Contractile tissue that produces movement in animals.
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
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 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.
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.
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 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.
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.
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 resection or removal of the innervation 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.
Non-striated, elongated, spindle-shaped cells found lining the digestive tract, uterus, and blood vessels. They are derived from specialized myoblasts (MYOBLASTS, SMOOTH MUSCLE).
Mitochondria of skeletal and smooth muscle. It does not include myocardial mitochondria for which MITOCHONDRIA, HEART is available.
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).
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.
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.
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.
These include the muscles of the DIAPHRAGM and the INTERCOSTAL MUSCLES.
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)
Conical muscular projections from the walls of the cardiac ventricles, attached to the cusps of the atrioventricular valves by the chordae tendineae.
Muscles forming the ABDOMINAL WALL including RECTUS ABDOMINIS, external and internal oblique muscles, transversus abdominis, and quadratus abdominis. (from Stedman, 25th ed)
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.
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.
A masticatory muscle whose action is closing the jaws.
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)
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)
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)
Recording of the changes in electric potential of muscle by means of surface or needle electrodes.
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.
Muscular contractions characterized by increase in tension without change in 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 pectoralis major and pectoralis minor muscles that make up the upper and fore part of the chest in front of the AXILLA.
Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.
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.
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 .
A masticatory muscle whose action is closing the jaws; its posterior portion retracts the mandible.
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)
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.
Use of electric potential or currents to elicit biological responses.
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.
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.
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.
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.
Elements of limited time intervals, contributing to particular results or situations.
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 properties, processes, and behavior of biological systems under the action of mechanical forces.
Neurons which activate MUSCLE CELLS.
The synapse between a neuron and a muscle.
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).
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.
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.
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)
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.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
The physiological renewal, repair, or replacement of tissue.
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.
The repeating contractile units of the MYOFIBRIL, delimited by Z bands along its length.
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.
A myogenic regulatory factor that controls myogenesis. Though it is not clear how its function differs from the other myogenic regulatory factors, MyoD appears to be related to fusion and terminal differentiation of the muscle cell.
The inferior part of the lower extremity between the KNEE and the ANKLE.
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.
Exercises that stretch the muscle fibers with the aim to increase muscle-tendon FLEXIBILITY, improve RANGE OF MOTION or musculoskeletal function, and prevent injuries. There are various types of stretching techniques including active, passive (relaxed), static, dynamic (gentle), ballistic (forced), isometric, and others.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
Continuous involuntary sustained muscle contraction which is often a manifestation of BASAL GANGLIA DISEASES. When an affected muscle is passively stretched, the degree of resistance remains constant regardless of the rate at which the muscle is stretched. This feature helps to distinguish rigidity from MUSCLE SPASTICITY. (From Adams et al., Principles of Neurology, 6th ed, p73)
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.
General increase in bulk of a part or organ due to CELL ENLARGEMENT and accumulation of FLUIDS AND SECRETIONS, not due to tumor formation, nor to an increase in the number of cells (HYPERPLASIA).
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.
The time span between the beginning of physical activity by an individual and the termination because of exhaustion.
Precursor cells destined to differentiate into skeletal myocytes (MYOCYTES, SKELETAL).
The main trunk of the systemic arteries.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Fibrous bands or cords of CONNECTIVE TISSUE at the ends of SKELETAL MUSCLE FIBERS that serve to attach the MUSCLES to bones and other structures.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
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.
Technique for limiting use, activity, or movement by immobilizing or restraining animal by suspending from hindlimbs or tails. This immobilization is used to simulate some effects of reduced gravity and study weightlessness physiology.
The rate dynamics in chemical or physical systems.
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)
The portion of the leg in humans and other animals found between the HIP and KNEE.
Tumors or cancer located in muscle tissue or specific muscles. They are differentiated from NEOPLASMS, MUSCLE TISSUE which are neoplasms composed of skeletal, cardiac, or smooth muscle tissue, such as MYOSARCOMA or LEIOMYOMA.
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.
Two of the masticatory muscles: the internal, or medial, pterygoid muscle and external, or lateral, pterygoid muscle. Action of the former is closing the jaws and that of the latter is opening the jaws, protruding the mandible, and moving the mandible from side to side.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
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 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.
Myosin type II isoforms found in skeletal muscle.
An order of the class Amphibia, which includes several families of frogs and toads. They are characterized by well developed hind limbs adapted for jumping, fused head and trunk and webbed toes. The term "toad" is ambiguous and is properly applied only to the family Bufonidae.
The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
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 heterogeneous group of drugs used to produce muscle relaxation, excepting the neuromuscular blocking agents. They have their primary clinical and therapeutic uses in the treatment of muscle spasm and immobility associated with strains, sprains, and injuries of the back and, to a lesser degree, injuries to the neck. They have been used also for the treatment of a variety of clinical conditions that have in common only the presence of skeletal muscle hyperactivity, for example, the muscle spasms that can occur in MULTIPLE SCLEROSIS. (From Smith and Reynard, Textbook of Pharmacology, 1991, p358)
The excitable plasma membrane of a muscle cell. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
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)
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)
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 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.
Inflammation of a muscle or muscle tissue.
A myogenic regulatory factor that controls myogenesis. Myogenin is induced during differentiation of every skeletal muscle cell line that has been investigated, in contrast to the other myogenic regulatory factors that only appear in certain cell types.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
Common name for the species Gallus gallus, the domestic fowl, in the family Phasianidae, order GALLIFORMES. It is descended from the red jungle fowl of SOUTHEAST ASIA.
An endogenous substance found mainly in skeletal muscle of vertebrates. It has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1996)
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.
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.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
