in the head and neck.

It is important to note that electric stimulation should only be administered under the guidance of a qualified healthcare professional, as improper use can cause harm or discomfort.

"Torque" is not a term that has a specific medical definition. It is a physical concept used in the fields of physics and engineering, referring to a twisting force that causes rotation around an axis. However, in certain medical contexts, such as in discussions of spinal or joint biomechanics, the term "torque" may be used to describe a rotational force applied to a body part. But generally speaking, "torque" is not a term commonly used in medical terminology.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.

Myotonic disorders are a group of genetic muscle diseases characterized by the inability to relax muscles (myotonia) after contraction. Myotonia can cause symptoms such as stiffness, muscle spasms, and prolonged muscle contractions or cramps. These disorders may also be associated with other symptoms, including muscle weakness, wasting, and various systemic features.

The most common myotonic disorder is myotonic dystrophy type 1 (DM1), which is caused by a mutation in the DMPK gene. Myotonic dystrophy type 2 (DM2) is another form of myotonic dystrophy, resulting from a mutation in the CNBP gene. These two forms of myotonic dystrophy have distinct genetic causes but share similar clinical features, such as myotonia and muscle weakness.

Other less common myotonic disorders include:

1. Myotonia congenita - A group of inherited conditions characterized by muscle stiffness from birth or early childhood. There are two main types: Thomsen's disease (autosomal dominant) and Becker's disease (autosomal recessive).
2. Paramyotonia congenita - An autosomal dominant disorder characterized by muscle stiffness triggered by cold temperatures or physical exertion.
3. Potassium-aggravated myotonia (PAM) - A rare, autosomal dominant condition with symptoms similar to paramyotonia congenita but without the cold sensitivity.
4. Myotonia fluctuans - A rare, autosomal dominant disorder characterized by fluctuating muscle stiffness and cramps.
5. Acquired myotonia - Rare cases of myotonia caused by factors other than genetic mutations, such as medication side effects or underlying medical conditions.

Myotonic disorders can significantly impact a person's quality of life, making daily activities challenging. Proper diagnosis and management are essential to help alleviate symptoms and improve overall well-being.

Neural conduction is the process by which electrical signals, known as action potentials, are transmitted along the axon of a neuron (nerve cell) to transmit information between different parts of the nervous system. This electrical impulse is generated by the movement of ions across the neuronal membrane, and it propagates down the length of the axon until it reaches the synapse, where it can then stimulate the release of neurotransmitters to communicate with other neurons or target cells. The speed of neural conduction can vary depending on factors such as the diameter of the axon, the presence of myelin sheaths (which act as insulation and allow for faster conduction), and the temperature of the environment.

Breathing exercises are a series of deliberate breathing techniques that aim to improve respiratory function, reduce stress and anxiety, and promote relaxation. These exercises can involve various methods such as deep, slow, or rhythmic breathing, often combined with other practices like pursed-lips breathing, diaphragmatic breathing, or alternate nostril breathing. By focusing on the breath and controlling its pace and depth, individuals can experience numerous health benefits, including improved lung capacity, reduced heart rate, increased oxygenation of the blood, and a greater sense of calm and well-being. Breathing exercises are often used as a complementary therapy in various medical and holistic practices, such as yoga, meditation, and stress management programs.

The pectoralis muscles are a group of chest muscles that are primarily involved in the movement and stabilization of the shoulder joint. They consist of two individual muscles: the pectoralis major and the pectoralis minor.

1. Pectoralis Major: This is the larger and more superficial of the two muscles, lying just under the skin and fat of the chest wall. It has two heads of origin - the clavicular head arises from the medial half of the clavicle (collarbone), while the sternocostal head arises from the anterior surface of the sternum (breastbone) and the upper six costal cartilages. Both heads insert onto the lateral lip of the bicipital groove of the humerus (upper arm bone). The primary actions of the pectoralis major include flexion, adduction, and internal rotation of the shoulder joint.

2. Pectoralis Minor: This is a smaller, triangular muscle that lies deep to the pectoralis major. It originates from the third, fourth, and fifth ribs near their costal cartilages and inserts onto the coracoid process of the scapula (shoulder blade). The main function of the pectoralis minor is to pull the scapula forward and downward, helping to stabilize the shoulder joint and aiding in deep inspiration during breathing.

Together, these muscles play essential roles in various movements such as pushing, pulling, and hugging, making them crucial for daily activities and athletic performance.

Respiratory insufficiency is a condition characterized by the inability of the respiratory system to maintain adequate gas exchange, resulting in an inadequate supply of oxygen and/or removal of carbon dioxide from the body. This can occur due to various causes, such as lung diseases (e.g., chronic obstructive pulmonary disease, pneumonia), neuromuscular disorders (e.g., muscular dystrophy, spinal cord injury), or other medical conditions that affect breathing mechanics and/or gas exchange.

Respiratory insufficiency can manifest as hypoxemia (low oxygen levels in the blood) and/or hypercapnia (high carbon dioxide levels in the blood). Symptoms of respiratory insufficiency may include shortness of breath, rapid breathing, fatigue, confusion, and in severe cases, loss of consciousness or even death. Treatment depends on the underlying cause and severity of the condition and may include oxygen therapy, mechanical ventilation, medications, and/or other supportive measures.

Progressive bulbar palsy (PBP) is a form of motor neuron disease (MND), also known as Amyotrophic Lateral Sclerosis (ALS). It is characterized by the progressive degeneration of the motor neurons in the brainstem, which control vital functions such as swallowing, speaking, chewing, and breathing.

In PBP, these symptoms gradually worsen over time, often resulting in severe disability and ultimately death due to respiratory failure. The progression of the disease can vary from person to person, but it typically advances more slowly than other forms of ALS. There is currently no cure for PBP or any other form of MND, and treatment is focused on managing symptoms and maintaining quality of life.

Oculopharyngeal Muscular Dystrophy (OPMD) is a genetic disorder that affects the muscles, particularly those around the eyes and throat. The medical definition of OPMD, as per the National Organization for Rare Disorders (NORD), is:

"Oculopharyngeal Muscular Dystrophy (OPMD) is an inherited neuromuscular disorder characterized by progressive weakness of specific muscle groups, particularly those around the eyes (ocular) and throat (pharyngeal). The symptoms may include drooping of the eyelids (ptosis), difficulty swallowing (dysphagia), and, in some cases, proximal limb weakness. Onset of the disorder usually occurs in adulthood, typically after age 40, but earlier onsets have been reported."

The underlying cause of OPMD is a genetic mutation that leads to the production of an abnormal protein in muscle cells, ultimately resulting in muscle degeneration and weakness.

A syndrome, in medical terms, is a set of symptoms that collectively indicate or characterize a disease, disorder, or underlying pathological process. It's essentially a collection of signs and/or symptoms that frequently occur together and can suggest a particular cause or condition, even though the exact physiological mechanisms might not be fully understood.

For example, Down syndrome is characterized by specific physical features, cognitive delays, and other developmental issues resulting from an extra copy of chromosome 21. Similarly, metabolic syndromes like diabetes mellitus type 2 involve a group of risk factors such as obesity, high blood pressure, high blood sugar, and abnormal cholesterol or triglyceride levels that collectively increase the risk of heart disease, stroke, and diabetes.

It's important to note that a syndrome is not a specific diagnosis; rather, it's a pattern of symptoms that can help guide further diagnostic evaluation and management.

A biopsy is a medical procedure in which a small sample of tissue is taken from the body to be examined under a microscope for the presence of disease. This can help doctors diagnose and monitor various medical conditions, such as cancer, infections, or autoimmune disorders. The type of biopsy performed will depend on the location and nature of the suspected condition. Some common types of biopsies include:

1. Incisional biopsy: In this procedure, a surgeon removes a piece of tissue from an abnormal area using a scalpel or other surgical instrument. This type of biopsy is often used when the lesion is too large to be removed entirely during the initial biopsy.

2. Excisional biopsy: An excisional biopsy involves removing the entire abnormal area, along with a margin of healthy tissue surrounding it. This technique is typically employed for smaller lesions or when cancer is suspected.

3. Needle biopsy: A needle biopsy uses a thin, hollow needle to extract cells or fluid from the body. There are two main types of needle biopsies: fine-needle aspiration (FNA) and core needle biopsy. FNA extracts loose cells, while a core needle biopsy removes a small piece of tissue.

4. Punch biopsy: In a punch biopsy, a round, sharp tool is used to remove a small cylindrical sample of skin tissue. This type of biopsy is often used for evaluating rashes or other skin abnormalities.

5. Shave biopsy: During a shave biopsy, a thin slice of tissue is removed from the surface of the skin using a sharp razor-like instrument. This technique is typically used for superficial lesions or growths on the skin.

After the biopsy sample has been collected, it is sent to a laboratory where a pathologist will examine the tissue under a microscope and provide a diagnosis based on their findings. The results of the biopsy can help guide further treatment decisions and determine the best course of action for managing the patient's condition.

Brachial plexus neuritis, also known as Parsonage-Turner syndrome or neuralgic amyotrophy, is a medical condition characterized by inflammation and damage to the brachial plexus. The brachial plexus is a network of nerves that originates from the spinal cord in the neck and travels down the arm, controlling movement and sensation in the shoulder, arm, and hand.

In Brachial plexus neuritis, the insulating covering of the nerves (myelin sheath) is damaged or destroyed, leading to impaired nerve function. The exact cause of this condition is not fully understood, but it can be associated with viral infections, trauma, surgery, or immunological disorders.

Symptoms of Brachial plexus neuritis may include sudden onset of severe pain in the shoulder and arm, followed by weakness or paralysis of the affected muscles. There may also be numbness, tingling, or loss of sensation in the affected areas. In some cases, recovery can occur spontaneously within a few months, while others may experience persistent weakness or disability. Treatment typically involves pain management, physical therapy, and in some cases, corticosteroids or other medications to reduce inflammation.

Facioscapulohumeral Muscular Dystrophy (FSHD) is a genetic muscle disorder characterized by the progressive weakness and wasting (atrophy) of muscles in the face, shoulders, arms, and legs. It is caused by the abnormal expression of a gene called DUX4, which is normally only active during early embryonic development. In FSHD, this gene becomes reactivated in muscle cells, leading to their degeneration and death.

The symptoms of FSHD typically begin in late childhood or adolescence, although they can also appear in adulthood. The first noticeable sign is often difficulty raising the arms above the head or a weakened grip. Over time, the muscles of the face may become affected, leading to problems with smiling, swallowing, and speaking. The muscle weakness in FSHD tends to progress slowly, but it can vary widely from person to person. Some people with FSHD may require wheelchair assistance, while others may continue to walk with only minor limitations.

FSHD is inherited in an autosomal dominant manner, which means that a child has a 50% chance of inheriting the disease-causing gene from an affected parent. However, about 30% of cases are the result of new mutations and occur in people with no family history of the disorder. Currently, there is no cure for FSHD, but various treatments can help manage its symptoms and improve quality of life. These may include physical therapy, orthotics, assistive devices, and medications to treat pain or other complications.

Respiratory aspiration is defined as the entry of foreign materials (such as food, liquids, or vomit) into the lower respiratory tract during swallowing, which includes the trachea and lungs. This can lead to respiratory complications such as pneumonia, bronchitis, or lung abscesses. Aspiration can occur in individuals with impaired swallowing function due to various conditions like neurological disorders, stroke, or anesthesia.

Muscle spasticity is a motor disorder characterized by an involuntary increase in muscle tone, leading to stiffness and difficulty in moving muscles. It is often seen in people with damage to the brain or spinal cord, such as those with cerebral palsy, multiple sclerosis, or spinal cord injuries.

In muscle spasticity, the muscles may contract excessively, causing rigid limbs, awkward movements, and abnormal postures. The severity of muscle spasticity can vary from mild stiffness to severe contractures that limit mobility and function.

Muscle spasticity is caused by an imbalance between excitatory and inhibitory signals in the central nervous system, leading to overactivity of the alpha motor neurons that control muscle contraction. This can result in hyperreflexia (overactive reflexes), clonus (rapid, rhythmic muscle contractions), and flexor or extensor spasms.

Effective management of muscle spasticity may involve a combination of physical therapy, medication, surgery, or other interventions to improve function, reduce pain, and prevent complications such as contractures and pressure sores.

Neuromuscular junction diseases are a group of disorders that affect the functioning of the neuromuscular junction, which is the site where nerve impulses are transmitted to muscles. These diseases are characterized by muscle weakness and fatigue, and can be caused by various factors such as autoimmune disorders, genetic mutations, or toxins.

Examples of neuromuscular junction diseases include myasthenia gravis, Lambert-Eaton myasthenic syndrome (LEMS), congenital myasthenic syndromes (CMS), and botulism. Myasthenia gravis is an autoimmune disorder that causes the immune system to attack the receptors in the neuromuscular junction, leading to muscle weakness and fatigue. LEMS is a rare autoimmune disorder that affects the nerve endings at the neuromuscular junction, causing muscle weakness and decreased reflexes.

Congenital myasthenic syndromes are genetic disorders that affect the functioning of the neuromuscular junction from birth, leading to muscle weakness and fatigue. Botulism is a rare but serious condition caused by the ingestion of botulinum toxin, which can lead to paralysis of the muscles due to interference with nerve impulse transmission at the neuromuscular junction.

Treatment for neuromuscular junction diseases may include medications such as cholinesterase inhibitors, immunosuppressive drugs, or plasma exchange therapy, depending on the specific diagnosis and severity of the condition.

An abnormal reflex in a medical context refers to an involuntary and exaggerated response or lack of response to a stimulus that is not expected in the normal physiological range. These responses can be indicative of underlying neurological disorders or damage to the nervous system. Examples include hyperreflexia (overactive reflexes) and hyporeflexia (underactive reflexes). The assessment of reflexes is an important part of a physical examination, as it can provide valuable information about the functioning of the nervous system.

In the context of human anatomy, the thigh is the part of the lower limb that extends from the hip to the knee. It is the upper and largest portion of the leg and is primarily composed of the femur bone, which is the longest and strongest bone in the human body, as well as several muscles including the quadriceps femoris (front thigh), hamstrings (back thigh), and adductors (inner thigh). The major blood vessels and nerves that supply the lower limb also pass through the thigh.

Desmin is a type of intermediate filament protein that is primarily found in the cardiac and skeletal muscle cells, as well as in some types of smooth muscle cells. It is an important component of the cytoskeleton, which provides structural support to the cell and helps maintain its shape. Desmin plays a crucial role in maintaining the integrity of the sarcomere, which is the basic contractile unit of the muscle fiber. Mutations in the desmin gene can lead to various forms of muscular dystrophy and other inherited muscle disorders.

NAV1.4, also known as SCN4A, is a gene that encodes for the α subunit of the voltage-gated sodium channel in humans. This channel, specifically located in the skeletal muscle, is responsible for the rapid influx of sodium ions during the initiation and propagation of action potentials, which are critical for muscle contraction.

The NAV1.4 Voltage-Gated Sodium Channel plays a crucial role in the functioning of skeletal muscles. Mutations in this gene can lead to various neuromuscular disorders such as hyperkalemic periodic paralysis, paramyotonia congenita, and potassium-aggravated myotonia, which are characterized by muscle stiffness, cramps, and episodes of weakness or paralysis.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Uranyl nitrate is not typically defined in the context of medical terminology, but it is a chemical compound with the formula UO2(NO3)2·6H2O. It is used in various industrial and laboratory applications, including as a radiographic contrast agent for visualizing blood vessels and gastrointestinal tracts. However, due to its radioactive properties and potential health hazards, its use in medical settings is highly regulated and generally not common.

It's important to note that uranyl nitrate should be handled with appropriate precautions and safety measures, as it can be harmful if ingested or inhaled, and may pose radiation risks.

Mitochondrial myopathies are a group of genetic disorders caused by mutations in the mitochondrial DNA or nuclear DNA that affect the function of the mitochondria, which are the energy-producing structures in cells. These mutations can result in impaired muscle function and other symptoms, depending on the specific type and severity of the disorder.

Mitochondrial myopathies can present at any age and can cause a range of symptoms, including muscle weakness, exercise intolerance, fatigue, muscle pain, and difficulty with coordination and balance. Some people with mitochondrial myopathies may also experience neurological symptoms such as seizures, developmental delays, and hearing or vision loss.

The diagnosis of mitochondrial myopathies typically involves a combination of clinical evaluation, muscle biopsy, genetic testing, and other diagnostic tests to assess mitochondrial function. Treatment is generally supportive and may include physical therapy, medications to manage symptoms, and nutritional support. In some cases, specific therapies such as vitamin or coenzyme Q10 supplementation may be recommended based on the underlying genetic defect.

Actin is a type of protein that forms part of the contractile apparatus in muscle cells, and is also found in various other cell types. It is a globular protein that polymerizes to form long filaments, which are important for many cellular processes such as cell division, cell motility, and the maintenance of cell shape. In muscle cells, actin filaments interact with another type of protein called myosin to enable muscle contraction. Actins can be further divided into different subtypes, including alpha-actin, beta-actin, and gamma-actin, which have distinct functions and expression patterns in the body.

Neoplasms of connective tissue are abnormal growths or tumors that develop from the cells that form the body's supportive framework, including bones, cartilage, tendons, ligaments, and other connective tissues. These neoplasms can be benign (non-cancerous) or malignant (cancerous), and they can cause various symptoms depending on their location and size.

There are several types of connective tissue neoplasms, including:

1. Fibroma: A benign tumor that arises from fibrous connective tissue.
2. Fibrosarcoma: A malignant tumor that develops from fibrous connective tissue.
3. Lipoma: A benign tumor that arises from fat cells.
4. Liposarcoma: A malignant tumor that develops from fat cells.
5. Chondroma: A benign tumor that arises from cartilage.
6. Chondrosarcoma: A malignant tumor that develops from cartilage.
7. Osteoma: A benign tumor that arises from bone.
8. Osteosarcoma: A malignant tumor that develops from bone.
9. Giant cell tumors: Benign or malignant tumors that contain many giant cells, which are large, multinucleated cells.
10. Synovial sarcoma: A malignant tumor that arises from the synovial tissue that lines joints and tendons.

Connective tissue neoplasms can cause various symptoms depending on their location and size. For example, a benign lipoma may cause a painless lump under the skin, while a malignant osteosarcoma may cause bone pain, swelling, and fractures. Treatment options for connective tissue neoplasms include surgery, radiation therapy, chemotherapy, or a combination of these approaches.

Tropomyosin is a protein that plays a crucial role in muscle contraction. It is a long, thin filamentous protein that runs along the length of actin filaments in muscle cells, forming part of the troponin-tropomyosin complex. This complex regulates the interaction between actin and myosin, which are the other two key proteins involved in muscle contraction.

In a relaxed muscle, tropomyosin blocks the myosin-binding sites on actin, preventing muscle contraction from occurring. When a signal is received to contract, calcium ions are released into the muscle cell, which binds to troponin and causes a conformational change that moves tropomyosin out of the way, exposing the myosin-binding sites on actin. This allows myosin to bind to actin and generate force, leading to muscle contraction.

Tropomyosin is composed of two alpha-helical chains that wind around each other in a coiled-coil structure. There are several isoforms of tropomyosin found in different types of muscle cells, including skeletal, cardiac, and smooth muscle. Mutations in the genes encoding tropomyosin have been associated with various inherited muscle disorders, such as hypertrophic cardiomyopathy and distal arthrogryposis.

Polyneuropathy is a medical condition that refers to the damage or dysfunction of peripheral nerves (nerves outside the brain and spinal cord) in multiple areas of the body. These nerves are responsible for transmitting sensory, motor, and autonomic signals between the central nervous system and the rest of the body.

In polyneuropathies, this communication is disrupted, leading to various symptoms depending on the type and extent of nerve damage. Commonly reported symptoms include:

1. Numbness or tingling in the hands and feet
2. Muscle weakness and cramps
3. Loss of reflexes
4. Burning or stabbing pain
5. Balance and coordination issues
6. Increased sensitivity to touch
7. Autonomic dysfunction, such as bowel, bladder, or digestive problems, and changes in blood pressure

Polyneuropathies can be caused by various factors, including diabetes, alcohol abuse, nutritional deficiencies, autoimmune disorders, infections, toxins, inherited genetic conditions, or idiopathic (unknown) causes. The treatment for polyneuropathy depends on the underlying cause and may involve managing underlying medical conditions, physical therapy, pain management, and lifestyle modifications.

The psoas muscles are a pair of muscles that are located in the lower lumbar region of the spine and run through the pelvis to attach to the femur (thigh bone). They are deep muscles, meaning they are located close to the body's core, and are surrounded by other muscles, bones, and organs.

The psoas muscles are composed of two separate muscles: the psoas major and the psoas minor. The psoas major is the larger of the two muscles and originates from the lumbar vertebrae (T12 to L5) and runs through the pelvis to attach to the lesser trochanter of the femur. The psoas minor, which is smaller and tends to be absent in some people, originates from the lower thoracic vertebrae (T12) and upper lumbar vertebrae (L1-L3) and runs down to attach to the iliac fascia and the pectineal line of the pubis.

The primary function of the psoas muscles is to flex the hip joint, which means they help to bring the knee towards the chest. They also play a role in stabilizing the lumbar spine and pelvis during movement. Tightness or weakness in the psoas muscles can contribute to lower back pain, postural issues, and difficulty with mobility and stability.

Guillain-Barré syndrome (GBS) is a rare autoimmune disorder in which the body's immune system mistakenly attacks the peripheral nervous system, leading to muscle weakness, tingling sensations, and sometimes paralysis. The peripheral nervous system includes the nerves that control our movements and transmit signals from our skin, muscles, and joints to our brain.

The onset of GBS usually occurs after a viral or bacterial infection, such as respiratory or gastrointestinal infections, or following surgery, vaccinations, or other immune system triggers. The exact cause of the immune response that leads to GBS is not fully understood.

GBS typically progresses rapidly over days or weeks, with symptoms reaching their peak within 2-4 weeks after onset. Most people with GBS experience muscle weakness that starts in the lower limbs and spreads upward to the upper body, arms, and face. In severe cases, the diaphragm and chest muscles may become weakened, leading to difficulty breathing and requiring mechanical ventilation.

The diagnosis of GBS is based on clinical symptoms, nerve conduction studies, and sometimes cerebrospinal fluid analysis. Treatment typically involves supportive care, such as pain management, physical therapy, and respiratory support if necessary. In addition, plasma exchange (plasmapheresis) or intravenous immunoglobulin (IVIG) may be used to reduce the severity of symptoms and speed up recovery.

While most people with GBS recover completely or with minimal residual symptoms, some may experience long-term disability or require ongoing medical care. The prognosis for GBS varies depending on the severity of the illness and the individual's age and overall health.

Central core myopathy is a rare genetic muscle disorder that is typically present at birth or appears in early childhood. It is characterized by the presence of distinctive rod-like structures, called cores, in the center of the muscle fibers. These cores are devoid of normal mitochondria and other organelles, which can lead to muscle weakness and wasting.

Central core myopathy is often associated with mutations in the ryanodine receptor 1 (RYR1) gene, which provides instructions for making a protein that plays a critical role in calcium signaling within muscles. Abnormalities in calcium signaling can lead to muscle weakness and wasting.

The symptoms of central core myopathy can vary widely, even among members of the same family with the same genetic mutation. Some people with this condition may have only mild muscle weakness, while others may be severely affected and have difficulty walking or performing other physical activities. The condition typically does not worsen over time, and life expectancy is usually normal. However, some people with central core myopathy may be at increased risk of malignant hyperthermia, a potentially life-threatening reaction to certain anesthetics.

Asthenia is a medical term that refers to a condition of unusual physical weakness or exhaustion that is not relieved by rest. It can be a symptom of various underlying health issues, such as infections, neurological disorders, endocrine diseases, and mental health conditions. Asthenia should not be confused with general fatigue or tiredness, as it is more severe, persistent, and debilitating.

The term "asthenia" comes from the Greek words "a" (without) and "sthenos" (strength), which together mean "without strength." In medical contexts, asthenia is often used to describe a significant decrease in muscle strength or energy levels that interferes with daily activities and reduces the overall quality of life.

Asthenia can manifest as a general feeling of weakness, fatigue, lethargy, or lack of stamina. In some cases, it may be accompanied by other symptoms such as dizziness, lightheadedness, headaches, irritability, and depression. Depending on the underlying cause, asthenia may be treated with various interventions, including medication, lifestyle changes, physical therapy, or counseling.

A hindlimb, also known as a posterior limb, is one of the pair of extremities that are located distally to the trunk in tetrapods (four-legged vertebrates) and include mammals, birds, reptiles, and amphibians. In humans and other primates, hindlimbs are equivalent to the lower limbs, which consist of the thigh, leg, foot, and toes.

The primary function of hindlimbs is locomotion, allowing animals to move from one place to another. However, they also play a role in other activities such as balance, support, and communication. In humans, the hindlimbs are responsible for weight-bearing, standing, walking, running, and jumping.

In medical terminology, the term "hindlimb" is not commonly used to describe human anatomy. Instead, healthcare professionals use terms like lower limbs or lower extremities to refer to the same region of the body. However, in comparative anatomy and veterinary medicine, the term hindlimb is still widely used to describe the corresponding structures in non-human animals.

Sufentanil is a potent, synthetic opioid analgesic that is approximately 5-10 times more potent than fentanyl and 1000 times more potent than morphine. It is primarily used for the treatment of moderate to severe pain in surgical settings, as an adjunct to anesthesia, or for obstetrical analgesia during labor and delivery.

Sufentanil works by binding to opioid receptors in the brain and spinal cord, which inhibits the transmission of pain signals to the brain. It has a rapid onset of action and a short duration of effect, making it useful for procedures that require intense analgesia for brief periods.

Like other opioids, sufentanil can cause respiratory depression, sedation, nausea, vomiting, and constipation. It should be used with caution in patients with compromised respiratory function or those who are taking other central nervous system depressants.

Aging is a complex, progressive and inevitable process of bodily changes over time, characterized by the accumulation of cellular damage and degenerative changes that eventually lead to increased vulnerability to disease and death. It involves various biological, genetic, environmental, and lifestyle factors that contribute to the decline in physical and mental functions. The medical field studies aging through the discipline of gerontology, which aims to understand the underlying mechanisms of aging and develop interventions to promote healthy aging and extend the human healthspan.

Hereditary Sensory and Motor Neuropathy (HSMN) is a group of inherited disorders that affect the peripheral nerves, which are the nerves outside the brain and spinal cord. These nerves transmit information between the brain and muscles, as well as sensations such as touch, pain, heat, and cold.

HSMN is characterized by progressive degeneration of these peripheral nerves, leading to muscle weakness, numbness, and tingling sensations, particularly in the hands and feet. The condition can also affect the autonomic nervous system, which controls involuntary functions such as heart rate, blood pressure, and digestion.

HSMN is caused by genetic mutations that are inherited from one or both parents. There are several types of HSMN, each with its own specific symptoms, severity, and pattern of inheritance. The most common form is Charcot-Marie-Tooth disease (CMT), which affects both motor and sensory nerves.

Treatment for HSMN typically focuses on managing the symptoms and preventing complications. This may include physical therapy, bracing or orthopedic surgery to support weakened muscles, pain management, and lifestyle modifications such as avoiding activities that aggravate symptoms. There is currently no cure for HSMN, but ongoing research is aimed at developing new treatments and therapies to slow or halt the progression of the disease.

Gait is a medical term used to describe the pattern of movement of the limbs during walking or running. It includes the manner or style of walking, including factors such as rhythm, speed, and step length. A person's gait can provide important clues about their physical health and neurological function, and abnormalities in gait may indicate the presence of underlying medical conditions, such as neuromuscular disorders, orthopedic problems, or injuries.

A typical human gait cycle involves two main phases: the stance phase, during which the foot is in contact with the ground, and the swing phase, during which the foot is lifted and moved forward in preparation for the next step. The gait cycle can be further broken down into several sub-phases, including heel strike, foot flat, midstance, heel off, and toe off.

Gait analysis is a specialized field of study that involves observing and measuring a person's gait pattern using various techniques, such as video recordings, force plates, and motion capture systems. This information can be used to diagnose and treat gait abnormalities, improve mobility and function, and prevent injuries.

C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.

The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.

C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.

One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.

Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.

Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disorder that affects nerve cells in the brain and spinal cord responsible for controlling voluntary muscle movements, such as speaking, walking, breathing, and swallowing. The condition is characterized by the degeneration of motor neurons in the brain (upper motor neurons) and spinal cord (lower motor neurons), leading to their death.

The term "amyotrophic" comes from the Greek words "a" meaning no or negative, "myo" referring to muscle, and "trophic" relating to nutrition. When a motor neuron degenerates and can no longer send impulses to the muscle, the muscle becomes weak and eventually atrophies due to lack of use.

The term "lateral sclerosis" refers to the hardening or scarring (sclerosis) of the lateral columns of the spinal cord, which are primarily composed of nerve fibers that carry information from the brain to the muscles.

ALS is often called Lou Gehrig's disease, named after the famous American baseball player who was diagnosed with the condition in 1939. The exact cause of ALS remains unknown, but it is believed to involve a combination of genetic and environmental factors. There is currently no cure for ALS, and treatment primarily focuses on managing symptoms and maintaining quality of life.

The progression of ALS varies from person to person, with some individuals experiencing rapid decline over just a few years, while others may have a more slow-progressing form of the disease that lasts several decades. The majority of people with ALS die from respiratory failure within 3 to 5 years after the onset of symptoms. However, approximately 10% of those affected live for 10 or more years following diagnosis.

The temporalis muscle is a fan-shaped muscle located in the lateral aspect of the head, in the temporal fossa region. It belongs to the group of muscles known as muscles of mastication, responsible for chewing movements. The temporalis muscle has its origin at the temporal fossa and inserts into the coronoid process and ramus of the mandible. Its main function is to retract the mandible and assist in closing the jaw.

The pharyngeal muscles, also known as the musculature of the pharynx, are a group of skeletal muscles that make up the walls of the pharynx, which is the part of the throat located just above the esophagus and behind the nasal and oral cavities. These muscles play a crucial role in several vital functions, including:

1. Swallowing (deglutition): The pharyngeal muscles contract in a coordinated sequence to propel food or liquids from the mouth through the pharynx and into the esophagus during swallowing.
2. Speech: The contraction and relaxation of these muscles help shape the sounds produced by the vocal cords, contributing to the production of speech.
3. Respiration: The pharyngeal muscles assist in maintaining an open airway during breathing, especially during sleep and when the upper airways are obstructed.

The pharyngeal muscles consist of three layers: the outer circular muscle layer, the middle longitudinal muscle layer, and the inner inferior constrictor muscle layer. The specific muscles that make up these layers include:

1. Superior constrictor muscle (outer circular layer)
2. Middle constrictor muscle (middle longitudinal layer)
3. Inferior constrictor muscle (inner inferior constrictor layer)
4. Stylopharyngeus muscle
5. Salpingopharyngeus muscle
6. Palatopharyngeus muscle
7. Buccinator muscle (partially contributes to the middle longitudinal layer)

These muscles work together to perform their various functions, and any dysfunction in these muscles can lead to problems like swallowing difficulties (dysphagia), speech impairments, or respiratory issues.

Exercise is defined in the medical context as a physical activity that is planned, structured, and repetitive, with the primary aim of improving or maintaining one or more components of physical fitness. Components of physical fitness include cardiorespiratory endurance, muscular strength, muscular endurance, flexibility, and body composition. Exercise can be classified based on its intensity (light, moderate, or vigorous), duration (length of time), and frequency (number of times per week). Common types of exercise include aerobic exercises, such as walking, jogging, cycling, and swimming; resistance exercises, such as weightlifting; flexibility exercises, such as stretching; and balance exercises. Exercise has numerous health benefits, including reducing the risk of chronic diseases, improving mental health, and enhancing overall quality of life.

I believe there may be some confusion in your question. "Rabbits" is a common name used to refer to the Lagomorpha species, particularly members of the family Leporidae. They are small mammals known for their long ears, strong legs, and quick reproduction.

However, if you're referring to "rabbits" in a medical context, there is a term called "rabbit syndrome," which is a rare movement disorder characterized by repetitive, involuntary movements of the fingers, resembling those of a rabbit chewing. It is also known as "finger-chewing chorea." This condition is usually associated with certain medications, particularly antipsychotics, and typically resolves when the medication is stopped or adjusted.

Pyridostigmine Bromide is a medication that belongs to the class of drugs known as cholinesterase inhibitors. It is primarily used in the treatment of myasthenia gravis, a neuromuscular disorder characterized by muscle weakness and fatigue.

Pyridostigmine works by blocking the action of acetylcholinesterase, an enzyme that breaks down acetylcholine, a neurotransmitter essential for muscle contraction. By preventing the breakdown of acetylcholine, pyridostigmine helps to increase its levels at the neuromuscular junction, thereby improving muscle strength and function.

The bromide salt form of pyridostigmine is commonly used because it is more soluble in water, which makes it easier to administer orally as a liquid or tablet. The medication's effects typically last for several hours, and its dosage may be adjusted based on the patient's response and any side effects experienced.

Common side effects of pyridostigmine include nausea, vomiting, diarrhea, increased salivation, sweating, and muscle cramps. In some cases, higher doses of the medication can lead to more severe side effects such as respiratory distress, seizures, or cardiac arrhythmias. Therefore, it is essential to monitor patients closely while they are taking pyridostigmine and adjust the dosage as necessary to minimize side effects and optimize treatment outcomes.

Vital capacity (VC) is a term used in pulmonary function tests to describe the maximum volume of air that can be exhaled after taking a deep breath. It is the sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume. In other words, it's the total amount of air you can forcibly exhale after inhaling as deeply as possible. Vital capacity is an important measurement in assessing lung function and can be reduced in conditions such as chronic obstructive pulmonary disease (COPD), asthma, and other respiratory disorders.

Transgenic mice are genetically modified rodents that have incorporated foreign DNA (exogenous DNA) into their own genome. This is typically done through the use of recombinant DNA technology, where a specific gene or genetic sequence of interest is isolated and then introduced into the mouse embryo. The resulting transgenic mice can then express the protein encoded by the foreign gene, allowing researchers to study its function in a living organism.

The process of creating transgenic mice usually involves microinjecting the exogenous DNA into the pronucleus of a fertilized egg, which is then implanted into a surrogate mother. The offspring that result from this procedure are screened for the presence of the foreign DNA, and those that carry the desired genetic modification are used to establish a transgenic mouse line.

Transgenic mice have been widely used in biomedical research to model human diseases, study gene function, and test new therapies. They provide a valuable tool for understanding complex biological processes and developing new treatments for a variety of medical conditions.

Myotonia Congenita is a genetic muscle disorder characterized by delayed relaxation after voluntary muscle contraction, leading to stiffness or difficulty in relaxing the muscles following use. This muscle stiffness is called myotonia and can be aggravated by voluntary muscle action, such as handgrip or walking, and also occurs after periods of rest.

There are two main forms of Myotonia Congenita: Thomsen's disease (autosomal dominant inheritance) and Becker's disease (autosomal recessive inheritance). The disorder is caused by mutations in the CLCN1 gene, which encodes a chloride channel that helps regulate muscle excitability.

Myotonia Congenita primarily affects skeletal muscles, causing stiffness and cramping, but it does not typically affect muscle strength or size. Symptoms usually begin in childhood and may improve with repeated muscle use (warm-up phenomenon). Treatment options include medication to reduce muscle stiffness and physical therapy to maintain muscle flexibility and strength.

Edrophonium is a type of medication called an anticholinesterase agent. It works by blocking the breakdown of acetylcholine, a neurotransmitter in the body that is important for muscle contraction. This results in an increase in the amount of acetylcholine available to stimulate muscle contraction.

Edrophonium is used as a diagnostic aid in the diagnosis of myasthenia gravis, a neuromuscular disorder characterized by muscle weakness and fatigue. It is also used to reverse the effects of non-depolarizing muscle relaxants, which are medications that are sometimes given during surgery to temporarily paralyze muscles.

Edrophonium is administered intravenously (through a vein) and its effects usually begin within 30 seconds to 1 minute after injection and last for about 5 to 10 minutes. Common side effects of edrophonium include sweating, increased salivation, and muscle twitching. More serious side effects, such as seizures or cardiac arrest, can occur but are rare.

It is important to note that edrophonium should only be used under the supervision of a healthcare professional, as it can cause serious side effects if not used properly.

Physical endurance is the ability of an individual to withstand and resist physical fatigue over prolonged periods of strenuous activity, exercise, or exertion. It involves the efficient functioning of various body systems, including the cardiovascular system (heart, blood vessels, and blood), respiratory system (lungs and airways), and musculoskeletal system (muscles, bones, tendons, ligaments, and cartilage).

Physical endurance is often measured in terms of aerobic capacity or stamina, which refers to the body's ability to supply oxygen to muscles during sustained physical activity. It can be improved through regular exercise, such as running, swimming, cycling, or weightlifting, that challenges the body's major muscle groups and raises the heart rate for extended periods.

Factors that influence physical endurance include genetics, age, sex, fitness level, nutrition, hydration, sleep quality, stress management, and overall health status. It is essential to maintain good physical endurance to perform daily activities efficiently, reduce the risk of chronic diseases, and enhance overall well-being.

Sensation disorders are conditions that affect the nervous system's ability to receive and interpret sensory information from the environment. These disorders can affect any of the five senses, including sight, hearing, touch, taste, and smell. They can result in symptoms such as numbness, tingling, pain, or loss of sensation in various parts of the body.