The chemical reactions involved in the production and utilization of various forms of energy in cells.
Myosin type II isoforms found in smooth muscle.
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.
The act, process, or result of passing from one place or position to another. It differs from LOCOMOTION in that locomotion is restricted to the passing of the whole body from one place to another, while movement encompasses both locomotion but also a change of the position of the whole body or any of its parts. Movement may be used with reference to humans, vertebrate and invertebrate animals, and microorganisms. Differentiate also from MOTOR ACTIVITY, movement associated with behavior.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
Reflex contraction of a muscle in response to stretching, which stimulates muscle proprioceptors.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
The relationship between the dose of an administered drug and the response of the organism to the drug.
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 protein found in the thin filaments of muscle fibers. It inhibits contraction of the muscle unless its position is modified by TROPONIN.
The measurement of an organ in volume, mass, or heaviness.
A purely physical condition which exists within any material because of strain or deformation by external forces or by non-uniform thermal expansion; expressed quantitatively in units of force per unit area.
The non-genetic biological changes of an organism in response to challenges in its ENVIRONMENT.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Enzyme that catalyzes the first step of the tricarboxylic acid cycle (CITRIC ACID CYCLE). It catalyzes the reaction of oxaloacetate and acetyl CoA to form citrate and coenzyme A. This enzyme was formerly listed as EC 4.1.3.7.
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.
The flow of BLOOD through or around an organ or region of the body.
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
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.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
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.
Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms.
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.
Progressive decline in muscle mass due to aging which results in decreased functional capacity of muscles.
Study of intracellular distribution of chemicals, reaction sites, enzymes, etc., by means of staining reactions, radioactive isotope uptake, selective metal distribution in electron microscopy, or other methods.
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.
A species of the family Ranidae occurring in a wide variety of habitats from within the Arctic Circle to South Africa, Australia, etc.
Thick triangular muscle in the SHOULDER whose function is to abduct, flex, and extend the arm. It is a common site of INTRAMUSCULAR INJECTIONS.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
The hollow, muscular organ that maintains the circulation of the blood.
A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed)
A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes SMOOTH MUSCLE, stimulates CARDIAC MUSCLE, stimulates DIURESIS, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide PHOSPHODIESTERASES, antagonism of ADENOSINE RECEPTORS, and modulation of intracellular calcium handling.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
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.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
A family of muscle-specific transcription factors which bind to DNA in control regions and thus regulate myogenesis. All members of this family contain a conserved helix-loop-helix motif which is homologous to the myc family proteins. These factors are only found in skeletal muscle. Members include the myoD protein (MYOD PROTEIN); MYOGENIN; myf-5, and myf-6 (also called MRF4 or herculin).
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.
An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord.
A glucose transport protein found in mature MUSCLE CELLS and ADIPOCYTES. It promotes transport of glucose from the BLOOD into target TISSUES. The inactive form of the protein is localized in CYTOPLASMIC VESICLES. In response to INSULIN, it is translocated to the PLASMA MEMBRANE where it facilitates glucose uptake.
Characteristic restricted to a particular organ of the body, such as a cell type, metabolic response or expression of a particular protein or antigen.
A highly variable species of the family Ranidae in Canada, the United States and Central America. It is the most widely used Anuran in biomedical research.
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
The use of wings or wing-like appendages to remain aloft and move through the air.
An isoenzyme of creatine kinase found in the MUSCLE.
An activity in which the body is propelled by moving the legs rapidly. Running is performed at a moderate to rapid pace and should be differentiated from JOGGING, which is performed at a much slower pace.
The restriction of the MOVEMENT of whole or part of the body by physical means (RESTRAINT, PHYSICAL) or chemically by ANALGESIA, or the use of TRANQUILIZING AGENTS or NEUROMUSCULAR NONDEPOLARIZING AGENTS. It includes experimental protocols used to evaluate the physiologic effects of immobility.
A paired box transcription factor that is involved in EMBRYONIC DEVELOPMENT of the CENTRAL NERVOUS SYSTEM and SKELETAL MUSCLE.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.
Abnormal increase in skeletal or smooth muscle tone. Skeletal muscle hypertonicity may be associated with PYRAMIDAL TRACT lesions or BASAL GANGLIA DISEASES.
Established cell cultures that have the potential to propagate indefinitely.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
The vessels carrying blood away from the heart.
The farthest or outermost projections of the body, such as the HAND and FOOT.
A SKELETAL MUSCLE-specific transcription factor that contains a basic HELIX-LOOP-HELIX MOTIF. It plays an essential role in MUSCLE DEVELOPMENT.
Deep muscles in the BACK whose function is to extend and rotate the SPINE and maintain POSTURE. It consists splenius, semispinalis, multifidus, rotatores, interspinales, intertransversarii and sacrospinalis.
The position or attitude of the body.
The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
The developmental entity of a fertilized chicken egg (ZYGOTE). The developmental process begins about 24 h before the egg is laid at the BLASTODISC, a small whitish spot on the surface of the EGG YOLK. After 21 days of incubation, the embryo is fully developed before hatching.
Specialized connective tissue composed of fat cells (ADIPOCYTES). It is the site of stored FATS, usually in the form of TRIGLYCERIDES. In mammals, there are two types of adipose tissue, the WHITE FAT and the BROWN FAT. Their relative distributions vary in different species with most adipose tissue being white.
The superior part of the upper extremity between the SHOULDER and the ELBOW.
One of the minor protein components of skeletal muscle. Its function is to serve as the calcium-binding component in the troponin-tropomyosin B-actin-myosin complex by conferring calcium sensitivity to the cross-linked actin and myosin filaments.
Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios.
A front limb of a quadruped. (The Random House College Dictionary, 1980)
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.
The minute vessels that connect the arterioles and venules.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
A white crystal or crystalline powder used in BUFFERS; FERTILIZERS; and EXPLOSIVES. It can be used to replenish ELECTROLYTES and restore WATER-ELECTROLYTE BALANCE in treating HYPOKALEMIA.
A region of the lower extremity immediately surrounding and including the KNEE JOINT.
The spread of response if stimulation is prolonged. (Campbell's Psychiatric Dictionary, 8th ed.)
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.
Disorders characterized by an abnormal reduction in muscle volume due to a decrease in the size or number of muscle fibers. Atrophy may result from diseases intrinsic to muscle tissue (e.g., MUSCULAR DYSTROPHY) or secondary to PERIPHERAL NERVOUS SYSTEM DISEASES that impair innervation to muscle tissue (e.g., MUSCULAR ATROPHY, SPINAL).
Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.
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)
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.
The rear surface of an upright primate from the shoulders to the hip, or the dorsal surface of tetrapods.
Neurons which conduct NERVE IMPULSES to the CENTRAL NERVOUS SYSTEM.
A slowly hydrolyzed CHOLINERGIC AGONIST that acts at both MUSCARINIC RECEPTORS and NICOTINIC RECEPTORS.
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
The relative amounts of various components in the body, such as percentage of body fat.
A sport in which weights are lifted competitively or as an exercise.
A diminution of the skeletal muscle tone marked by a diminished resistance to passive stretching.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.

Requirement of a novel gene, Xin, in cardiac morphogenesis. (1/28646)

A novel gene, Xin, from chick (cXin) and mouse (mXin) embryonic hearts, may be required for cardiac morphogenesis and looping. Both cloned cDNAs have a single open reading frame, encoding proteins with 2,562 and 1,677 amino acids for cXin and mXin, respectively. The derived amino acid sequences share 46% similarity. The overall domain structures of the predicted cXin and mXin proteins, including proline-rich regions, 16 amino acid repeats, DNA-binding domains, SH3-binding motifs and nuclear localization signals, are highly conserved. Northern blot analyses detect a single message of 8.9 and 5.8 kilo base (kb) from both cardiac and skeletal muscle of chick and mouse, respectively. In situ hybridization reveals that the cXin gene is specifically expressed in cardiac progenitor cells of chick embryos as early as stage 8, prior to heart tube formation. cXin continues to be expressed in the myocardium of developing hearts. By stage 15, cXin expression is also detected in the myotomes of developing somites. Immunofluorescence microscopy reveals that the mXin protein is colocalized with N-cadherin and connexin-43 in the intercalated discs of adult mouse hearts. Incubation of stage 6 chick embryos with cXin antisense oligonucleotides results in abnormal cardiac morphogenesis and an alteration of cardiac looping. The myocardium of the affected hearts becomes thickened and tends to form multiple invaginations into the heart cavity. This abnormal cellular process may account in part for the abnormal looping. cXin expression can be induced by bone morphogenetic protein (BMP) in explants of anterior medial mesoendoderm from stage 6 chick embryos, a tissue that is normally non-cardiogenic. This induction occurs following the BMP-mediated induction of two cardiac-restricted transcription factors, Nkx2.5 and MEF2C. Furthermore, either MEF2C or Nkx2.5 can transactivate a luciferase reporter driven by the mXin promoter in mouse fibroblasts. These results suggest that Xin may participate in a BMP-Nkx2.5-MEF2C pathway to control cardiac morphogenesis and looping.  (+info)

Coupling of the cell cycle and myogenesis through the cyclin D1-dependent interaction of MyoD with cdk4. (2/28646)

Proliferating myoblasts express the muscle determination factor, MyoD, throughout the cell cycle in the absence of differentiation. Here we show that a mitogen-sensitive mechanism, involving the direct interaction between MyoD and cdk4, restricts myoblast differentiation to cells that have entered into the G0 phase of the cell cycle under mitogen withdrawal. Interaction between MyoD and cdk4 disrupts MyoD DNA-binding, muscle-specific gene activation and myogenic conversion of 10T1/2 cells independently of cyclin D1 and the CAK activation of cdk4. Forced induction of cyclin D1 in myotubes results in the cytoplasmic to nuclear translocation of cdk4. The specific MyoD-cdk4 interaction in dividing myoblasts, coupled with the cyclin D1-dependent nuclear targeting of cdk4, suggests a mitogen-sensitive mechanism whereby cyclin D1 can regulate MyoD function and the onset of myogenesis by controlling the cellular location of cdk4 rather than the phosphorylation status of MyoD.  (+info)

Cloning and characterization of the promoters of the maxiK channel alpha and beta subunits. (3/28646)

Large conductance, calcium-activated potassium (maxiK) channels are expressed in nerve, muscle, and other cell types and are important determinants of smooth muscle tone. To determine the mechanisms involved in the transcriptional regulation of maxiK channels, we characterized the promoter regions of the pore forming (alpha) and regulatory (beta) subunits of the human channel complex. Maximum promoter activity (up to 12.3-fold over control) occurred between nucleotides -567 and -220 for the alpha subunit (hSlo) gene. The minimal promoter is GC-rich with 5 Sp-1 binding sites and several TCC repeats. Other transcription factor-binding motifs, including c/EBP, NF-kB, PU.1, PEA-3, Myo-D, and E2A, were observed in the 5'-flanking sequence. Additionally, a CCTCCC sequence, which increases the transcriptional activity of the SM1/2 gene in smooth muscle, is located 27 bp upstream of the TATA-like sequence, a location identical to that found in the SM1/2 5'-flanking region. However, the promoter directed equivalent expression when transfected into smooth muscle and other cell types. Analysis of the hSlo beta subunit 5'-flanking region revealed a TATA box at position -77 and maximum promoter activity (up to 11.0-fold) in a 200 bp region upstream from the cap site. Binding sites for GATA-1, Myo-D, c-myb, Ets-1/Elk-1, Ap-1, and Ik-2 were identified within this sequence. Two CCTCCC elements are present in the hSlo beta subunit promoter, but tissue-specific transcriptional activity was not observed. The lack of tissue-specific promoter activity, particularly the finding of promoter activity in cells from tissues in which the maxiK gene is not expressed, suggests a complex channel regulatory mechanism for hSlo genes. Moreover, the lack of similarity of the promoters of the two genes suggests that regulation of coordinate expression of the subunits does not occur through equivalent cis-acting sequences.  (+info)

Perioperative growth hormone treatment and functional outcome after major abdominal surgery: a randomized, double-blind, controlled study. (4/28646)