Some common types of sensation disorders include:

1. Neuropathy: A disorder that affects the nerves, often causing numbness, tingling, or pain in the hands and feet.
2. Central pain syndrome: A condition that results from damage to the brain or spinal cord, leading to chronic pain.
3. Tinnitus: A ringing or buzzing sound in the ears that can be a symptom of an underlying hearing disorder.
4. Ageusia: The loss of taste sensation, often caused by damage to the tongue or nerves that transmit taste information to the brain.
5. Anosmia: The loss of smell sensation, which can result from a variety of causes including injury, infection, or neurological disorders.

Sensation disorders can have significant impacts on a person's quality of life and ability to perform daily activities. Treatment may involve medication, physical therapy, or other interventions aimed at addressing the underlying cause of the disorder.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

Quadriplegia, also known as tetraplegia, is a medical condition characterized by paralysis affecting all four limbs and the trunk of the body. It results from damage to the cervical spinal cord, typically at levels C1-C8, which controls signals to the muscles in the arms, hands, trunk, legs, and pelvic organs. The extent of quadriplegia can vary widely, ranging from weakness to complete loss of movement and sensation below the level of injury. Other symptoms may include difficulty breathing, bowel and bladder dysfunction, and sexual dysfunction. The severity and prognosis depend on the location and extent of the spinal cord injury.

Resistance training is a form of exercise that involves working your muscles against some form of external resistance, such as free weights, resistance bands, or your own body weight. The goal of resistance training is to increase muscle strength, power, endurance, and size. It can also help improve overall physical function, bone density, and metabolic health.

In a medical context, resistance training may be recommended as part of a treatment plan for various conditions, such as chronic pain, arthritis, or mobility limitations. When performed regularly and with proper form, resistance training can help reduce symptoms, improve functional ability, and enhance quality of life for individuals with these conditions.

It is important to note that resistance training should be tailored to the individual's fitness level, goals, and any medical considerations. It is always recommended to consult with a healthcare provider or a qualified fitness professional before starting a new exercise program.

Sarcoglycans are a group of proteins that are part of the dystrophin-glycoprotein complex in muscle cells. This complex helps to maintain the structural integrity of the muscle fiber by forming a link between the cytoskeleton and the extracellular matrix. Sarcoglycans are located on the surface of the muscle fiber and play a critical role in protecting the muscle from damage during contraction.

There are four main sarcoglycans, known as alpha, beta, gamma, and delta-sarcoglycan. Mutations in any one of these proteins can lead to a group of genetic disorders known as the sarcoglycanopathies, which are characterized by progressive muscle weakness and wasting. The most severe form of this disorder is called limb-girdle muscular dystrophy type 2C (LGMD2C), which is caused by mutations in the gamma-sarcoglycan gene.

In addition to their role in muscle cells, sarcoglycans have also been found to be expressed in other tissues, including the brain and the lungs, suggesting that they may have additional functions beyond their structural role in muscle.

Brachial plexus neuropathies refer to a group of conditions that affect the brachial plexus, which is a network of nerves that originates from the spinal cord in the neck and travels down the arm. These nerves are responsible for providing motor and sensory function to the shoulder, arm, and hand.

Brachial plexus neuropathies can occur due to various reasons, including trauma, compression, inflammation, or tumors. The condition can cause symptoms such as pain, numbness, weakness, or paralysis in the affected arm and hand.

The specific medical definition of brachial plexus neuropathies is:

"A group of conditions that affect the brachial plexus, characterized by damage to the nerves that results in motor and/or sensory impairment of the upper limb. The condition can be congenital or acquired, with causes including trauma, compression, inflammation, or tumors."

Medical Definition:

Magnetic Resonance Imaging (MRI) is a non-invasive diagnostic imaging technique that uses a strong magnetic field and radio waves to create detailed cross-sectional or three-dimensional images of the internal structures of the body. The patient lies within a large, cylindrical magnet, and the scanner detects changes in the direction of the magnetic field caused by protons in the body. These changes are then converted into detailed images that help medical professionals to diagnose and monitor various medical conditions, such as tumors, injuries, or diseases affecting the brain, spinal cord, heart, blood vessels, joints, and other internal organs. MRI does not use radiation like computed tomography (CT) scans.

Collagen Type VI is a type of collagen that is widely expressed in various tissues, including skeletal muscle, skin, and blood vessels. It is a major component of the extracellular matrix and plays important roles in maintaining tissue structure and function. Collagen Type VI forms microfilaments that provide structural support to the basement membrane and regulate cell-matrix interactions. Mutations in the genes encoding collagen Type VI can lead to several inherited connective tissue disorders, such as Bethlem myopathy and Ullrich congenital muscular dystrophy.

A contracture, in a medical context, refers to the abnormal shortening and hardening of muscles, tendons, or other tissue, which can result in limited mobility and deformity of joints. This condition can occur due to various reasons such as injury, prolonged immobilization, scarring, neurological disorders, or genetic conditions.

Contractures can cause significant impairment in daily activities and quality of life, making it difficult for individuals to perform routine tasks like dressing, bathing, or walking. Treatment options may include physical therapy, splinting, casting, medications, surgery, or a combination of these approaches, depending on the severity and underlying cause of the contracture.

A motor endplate, also known as the neuromuscular junction, is the site where a motor neuron's axon terminal synapses with a muscle fiber. It is a specialized chemical synapse that allows for the transmission of electrical signals from the nervous system to the skeletal muscles, resulting in muscle contraction. The motor endplate is composed of several structures including the presynaptic membrane, which contains neurotransmitter-filled vesicles, and the postsynaptic membrane, which contains numerous nicotinic acetylcholine receptors. When an action potential reaches the axon terminal, it triggers the release of acetylcholine into the synaptic cleft, where it binds to receptors on the postsynaptic membrane and causes the opening of ion channels, leading to the generation of an endplate potential that can trigger muscle contraction.

Peripheral Nervous System (PNS) diseases, also known as Peripheral Neuropathies, refer to conditions that affect the functioning of the peripheral nervous system, which includes all the nerves outside the brain and spinal cord. These nerves transmit signals between the central nervous system (CNS) and the rest of the body, controlling sensations, movements, and automatic functions such as heart rate and digestion.

PNS diseases can be caused by various factors, including genetics, infections, toxins, metabolic disorders, trauma, or autoimmune conditions. The symptoms of PNS diseases depend on the type and extent of nerve damage but often include:

1. Numbness, tingling, or pain in the hands and feet
2. Muscle weakness or cramps
3. Loss of reflexes
4. Decreased sensation to touch, temperature, or vibration
5. Coordination problems and difficulty with balance
6. Sexual dysfunction
7. Digestive issues, such as constipation or diarrhea
8. Dizziness or fainting due to changes in blood pressure

Examples of PNS diseases include Guillain-Barre syndrome, Charcot-Marie-Tooth disease, diabetic neuropathy, and peripheral nerve injuries. Treatment for these conditions varies depending on the underlying cause but may involve medications, physical therapy, lifestyle changes, or surgery.

Respiratory Function Tests (RFTs) are a group of medical tests that measure how well your lungs take in and exhale air, and how well they transfer oxygen and carbon dioxide into and out of your blood. They can help diagnose certain lung disorders, measure the severity of lung disease, and monitor response to treatment.

RFTs include several types of tests, such as:

1. Spirometry: This test measures how much air you can exhale and how quickly you can do it. It's often used to diagnose and monitor conditions like asthma, chronic obstructive pulmonary disease (COPD), and other lung diseases.
2. Lung volume testing: This test measures the total amount of air in your lungs. It can help diagnose restrictive lung diseases, such as pulmonary fibrosis or sarcoidosis.
3. Diffusion capacity testing: This test measures how well oxygen moves from your lungs into your bloodstream. It's often used to diagnose and monitor conditions like pulmonary fibrosis, interstitial lung disease, and other lung diseases that affect the ability of the lungs to transfer oxygen to the blood.
4. Bronchoprovocation testing: This test involves inhaling a substance that can cause your airways to narrow, such as methacholine or histamine. It's often used to diagnose and monitor asthma.
5. Exercise stress testing: This test measures how well your lungs and heart work together during exercise. It's often used to diagnose lung or heart disease.

Overall, Respiratory Function Tests are an important tool for diagnosing and managing a wide range of lung conditions.

The term "extremities" in a medical context refers to the most distant parts of the body, including the hands and feet (both fingers and toes), as well as the arms and legs. These are the farthest parts from the torso and head. Medical professionals may examine a patient's extremities for various reasons, such as checking circulation, assessing nerve function, or looking for injuries or abnormalities.

Immunohistochemistry (IHC) is a technique used in pathology and laboratory medicine to identify specific proteins or antigens in tissue sections. It combines the principles of immunology and histology to detect the presence and location of these target molecules within cells and tissues. This technique utilizes antibodies that are specific to the protein or antigen of interest, which are then tagged with a detection system such as a chromogen or fluorophore. The stained tissue sections can be examined under a microscope, allowing for the visualization and analysis of the distribution and expression patterns of the target molecule in the context of the tissue architecture. Immunohistochemistry is widely used in diagnostic pathology to help identify various diseases, including cancer, infectious diseases, and immune-mediated disorders.

Cholinesterase inhibitors are a class of drugs that work by blocking the action of cholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine in the body. By inhibiting this enzyme, the levels of acetylcholine in the brain increase, which can help to improve symptoms of cognitive decline and memory loss associated with conditions such as Alzheimer's disease and other forms of dementia.

Cholinesterase inhibitors are also used to treat other medical conditions, including myasthenia gravis, a neuromuscular disorder that causes muscle weakness, and glaucoma, a condition that affects the optic nerve and can lead to vision loss. Some examples of cholinesterase inhibitors include donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon).

It's important to note that while cholinesterase inhibitors can help to improve symptoms in some people with dementia, they do not cure the underlying condition or stop its progression. Side effects of these drugs may include nausea, vomiting, diarrhea, and increased salivation. In rare cases, they may also cause seizures, fainting, or cardiac arrhythmias.

"Motor activity" is a general term used in the field of medicine and neuroscience to refer to any kind of physical movement or action that is generated by the body's motor system. The motor system includes the brain, spinal cord, nerves, and muscles that work together to produce movements such as walking, talking, reaching for an object, or even subtle actions like moving your eyes.

Motor activity can be voluntary, meaning it is initiated intentionally by the individual, or involuntary, meaning it is triggered automatically by the nervous system without conscious control. Examples of voluntary motor activity include deliberately lifting your arm or kicking a ball, while examples of involuntary motor activity include heartbeat, digestion, and reflex actions like jerking your hand away from a hot stove.

Abnormalities in motor activity can be a sign of neurological or muscular disorders, such as Parkinson's disease, cerebral palsy, or multiple sclerosis. Assessment of motor activity is often used in the diagnosis and treatment of these conditions.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

Urodynamics is a medical test that measures the function and performance of the lower urinary tract, which includes the bladder, urethra, and sphincters. It involves the use of specialized equipment to record measurements such as bladder pressure, urine flow rate, and residual urine volume. The test can help diagnose various urinary problems, including incontinence, urinary retention, and overactive bladder.

During the test, a small catheter is inserted into the bladder through the urethra to measure bladder pressure while filling it with sterile water or saline solution. Another catheter may be placed in the rectum to record abdominal pressure. The patient is then asked to urinate, and the flow rate and any leaks are recorded.

Urodynamics can help identify the underlying cause of urinary symptoms and guide treatment decisions. It is often recommended for patients with complex or persistent urinary problems that have not responded to initial treatments.

Paraneoplastic syndromes refer to a group of rare disorders that are caused by an abnormal immune system response to a cancerous (malignant) tumor. These syndromes are characterized by symptoms or signs that do not result directly from the growth of the tumor itself, but rather from substances produced by the tumor or the body's immune system in response to the tumor.

Paraneoplastic syndromes can affect various organs and systems in the body, including the nervous system, endocrine system, skin, and joints. Examples of paraneoplastic syndromes include Lambert-Eaton myasthenic syndrome (LEMS), which affects nerve function and causes muscle weakness; cerebellar degeneration, which can cause difficulty with coordination and balance; and dermatomyositis, which is an inflammatory condition that affects the skin and muscles.

Paraneoplastic syndromes can occur in association with a variety of different types of cancer, including lung cancer, breast cancer, ovarian cancer, and lymphoma. Treatment typically involves addressing the underlying cancer, as well as managing the symptoms of the paraneoplastic syndrome.

Exercise tolerance is a term used to describe the ability of an individual to perform physical activity or exercise without experiencing symptoms such as shortness of breath, chest pain, or undue fatigue. It is often used as a measure of cardiovascular fitness and can be assessed through various tests, such as a stress test or a six-minute walk test. Exercise intolerance may indicate the presence of underlying medical conditions, such as heart disease, lung disease, or deconditioning.

In medical terms, the hip is a ball-and-socket joint where the rounded head of the femur (thigh bone) fits into the cup-shaped socket, also known as the acetabulum, of the pelvis. This joint allows for a wide range of movement in the lower extremities and supports the weight of the upper body during activities such as walking, running, and jumping. The hip joint is surrounded by strong ligaments, muscles, and tendons that provide stability and enable proper functioning.

The "age of onset" is a medical term that refers to the age at which an individual first develops or displays symptoms of a particular disease, disorder, or condition. It can be used to describe various medical conditions, including both physical and mental health disorders. The age of onset can have implications for prognosis, treatment approaches, and potential causes of the condition. In some cases, early onset may indicate a more severe or progressive course of the disease, while late-onset symptoms might be associated with different underlying factors or etiologies. It is essential to provide accurate and precise information regarding the age of onset when discussing a patient's medical history and treatment plan.

Dyspnea is defined as difficulty or discomfort in breathing, often described as shortness of breath. It can range from mild to severe, and may occur during rest, exercise, or at any time. Dyspnea can be caused by various medical conditions, including heart and lung diseases, anemia, and neuromuscular disorders. It is important to seek medical attention if experiencing dyspnea, as it can be a sign of a serious underlying condition.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

Oxygen consumption, also known as oxygen uptake, is the amount of oxygen that is consumed or utilized by the body during a specific period of time, usually measured in liters per minute (L/min). It is a common measurement used in exercise physiology and critical care medicine to assess an individual's aerobic metabolism and overall health status.

In clinical settings, oxygen consumption is often measured during cardiopulmonary exercise testing (CPET) to evaluate cardiovascular function, pulmonary function, and exercise capacity in patients with various medical conditions such as heart failure, chronic obstructive pulmonary disease (COPD), and other respiratory or cardiac disorders.

During exercise, oxygen is consumed by the muscles to generate energy through a process called oxidative phosphorylation. The amount of oxygen consumed during exercise can provide important information about an individual's fitness level, exercise capacity, and overall health status. Additionally, measuring oxygen consumption can help healthcare providers assess the effectiveness of treatments and rehabilitation programs in patients with various medical conditions.

Triamterene is a potassium-sparing diuretic (a type of "water pill") that is used to treat fluid retention (edema) and high blood pressure. It works by preventing your body from absorbing too much salt and keeps your potassium levels from getting too low.

The medical definition of Triamterene, according to the National Library of Medicine's MedlinePlus, is: "A medication that helps to reduce the amount of fluid in the body by increasing the amount of urine produced. It is used to treat high blood pressure and edema (fluid retention)."

Triamterene is available only with a prescription and is typically taken by mouth in the form of a tablet, usually two or three times a day after meals. Common side effects include headache, dizziness, and stomach upset. It is important to follow your healthcare provider's instructions carefully when taking this medication, as it can have serious interactions with other medications and may cause an imbalance of electrolytes in the body if not used properly.

Hypoventilation is a medical condition that refers to the decreased rate and depth of breathing, which leads to an inadequate exchange of oxygen and carbon dioxide in the lungs. As a result, there is an increase in the levels of carbon dioxide (hypercapnia) and a decrease in the levels of oxygen (hypoxemia) in the blood. Hypoventilation can occur due to various reasons such as respiratory muscle weakness, sedative or narcotic overdose, chest wall deformities, neuromuscular disorders, obesity hypoventilation syndrome, and sleep-disordered breathing. Prolonged hypoventilation can lead to serious complications such as respiratory failure, cardiac arrhythmias, and even death.

Multiple Acyl Coenzyme A Dehydrogenase Deficiency (MADD) is a rare inherited metabolic disorder that affects the body's ability to break down certain fats and proteins. It is caused by mutations in genes that code for enzymes involved in the electron transfer flavoprotein-ubiquinone (ETF-QO) complex, which is responsible for transferring electrons from various acyl-CoA dehydrogenases to the electron transport chain during fatty acid and amino acid oxidation.

As a result of these genetic defects, there is a buildup of unoxidized acyl-CoA molecules in the body, leading to the accumulation of toxic intermediates that can damage organs and tissues. This can cause a wide range of symptoms, including hypoglycemia, metabolic acidosis, cardiac arrhythmias, muscle weakness, and developmental delays.

MADD is typically classified into three types based on the age of onset and severity of symptoms: neonatal, infantile, and late-onset. The neonatal form is the most severe and often leads to death in early infancy, while the infantile and late-onset forms can present with milder symptoms that may not become apparent until later in life.

Treatment for MADD typically involves a combination of dietary modifications, such as restricting long-chain fatty acids and supplementing with medium-chain triglycerides, and oral supplementation with riboflavin (vitamin B2), which has been shown to improve the activity of the ETF-QO complex in some cases.

A "knockout" mouse is a genetically engineered mouse in which one or more genes have been deleted or "knocked out" using molecular biology techniques. This allows researchers to study the function of specific genes and their role in various biological processes, as well as potential associations with human diseases. The mice are generated by introducing targeted DNA modifications into embryonic stem cells, which are then used to create a live animal. Knockout mice have been widely used in biomedical research to investigate gene function, disease mechanisms, and potential therapeutic targets.

'Gene expression regulation' refers to the processes that control whether, when, and where a particular gene is expressed, meaning the production of a specific protein or functional RNA encoded by that gene. This complex mechanism can be influenced by various factors such as transcription factors, chromatin remodeling, DNA methylation, non-coding RNAs, and post-transcriptional modifications, among others. Proper regulation of gene expression is crucial for normal cellular function, development, and maintaining homeostasis in living organisms. Dysregulation of gene expression can lead to various diseases, including cancer and genetic disorders.

Neuromuscular blocking agents (NMBAs) are a class of drugs that act on the neuromuscular junction, the site where nerve impulses transmit signals to muscles to cause contraction. NMBAs prevent the transmission of these signals, leading to muscle paralysis. They are used in medical settings during surgical procedures and mechanical ventilation to facilitate intubation, control ventilation, and prevent patient movement. It is important to note that NMBAs do not have any effect on consciousness or pain perception; therefore, they are always used in conjunction with anesthetics and analgesics.