OBJECTIVE: To evaluate short- and long-term effects of perioperative human growth hormone (hGH) treatment on physical performance and fatigue in younger patients undergoing a major abdominal operation in a normal postoperative regimen with oral nutrition. SUMMARY BACKGROUND DATA: Muscle wasting and functional impairment follow major abdominal surgery. METHODS: Twenty-four patients with ulcerative colitis undergoing ileoanal J-pouch surgery were randomized to hGH (12 IU/day) or placebo treatment from 2 days before to 7 days after surgery. Measurements were performed 2 days before and 10, 30, and 90 days after surgery. RESULTS: The total muscle strength of four limb muscle groups was reduced by 7.6% in the hGH group and by 17.1% in the placebo group at postoperative day 10 compared with baseline values. There was also a significant difference between treatment groups in total muscle strength at day 30, and at the 90-day follow-up total muscle strength was equal to baseline values in the hGH group, but still significantly 5.9% below in the placebo group. The work capacity decreased by approximately 20% at day 10 after surgery, with no significant difference between treatment groups. Both groups were equally fatigued at day 10 after surgery, but at day 30 and 90 the hGH patients were less fatigued than the placebo patients. During the treatment period, patients receiving hGH had reduced loss of limb lean tissue mass, and 3 months after surgery the hGH patients had regained more lean tissue mass than placebo patients. CONCLUSIONS: Perioperative hGH treatment of younger patients undergoing major abdominal surgery preserved limb lean tissue mass, increased postoperative muscular strength, and reduced long-term postoperative fatigue.  (+info)

Spinal cord-evoked potentials and muscle responses evoked by transcranial magnetic stimulation in 10 awake human subjects. (5/28646)

Transcranial magnetic stimulation (TCMS) causes leg muscle contractions, but the neural structures in the brain that are activated by TCMS and their relationship to these leg muscle responses are not clearly understood. To elucidate this, we concomitantly recorded leg muscle responses and thoracic spinal cord-evoked potentials (SCEPs) after TCMS for the first time in 10 awake, neurologically intact human subjects. In this report we provide evidence of direct and indirect activation of corticospinal neurons after TCMS. In three subjects, SCEP threshold (T) stimulus intensities recruited both the D wave (direct activation of corticospinal neurons) and the first I wave (I1, indirect activation of corticospinal neurons). In one subject, the D, I1, and I2 waves were recruited simultaneously, and in another subject, the I1 and I2 waves were recruited simultaneously. In the remaining five subjects, only the I1 wave was recruited first. More waves were recruited as the stimulus intensity increased. The presence of D and I waves in all subjects at low stimulus intensities verified that TCMS directly and indirectly activated corticospinal neurons supplying the lower extremities. Leg muscle responses were usually contingent on the SCEP containing at least four waves (D, I1, I2, and I3).  (+info)

Wasting of the small hand muscles in upper and mid-cervical cord lesions. (6/28646)

Four patients are described with destructive rheumatoid arthritis of the cervical spine and neurogenic wasting of forearm and hand muscles. The pathological connection is not immediately obvious, but a relationship between these two observations is described here with clinical, radiological, electrophysiological and necropsy findings. Compression of the anterior spinal artery at upper and mid-cervical levels is demonstrated to be the likely cause of changes lower in the spinal cord. These are shown to be due to the resulting ischaemia of the anterior part of the lower cervical spinal cord, with degeneration of the neurones innervating the forearm and hand muscles. These findings favour external compression of the anterior spinal artery leading to ischaemia in a watershed area as the likeliest explanation for this otherwise inappropriate and bizarre phenomenon.  (+info)

Fas and Fas ligand interaction induces apoptosis in inflammatory myopathies: CD4+ T cells cause muscle cell injury directly in polymyositis. (7/28646)

OBJECTIVE: To investigate the involvement of the Fas/Fas ligand (Fas/FasL) system in the inflammatory myopathies. METHODS: Frozen muscle sections obtained from 7 patients with polymyositis (PM), 4 patients with dermatomyositis (DM), and 3 controls were studied by immunochemistry. Apoptosis was detected by DNA electrophoresis and in situ labeling using the TUNEL method. RESULTS: Fas was detected on muscle fibers and infiltrating mononuclear cells (MNC) in 6 PM patients and 2 DM patients. FasL was expressed mainly on CD4+ T cells and some CD8+ T cells, and on macrophages surrounding Fas-positive muscles in 4 PM patients and 1 DM patient. In 3 of the 5 patients with FasL-positive MNC, the TUNEL method showed that both invaded myonuclei and MNC underwent apoptosis. Chromosomal DNA from the muscle tissue of these patients showed ladder formation. CONCLUSION: Fas/FasL is involved in muscle cell apoptosis in at least 2 of the inflammatory myopathies, PM and DM. Although CD8+-mediated cytotoxicity is thought to be the main mechanism of muscle injury in PM, our data suggest that CD4+ T cells also directly cause muscle cell damage.  (+info)

A novel interaction mechanism accounting for different acylphosphatase effects on cardiac and fast twitch skeletal muscle sarcoplasmic reticulum calcium pumps. (8/28646)

In cardiac and skeletal muscle Ca2+ translocation from cytoplasm into sarcoplasmic reticulum (SR) is accomplished by different Ca2+-ATPases whose functioning involves the formation and decomposition of an acylphosphorylated phosphoenzyme intermediate (EP). In this study we found that acylphosphatase, an enzyme well represented in muscular tissues and which actively hydrolyzes EP, had different effects on heart (SERCA2a) and fast twitch skeletal muscle SR Ca2+-ATPase (SERCA1). With physiological acylphosphatase concentrations SERCA2a exhibited a parallel increase in the rates of both ATP hydrolysis and Ca2+ transport; in contrast, SERCA1 appeared to be uncoupled since the stimulation of ATP hydrolysis matched an inhibition of Ca2+ pump. These different effects probably depend on phospholamban, which is associated with SERCA2a but not SERCA1. Consistent with this view, the present study suggests that acylphosphatase-induced stimulation of SERCA2a, in addition to an enhanced EP hydrolysis, may be due to a displacement of phospholamban, thus to a removal of its inhibitory effect.  (+info)