NMBAs can be classified into two main categories based on their mechanism of action:

1. Depolarizing Neuromuscular Blocking Agents: These drugs, such as succinylcholine, cause muscle fasciculations (brief, involuntary contractions) before inducing paralysis. They work by binding to the acetylcholine receptors at the neuromuscular junction and depolarizing the membrane, which results in muscle paralysis. However, the continuous depolarization also causes desensitization of the receptors, leading to a loss of effectiveness over time. Depolarizing NMBAs have a relatively short duration of action.
2. Non-depolarizing Neuromuscular Blocking Agents: These drugs, such as rocuronium, vecuronium, and pancuronium, do not cause muscle fasciculations. They work by binding to the acetylcholine receptors at the neuromuscular junction without depolarizing the membrane, which prevents the transmission of nerve impulses to muscles and leads to paralysis. Non-depolarizing NMBAs have a longer duration of action compared to depolarizing NMBAs.

Close monitoring of neuromuscular function is essential when using NMBAs to ensure adequate reversal of their effects before the patient regains consciousness. This can be achieved through the use of nerve stimulators, which assess the degree of blockade and help guide the administration of reversal agents when necessary.

Myasthenia gravis is a neuromuscular disorder characterized by muscle weakness and fatigability. In autoimmune myasthenia gravis, the immune system produces antibodies that attack the receptors at the junction between the nerve and muscle (the neuromuscular junction), impairing communication between the nerve and muscle and leading to muscle weakness.

The term "experimental" in this context typically refers to a research setting where the condition is being studied, rather than a specific medical definition for a type of myasthenia gravis. Experiments may involve investigating new treatment approaches, understanding the underlying mechanisms of the disease, or exploring potential causes and risk factors.

Therefore, 'Myasthenia Gravis, Autoimmune, Experimental' generally means that researchers are studying autoimmune myasthenia gravis in an experimental setting to advance our knowledge and develop better treatment strategies for this condition.

Lung volume measurements are clinical tests that determine the amount of air inhaled, exhaled, and present in the lungs at different times during the breathing cycle. These measurements include:

1. Tidal Volume (TV): The amount of air inhaled or exhaled during normal breathing, usually around 500 mL in resting adults.
2. Inspiratory Reserve Volume (IRV): The additional air that can be inhaled after a normal inspiration, approximately 3,000 mL in adults.
3. Expiratory Reserve Volume (ERV): The extra air that can be exhaled after a normal expiration, about 1,000-1,200 mL in adults.
4. Residual Volume (RV): The air remaining in the lungs after a maximal exhalation, approximately 1,100-1,500 mL in adults.
5. Total Lung Capacity (TLC): The total amount of air the lungs can hold at full inflation, calculated as TV + IRV + ERV + RV, around 6,000 mL in adults.
6. Functional Residual Capacity (FRC): The volume of air remaining in the lungs after a normal expiration, equal to ERV + RV, about 2,100-2,700 mL in adults.
7. Inspiratory Capacity (IC): The maximum amount of air that can be inhaled after a normal expiration, equal to TV + IRV, around 3,500 mL in adults.
8. Vital Capacity (VC): The total volume of air that can be exhaled after a maximal inspiration, calculated as IC + ERV, approximately 4,200-5,600 mL in adults.

These measurements help assess lung function and identify various respiratory disorders such as chronic obstructive pulmonary disease (COPD), asthma, and restrictive lung diseases.

In medical terms, pressure is defined as the force applied per unit area on an object or body surface. It is often measured in millimeters of mercury (mmHg) in clinical settings. For example, blood pressure is the force exerted by circulating blood on the walls of the arteries and is recorded as two numbers: systolic pressure (when the heart beats and pushes blood out) and diastolic pressure (when the heart rests between beats).

Pressure can also refer to the pressure exerted on a wound or incision to help control bleeding, or the pressure inside the skull or spinal canal. High or low pressure in different body systems can indicate various medical conditions and require appropriate treatment.

Glycogen is a complex carbohydrate that serves as the primary form of energy storage in animals, fungi, and bacteria. It is a polysaccharide consisting of long, branched chains of glucose molecules linked together by glycosidic bonds. Glycogen is stored primarily in the liver and muscles, where it can be quickly broken down to release glucose into the bloodstream during periods of fasting or increased metabolic demand.

In the liver, glycogen plays a crucial role in maintaining blood glucose levels by releasing glucose when needed, such as between meals or during exercise. In muscles, glycogen serves as an immediate energy source for muscle contractions during intense physical activity. The ability to store and mobilize glycogen is essential for the proper functioning of various physiological processes, including athletic performance, glucose homeostasis, and overall metabolic health.

The sarcoplasmic reticulum (SR) is a specialized type of smooth endoplasmic reticulum found in muscle cells, particularly in striated muscles such as skeletal and cardiac muscles. It is a complex network of tubules that surrounds the myofibrils, the contractile elements of the muscle fiber.

The primary function of the sarcoplasmic reticulum is to store calcium ions (Ca2+) and regulate their release during muscle contraction and uptake during muscle relaxation. The SR contains a high concentration of calcium-binding proteins, such as calsequestrin, which help to maintain this storage.

The release of calcium ions from the sarcoplasmic reticulum is triggered by an action potential that travels along the muscle fiber's sarcolemma and into the muscle fiber's interior (the sarcoplasm). This action potential causes the voltage-gated calcium channels in the SR membrane, known as ryanodine receptors, to open, releasing Ca2+ ions into the sarcoplasm.

The increased concentration of Ca2+ ions in the sarcoplasm triggers muscle contraction by binding to troponin, a protein associated with actin filaments, causing a conformational change that exposes the active sites on actin for myosin heads to bind and generate force.

After muscle contraction, the calcium ions must be actively transported back into the sarcoplasmic reticulum by Ca2+ ATPase pumps, also known as sarco(endo)plasmic reticulum calcium ATPases (SERCAs). This process helps to lower the concentration of Ca2+ in the sarcoplasm and allows the muscle fiber to relax.

Overall, the sarcoplasmic reticulum plays a crucial role in excitation-contraction coupling, the process by which action potentials trigger muscle contraction.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

In medical terms, the leg refers to the lower portion of the human body that extends from the knee down to the foot. It includes the thigh (femur), lower leg (tibia and fibula), foot, and ankle. The leg is primarily responsible for supporting the body's weight and enabling movements such as standing, walking, running, and jumping.

The leg contains several important structures, including bones, muscles, tendons, ligaments, blood vessels, nerves, and joints. These structures work together to provide stability, support, and mobility to the lower extremity. Common medical conditions that can affect the leg include fractures, sprains, strains, infections, peripheral artery disease, and neurological disorders.

Electron microscopy (EM) is a type of microscopy that uses a beam of electrons to create an image of the sample being examined, resulting in much higher magnification and resolution than light microscopy. There are several types of electron microscopy, including transmission electron microscopy (TEM), scanning electron microscopy (SEM), and reflection electron microscopy (REM).

In TEM, a beam of electrons is transmitted through a thin slice of the sample, and the electrons that pass through the sample are focused to form an image. This technique can provide detailed information about the internal structure of cells, viruses, and other biological specimens, as well as the composition and structure of materials at the atomic level.

In SEM, a beam of electrons is scanned across the surface of the sample, and the electrons that are scattered back from the surface are detected to create an image. This technique can provide information about the topography and composition of surfaces, as well as the structure of materials at the microscopic level.

REM is a variation of SEM in which the beam of electrons is reflected off the surface of the sample, rather than scattered back from it. This technique can provide information about the surface chemistry and composition of materials.

Electron microscopy has a wide range of applications in biology, medicine, and materials science, including the study of cellular structure and function, disease diagnosis, and the development of new materials and technologies.

Prednisolone is a synthetic glucocorticoid drug, which is a class of steroid hormones. It is commonly used in the treatment of various inflammatory and autoimmune conditions due to its potent anti-inflammatory and immunosuppressive effects. Prednisolone works by binding to specific receptors in cells, leading to changes in gene expression that reduce the production of substances involved in inflammation, such as cytokines and prostaglandins.

Prednisolone is available in various forms, including tablets, syrups, and injectable solutions. It can be used to treat a wide range of medical conditions, including asthma, rheumatoid arthritis, inflammatory bowel disease, allergies, skin conditions, and certain types of cancer.

Like other steroid medications, prednisolone can have significant side effects if used in high doses or for long periods of time. These may include weight gain, mood changes, increased risk of infections, osteoporosis, diabetes, and adrenal suppression. As a result, the use of prednisolone should be closely monitored by a healthcare professional to ensure that its benefits outweigh its risks.

Paresis is a medical term that refers to a partial loss of voluntary muscle function. It is often described as muscle weakness, and it can affect one or several parts of the body. Paresis can be caused by various conditions, including nerve damage, stroke, spinal cord injuries, multiple sclerosis, and infections like polio or botulism. The severity of paresis can range from mild to severe, depending on the underlying cause and the specific muscles involved. Treatment for paresis typically focuses on addressing the underlying condition causing it.

Carnitine is a naturally occurring substance in the body that plays a crucial role in energy production. It transports long-chain fatty acids into the mitochondria, where they can be broken down to produce energy. Carnitine is also available as a dietary supplement and is often used to treat or prevent carnitine deficiency.

The medical definition of Carnitine is:

"A quaternary ammonium compound that occurs naturally in animal tissues, especially in muscle, heart, brain, and liver. It is essential for the transport of long-chain fatty acids into the mitochondria, where they can be oxidized to produce energy. Carnitine also functions as an antioxidant and has been studied as a potential treatment for various conditions, including heart disease, diabetes, and kidney disease."

Carnitine is also known as L-carnitine or levocarnitine. It can be found in foods such as red meat, dairy products, fish, poultry, and tempeh. In the body, carnitine is synthesized from the amino acids lysine and methionine with the help of vitamin C and iron. Some people may have a deficiency in carnitine due to genetic factors, malnutrition, or certain medical conditions, such as kidney disease or liver disease. In these cases, supplementation may be necessary to prevent or treat symptoms of carnitine deficiency.

Spinal muscular atrophies (SMAs) of childhood are a group of inherited neuromuscular disorders characterized by degeneration and loss of lower motor neurons in the spinal cord, leading to progressive muscle weakness and atrophy. The severity and age of onset can vary significantly, with some forms presenting in infancy and others in later childhood or even adulthood.

The most common form of SMA is 5q autosomal recessive SMA, also known as survival motor neuron (SMN) disease, which results from mutations in the SMN1 gene. The severity of this form can range from severe (type I or Werdnig-Hoffmann disease), intermediate (type II or chronic infantile neurodegenerative disorder), to mild (type III or Kugelberg-Welander disease).

Type I SMA is the most severe form, with onset before 6 months of age and rapid progression leading to death within the first two years of life if left untreated. Type II SMA has an onset between 6 and 18 months of age, with affected children never achieving the ability to walk independently. Type III SMA has a later onset, typically after 18 months of age, and is characterized by a slower progression, allowing for the ability to walk unaided, although mobility may be lost over time.

Other forms of childhood-onset SMA include autosomal dominant distal SMA, X-linked SMA, and spinal bulbar muscular atrophy (SBMA or Kennedy's disease). These forms have distinct genetic causes and clinical presentations.

In general, SMAs are characterized by muscle weakness, hypotonia, fasciculations, tongue atrophy, and depressed or absent deep tendon reflexes. Respiratory and nutritional support is often required in more severe cases. Recent advances in gene therapy have led to the development of disease-modifying treatments for some forms of SMA.

Fatigue is a state of feeling very tired, weary, or exhausted, which can be physical, mental, or both. It is a common symptom that can be caused by various factors, including lack of sleep, poor nutrition, stress, medical conditions (such as anemia, diabetes, heart disease, or cancer), medications, and substance abuse. Fatigue can also be a symptom of depression or other mental health disorders. In medical terms, fatigue is often described as a subjective feeling of tiredness that is not proportional to recent activity levels and interferes with usual functioning. It is important to consult a healthcare professional if experiencing persistent or severe fatigue to determine the underlying cause and develop an appropriate treatment plan.

Pharyngeal diseases refer to conditions that affect the pharynx, which is the part of the throat that lies behind the nasal cavity and mouth, and above the esophagus and larynx. The pharynx plays a crucial role in swallowing, speaking, and breathing. Pharyngeal diseases can cause symptoms such as sore throat, difficulty swallowing, pain during swallowing, swollen lymph nodes, and earaches.

Some common pharyngeal diseases include:

1. Pharyngitis: Inflammation of the pharynx, often caused by a viral or bacterial infection.
2. Tonsillitis: Inflammation of the tonsils, which are two masses of lymphoid tissue located on either side of the back of the throat.
3. Epiglottitis: Inflammation of the epiglottis, a flap of cartilage that covers the windpipe during swallowing to prevent food and liquids from entering the lungs.
4. Abscesses: A collection of pus in the pharynx caused by a bacterial infection.
5. Cancer: Malignant tumors that can develop in the pharynx, often caused by smoking or heavy alcohol use.
6. Dysphagia: Difficulty swallowing due to nerve damage, muscle weakness, or structural abnormalities in the pharynx.
7. Stridor: Noisy breathing caused by a narrowed or obstructed airway in the pharynx.

Treatment for pharyngeal diseases depends on the underlying cause and may include antibiotics, pain relievers, surgery, or radiation therapy.

A Severity of Illness Index is a measurement tool used in healthcare to assess the severity of a patient's condition and the risk of mortality or other adverse outcomes. These indices typically take into account various physiological and clinical variables, such as vital signs, laboratory values, and co-morbidities, to generate a score that reflects the patient's overall illness severity.

Examples of Severity of Illness Indices include the Acute Physiology and Chronic Health Evaluation (APACHE) system, the Simplified Acute Physiology Score (SAPS), and the Mortality Probability Model (MPM). These indices are often used in critical care settings to guide clinical decision-making, inform prognosis, and compare outcomes across different patient populations.

It is important to note that while these indices can provide valuable information about a patient's condition, they should not be used as the sole basis for clinical decision-making. Rather, they should be considered in conjunction with other factors, such as the patient's overall clinical presentation, treatment preferences, and goals of care.

A muscle cramp is an involuntary and forcibly contracted muscle that does not relax. It can involve partial or complete muscle groups, often occurring in the legs and feet (hamstrings, quadriceps, calves, and foot intrinsic muscles) during or after exercise, at night, or while resting. The exact cause of muscle cramps is unclear, but they can be associated with muscle fatigue, heavy exercising, dehydration, electrolyte imbalances, or underlying medical conditions (e.g., nerve compression or disorders, hormonal imbalances). The primary symptom is a sudden, sharp pain in the affected muscle, which may be visibly tightened and hard to touch. Most muscle cramps resolve on their own within a few minutes, but gentle stretching, massage, or applying heat/cold can help alleviate discomfort.

Medical Definition of Respiration:

Respiration, in physiology, is the process by which an organism takes in oxygen and gives out carbon dioxide. It's also known as breathing. This process is essential for most forms of life because it provides the necessary oxygen for cellular respiration, where the cells convert biochemical energy from nutrients into adenosine triphosphate (ATP), and releases waste products, primarily carbon dioxide.

In humans and other mammals, respiration is a two-stage process:

1. Breathing (or external respiration): This involves the exchange of gases with the environment. Air enters the lungs through the mouth or nose, then passes through the pharynx, larynx, trachea, and bronchi, finally reaching the alveoli where the actual gas exchange occurs. Oxygen from the inhaled air diffuses into the blood, while carbon dioxide, a waste product of metabolism, diffuses from the blood into the alveoli to be exhaled.

2. Cellular respiration (or internal respiration): This is the process by which cells convert glucose and other nutrients into ATP, water, and carbon dioxide in the presence of oxygen. The carbon dioxide produced during this process then diffuses out of the cells and into the bloodstream to be exhaled during breathing.

In summary, respiration is a vital physiological function that enables organisms to obtain the necessary oxygen for cellular metabolism while eliminating waste products like carbon dioxide.

Hypophosphatemia is a medical condition characterized by abnormally low levels of phosphate (phosphorus) in the blood, specifically below 2.5 mg/dL. Phosphate is an essential electrolyte that plays a crucial role in various bodily functions such as energy production, bone formation, and maintaining acid-base balance.

Hypophosphatemia can result from several factors, including malnutrition, vitamin D deficiency, alcoholism, hormonal imbalances, and certain medications. Symptoms of hypophosphatemia may include muscle weakness, fatigue, bone pain, confusion, and respiratory failure in severe cases. Treatment typically involves correcting the underlying cause and administering phosphate supplements to restore normal levels.

Myostatin is a protein that is primarily known for its role in regulating muscle growth. It's also called "growth differentiation factor 8" or GDF-8. Produced by muscle cells, myostatin inhibits the process of muscle growth by preventing the transformation of stem cells into muscle fibers and promoting the breakdown of existing muscle proteins.

In essence, myostatin acts as a negative regulator of muscle mass, keeping it in check to prevent excessive growth. Mutations leading to reduced myostatin activity or expression have been associated with increased muscle mass and strength in both animals and humans, making it a potential target for therapeutic interventions in muscle-wasting conditions such as muscular dystrophy and age-related sarcopenia.

Osteomalacia is a medical condition characterized by the softening of bones due to defective bone mineralization, resulting from inadequate vitamin D, phosphate, or calcium. It mainly affects adults and is different from rickets, which occurs in children. The primary symptom is bone pain, but muscle weakness can also occur. Prolonged osteomalacia may lead to skeletal deformities and an increased risk of fractures. Treatment typically involves supplementation with vitamin D, calcium, and sometimes phosphate.

The Ryanodine Receptor (RyR) is a calcium release channel located on the sarcoplasmic reticulum (SR), a type of endoplasmic reticulum found in muscle cells. It plays a crucial role in excitation-contraction coupling, which is the process by which electrical signals are converted into mechanical responses in muscle fibers.

In more detail, when an action potential reaches the muscle fiber's surface membrane, it triggers the opening of voltage-gated L-type calcium channels (Dihydropyridine Receptors or DHPRs) in the sarcolemma (the cell membrane of muscle fibers). This influx of calcium ions into the cytoplasm causes a conformational change in the RyR, leading to its own opening and the release of stored calcium from the SR into the cytoplasm. The increased cytoplasmic calcium concentration then initiates muscle contraction through interaction with contractile proteins like actin and myosin.

There are three isoforms of RyR: RyR1, RyR2, and RyR3. RyR1 is primarily found in skeletal muscle, while RyR2 is predominantly expressed in cardiac muscle. Both RyR1 and RyR2 are large homotetrameric proteins with a molecular weight of approximately 2.2 million Daltons. They contain multiple domains including an ion channel pore, regulatory domains, and a foot structure that interacts with DHPRs. RyR3 is more widely distributed, being found in various tissues such as the brain, smooth muscle, and some types of neurons.

Dysfunction of these channels has been implicated in several diseases including malignant hyperthermia, central core disease, catecholaminergic polymorphic ventricular tachycardia (CPVT), and certain forms of heart failure.