There are several causes of muscle weakness, including:

1. Neuromuscular diseases: These are disorders that affect the nerves that control voluntary muscle movement, such as amyotrophic lateral sclerosis (ALS) and polio.
2. Musculoskeletal disorders: These are conditions that affect the muscles, bones, and joints, such as arthritis and fibromyalgia.
3. Metabolic disorders: These are conditions that affect the body's ability to produce energy, such as hypoglycemia and hypothyroidism.
4. Injuries: Muscle weakness can occur due to injuries such as muscle strains and tears.
5. Infections: Certain infections such as botulism and Lyme disease can cause muscle weakness.
6. Nutritional deficiencies: Deficiencies in vitamins and minerals such as vitamin D and B12 can cause muscle weakness.
7. Medications: Certain medications such as steroids and anticonvulsants can cause muscle weakness as a side effect.

The symptoms of muscle weakness can vary depending on the underlying cause, but may include:

1. Fatigue: Feeling tired or weak after performing simple tasks.
2. Lack of strength: Difficulty lifting objects or performing physical activities.
3. Muscle cramps: Spasms or twitches in the muscles.
4. Muscle wasting: Loss of muscle mass and tone.
5. Difficulty speaking or swallowing: In cases where the muscle weakness affects the face, tongue, or throat.
6. Difficulty walking or standing: In cases where the muscle weakness affects the legs or lower back.
7. Droopy facial features: In cases where the muscle weakness affects the facial muscles.

If you are experiencing muscle weakness, it is important to seek medical attention to determine the underlying cause and receive proper treatment. A healthcare professional will perform a physical examination and may order diagnostic tests such as blood tests or imaging studies to help diagnose the cause of the muscle weakness. Treatment will depend on the underlying cause, but may include medication, physical therapy, or lifestyle changes. In some cases, muscle weakness may be a sign of a serious underlying condition that requires prompt medical attention.

There are several types of muscular atrophy, including:

1. Disuse atrophy: This type of atrophy occurs when a muscle is not used for a long period, leading to its degeneration.
2. Neurogenic atrophy: This type of atrophy occurs due to damage to the nerves that control muscles.
3. Dystrophic atrophy: This type of atrophy occurs due to inherited genetic disorders that affect muscle fibers.
4. Atrophy due to aging: As people age, their muscles can degenerate and lose mass and strength.
5. Atrophy due to disease: Certain diseases such as cancer, HIV/AIDS, and muscular dystrophy can cause muscular atrophy.
6. Atrophy due to infection: Infections such as polio and tetanus can cause muscular atrophy.
7. Atrophy due to trauma: Traumatic injuries can cause muscular atrophy, especially if the injury is severe and leads to prolonged immobilization.

Muscular atrophy can lead to a range of symptoms depending on the type and severity of the condition. Some common symptoms include muscle weakness, loss of motor function, muscle wasting, and difficulty performing everyday activities. Treatment for muscular atrophy depends on the underlying cause and may include physical therapy, medication, and lifestyle changes such as exercise and dietary modifications. In severe cases, surgery may be necessary to restore muscle function.

1. Muscular dystrophy: A group of genetic disorders characterized by progressive muscle weakness and degeneration.
2. Myopathy: A condition where the muscles become damaged or diseased, leading to muscle weakness and wasting.
3. Fibromyalgia: A chronic condition characterized by widespread pain, fatigue, and muscle stiffness.
4. Rhabdomyolysis: A condition where the muscle tissue is damaged, leading to the release of myoglobin into the bloodstream and potentially causing kidney damage.
5. Polymyositis/dermatomyositis: Inflammatory conditions that affect the muscles and skin.
6. Muscle strain: A common injury caused by overstretching or tearing of muscle fibers.
7. Cervical dystonia: A movement disorder characterized by involuntary contractions of the neck muscles.
8. Myasthenia gravis: An autoimmune disorder that affects the nerve-muscle connection, leading to muscle weakness and fatigue.
9. Oculopharyngeal myopathy: A condition characterized by weakness of the muscles used for swallowing and eye movements.
10. Inclusion body myositis: An inflammatory condition that affects the muscles, leading to progressive muscle weakness and wasting.

These are just a few examples of the many different types of muscular diseases that can affect individuals. Each condition has its unique set of symptoms, causes, and treatment options. It's important for individuals experiencing muscle weakness or wasting to seek medical attention to receive an accurate diagnosis and appropriate care.

1. Duchenne muscular dystrophy: This is the most common form of muscular dystrophy in children, caused by a defect in the DMD gene that codes for dystrophin protein. It affects boys primarily and can lead to progressive muscle weakness and wasting, as well as cardiac and other complications.
2. Becker muscular dystrophy: This is a milder form of muscular dystrophy than Duchenne, caused by a defect in the DMD gene that codes for dystrophin protein. It primarily affects boys but can also affect girls.
3. Limb-girdle muscular dystrophy: This is a group of disorders characterized by progressive muscle weakness and degeneration, particularly affecting the shoulder and pelvic girdles. There are several types of limb-girdle muscular dystrophy, including type 1A, 1B, 2A, and 2B.
4. Facioscapulohumeral muscular dystrophy: This is a type of muscular dystrophy that affects the muscles of the face, shoulder blades, and upper arms. It can cause progressive muscle weakness, wasting, and fatigue.
5. Myotonic muscular dystrophy: This is the most common form of adult-onset muscular dystrophy, caused by a defect in the DMPK gene that codes for myotonia protein. It can cause progressive muscle stiffness, spasms, and weakness, as well as other complications such as cataracts and type 2 diabetes.

In animals, muscular dystrophy is similar to human forms of the disorder, caused by genetic mutations that affect muscle function and strength. It can be caused by a variety of factors, including genetics, nutrition, and environmental exposures.