Artificial respiration is an emergency procedure that can be used to provide oxygen to a person who is not breathing or is breathing inadequately. It involves manually forcing air into the lungs, either by compressing the chest or using a device to deliver breaths. The goal of artificial respiration is to maintain adequate oxygenation of the body's tissues and organs until the person can breathe on their own or until advanced medical care arrives. Artificial respiration may be used in conjunction with cardiopulmonary resuscitation (CPR) in cases of cardiac arrest.

Electrophysiology is a branch of medicine that deals with the electrical activities of the body, particularly the heart. In a medical context, electrophysiology studies (EPS) are performed to assess abnormal heart rhythms (arrhythmias) and to evaluate the effectiveness of certain treatments, such as medication or pacemakers.

During an EPS, electrode catheters are inserted into the heart through blood vessels in the groin or neck. These catheters can record the electrical activity of the heart and stimulate it to help identify the source of the arrhythmia. The information gathered during the study can help doctors determine the best course of treatment for each patient.

In addition to cardiac electrophysiology, there are also other subspecialties within electrophysiology, such as neuromuscular electrophysiology, which deals with the electrical activity of the nervous system and muscles.

Exercise therapy is a type of medical treatment that uses physical movement and exercise to improve a patient's physical functioning, mobility, and overall health. It is often used as a component of rehabilitation programs for individuals who have experienced injuries, illnesses, or surgeries that have impaired their ability to move and function normally.

Exercise therapy may involve a range of activities, including stretching, strengthening, balance training, aerobic exercise, and functional training. The specific exercises used will depend on the individual's needs, goals, and medical condition.

The benefits of exercise therapy include:

* Improved strength and flexibility
* Increased endurance and stamina
* Enhanced balance and coordination
* Reduced pain and inflammation
* Improved cardiovascular health
* Increased range of motion and joint mobility
* Better overall physical functioning and quality of life.

Exercise therapy is typically prescribed and supervised by a healthcare professional, such as a physical therapist or exercise physiologist, who has experience working with individuals with similar medical conditions. The healthcare professional will create an individualized exercise program based on the patient's needs and goals, and will provide guidance and support to ensure that the exercises are performed safely and effectively.

Posture is the position or alignment of body parts supported by the muscles, especially the spine and head in relation to the vertebral column. It can be described as static (related to a stationary position) or dynamic (related to movement). Good posture involves training your body to stand, walk, sit, and lie in positions where the least strain is placed on supporting muscles and ligaments during movement or weight-bearing activities. Poor posture can lead to various health issues such as back pain, neck pain, headaches, and respiratory problems.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Orthotic devices are custom-made or prefabricated appliances designed to align, support, prevent deformity, or improve the function of movable body parts. They are frequently used in the treatment of various musculoskeletal disorders, such as foot and ankle conditions, knee problems, spinal alignment issues, and hand or wrist ailments. These devices can be adjustable or non-adjustable and are typically made from materials like plastic, metal, leather, or fabric. They work by redistributing forces across joints, correcting alignment, preventing unwanted movements, or accommodating existing deformities. Examples of orthotic devices include ankle-foot orthoses, knee braces, back braces, wrist splints, and custom-made foot insoles.

Physical exertion is defined as the act of applying energy to physically demandable activities or tasks, which results in various body systems working together to produce movement and maintain homeostasis. It often leads to an increase in heart rate, respiratory rate, and body temperature, among other physiological responses. The level of physical exertion can vary based on the intensity, duration, and frequency of the activity.

It's important to note that engaging in regular physical exertion has numerous health benefits, such as improving cardiovascular fitness, strengthening muscles and bones, reducing stress, and preventing chronic diseases like obesity, diabetes, and heart disease. However, it is also crucial to balance physical exertion with adequate rest and recovery time to avoid overtraining or injury.

Peripheral nerves are nerve fibers that transmit signals between the central nervous system (CNS, consisting of the brain and spinal cord) and the rest of the body. These nerves convey motor, sensory, and autonomic information, enabling us to move, feel, and respond to changes in our environment. They form a complex network that extends from the CNS to muscles, glands, skin, and internal organs, allowing for coordinated responses and functions throughout the body. Damage or injury to peripheral nerves can result in various neurological symptoms, such as numbness, weakness, or pain, depending on the type and severity of the damage.

Alpha-glucosidases are a group of enzymes that break down complex carbohydrates into simpler sugars, such as glucose, by hydrolyzing the alpha-1,4 and alpha-1,6 glycosidic bonds in oligosaccharides, disaccharides, and polysaccharides. These enzymes are located on the brush border of the small intestine and play a crucial role in carbohydrate digestion and absorption.

Inhibitors of alpha-glucosidases, such as acarbose and miglitol, are used in the treatment of type 2 diabetes to slow down the digestion and absorption of carbohydrates, which helps to reduce postprandial glucose levels and improve glycemic control.

A neurological examination is a series of tests used to evaluate the functioning of the nervous system, including both the central nervous system (the brain and spinal cord) and peripheral nervous system (the nerves that extend from the brain and spinal cord to the rest of the body). It is typically performed by a healthcare professional such as a neurologist or a primary care physician with specialized training in neurology.

During a neurological examination, the healthcare provider will assess various aspects of neurological function, including:

1. Mental status: This involves evaluating a person's level of consciousness, orientation, memory, and cognitive abilities.
2. Cranial nerves: There are 12 cranial nerves that control functions such as vision, hearing, smell, taste, and movement of the face and neck. The healthcare provider will test each of these nerves to ensure they are functioning properly.
3. Motor function: This involves assessing muscle strength, tone, coordination, and reflexes. The healthcare provider may ask the person to perform certain movements or tasks to evaluate these functions.
4. Sensory function: The healthcare provider will test a person's ability to feel different types of sensations, such as touch, pain, temperature, vibration, and proprioception (the sense of where your body is in space).
5. Coordination and balance: The healthcare provider may assess a person's ability to perform coordinated movements, such as touching their finger to their nose or walking heel-to-toe.
6. Reflexes: The healthcare provider will test various reflexes throughout the body using a reflex hammer.

The results of a neurological examination can help healthcare providers diagnose and monitor conditions that affect the nervous system, such as stroke, multiple sclerosis, Parkinson's disease, or peripheral neuropathy.

Western blotting is a laboratory technique used in molecular biology to detect and quantify specific proteins in a mixture of many different proteins. This technique is commonly used to confirm the expression of a protein of interest, determine its size, and investigate its post-translational modifications. The name "Western" blotting distinguishes this technique from Southern blotting (for DNA) and Northern blotting (for RNA).

The Western blotting procedure involves several steps:

1. Protein extraction: The sample containing the proteins of interest is first extracted, often by breaking open cells or tissues and using a buffer to extract the proteins.
2. Separation of proteins by electrophoresis: The extracted proteins are then separated based on their size by loading them onto a polyacrylamide gel and running an electric current through the gel (a process called sodium dodecyl sulfate-polyacrylamide gel electrophoresis or SDS-PAGE). This separates the proteins according to their molecular weight, with smaller proteins migrating faster than larger ones.
3. Transfer of proteins to a membrane: After separation, the proteins are transferred from the gel onto a nitrocellulose or polyvinylidene fluoride (PVDF) membrane using an electric current in a process called blotting. This creates a replica of the protein pattern on the gel but now immobilized on the membrane for further analysis.
4. Blocking: The membrane is then blocked with a blocking agent, such as non-fat dry milk or bovine serum albumin (BSA), to prevent non-specific binding of antibodies in subsequent steps.
5. Primary antibody incubation: A primary antibody that specifically recognizes the protein of interest is added and allowed to bind to its target protein on the membrane. This step may be performed at room temperature or 4°C overnight, depending on the antibody's properties.
6. Washing: The membrane is washed with a buffer to remove unbound primary antibodies.
7. Secondary antibody incubation: A secondary antibody that recognizes the primary antibody (often coupled to an enzyme or fluorophore) is added and allowed to bind to the primary antibody. This step may involve using a horseradish peroxidase (HRP)-conjugated or alkaline phosphatase (AP)-conjugated secondary antibody, depending on the detection method used later.
8. Washing: The membrane is washed again to remove unbound secondary antibodies.
9. Detection: A detection reagent is added to visualize the protein of interest by detecting the signal generated from the enzyme-conjugated or fluorophore-conjugated secondary antibody. This can be done using chemiluminescent, colorimetric, or fluorescent methods.
10. Analysis: The resulting image is analyzed to determine the presence and quantity of the protein of interest in the sample.

Western blotting is a powerful technique for identifying and quantifying specific proteins within complex mixtures. It can be used to study protein expression, post-translational modifications, protein-protein interactions, and more. However, it requires careful optimization and validation to ensure accurate and reproducible results.

Survival of Motor Neuron 1 (SMN1) protein is a critical component for the survival of motor neurons, which are nerve cells that control muscle movements. The SMN1 protein is produced by the Survival of Motor Neuron 1 gene, located on human chromosome 5q13.

The primary function of the SMN1 protein is to assist in the biogenesis of small nuclear ribonucleoproteins (snRNPs), which are essential for spliceosomes - complex molecular machines responsible for RNA processing in the cell. The absence or significant reduction of SMN1 protein leads to defective snRNP assembly, impaired RNA splicing, and ultimately results in motor neuron degeneration.

Mutations in the SMN1 gene can cause Spinal Muscular Atrophy (SMA), a genetic disorder characterized by progressive muscle weakness, atrophy, and paralysis due to the loss of lower motor neurons in the spinal cord. The severity of SMA depends on the amount of functional SMN1 protein produced, with less protein leading to more severe symptoms.

Potassium is a essential mineral and an important electrolyte that is widely distributed in the human body. The majority of potassium in the body (approximately 98%) is found within cells, with the remaining 2% present in blood serum and other bodily fluids. Potassium plays a crucial role in various physiological processes, including:

1. Regulation of fluid balance and maintenance of normal blood pressure through its effects on vascular tone and sodium excretion.
2. Facilitation of nerve impulse transmission and muscle contraction by participating in the generation and propagation of action potentials.
3. Protein synthesis, enzyme activation, and glycogen metabolism.
4. Regulation of acid-base balance through its role in buffering systems.

The normal serum potassium concentration ranges from 3.5 to 5.0 mEq/L (milliequivalents per liter) or mmol/L (millimoles per liter). Potassium levels outside this range can have significant clinical consequences, with both hypokalemia (low potassium levels) and hyperkalemia (high potassium levels) potentially leading to serious complications such as cardiac arrhythmias, muscle weakness, and respiratory failure.

Potassium is primarily obtained through the diet, with rich sources including fruits (e.g., bananas, oranges, and apricots), vegetables (e.g., leafy greens, potatoes, and tomatoes), legumes, nuts, dairy products, and meat. In cases of deficiency or increased needs, potassium supplements may be recommended under the guidance of a healthcare professional.

Analysis of Variance (ANOVA) is a statistical technique used to compare the means of two or more groups and determine whether there are any significant differences between them. It is a way to analyze the variance in a dataset to determine whether the variability between groups is greater than the variability within groups, which can indicate that the groups are significantly different from one another.

ANOVA is based on the concept of partitioning the total variance in a dataset into two components: variance due to differences between group means (also known as "between-group variance") and variance due to differences within each group (also known as "within-group variance"). By comparing these two sources of variance, ANOVA can help researchers determine whether any observed differences between groups are statistically significant, or whether they could have occurred by chance.

ANOVA is a widely used technique in many areas of research, including biology, psychology, engineering, and business. It is often used to compare the means of two or more experimental groups, such as a treatment group and a control group, to determine whether the treatment had a significant effect. ANOVA can also be used to compare the means of different populations or subgroups within a population, to identify any differences that may exist between them.

A fatal outcome is a term used in medical context to describe a situation where a disease, injury, or illness results in the death of an individual. It is the most severe and unfortunate possible outcome of any medical condition, and is often used as a measure of the severity and prognosis of various diseases and injuries. In clinical trials and research, fatal outcome may be used as an endpoint to evaluate the effectiveness and safety of different treatments or interventions.

A case-control study is an observational research design used to identify risk factors or causes of a disease or health outcome. In this type of study, individuals with the disease or condition (cases) are compared with similar individuals who do not have the disease or condition (controls). The exposure history or other characteristics of interest are then compared between the two groups to determine if there is an association between the exposure and the disease.

Case-control studies are often used when it is not feasible or ethical to conduct a randomized controlled trial, as they can provide valuable insights into potential causes of diseases or health outcomes in a relatively short period of time and at a lower cost than other study designs. However, because case-control studies rely on retrospective data collection, they are subject to biases such as recall bias and selection bias, which can affect the validity of the results. Therefore, it is important to carefully design and conduct case-control studies to minimize these potential sources of bias.

Spinal cord diseases refer to a group of conditions that affect the spinal cord, which is a part of the central nervous system responsible for transmitting messages between the brain and the rest of the body. These diseases can cause damage to the spinal cord, leading to various symptoms such as muscle weakness, numbness, pain, bladder and bowel dysfunction, and difficulty with movement and coordination.

Spinal cord diseases can be congenital or acquired, and they can result from a variety of causes, including infections, injuries, tumors, degenerative conditions, autoimmune disorders, and genetic factors. Some examples of spinal cord diseases include multiple sclerosis, spina bifida, spinal cord injury, herniated discs, spinal stenosis, and motor neuron diseases such as amyotrophic lateral sclerosis (ALS).

The treatment for spinal cord diseases varies depending on the underlying cause and severity of the condition. Treatment options may include medication, physical therapy, surgery, and rehabilitation. In some cases, the damage to the spinal cord may be irreversible, leading to permanent disability or paralysis.

Intravenous Immunoglobulins (IVIG) are a preparation of antibodies, specifically immunoglobulins, that are derived from the plasma of healthy donors. They are administered intravenously to provide passive immunity and help boost the immune system's response in individuals with weakened or compromised immune systems. IVIG can be used for various medical conditions such as primary immunodeficiency disorders, secondary immunodeficiencies, autoimmune diseases, and some infectious diseases. The administration of IVIG can help prevent infections, reduce the severity and frequency of infections, and manage the symptoms of certain autoimmune disorders. It is important to note that while IVIG provides temporary immunity, it does not replace a person's own immune system.

Regeneration in a medical context refers to the process of renewal, restoration, and growth that replaces damaged or missing cells, tissues, organs, or even whole limbs in some organisms. This complex biological process involves various cellular and molecular mechanisms, such as cell proliferation, differentiation, and migration, which work together to restore the structural and functional integrity of the affected area.

In human medicine, regeneration has attracted significant interest due to its potential therapeutic applications in treating various conditions, including degenerative diseases, trauma, and congenital disorders. Researchers are actively studying the underlying mechanisms of regeneration in various model organisms to develop novel strategies for promoting tissue repair and regeneration in humans.

Examples of regeneration in human medicine include liver regeneration after partial hepatectomy, where the remaining liver lobes can grow back to their original size within weeks, and skin wound healing, where keratinocytes migrate and proliferate to close the wound and restore the epidermal layer. However, the regenerative capacity of humans is limited compared to some other organisms, such as planarians and axolotls, which can regenerate entire body parts or even their central nervous system.

Medical science often defines and describes "walking" as a form of locomotion or mobility where an individual repeatedly lifts and sets down each foot to move forward, usually bearing weight on both legs. It is a complex motor activity that requires the integration and coordination of various systems in the human body, including the musculoskeletal, neurological, and cardiovascular systems.

Walking involves several components such as balance, coordination, strength, and endurance. The ability to walk independently is often used as a measure of functional mobility and overall health status. However, it's important to note that the specific definition of walking may vary depending on the context and the medical or scientific field in question.

Sarcopenia is a medical term that refers to the age-related decline in muscle mass, strength, and function. It's a natural process that occurs as we get older, but it can also be accelerated by various factors such as sedentary lifestyle, poor nutrition, and chronic diseases. Sarcopenia can lead to decreased mobility, weakness, frailty, and increased risk of falls and fractures in older adults. It's important to note that sarcopenia is different from cachexia, which is a muscle wasting condition associated with chronic illnesses such as cancer, HIV/AIDS, and heart failure.

The knee joint, also known as the tibiofemoral joint, is the largest and one of the most complex joints in the human body. It is a synovial joint that connects the thighbone (femur) to the shinbone (tibia). The patella (kneecap), which is a sesamoid bone, is located in front of the knee joint and helps in the extension of the leg.

The knee joint is made up of three articulations: the femorotibial joint between the femur and tibia, the femoropatellar joint between the femur and patella, and the tibiofibular joint between the tibia and fibula. These articulations are surrounded by a fibrous capsule that encloses the synovial membrane, which secretes synovial fluid to lubricate the joint.

The knee joint is stabilized by several ligaments, including the medial and lateral collateral ligaments, which provide stability to the sides of the joint, and the anterior and posterior cruciate ligaments, which prevent excessive forward and backward movement of the tibia relative to the femur. The menisci, which are C-shaped fibrocartilaginous structures located between the femoral condyles and tibial plateaus, also help to stabilize the joint by absorbing shock and distributing weight evenly across the articular surfaces.

The knee joint allows for flexion, extension, and a small amount of rotation, making it essential for activities such as walking, running, jumping, and sitting.

Ataxia is a medical term that refers to a group of disorders affecting coordination, balance, and speech. It is characterized by a lack of muscle control during voluntary movements, causing unsteady or awkward movements, and often accompanied by tremors. Ataxia can affect various parts of the body, such as the limbs, trunk, eyes, and speech muscles. The condition can be congenital or acquired, and it can result from damage to the cerebellum, spinal cord, or sensory nerves. There are several types of ataxia, including hereditary ataxias, degenerative ataxias, cerebellar ataxias, and acquired ataxias, each with its own specific causes, symptoms, and prognosis. Treatment for ataxia typically focuses on managing symptoms and improving quality of life, as there is no cure for most forms of the disorder.

Body weight is the measure of the force exerted on a scale or balance by an object's mass, most commonly expressed in units such as pounds (lb) or kilograms (kg). In the context of medical definitions, body weight typically refers to an individual's total weight, which includes their skeletal muscle, fat, organs, and bodily fluids.

Healthcare professionals often use body weight as a basic indicator of overall health status, as it can provide insights into various aspects of a person's health, such as nutritional status, metabolic function, and risk factors for certain diseases. For example, being significantly underweight or overweight can increase the risk of developing conditions like malnutrition, diabetes, heart disease, and certain types of cancer.

It is important to note that body weight alone may not provide a complete picture of an individual's health, as it does not account for factors such as muscle mass, bone density, or body composition. Therefore, healthcare professionals often use additional measures, such as body mass index (BMI), waist circumference, and blood tests, to assess overall health status more comprehensively.

The myocardium is the middle layer of the heart wall, composed of specialized cardiac muscle cells that are responsible for pumping blood throughout the body. It forms the thickest part of the heart wall and is divided into two sections: the left ventricle, which pumps oxygenated blood to the rest of the body, and the right ventricle, which pumps deoxygenated blood to the lungs.