Symptoms of muscular dystrophy in animals can include:

1. Progressive muscle weakness and wasting
2. Loss of coordination and balance
3. Difficulty walking or running
4. Muscle cramps and spasms
5. Poor appetite and weight loss
6. Increased breathing rate and difficulty breathing
7. Cardiac problems, such as arrhythmias and heart failure
8. Cognitive decline and seizures

Diagnosis of muscular dystrophy in animals is similar to human patients, involving a combination of physical examination, medical history, and diagnostic tests such as blood tests, imaging studies, and muscle biopsy.

Treatment for muscular dystrophy in animals is limited, but may include:

1. Supportive care, such as antibiotics for respiratory infections and pain management
2. Physical therapy to maintain joint mobility and prevent deformities
3. Nutritional support to ensure adequate nutrition and hydration
4. Medications to manage symptoms such as muscle spasms and seizures
5. Assistive devices, such as wheelchairs or slings, to improve mobility and quality of life

Prevention of muscular dystrophy in animals is not possible at present, but research into the genetic causes and potential treatments for the disease is ongoing. It is important for pet owners to be aware of the signs of muscular dystrophy and seek veterinary care if they suspect their pet may be affected.

Example sentences:

1. The runner experienced a muscle cramp in her leg during the marathon, causing her to slow down and almost drop out.
2. After experiencing frequent muscle cramps, the patient was diagnosed with hypokalemia, a condition characterized by low potassium levels.
3. During pregnancy, muscle cramps are common due to changes in hormone levels and increased pressure on the musculoskeletal system.
4. The elderly man's muscle cramps were caused by a lack of physical activity and dehydration, which can be a challenge for older adults.
5. Proper stretching and warm-up exercises can help prevent muscle cramps in athletes, especially those participating in endurance sports.

There are several possible causes of muscle rigidity, including:

1. Injury: Muscle rigidity can be a result of direct trauma to the muscle, such as a strain or sprain.
2. Infection: Certain infections, such as Lyme disease or endocarditis, can cause muscle rigidity as a symptom.
3. Neurological disorders: Conditions such as multiple sclerosis, Parkinson's disease, and stroke can all cause muscle rigidity due to damage to the nervous system.
4. Medication side effects: Certain medications, such as steroids and certain antidepressants, can cause muscle rigidity as a side effect.
5. Metabolic disorders: Conditions such as hypocalcemia (low calcium levels) and hyperthyroidism can cause muscle rigidity.
6. Autoimmune disorders: Conditions such as polymyositis and dermatomyositis can cause muscle rigidity due to inflammation of the muscles.

Symptoms of muscle rigidity may include:

* Stiffness or inflexibility in the affected muscles
* Pain or tenderness in the affected area
* Limited range of motion in the affected joints
* Muscle spasms or cramps
* Fatigue or weakness

Treatment for muscle rigidity will depend on the underlying cause. In some cases, medication may be prescribed to relax the muscles and improve mobility. Physical therapy and exercise may also be helpful in improving range of motion and strength. In other cases, treatment may involve addressing the underlying condition or disorder that is causing the muscle rigidity.

There are several types of hypertrophy, including:

1. Muscle hypertrophy: The enlargement of muscle fibers due to increased protein synthesis and cell growth, often seen in individuals who engage in resistance training exercises.
2. Cardiac hypertrophy: The enlargement of the heart due to an increase in cardiac workload, often seen in individuals with high blood pressure or other cardiovascular conditions.
3. Adipose tissue hypertrophy: The excessive growth of fat cells, often seen in individuals who are obese or have insulin resistance.
4. Neurological hypertrophy: The enlargement of neural structures such as brain or spinal cord due to an increase in the number of neurons or glial cells, often seen in individuals with neurodegenerative diseases such as Alzheimer's or Parkinson's.
5. Hepatic hypertrophy: The enlargement of the liver due to an increase in the number of liver cells, often seen in individuals with liver disease or cirrhosis.
6. Renal hypertrophy: The enlargement of the kidneys due to an increase in blood flow and filtration, often seen in individuals with kidney disease or hypertension.
7. Ovarian hypertrophy: The enlargement of the ovaries due to an increase in the number of follicles or hormonal imbalances, often seen in individuals with polycystic ovary syndrome (PCOS).

Hypertrophy can be diagnosed through various medical tests such as imaging studies (e.g., CT scans, MRI), biopsies, and blood tests. Treatment options for hypertrophy depend on the underlying cause and may include medications, lifestyle changes, and surgery.

In conclusion, hypertrophy is a growth or enlargement of cells, tissues, or organs in response to an excessive stimulus. It can occur in various parts of the body, including the brain, liver, kidneys, heart, muscles, and ovaries. Understanding the underlying causes and diagnosis of hypertrophy is crucial for effective treatment and management of related health conditions.

There are several types of muscle neoplasms, including:

1. Leiomyoma: A benign tumor that develops in the smooth muscle tissue of the uterus. It is the most common type of uterine tumor and is usually found in women over the age of 30.
2. Rhabdomyosarcoma: A rare type of cancerous muscle tumor that can develop in children and young adults. It can occur in any part of the body, but is most commonly found in the head, neck, or genitourinary tract.
3. Liposarcoma: A rare type of cancerous muscle tumor that develops in the fat cells of the soft tissue. It can occur in any part of the body and is more common in older adults.
4. Fibromyxoid tumor: A rare benign tumor that develops in the muscles and connective tissue. It usually affects the arms or legs and can be diagnosed at any age, but is most commonly found in children and young adults.
5. Alveolar soft part sarcoma: A rare type of cancerous muscle tumor that develops in the soft tissue of the body. It is more common in younger adults and can occur anywhere in the body, but is most commonly found in the legs or arms.

The symptoms of muscle neoplasms vary depending on the location and size of the tumor. They may include pain, swelling, redness, and limited mobility in the affected area. Diagnosis is usually made through a combination of imaging tests such as X-rays, CT scans, or MRI, and a biopsy to confirm the presence of cancerous cells.