The myocardium contains several types of cells, including cardiac muscle fibers, connective tissue, nerves, and blood vessels. The muscle fibers are arranged in a highly organized pattern that allows them to contract in a coordinated manner, generating the force necessary to pump blood through the heart and circulatory system.

Damage to the myocardium can occur due to various factors such as ischemia (reduced blood flow), infection, inflammation, or genetic disorders. This damage can lead to several cardiac conditions, including heart failure, arrhythmias, and cardiomyopathy.

Osteitis deformans, also known as Paget's disease of bone, is a chronic disorder of the bone characterized by abnormal turnover and remodeling of the bone. In this condition, the bone becomes enlarged, thickened, and deformed due to excessive and disorganized bone formation and resorption.

The process begins when the bone-remodeling cycle is disrupted, leading to an imbalance between the activity of osteoclasts (cells that break down bone) and osteoblasts (cells that form new bone). In Paget's disease, osteoclasts become overactive and increase bone resorption, followed by an overzealous response from osteoblasts, which attempt to repair the damage but do so in a disorganized manner.

The affected bones can become weakened, prone to fractures, and may cause pain, deformities, or other complications such as arthritis, hearing loss, or neurological symptoms if the skull or spine is involved. The exact cause of Paget's disease remains unknown, but it is believed that genetic and environmental factors play a role in its development.

Early diagnosis and treatment can help manage the symptoms and prevent complications associated with osteitis deformans. Treatment options include medications to slow down bone turnover, pain management, and orthopedic interventions when necessary.

MyoD protein is a member of the family of muscle regulatory factors (MRFs) that play crucial roles in the development and regulation of skeletal muscle. MyoD is a transcription factor, which means it binds to specific DNA sequences and helps control the transcription of nearby genes into messenger RNA (mRNA).

MyoD protein is encoded by the MYOD1 gene and is primarily expressed in skeletal muscle cells, where it functions as a master regulator of muscle differentiation. During myogenesis, MyoD is activated and initiates the expression of various genes involved in muscle-specific functions, such as contractile proteins and ion channels.

MyoD protein can also induce cell cycle arrest and promote the differentiation of non-muscle cells into muscle cells, a process known as transdifferentiation. This property has been explored in regenerative medicine for potential therapeutic applications.

In summary, MyoD protein is a key regulator of skeletal muscle development, differentiation, and maintenance, and it plays essential roles in the regulation of gene expression during myogenesis.

Hypertrophy, in the context of physiology and pathology, refers to an increase in the size of an organ or tissue due to an enlargement of its constituent cells. It is often used to describe the growth of muscle cells (myocytes) in response to increased workload or hormonal stimulation, resulting in an increase in muscle mass. However, hypertrophy can also occur in other organs such as the heart (cardiac hypertrophy) in response to high blood pressure or valvular heart disease.

It is important to note that while hypertrophy involves an increase in cell size, hyperplasia refers to an increase in cell number. In some cases, both hypertrophy and hyperplasia can occur together, leading to a significant increase in the overall size and function of the organ or tissue.

A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.

An amino acid sequence is the specific order of amino acids in a protein or peptide molecule, formed by the linking of the amino group (-NH2) of one amino acid to the carboxyl group (-COOH) of another amino acid through a peptide bond. The sequence is determined by the genetic code and is unique to each type of protein or peptide. It plays a crucial role in determining the three-dimensional structure and function of proteins.

A chronic disease is a long-term medical condition that often progresses slowly over a period of years and requires ongoing management and care. These diseases are typically not fully curable, but symptoms can be managed to improve quality of life. Common chronic diseases include heart disease, stroke, cancer, diabetes, arthritis, and COPD (chronic obstructive pulmonary disease). They are often associated with advanced age, although they can also affect children and younger adults. Chronic diseases can have significant impacts on individuals' physical, emotional, and social well-being, as well as on healthcare systems and society at large.

Recessive genes refer to the alleles (versions of a gene) that will only be expressed when an individual has two copies of that particular allele, one inherited from each parent. If an individual inherits one recessive allele and one dominant allele for a particular gene, the dominant allele will be expressed and the recessive allele will have no effect on the individual's phenotype (observable traits).

Recessive genes can still play a role in determining an individual's genetic makeup and can be passed down through generations even if they are not expressed. If two carriers of a recessive gene have children, there is a 25% chance that their offspring will inherit two copies of the recessive allele and exhibit the associated recessive trait.

Examples of genetic disorders caused by recessive genes include cystic fibrosis, sickle cell anemia, and albinism.

Hindlimb suspension is a commonly used animal model in biomedical research, particularly in the study of muscle atrophy and disuse osteoporosis. In this model, the hindlimbs of rodents (such as rats or mice) are suspended using a tape or a harness system, which elevates their limbs off the ground and prevents them from bearing weight. This state of disuse leads to significant changes in the musculoskeletal system, including muscle atrophy, bone loss, and alterations in muscle fiber type composition and architecture.

The hindlimb suspension model is often used to investigate the mechanisms underlying muscle wasting and bone loss in conditions such as spinal cord injury, bed rest, and spaceflight-induced disuse. By understanding these mechanisms, researchers can develop potential therapeutic interventions to prevent or mitigate the negative effects of disuse on the musculoskeletal system.

Neuromuscular non-depolarizing agents are a type of muscle relaxant medication used in anesthesia and critical care settings to facilitate endotracheal intubation, mechanical ventilation, and to prevent muscle contractions during surgery. These agents work by competitively binding to the acetylcholine receptors at the neuromuscular junction, without activating them, thereby preventing the initiation of muscle contraction.

Examples of non-depolarizing neuromuscular blocking agents include:

* Vecuronium
* Rocuronium
* Pancuronium
* Atracurium
* Cisatracurium
* Mivacurium

These medications have a reversible effect and their duration of action can be prolonged in patients with impaired renal or hepatic function, acid-base imbalances, electrolyte abnormalities, or in those who are taking other medications that interact with these agents. Therefore, it is important to monitor the patient's neuromuscular function during and after the administration of non-depolarizing neuromuscular blocking agents.

A tendon is the strong, flexible band of tissue that connects muscle to bone. It helps transfer the force produced by the muscle to allow various movements of our body parts. Tendons are made up of collagen fibers arranged in parallel bundles and have a poor blood supply, making them prone to injuries and slow to heal. Examples include the Achilles tendon, which connects the calf muscle to the heel bone, and the patellar tendon, which connects the kneecap to the shinbone.

Muscle stretching exercises are physical movements that aim to gradually lengthen the muscle to its full capacity, beyond its regular resting length, in order to improve flexibility and overall joint mobility. These exercises often involve slowly moving parts of the body into a position that will stretch certain muscles and then maintaining that position for a period of time, typically between 15-30 seconds.

There are various techniques for muscle stretching, including static stretching, dynamic stretching, ballistic stretching, and proprioceptive neuromuscular facilitation (PNF) stretches. Regular practice of these exercises can help enhance athletic performance, reduce the risk of injury, alleviate muscle tension, improve posture, and promote relaxation. However, it's important to perform muscle stretching exercises correctly and consistently, under the guidance of a fitness professional or healthcare provider, to ensure safety and effectiveness.

Muscle rigidity is a term used to describe an increased resistance to passive movement or muscle tone that is present at rest, which cannot be overcome by the person. It is a common finding in various neurological conditions such as Parkinson's disease, stiff-person syndrome, and tetanus. In these conditions, muscle rigidity can result from hyperexcitability of the stretch reflex arc or abnormalities in the basal ganglia circuitry.

Muscle rigidity should be distinguished from spasticity, which is a velocity-dependent increase in muscle tone that occurs during voluntary movement or passive stretching. Spasticity is often seen in upper motor neuron lesions such as stroke or spinal cord injury.

It's important to note that the assessment of muscle rigidity requires a careful physical examination and may need to be evaluated in conjunction with other signs and symptoms to determine an underlying cause.

Dominant genes refer to the alleles (versions of a gene) that are fully expressed in an individual's phenotype, even if only one copy of the gene is present. In dominant inheritance patterns, an individual needs only to receive one dominant allele from either parent to express the associated trait. This is in contrast to recessive genes, where both copies of the gene must be the recessive allele for the trait to be expressed. Dominant genes are represented by uppercase letters (e.g., 'A') and recessive genes by lowercase letters (e.g., 'a'). If an individual inherits one dominant allele (A) from either parent, they will express the dominant trait (A).

Signal transduction is the process by which a cell converts an extracellular signal, such as a hormone or neurotransmitter, into an intracellular response. This involves a series of molecular events that transmit the signal from the cell surface to the interior of the cell, ultimately resulting in changes in gene expression, protein activity, or metabolism.

The process typically begins with the binding of the extracellular signal to a receptor located on the cell membrane. This binding event activates the receptor, which then triggers a cascade of intracellular signaling molecules, such as second messengers, protein kinases, and ion channels. These molecules amplify and propagate the signal, ultimately leading to the activation or inhibition of specific cellular responses.

Signal transduction pathways are highly regulated and can be modulated by various factors, including other signaling molecules, post-translational modifications, and feedback mechanisms. Dysregulation of these pathways has been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.

Autoantibodies are defined as antibodies that are produced by the immune system and target the body's own cells, tissues, or organs. These antibodies mistakenly identify certain proteins or molecules in the body as foreign invaders and attack them, leading to an autoimmune response. Autoantibodies can be found in various autoimmune diseases such as rheumatoid arthritis, lupus, and thyroiditis. The presence of autoantibodies can also be used as a diagnostic marker for certain conditions.

Central muscle relaxants are a class of pharmaceutical agents that act on the central nervous system (CNS) to reduce skeletal muscle tone and spasticity. These medications do not directly act on the muscles themselves but rather work by altering the messages sent between the brain and the muscles, thereby reducing excessive muscle contraction and promoting relaxation.

Central muscle relaxants are often prescribed for the management of various neuromuscular disorders, such as multiple sclerosis, spinal cord injuries, cerebral palsy, and stroke-induced spasticity. They may also be used to treat acute musculoskeletal conditions like strains, sprains, or other muscle injuries.

Examples of central muscle relaxants include baclofen, tizanidine, cyclobenzaprine, methocarbamol, and diazepam. It is important to note that these medications can have side effects such as drowsiness, dizziness, and impaired cognitive function, so they should be used with caution and under the guidance of a healthcare professional.

Mitochondrial diseases are a group of disorders caused by dysfunctions in the mitochondria, which are the energy-producing structures in cells. These diseases can affect people of any age and can manifest in various ways, depending on which organs or systems are affected. Common symptoms include muscle weakness, neurological problems, cardiac disease, diabetes, and vision/hearing loss. Mitochondrial diseases can be inherited from either the mother's or father's side, or they can occur spontaneously due to genetic mutations. They can range from mild to severe and can even be life-threatening in some cases.

The spinal cord is a major part of the nervous system, extending from the brainstem and continuing down to the lower back. It is a slender, tubular bundle of nerve fibers (axons) and support cells (glial cells) that carries signals between the brain and the rest of the body. The spinal cord primarily serves as a conduit for motor information, which travels from the brain to the muscles, and sensory information, which travels from the body to the brain. It also contains neurons that can independently process and respond to information within the spinal cord without direct input from the brain.

The spinal cord is protected by the bony vertebral column (spine) and is divided into 31 segments: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. Each segment corresponds to a specific region of the body and gives rise to pairs of spinal nerves that exit through the intervertebral foramina at each level.

The spinal cord is responsible for several vital functions, including:

1. Reflexes: Simple reflex actions, such as the withdrawal reflex when touching a hot surface, are mediated by the spinal cord without involving the brain.
2. Muscle control: The spinal cord carries motor signals from the brain to the muscles, enabling voluntary movement and muscle tone regulation.
3. Sensory perception: The spinal cord transmits sensory information, such as touch, temperature, pain, and vibration, from the body to the brain for processing and awareness.
4. Autonomic functions: The sympathetic and parasympathetic divisions of the autonomic nervous system originate in the thoracolumbar and sacral regions of the spinal cord, respectively, controlling involuntary physiological responses like heart rate, blood pressure, digestion, and respiration.

Damage to the spinal cord can result in various degrees of paralysis or loss of sensation below the level of injury, depending on the severity and location of the damage.

Biological models, also known as physiological models or organismal models, are simplified representations of biological systems, processes, or mechanisms that are used to understand and explain the underlying principles and relationships. These models can be theoretical (conceptual or mathematical) or physical (such as anatomical models, cell cultures, or animal models). They are widely used in biomedical research to study various phenomena, including disease pathophysiology, drug action, and therapeutic interventions.

Examples of biological models include:

1. Mathematical models: These use mathematical equations and formulas to describe complex biological systems or processes, such as population dynamics, metabolic pathways, or gene regulation networks. They can help predict the behavior of these systems under different conditions and test hypotheses about their underlying mechanisms.
2. Cell cultures: These are collections of cells grown in a controlled environment, typically in a laboratory dish or flask. They can be used to study cellular processes, such as signal transduction, gene expression, or metabolism, and to test the effects of drugs or other treatments on these processes.
3. Animal models: These are living organisms, usually vertebrates like mice, rats, or non-human primates, that are used to study various aspects of human biology and disease. They can provide valuable insights into the pathophysiology of diseases, the mechanisms of drug action, and the safety and efficacy of new therapies.
4. Anatomical models: These are physical representations of biological structures or systems, such as plastic models of organs or tissues, that can be used for educational purposes or to plan surgical procedures. They can also serve as a basis for developing more sophisticated models, such as computer simulations or 3D-printed replicas.

Overall, biological models play a crucial role in advancing our understanding of biology and medicine, helping to identify new targets for therapeutic intervention, develop novel drugs and treatments, and improve human health.

Insulin is a hormone produced by the beta cells of the pancreatic islets, primarily in response to elevated levels of glucose in the circulating blood. It plays a crucial role in regulating blood glucose levels and facilitating the uptake and utilization of glucose by peripheral tissues, such as muscle and adipose tissue, for energy production and storage. Insulin also inhibits glucose production in the liver and promotes the storage of excess glucose as glycogen or triglycerides.

Deficiency in insulin secretion or action leads to impaired glucose regulation and can result in conditions such as diabetes mellitus, characterized by chronic hyperglycemia and associated complications. Exogenous insulin is used as a replacement therapy in individuals with diabetes to help manage their blood glucose levels and prevent long-term complications.

In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."

1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.

2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.

3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.

4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).

Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.

Nervous system diseases, also known as neurological disorders, refer to a group of conditions that affect the nervous system, which includes the brain, spinal cord, nerves, and muscles. These diseases can affect various functions of the body, such as movement, sensation, cognition, and behavior. They can be caused by genetics, infections, injuries, degeneration, or tumors. Examples of nervous system diseases include Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy, migraine, stroke, and neuroinfections like meningitis and encephalitis. The symptoms and severity of these disorders can vary widely, ranging from mild to severe and debilitating.

Postural balance is the ability to maintain, achieve, or restore a state of equilibrium during any posture or activity. It involves the integration of sensory information (visual, vestibular, and proprioceptive) to control and adjust body position in space, thereby maintaining the center of gravity within the base of support. This is crucial for performing daily activities and preventing falls, especially in older adults and individuals with neurological or orthopedic conditions.

Membrane potential is the electrical potential difference across a cell membrane, typically for excitable cells such as nerve and muscle cells. It is the difference in electric charge between the inside and outside of a cell, created by the selective permeability of the cell membrane to different ions. The resting membrane potential of a typical animal cell is around -70 mV, with the interior being negative relative to the exterior. This potential is generated and maintained by the active transport of ions across the membrane, primarily through the action of the sodium-potassium pump. Membrane potentials play a crucial role in many physiological processes, including the transmission of nerve impulses and the contraction of muscle cells.

Protein Tyrosine Phosphatases, Non-Receptor (PTPNs) are a type of enzymes that play a crucial role in the regulation of various cellular processes by removing phosphate groups from tyrosine residues of proteins. Unlike receptor protein tyrosine phosphatases, PTPNs do not have a transmembrane domain and are located in the cytoplasm. They are involved in several signaling pathways that control cell growth, differentiation, migration, and survival. Dysregulation of PTPN function has been implicated in various diseases, including cancer, diabetes, and neurological disorders.

Skeletal myoblasts are the precursor cells responsible for the formation and repair of skeletal muscle fibers. They are also known as satellite cells, located in a quiescent state between the basal lamina and sarcolemma of mature muscle fibers. Upon muscle injury or damage, these cells become activated, proliferate, differentiate into myocytes, align with existing muscle fibers, and fuse to form new muscle fibers or repair damaged ones. This process is crucial for postnatal growth, maintenance, and regeneration of skeletal muscles.

The aorta is the largest artery in the human body, which originates from the left ventricle of the heart and carries oxygenated blood to the rest of the body. It can be divided into several parts, including the ascending aorta, aortic arch, and descending aorta. The ascending aorta gives rise to the coronary arteries that supply blood to the heart muscle. The aortic arch gives rise to the brachiocephalic, left common carotid, and left subclavian arteries, which supply blood to the head, neck, and upper extremities. The descending aorta travels through the thorax and abdomen, giving rise to various intercostal, visceral, and renal arteries that supply blood to the chest wall, organs, and kidneys.

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Additionally, lower motor neurons are characterized by muscle weakness, hypotonia, hyporeflexia and muscle atrophy. Spinal ... Neurogenic shock lasts for weeks and can lead to a loss of muscle tone due to disuse of the muscles below the injured site. The ... These include hyperreflexia, hypertonia and muscle weakness. Lower motor neuronal damage results in its own characteristic ... Overall, spontaneous embryonic activity has been shown to play a role in neuron and muscle development but is probably not ...
Atypical breathing patterns then arise from the overactivation of secondary muscles of inspiration due to their weakness. This ... Muscle strength testing are also utilised to evaluate RSP. The following tests can assess the strength of muscles: With this ... Friedrich, Cathe (14 October 2018). "Rounded Shoulders? It's Probably Weakness in These Two Muscles".[self-published source?] ... Muscle strength deficits in the lower trapezius muscles are also a common clinical finding in patients with rounded shoulders ...
IBM2 causes progressive muscle weakness and wasting. Muscle wasting usually starts around the age of 20 - 30 years, although ... A 2009 review noted that muscle weakness usually begins after age 20 and after 20-30 years, the person usually requires a wheel ... The weakness and severity can vary from person to person. In some, weakness in the legs is noticed first. In some others, the ... Generally, they are neuromuscular disorders characterized by muscle weakness developing in young adults. Hereditary inclusion ...
Danon first described the disease in 2 boys with heart and skeletal muscle disease (muscle weakness), and intellectual ... Muscle weakness is often absent or subtle. Some females will tire easily with exercise Cardiomyopathy is often absent in ... Features of Danon disease in males are:[citation needed] An early age of onset of muscle weakness and heart disease (onset in ... Microscopically, muscles from Danon disease patients appear similar to muscles from Pompe disease patients. However, ...
In general, the symptoms are: Muscle weakness. Difficulty in motor acquisitions or absence of them. Poor control of the head ... muscle weakness, motor difficulties and lack of control in the movement of the head, respiratory failure and cardiac ... Unlike most muscular dystrophies, lamin A/C CMD does not present a breakdown of muscular fibres caused by muscle degeneration. ...
... generalized body weakness, aphasia, and somnolence. Severe cases might exhibit proximal muscle weakness. There are various ... by childhood-onset progressive severe muscle weakness and atrophy of the distal lower limbs and intrinsic hand muscles, ... progressive distal muscle weakness and atrophy which begins in the lower limbs and spreads to the upper limbs, distal upper and ... muscle weakness and atrophy of the distal extremities (mostly involving feet, legs, and the thenar eminence of the hands), loss ...
Weakness or muscle weakness (especially in the large muscles of the arms and legs). This latter occurs in 60 to 80 percent of ... Muscle weakness is rarely the chief complaint. The likelihood and degree of muscle weakness is correlated with the duration and ... Muscle strength returns gradually over several months after the hyperthyroidism has been treated. Muscle degeneration Shortness ... Limitation of eye movement (due to impairment of eye muscle function). Periorbital and conjunctival edema (accumulation of ...
Muscle weakness may persist for several days following treatment.[medical citation needed] It is unclear whether dantrolene has ... Benzodiazepines may also cause additive muscle weakness. Combined oral contraceptives and hormone replacement therapy with ... is a postsynaptic muscle relaxant that lessens excitation-contraction coupling in muscle cells. It achieves this by inhibiting ... It is also used in the management of neuroleptic malignant syndrome, muscle spasticity (e.g. after strokes, in paraplegia, ...
This causes some muscle weakness in the legs. A full recovery is usually expected. Lumbosacral trunk Ramus communicans.Sacral ... then emerges from the medial border of the psoas muscle to unite with the anterior ramus of L5 just superior to the pelvic brim ...
Muscle weakness can be found with either presentation. In countries with expanded newborn screening, SPCD can be identified ... Later cases were reported with cardiomyopathy and muscle weakness. Newborn screening expanded the potential phenotypes ... leading to a variety of symptoms such as chronic muscle weakness, cardiomyopathy, hypoglycemia and liver dysfunction. The ... Early cases were reported with liver dysfunction, muscular findings (weakness and underdevelopment), hypoketotic hypoglycemia, ...
Long term deficiency in vitamin E might cause muscle weakness as well as loss of muscle mass, abnormal eye movements and even ... such as weakness, muscle atrophy, twitching); headaches; disturbances in sensations; changes in nerve responses; performance ...
This disease causes fluctuating muscle weakness and fatigue. The disease occurs due to detectable antibodies produced against ... The use of transgenic models such as those used for discovery of the mimicry events leading to diseases of the CNS and muscle ...
Muscle weakness and cramping are not uncommon symptoms, but they are not as common as they are in human PFKM deficiency.[ ... Muscle weakness and pain are not as common in patients with hemolytic PFK deficiency.[citation needed] Presentation of the ... This type presents with exercise-induced muscle cramps and weakness (sometimes rhabdomyolysis), myoglobinuria, as well as with ... "Juvenile-onset permanent weakness in muscle phosphofructokinase deficiency". Journal of the Neurological Sciences. 316 (1-2): ...
... is a medical term for muscle weakness. The term may also refer to: Myasthenia gravis Ocular myasthenia Lambert-Eaton ...
Symptoms may include lethargy, impaired mental functioning; irritability; shaking, twitching, weakness in arm and leg muscles; ... Epinephrine prepares the muscles and respiratory system for activity in the case of a "fight or flight" response. Lastly, ... Glucose that is not circulating in the blood is stored in skeletal muscle and liver cells in the form of glycogen; in fasting ... insulin tells muscles to take up excess glucose for storage in the form of glycogen. Glucagon responds to too low of a blood ...
Signs and symptoms vary between people and may include irritability, muscle weakness, sleeping problems, a fast heartbeat, heat ... Extraocular muscle weakness may present with double vision. In lid-lag (von Graefe's sign), when the person tracks an object ... extraocular muscle weakness, and lid-lag. In hyperthyroid stare (Dalrymple sign) the eyelids are retracted upward more than ... muscle aches, weakness, fatigue, hyperactivity, irritability, high blood sugar, excessive urination, excessive thirst, delirium ...
... muscle weakness, and incoordination; occupational therapy contributing to restoration of function (23 min). PMF 5116C (1950) - ... cords to selected muscle and then to prosthetic appliance so that patient can operate appliance by contracting muscles in ... overcoming a definite weakness or loss of function; heavy resistance phase (29 min). PMF 5057 - PMF 5058 (1950) - The Medical ... motor power from muscles controlled by peripheral nerves originating in spinal cord; motor impulses from brain through ...
Proximal muscle weakness affects muscles closest to the bodys midline, while distal muscle weakness affects muscles further ... True muscle weakness (or neuromuscular weakness) describes a condition where the force exerted by the muscles is less than ... Proximal muscle weakness can be seen in Cushings syndrome and hyperthyroidism.[citation needed] Muscle weakness can be ... Its causes are many and can be divided into conditions that have either true or perceived muscle weakness. True muscle weakness ...
Muscle Weakness And Nausea Or Vomiting and their most common related conditions. ... Decreased Appetite, Fatigue, Muscle Weakness And Nausea Or Vomiting. *Medical Author: Dan Brennan, MD ...
The purposes of this study were to evaluate, in patients with COPD: (1) the relationship between muscle strength and cross- ... Peripheral muscle weakness is commonly found in patients with chronic obstructive pulmonary disease (COPD) and may play a role ... suggesting that weakness in COPD is due to muscle atrophy. In COPD, the distribution of peripheral muscle weakness and the ... the distribution of peripheral muscle weakness, and (3) the relationship between muscle strength and the severity of lung ...
... - Featured Topics from the National Center for Health Statistics ... Prevalence of Reduced Muscle Strength in Older U.S. Adults: United States, 2011-2012. Muscle weakness is linked to impaired ... Sarcopenia Project recently developed sex-specific criteria to diagnose different degrees of muscle strength (i.e., weak, ...
... researchers have discovered the likely cause of a childs rare type of severe muscle weakness. The child was one of six cases ... Likely genetic source of muscle weakness found in six previously undiagnosed children. Date:. April 9, 2015. Source:. The ... Bernes referred all five cases to TGen for genetic sequencing in an effort to find the causes of the childrens muscle weakness ... In still another case, TGen testing identified the genetic culprit of the childs muscle weakness as a pathogenic EMD variant ...
... - ABC Homeopathy Forum. 4 replies to 2013-07-06. ... shoulder muscle weakness and enlarged the breast size. hi my age is 33y married wt 51kg height 5 my problem is sharp shoulder ... muscle weakness my diet is weak thirst is good and feeding of the 2nd baby my breast size is too small i have been allopathic ...
Muscle wasting in MND causes weakness and can affect balance and posture, with the risk of falls. ... Muscle weakness and pain Management. Consider:. *physiotherapy (including walking aids, orthotics, splints, active and passive ... Muscle wasting in MND causes weakness and can affect balance and posture, with the risk of falls. ... General muscle tightness or spasticity (stiffness, rigidity and spasms) can affect mobility, coordination of movement and may ...
Fix Your Bench Pressing Weaknesses. Perfect one of the most popular workouts with these bench pressing tips and fixes.. by ... Copyright 2023 JW Media, LLC, parent company of Muscle & Fitness. All rights reserved. ... This old-school exercise can benefit a wide range of muscle groups. ...
Resources , News , ICU acquired muscle weakness (ICUAW), early mobilisation and nutrition. ICU acquired muscle weakness (ICUAW ...
... muscle fatigue and muscle fibers. There was not a clear indication of mitochondrial limitation between the two groups either.. ... Integrative and Comparative Physiology comparing the soleus muscle in mice with Down syndrome and mice without Down syndrome.. ... that there was not a significant difference between the two groups of mice with regards to the force production of the muscle, ...
MHRC Faculty Member Christopher Perry and team working toward new therapies that treat muscle weakness in Duchenne muscular ... MHRC Faculty Member Christopher Perry and team working toward new therapies that treat muscle weakness in Duchenne muscular ...
Tag Archives: muscle weakness Get to know the disease "weak eye muscles", a disorder from the nervous system. Get to know the ... casino casino games Chelsea Cristiano Ronaldo eye muscle weakness disease FA Cup fish shooting Fish shooting game Football ... gambling games game Health Hugo Lloris Karim Benzema League Cup Lloris Luis Sanchez Madrid Manchester United muscle weakness ... Get to know the disease "weak eye muscles", a disorder from the nervous system ...
Compensatory strategies for muscle weakness during stair ascent in subjects with total knee arthroplasty. Download Prime PubMed ... Biomechanical PhenomenaCross-Sectional StudiesElectromyographyFemaleGaitHumansKnee JointLegMaleMiddle AgedMuscle WeaknessMuscle ... "Compensatory Strategies for Muscle Weakness During Stair Ascent in Subjects With Total Knee Arthroplasty." The Journal of ... Compensatory Strategies for Muscle Weakness During Stair Ascent in Subjects With Total Knee Arthroplasty. J Arthroplasty. 2014; ...
Muscle testing reveals continued glute weakness…. Posted: Sun, February 22, 2009. On occasion, I will have some patients that ... They typically are neutral and can find and feel the glute, but muscle testing reveals continued weakness and femurs remain ...
Muscle weakness often occurs after an injury where certain parts of the body are unable to get exercise due to the damaged ... MUSCLE WEAKNESS. If a muscle is not given any work to do each little muscle fibre becomes thinner and the whole muscle begins ... For instance a calf injury will result in weakness of the muscles and if not restored to normal strength running and even ... Muscles only respond to the demands placed on them. When an injury has healed the muscles will recover in response to the ...
BACKGROUND--It is well established that patients with longstanding weakness of the respiratory muscles have a reduction in lung ... CONCLUSIONS--In many patients with chronic weakness of the respiratory muscles the reduced lung distensibility does not appear ... Lung volume restriction in patients with chronic respiratory muscle weakness: the role of microatelectasis. ... Lung volume restriction in patients with chronic respiratory muscle weakness: the role of microatelectasis. ...
We found that TWK10 not only enhanced muscle strength in young mice, but also prevented the aging-related loss of muscle ... We found that TWK10 not only enhanced muscle strength in young mice, but also prevented the aging-related loss of muscle ... improved muscle strength, exercise endurance, and overall body composition in healthy humans. In this study, the effect of ... strength in aged mice, which was accompanied by elevated muscle glycogen levels. Furthermore, TWK10 attenuated the aging- ...
Oftentimes on commercials advertising prescription medicines, they say that if you experience muscle pain or weakness while ...
APSF Survey Results: Drug-Induced Muscle Weakness in the Postoperative Period Safety Initiative Robert K. Stoelting, MD Share ... The view as to the frequency of muscle weakness in the PACU due to residual neuromuscular blockade was mixed (Figure 2) but 82 ... A recent APSF survey of anesthesia professionals on residual muscle relaxant-induced weakness in the postoperative period was a ... Survey: APSF Survey Results: Drug-Induced Muscle Weakness in the Postoperative Period Safety Initiative ...
... issues such as weakness in chest muscles or ligaments are usually evident. Those afflicted with SRS would often present with ...
Idiopathic spinal cord herniation of the cervical cord: unusual cause of proximal muscle weakness in upper limbs ... Idiopathic spinal cord herniation of the cervical cord: unusual cause of proximal muscle weakness in upper limbs ... Idiopathic spinal cord herniation of the cervical cord: unusual cause of proximal muscle weakness in upper limbs ...
For those suffering from muscle weakness and fatigue, Carex offers a wide array of products to meet many individual needs. Use ... Muscle Weakness and Fatigue Treatment Products. Collection Menu Filter. Arm Rest Style. *Flip Back Desk-Length ... Home / Muscle Weakness and Fatigue Treatment Products / Height Range 28" to 37" * ... For those suffering from muscle weakness and fatigue, Carex offers a wide array of products to meet many individual needs. Use ...
Progressive Muscle Weakness and Atrophy Symptom Checker: Possible causes include Progressive Muscular Atrophy. Check the full ... Symptoms include pharyngeal muscle weakness (muscles that are involved in swallowing), weak facial muscles, progressive loss of ... Symptoms include pharyngeal muscle weakness (muscles that are involved in swallowing), weak facial muscles, progressive loss of ... weakness and atrophy, initially of the peroneal muscles and later of the distal muscles of the arms. [antibodyplus.com] ...
Intravenous immunoglobulin therapy (IVIg 0.4 g/kg x 5 days) markedly reduced the severe pain and muscle weakness in the legs. ... Intravenous immunoglobulin therapy markedly ameliorates muscle weakness and severe pain in proximal diabetic neuropathy.. Y ... A 57-year-old man with type 2 diabetes mellitus for 10 years showed progressive loss of muscle strength in both legs, pain and ... Eventually, pain assessed by the Visual Analogue Scale was relieved by 80% and muscle strength was also well recovered, thereby ...
Understand and effectively manage muscle weakness in MS. Discover adaptive strategies and tips to cope with it. ... Muscle Weakness in Multiple Sclerosis (MS) Muscle weakness is a common symptom experienced by many individuals with multiple ... Understand and effectively manage muscle weakness in MS. Discover adaptive strategies and tips to cope with it. ...
MUSCLE WEAKNESS and CONGENITAL MUSCULAR DYSTROPHY related symptoms, diseases, and genetic alterations. Get the complete ... Muscle weakness, and Congenital muscular dystrophy. .site-footer{margin-bottom:80px}. If you liked this article maybe you will ...
Muscle weakness. Little evidence suggests that intrinsic muscle weakness is a major contributor to upper airway dysfunction in ... Therefore, even if a major weakness is not present, the mechanical disadvantage imposed by muscle shortening or by displacement ... During wakefulness, neural input to a number of small muscle groups in the pharynx maintains muscle tone and airway patency. ... and sternohyoid muscles. These muscles tend to promote a patent pharyngeal lumen and receive phasic activation in synchrony ...
"Muscle tightness is secondary to muscle weakness." Solve the weakness and you just may solve the tightness. ... What causes muscle weakness?. A multitude of factors such as trauma, stress, or overuse can contribute to a muscle becoming ... What are the indications of muscle weakness - how do I know if I have a weak muscle? ... These lengthening muscles may lose their ability to lengthen as a function of the other muscles loss of ability to contract and ...
Muscle weakness and neurologic deficits. Muscle weakness and focal neurologic deficits such as tetraparesis [40] may be the ... Aggressively treat respiratory failure, which may ensue once muscle weakness involves the diaphragm, and support ventilation in ...
Muscle weakness. This drug can cause muscle weakness (myasthenia) in different parts of the body. ... You might feel some pain in your muscles and joints. Or you might have pain in your back, neck, chest, bones, or arms and legs. ... Tiredness and weakness. You might feel very tired and as though you lack energy. ... Symptoms include a change in temperature, aching muscles, headaches, feeling cold and shivery and generally unwell. You might ...
  • Central muscle fatigue manifests as an overall sense of energy deprivation, while peripheral muscle fatigue manifests as a local, muscle-specific inability to do work. (wikipedia.org)
  • When a nerve experiences synaptic fatigue it becomes unable to stimulate the muscle that it innervates. (wikipedia.org)
  • Most movements require a force far below what a muscle could potentially generate, and barring pathology, neuromuscular fatigue is seldom an issue. (wikipedia.org)
  • citation needed] Central fatigue is a reduction in the neural drive or nerve-based motor command to working muscles that results in a decline in the force output. (wikipedia.org)
  • Peripheral muscle fatigue during physical work is an inability for the body to supply sufficient energy or other metabolites to the contracting muscles to meet the increased energy demand. (wikipedia.org)
  • The insufficiency of energy, i.e. sub-optimal aerobic metabolism, generally results in the accumulation of lactic acid and other acidic anaerobic metabolic by-products in the muscle, causing the stereotypical burning sensation of local muscle fatigue, though recent studies have indicated otherwise, actually finding that lactic acid is a source of energy. (wikipedia.org)
  • The fundamental difference between the peripheral and central theories of muscle fatigue is that the peripheral model of muscle fatigue assumes failure at one or more sites in the chain that initiates muscle contraction. (wikipedia.org)
  • Peripheral regulation therefore depends on the localized metabolic chemical conditions of the local muscle affected, whereas the central model of muscle fatigue is an integrated mechanism that works to preserve the integrity of the system by initiating muscle fatigue through muscle derecruitment, based on collective feedback from the periphery, before cellular or organ failure occurs. (wikipedia.org)
  • Though Gainers are used primarily for bulking up, nevertheless many health execs use gainers as a publish-workout due to their ability to rebuild glycogen stores in the muscular tissues and support in muscle tissue growth, and likewise as a pre-exercise because gainers add vitality and delay fatigue throughout exercise. (wijvallenaf.nl)
  • For those suffering from muscle weakness and fatigue, Carex offers a wide array of products to meet many individual needs. (carex.com)
  • Carex's versatile offering is sure to have a device to make living with muscle weakness and fatigue more comfortable and improve patient outcomes. (carex.com)
  • They get muscle fatigue. (yeastinfection.org)
  • Although pain, fatigue, and weakness can all hinder muscle use, they're actually discrete symptom classifications. (getluna.com)
  • Fatigue is a feeling of tiredness, exhaustion, or lack of energy, which may make it difficult to use the muscles. (getluna.com)
  • A stroke or spinal cord injury can cause sudden muscle weakness, as can chronic fatigue syndrome, muscular dystrophy, Graves disease, Guillain-Barre syndrome, ALS, or prolonged immobilization (i.e. bed rest). (getluna.com)
  • In layman's terms, it is a disorder of brain chemicals, which is characterized by Chronic Diffuse Bodywide Muscle Pain, Stiffness, Chronic Fatigue and Sleep Disturbances, which result in decreased Deep Stage 4 Sleep (the restful/replenishing part of the sleep cycle). (tripod.com)