Treatment for muscle neoplasms depends on the type and location of the tumor, as well as the stage of the disease. Surgery is often the first line of treatment, followed by radiation therapy or chemotherapy if the tumor is malignant. In some cases, observation and monitoring may be recommended if the tumor is benign and not causing any symptoms.

It's important to note that muscle neoplasms are relatively rare, and most muscle masses are benign and non-cancerous. However, it's always best to consult a medical professional if you notice any unusual lumps or bumps on your body to determine the cause and appropriate treatment.

There are several types of muscular dystrophies, including:

1. Duchenne muscular dystrophy (DMD): This is the most common form of muscular dystrophy, affecting males primarily. It is caused by a mutation in the dystrophin gene and is characterized by progressive muscle weakness, wheelchair dependence, and shortened lifespan.
2. Becker muscular dystrophy (BMD): This is a less severe form of muscular dystrophy than DMD, affecting both males and females. It is caused by a mutation in the dystrophin gene and is characterized by progressive muscle weakness, but with a milder course than DMD.
3. Limb-girdle muscular dystrophy (LGMD): This is a group of disorders that affect the muscles around the shoulders and hips, leading to progressive weakness and degeneration. There are several subtypes of LGMD, each with different symptoms and courses.
4. Facioscapulohumeral muscular dystrophy (FSHD): This is a rare form of muscular dystrophy that affects the muscles of the face, shoulder, and upper arm. It is caused by a mutation in the D4Z4 repeat on chromosome 4.
5. Myotonic dystrophy: This is the most common adult-onset form of muscular dystrophy, affecting both males and females. It is characterized by progressive muscle stiffness, weakness, and wasting, as well as other symptoms such as cataracts, myotonia, and cognitive impairment.

There is currently no cure for muscular dystrophies, but various treatments are available to manage the symptoms and slow the progression of the disease. These include physical therapy, orthotics and assistive devices, medications to manage pain and other symptoms, and in some cases, surgery. Researchers are actively working to develop new treatments and a cure for muscular dystrophies, including gene therapy, stem cell therapy, and small molecule therapies.

It's important to note that muscular dystrophy can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner, depending on the specific type of dystrophy. This means that the risk of inheriting the condition depends on the mode of inheritance and the presence of mutations in specific genes.

In summary, muscular dystrophy is a group of genetic disorders characterized by progressive muscle weakness and degeneration. There are several types of muscular dystrophy, each with different symptoms and courses. While there is currently no cure for muscular dystrophy, various treatments are available to manage the symptoms and slow the progression of the disease. Researchers are actively working to develop new treatments and a cure for muscular dystrophy.

Muscle spasticity can cause a range of symptoms, including:

* Increased muscle tone, leading to stiffness and rigidity
* Spasms or sudden contractions of the affected muscles
* Difficulty moving the affected limbs
* Pain or discomfort in the affected area
* Abnormal postures or movements

There are several potential causes of muscle spasticity, including:

* Neurological disorders such as cerebral palsy, multiple sclerosis, and spinal cord injuries
* Stroke or other brain injuries
* Muscle damage or inflammation
* Infections such as meningitis or encephalitis
* Metabolic disorders such as hypokalemia (low potassium levels) or hyperthyroidism

Treatment options for muscle spasticity include:

* Physical therapy to improve range of motion and strength
* Medications such as baclofen, tizanidine, or dantrolene to reduce muscle spasms
* Injectable medications such as botulinum toxin or phenol to destroy excess nerve fibers
* Surgery to release or sever affected nerve fibers
* Electrical stimulation therapy to improve muscle function and reduce spasticity.

It is important to note that muscle spasticity can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, maintain independence, and engage in social and recreational activities. As such, it is important to seek medical attention if symptoms of muscle spasticity are present to determine the underlying cause and develop an appropriate treatment plan.

The symptoms of DMD typically become apparent in early childhood and progress rapidly. They include:

* Delayed motor development
* Weakness and wasting of muscles, particularly in the legs and pelvis
* Muscle weakness that worsens over time
* Loss of muscle mass and fatigue
* Difficulty walking, running, or standing
* Heart problems, such as cardiomyopathy and arrhythmias
* Respiratory difficulties, such as breathing problems and pneumonia

DMD is diagnosed through a combination of clinical evaluation, muscle biopsy, and genetic testing. Treatment options are limited and focus on managing symptoms and improving quality of life. These may include:

* Physical therapy to maintain muscle strength and function
* Medications to manage pain, spasms, and other symptoms
* Assistive devices, such as braces and wheelchairs, to improve mobility and independence
* Respiratory support, such as ventilation assistance, to manage breathing difficulties

The progression of DMD is highly variable, with some individuals experiencing a more rapid decline in muscle function than others. The average life expectancy for individuals with DMD is approximately 25-30 years, although some may live into their 40s or 50s with appropriate medical care and support.

Duchenne muscular dystrophy is a devastating and debilitating condition that affects thousands of individuals worldwide. While there is currently no cure for the disorder, ongoing research and advancements in gene therapy and other treatments offer hope for improving the lives of those affected by DMD.

1. Polymyositis: This is an inflammatory disease that affects the muscles and can cause muscle weakness, pain, and stiffness.
2. Dercum's disease: This is a rare condition that causes fatty degeneration of the muscles, leading to muscle pain, weakness, and wasting.
3. Inflammatory myopathy: This is a group of conditions that cause inflammation in the muscles, leading to muscle weakness and pain.
4. Dermatomyositis: This is an inflammatory condition that affects both the skin and the muscles, causing skin rashes and muscle weakness.
5. Juvenile myositis: This is a rare condition that affects children and can cause muscle weakness, pain, and stiffness.

The symptoms of myositis can vary depending on the type of condition and its severity. Common symptoms include muscle weakness, muscle pain, stiffness, and fatigue. Other symptoms may include skin rashes, fever, and joint pain.