  • Vitamin D deficiency has become increasingly common in the United States, with nearly 1 in 4 adults considered to be low in vitamin D. Symptoms of deficiency include fatigue, poor sleep, bone pain, depression, muscle weakness, and increased susceptibility to illness. (bacchusgamma.org)
  • In addition to fatigue, individuals with vitamin D deficiency may also experience poor sleep, depression, muscle weakness, and increased susceptibility to illness. (bacchusgamma.org)
  • Fatigue, poor sleep, depression, muscle weakness, and increased susceptibility to illness are all symptoms that may arise from low levels of vitamin D. It is important to address a deficiency through a combination of dietary changes, sunlight exposure, and supplementation, under the guidance of a healthcare professional. (bacchusgamma.org)
  • Mr. Nimmo age 66, has noticed excessive fatigue muscle aches and weakness in his legs for some time. (academicresearchexperts.net)
  • Fatigue or weakness. (mayoclinic.org)
  • In this article, we'll discuss the various causes of weakness in muscles and ligaments, as well as the signs and symptoms that can indicate weakness. (spinalligamentinjury.com)
  • Muscle weakness" can refer to a wide array of symptoms, ranging from mild to severe and from acute to diffuse. (getluna.com)
  • Some symptoms of wound botulism can look like symptoms of opioid overdose, such as slurred speech or inability to talk, weakness, and trouble breathing. (cdc.gov)
  • Usually, symptoms develop during the teen years, with most people noticing some problems by age 20, although weakness in some muscles can begin as early as infancy and as late as the 50s. (mda.org)
  • Poor circulation can worsen the symptoms of arthritis, causing joint inflammation, degeneration, and muscle weakness. (quenchers.com)
  • True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. (wikipedia.org)
  • Both skeletal muscle and cardiac muscle no longer operated normally, and this was true when the mice and fish were tested themselves, or their muscle fibers were examined individually in a test tube. (go.com)
  • Skeletal muscle constantly relies on mitochondria for power. (nih.gov)
  • Although well known in many other tissues, the current study is the first to show that mitochondria in skeletal muscle are capable of undergoing fusion as a repair mechanism. (nih.gov)
  • It had been thought that this type of mitochondrial self-repair was unlikely in the packed fibers of the skeletal muscle cells, as mitochondria have little opportunity to interact in the narrow space between the thread-like structures called myofilaments that make up muscle. (nih.gov)
  • The severe end of the spectrum includes progressive muscle diseases that are classified as Duchenne/Becker muscular dystrophy when skeletal muscle is primarily affected and as DMD-associated DCM when the heart is primarily affected. (nih.gov)
  • Becker muscular dystrophy (BMD) is characterized by later-onset skeletal muscle weakness. (nih.gov)
  • Despite the milder skeletal muscle involvement, heart failure from DCM is a common cause of morbidity and the most common cause of death in BMD. (nih.gov)
  • This leads to muscle wasting and a decrease in skeletal muscle mass and strength. (healthline.com)
  • MMT and MVIC have not been compared in Spinal and Bulbar Muscular Atrophy (SBMA), a progressive neuromuscular disease characterized by muscle weakness. (nih.gov)
  • Also, midfacial hypoplasia may develop with long-term use, particularly in children with neuromuscular weakness. (medscape.com)
  • Tramadol should also not be used in used in children 12 to 18 years of age who are obese or who have a neuromuscular disease (disease that affects the nerves that control voluntary muscles), a lung disease, or obstructive sleep apnea (condition in which the airway becomes blocked or narrow and breathing stops for short periods during sleep) as these conditions may increase their risk of breathing problems. (medlineplus.gov)
  • In this retrospective case study, we report the apparent clinical effectiveness of neuromuscular electrical stimulation (NMES) in combination with voice therapy (VT) for rehabilitating dysphonia secondary to suspected superior laryngeal nerve (SLN) weakness in two female patients. (uandes.cl)
  • Contact your doctor right away if you develop unusual weight gain (especially in the face), muscle weakness, increased thirst or urination, confusion, unusual drowsiness, severe or persistent headache, or vision changes. (drugs.com)
  • Nerves control the contraction of muscles by determining the number, sequence, and force of muscular contraction. (wikipedia.org)
  • Muscle power of the quadriceps femoris, hip flexors and gluteus medius on both sides of the body was graded using the Modified Medical Research Council (MMRC) scale, which has been used in muscle diseases, such as Duchenne muscular dystrophy 14 . (ersjournals.com)
  • The intermediate syndrome is a delayed-onset of muscular weakness and paralysis following an episode of acute cholinesterase inhibitor poisoning. (cdc.gov)
  • For instance, some people may be born with conditions such as muscular dystrophy, which can cause weakness in the muscles and ligaments. (spinalligamentinjury.com)
  • Patients with chronic muscle disorders such as muscular dystrophy may experience weakness all over the body, while patients who have suffered an injury or stroke may have weakness in just one half or one part of the body. (getluna.com)
  • The dystrophinopathies cover a spectrum of X-linked muscle disease ranging from mild to severe that includes Duchenne muscular dystrophy, Becker muscular dystrophy, and DMD-associated dilated cardiomyopathy (DCM). (nih.gov)
  • The muscles used for breathing commonly are not affected in FSHD, as they are in other forms of muscular dystrophy. (mda.org)
  • Sometimes, especially in those types of dystrophy which mainly affect the major limb muscles, cramps and stiffness are quite common. (viquepedia.com)
  • However, severe cramps and stiffness are very unusual and, especially if the muscles are also tender, may indicate some other cause for the muscle weakness. (viquepedia.com)
  • The mild end of the spectrum includes the phenotypes of asymptomatic increase in serum concentration of creatine phosphokinase (CK) and muscle cramps with myoglobinuria. (nih.gov)
  • No one wants to experience aches and pains in their muscles and ligaments, yet it's an all-too-common occurrence in today's society. (spinalligamentinjury.com)
  • Aches in muscles or joints. (mayoclinic.org)
  • The absence of correlation with age and the presence, in some patients, of severe respiratory insufficiency without severe limb girdle muscle weakness indicate that respiratory function should be monitored independently from the degree of peripheral muscle weakness. (ersjournals.com)
  • Muscle weakness is a lack of muscle strength. (wikipedia.org)
  • Part of the process of strength training is increasing the nerve's ability to generate sustained, high frequency signals which allow a muscle to contract with their greatest force. (wikipedia.org)
  • The Foundation for the National Institutes of Health (FNIH) Sarcopenia Project recently developed sex-specific criteria to diagnose different degrees of muscle strength (i.e., weak, intermediate, and normal) in older adults based on maximum hand grip strength. (cdc.gov)
  • The finding gives insight into why chronic heavy drinking often saps muscle strength and it could also lead to new targets for medication development. (nih.gov)
  • The finding gives insight into why chronic heavy drinking often saps muscle strength and it could also lead to new targets for medication development," said Dr. George Koob, director of the National Institute on Alcohol Abuse and Alcoholism, the NIH institute that funded the study. (nih.gov)
  • Manual Muscle Testing (MMT) is the most common clinical strength assessment. (nih.gov)
  • Weakness is reduced strength in one or more muscles. (medlineplus.gov)
  • Genetic issues can affect the strength and flexibility of muscles and ligaments. (spinalligamentinjury.com)
  • Strengthening exercises are typically combined with flexibility and balance exercises to ensure that the patient is developing muscle strength safely and effectively. (getluna.com)
  • Strength training exercises can help to counteract muscle weakness and improve circulation. (quenchers.com)
  • The spectrum of this disease is wide and varies from a rapidly progressive infantile disease with cardiorespiratory insufficiency, which is usually fatal before 1 yr of age 1 , to a slowly progressive adult-onset disease with muscle weakness, respiratory insufficiency 1 , 2 and sleep-disordered breathing 3 . (ersjournals.com)
  • Although respiratory muscle involvement is rarely inaugural 5 , 6 , it may occur early in the course of the disease and may cause death. (ersjournals.com)
  • These characteristics, and the likelihood that new treatments recently tested in infantile and juvenile Pompe's disease 7 - 10 will require evaluation in adult-onset disease, indicate a need for investigations into the relationships between respiratory muscle weakness and weakness in other muscles. (ersjournals.com)
  • For example, muscle weakness may result from a disease which affects the nerve supply to the muscle. (viquepedia.com)
  • It is a disease which primarily affects muscle tissue, though in some dystrophies other tissues and organs may also be affected. (viquepedia.com)
  • For example, those with diabetes may experience weakened muscles due to nerve damage caused by the disease. (spinalligamentinjury.com)
  • Certain illnesses such as diabetes, arthritis, and kidney disease can cause muscle and ligament weakness. (spinalligamentinjury.com)
  • By tagging mitochondria in the skeletal tissue of rats with different colors, the researchers were able to observe the process in action and confirm that mitochondrial fusion occurs in muscle cells. (nih.gov)
  • Bodily exercise ensures that the protein ingested is used to burn fats and construct lean muscle tissue-which is essential if women wish to protect the youthful look of a well-constructed body. (wijvallenaf.nl)
  • The truth is, if your body does not have sufficient of the other 6 amino acids, then it should break down (catabolize) muscle tissue with a purpose to acquire it. (wijvallenaf.nl)
  • The cause of pseudohypertrophy is not entirely clear but is probably largely due to the muscle tissue becoming replaced by fat. (viquepedia.com)
  • Muscle weakness often occurs as the result of another health problem, such as a thyroid problem, a stroke, a spinal cord injury, or a chronic muscle disorder. (getluna.com)
  • Compression of the lumbar spine nerve root may trigger pain and/or weakness for some spinal stenosis and disc herniation patients. (mostchiropractic.com)
  • Muscle weakness from long-term alcoholism may stem from an inability of mitochondria, the powerhouses of cells, to self-repair, according to a study funded by the National Institutes of Health. (nih.gov)
  • A constant feature, and one of the earliest signs, was marked weakness of the neck flexors and inability of patients to raise their heads off their pillows. (cdc.gov)
  • Due to facial weakness, the eyes may remain partially open during sleep in patients with FSHD, 3 which can cause exposure keratitis (inflammation of the cornea). (mda.org)
  • Another reason for muscle weakness and pain in people with PsA may be chronic inflammation. (healthline.com)
  • High levels of inflammation as measured by markers in the blood, such as C-reactive protein, have been associated with smaller muscle size. (healthline.com)
  • Muscle wasting can also be caused by nutritional deficiencies, chronic inflammation, and reduced physical activity. (healthline.com)
  • Encephalitis (en-sef-uh-LIE-tis) is inflammation of the brain. (mayoclinic.org)
  • Poor Nutrition: A lack of essential vitamins and minerals can lead to weakened muscles and ligaments . (spinalligamentinjury.com)
  • Lack of Exercise: Regular physical activity is necessary for maintaining strong muscles and ligaments . (spinalligamentinjury.com)
  • The course and severity of muscle weakness, its prognosis, depend very much on the particular type of dystrophy from which a person suffers. (viquepedia.com)
  • Depending on the severity and cause of the weakness, patients may need intervention from specialists or intensive physical therapy. (getluna.com)
  • The evaluation consisted of an interview regarding occupational activities, ability to swallow without difficulty, ability to control urination and presence of chronic pain ( e.g. in the back, neck or muscles). (ersjournals.com)
  • Critical illness polyneuropathy (CIP) and myopathy (CIM) are complications of critical illness that present with muscle weakness and failure to wean from the ventilator. (nih.gov)
  • Illness: Certain illnesses can cause muscle or ligament weakness. (spinalligamentinjury.com)
  • Illness can also weaken the muscles and ligaments. (spinalligamentinjury.com)
  • Injury or illness associated with the brain, nervous system, or the muscles themselves can all result in chronic muscle weakness. (getluna.com)
  • From August 1 until October 20, there were 37 cases nationwide of muscle weakness with a preceding respiratory illness. (frontporchne.com)
  • The muscle weakness which occurs in all types of dystrophy has certain features in common. (viquepedia.com)
  • Serotonin binds to extrasynaptic receptors located on the axon initial segment of motoneurons with the result that nerve impulse initiation and thereby muscle contraction are inhibited. (wikipedia.org)
  • Structural changes associated with CIP and CIM include axonal nerve degeneration, muscle myosin loss, and muscle necrosis. (nih.gov)
  • An acquired sodium channelopathy causing reduced muscle membrane and nerve excitability is a possible unifying mechanism underlying CIP and CIM. (nih.gov)
  • If you have urge incontinence, your pelvic floor muscles may be too weak to hold back a bowel movement due to muscle injury or nerve damage . (nih.gov)
  • There is no way of knowing whether there is any permanent neurological damage from the weakness. (frontporchne.com)
  • Typically, a muscle strengthening plan will consist of gentle, low-impact exercises that target the affected muscles, gradually ramping up in intensity as the plan progresses. (getluna.com)
  • individuals with onset before age 12 months with cardiomyopathy) may be apparent in utero but more typically onset is at the median age of four months with hypotonia, generalized muscle weakness, feeding difficulties, failure to thrive, respiratory distress, and hypertrophic cardiomyopathy. (nih.gov)
  • Dermatomyositis (DM) is an autoimmune disorder, which belongs to a group of rare autoimmune dermatoses characterized by different skin features and variable muscle involvement. (nih.gov)
  • Muscle weakness is linked to impaired mobility and mortality in older persons. (cdc.gov)
  • As abdominal weakness progresses, a person develops a lordosis , an exaggerated curve in the lumbar (lower) region of the spine. (mda.org)
  • Used in antiseptic hand soaps, shaving gel, toothpaste, deodorant and other hygiene products, a new study has found the chemical can weaken muscle contraction. (go.com)
  • For example, a broken bone or a sprain can weaken the muscles and ligaments around the affected area. (spinalligamentinjury.com)
  • Muscle weakness, however, comprises its own classification. (getluna.com)
  • Drawbacks of MMT include poor sensitivity for strong muscles, subjective grading, and examiner stature influence. (nih.gov)
  • This is called subjective weakness. (medlineplus.gov)
  • When buying a mass gainer, you not only want one which helps you achieve weight and lean muscle mass, but you additionally want one that is wholesome and incorporates the vitamins you need. (wijvallenaf.nl)
  • Loss of lean muscle mass can lead to weakness and disability. (healthline.com)
  • In dystrophy, however, the enlarged muscles are weak, and their enlargement has therefore been referred to as pseudohypertrophy Opens in new window (which means false hypertrophy). (viquepedia.com)
  • Injury: An injury or trauma to the body can cause muscles and ligaments to become weak. (spinalligamentinjury.com)
  • The weakness sometimes referred to as "paresis" or "paralysis-like" can affect the arms, legs, face, eye muscles or throat. (frontporchne.com)
  • This toxin attacks your body's nerves, which can make it hard to breathe and can cause muscle weakness and even death. (cdc.gov)
  • Does psoriatic arthritis cause muscle pain and weakness? (healthline.com)
  • Poor circulation can cause muscle weakness , making it more difficult for the muscles to support the joints properly. (quenchers.com)
  • PsA patients who have chronic pain and joint stiffness are less likely to engage in weight-bearing exercises and are more likely to be sedentary or even bed-bound, which can lead to muscle wasting. (healthline.com)
  • In research conducted with rats, scientists found evidence that chronic heavy alcohol use affects a gene involved in mitochondrial repair and muscle regeneration. (nih.gov)
  • Fountain, Colorado, Luna's physical therapists specialize in treating patients suffering from chronic muscle weakness. (getluna.com)
  • The muscles surrounding the joints are responsible for providing support and stability. (quenchers.com)
  • The diagnosis of CIP, CIM, or combined CIP and CIM relies on clinical, electrophysiological, and muscle biopsy investigations. (nih.gov)
  • When patients experience muscle weakness, they may have difficulty performing even the most simple actions in their daily lives. (getluna.com)
  • People with FSHD often do not go to the doctor until their shoulder or leg muscles become involved and they experience difficulty reaching over their heads or going up and down stairs. (mda.org)
  • Dysphagia (difficulty in swallowing) is rare in patients with FSHD but can develop due to weakness of the jaw and lingual muscles. (mda.org)
  • There is no sensation of pain or discomfort, the muscle appears to simply 'stop listening' and gradually cease to move, often lengthening. (wikipedia.org)
  • Weakness is not usually associated with pain and the muscles are not tender to touch. (viquepedia.com)
  • Similarly, when patients are experiencing muscle pain, it may be uncomfortable to move the affected areas. (getluna.com)
  • Patients with PsA often complain of muscle pain and weakness. (healthline.com)
  • There are several reasons people with psoriatic arthritis can have muscle pain and weakness. (healthline.com)
  • The patient can sometimes have muscles that are like cement, due to the myofascial splinting (guarding from the pain). (tripod.com)
  • (2) Bring your Murfreesboro back pain and related muscle weakness to Most Chiropractic Clinic for Murfreesboro non-operative care first. (mostchiropractic.com)
  • Whether caused by an injury, a medical condition, or simply overuse, having weakness in your muscles and ligaments can have a significant impact on your quality of life. (spinalligamentinjury.com)
  • Injury is another common cause of muscle and ligament weakness. (spinalligamentinjury.com)
  • This pro-inflammatory state is associated with the development of psoriasis and psoriatic arthritis as well as causing greater arthritis activity with damage to the muscles, cartilage, and bones. (healthline.com)
  • Listen to this PODCAST with Dr. Dean Greenwood on The Back Doctor's Podcast with Dr. Michael Johnson about a patient with muscle weakness accompanying a synovial cyst that improved with chiropractic care utilizing the Cox® Technic System . (mostchiropractic.com)
  • Most Chiropractic Clinic is here to help you regain your muscle loss and develop your bones! (mostchiropractic.com)
  • During motor activity, serotonin released in synapses that contact motoneurons promotes muscle contraction. (wikipedia.org)
  • When researchers at the University of California at Davis exposed the individual muscle fibers of fish and mice to triclosan, they found it impaired the normal contraction mechanism. (go.com)
  • Inflammatory proteins in the blood can stimulate the breakdown of protein in the body as well as reduce the production of protein in the muscles. (healthline.com)
  • Background and purpose - Knee extensor (KE) muscle weakness is a modifiable feature commonly observed in individuals with knee osteoarthritis (KOA) and constitutes a potential target for patient-specific interventions. (nih.gov)
  • Therefore, in this study, we explored whether KE weakness is associated with radiographic (medial and/or lateral) KOA progression and how this relationship differs depending on frontal plane knee alignment and sex. (nih.gov)
  • With Luna, patients can receive physical therapy right at home - for muscle weakness and a range of other conditions. (getluna.com)
  • For patients experiencing muscle weakness, moving the muscles may not be a matter of overcoming exhaustion or discomfort - certain movements actually might not be possible. (getluna.com)
  • Physical therapy is a leading treatment option for patients experiencing persistent muscle weakness. (getluna.com)
  • The decrease in hand muscle volume was twice that in men than women among PsA patients. (healthline.com)
  • Muscle weakness appears in as many as 30% to 50% of disc herniation patients. (mostchiropractic.com)
  • 80% of disc herniation patients with weakness show improvement with 6 weeks of non-surgical care, 90% at 12 weeks, 93% at 24 weeks. (mostchiropractic.com)
  • Surgical patients discover that the most clinically significant weakness improvement happened within 6 weeks of spine surgery for a disc herniation. (mostchiropractic.com)
  • Both patients failed or plateaued with traditional VT but had significant improvement with the addition of NMES of the cricothyroid muscle and SLN using a VitalStim unit. (uandes.cl)
  • There are a few studies that have demonstrated muscle loss from psoriatic arthritis. (healthline.com)