The diagnosis of myositis typically involves a combination of physical examination, medical history, and laboratory tests such as blood tests and muscle biopsies. Treatment for myositis depends on the underlying cause and may include medications such as corticosteroids, immunosuppressive drugs, and physical therapy. In some cases, surgery may be necessary to remove affected muscle tissue.

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

Muscle mass is an important component of overall body strength, and as people age, their muscles naturally begin to atrophy due to a combination of hormonal changes and disuse. This leads to a decrease in the amount of protein available for other bodily functions, which can further exacerbate the decline in physical functioning.

Sarcopenia can be caused by various factors such as inactivity, malnutrition, chronic diseases like diabetes and heart disease, and genetics. It is a major risk factor for falls, disability, and cognitive decline in the elderly population.

There is no single test to diagnose sarcopenia, but healthcare professionals use a combination of physical examination, medical history, and laboratory tests to assess muscle mass and function. Treatment options include resistance training exercises, nutritional supplements, and medications such as selective estrogen receptor modulators (SERMs) and growth hormone-releasing peptides.

In conclusion, sarcopenia is a progressive condition that affects the muscles in older adults, leading to a loss of strength and physical functioning. It can be caused by various factors, and healthcare professionals use a combination of physical examination and laboratory tests to diagnose and treat it.

1. Muscular dystrophy: A group of genetic disorders that cause progressive muscle weakness and degeneration.
2. Amyotrophic lateral sclerosis (ALS): A progressive neurological disease that affects nerve cells in the brain and spinal cord, leading to muscle weakness, paralysis, and eventually death.
3. Spinal muscular atrophy: A genetic disorder that affects the nerve cells responsible for controlling voluntary muscle movement.
4. Peripheral neuropathy: A condition that causes damage to the peripheral nerves, leading to weakness, numbness, and pain in the hands and feet.
5. Myasthenia gravis: An autoimmune disorder that affects the nerve-muscle connection, causing muscle weakness and fatigue.
6. Neuropathy: A term used to describe damage to the nerves, which can cause a range of symptoms including numbness, tingling, and pain in the hands and feet.
7. Charcot-Marie-Tooth disease: A group of inherited disorders that affect the peripheral nerves, leading to muscle weakness and wasting.
8. Guillain-Barré syndrome: An autoimmune disorder that causes inflammation and damage to the nerves, leading to muscle weakness and paralysis.
9. Botulism: A bacterial infection that can cause muscle weakness and paralysis by blocking the release of the neurotransmitter acetylcholine.
10. Myotonia congenita: A genetic disorder that affects the nerve-muscle connection, causing muscle stiffness and rigidity.

These are just a few examples of neuromuscular diseases, and there are many more conditions that can cause muscle weakness and fatigue. It's important to see a doctor if you experience persistent or severe symptoms to receive an accurate diagnosis and appropriate treatment.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

There are several potential causes of muscle hypertonia, including:

1. Neurological disorders such as cerebral palsy, Parkinson's disease, or multiple sclerosis
2. Musculoskeletal injuries or inflammation
3. Infections such as Lyme disease or viral infections
4. Metabolic disorders such as hypokalemia (low potassium levels) or hyperthyroidism
5. Adverse reactions to certain medications
6. Emotional stress or anxiety

Symptoms of muscle hypertonia can vary depending on the severity and location of the condition, but may include:

1. Stiffness and rigidity of the affected muscles
2. Pain or tenderness in the muscles
3. Limited range of motion in the affected joints
4. Fatigue or weakness in the affected limbs
5. Difficulty with movement and balance
6. Muscle spasms or cramping

Treatment for muscle hypertonia typically involves a combination of physical therapy, medication, and lifestyle modifications. Physical therapy may include stretching and strengthening exercises to improve range of motion and reduce stiffness, as well as techniques such as heat or cold therapy to relax the muscles. Medications such as muscle relaxants or anti-inflammatory drugs may be prescribed to reduce muscle spasms and inflammation. Lifestyle modifications such as regular exercise, proper nutrition, and stress management techniques can also help to reduce symptoms of muscle hypertonia. In severe cases, surgery may be necessary to release or lengthen the affected muscles.

There are several factors that can contribute to the development of insulin resistance, including:

1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.

There are several ways to diagnose insulin resistance, including:

1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.

There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:

1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.

Medications that may be used to treat insulin resistance include:

1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.

It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.

Examples of atrophic muscular disorders include:

1. Muscular dystrophy: A group of inherited disorders that cause progressive loss of muscle mass and strength, leading to muscle wasting and weakness.
2. Myotonia congenita: An autosomal dominant disorder characterized by muscle stiffness and spasms, particularly in the neck, shoulder, and limb muscles.
3. Inclusion body myositis: An inflammatory muscle disease that leads to progressive muscle weakness and wasting, with deposits of abnormal protein called inclusion bodies in the muscle fibers.
4. Limb-girdle muscular dystrophy: A group of inherited disorders that cause progressive loss of muscle mass and strength in the arms and legs, leading to muscle wasting and weakness.
5. Facioscapulohumeral muscular dystrophy: An inherited disorder characterized by progressive weakness of the facial, shoulder, and upper arm muscles, with a loss of motor neurons in the spinal cord.

The symptoms of atrophic muscular disorders can vary depending on the specific disorder and its severity, but may include:

1. Muscle weakness and wasting
2. Muscle cramps and spasms
3. Difficulty walking or standing
4. Fatigue and decreased endurance
5. Loss of motor neurons in the spinal cord
6. Cognitive impairment
7. Developmental delays
8. Vision loss
9. Hearing loss
10. Skeletal deformities

Atrophic muscular disorders can be diagnosed through a combination of clinical evaluation, electromyography (EMG), and muscle biopsy. Treatment is focused on managing the symptoms and slowing the progression of the disease, and may include:

1. Physical therapy to maintain muscle strength and function
2. Medications to manage pain and spasms
3. Assistive devices such as braces and walkers
4. Respiratory support in advanced cases
5. Gene therapy is an area of ongoing research, but it is not yet widely available for the treatment of atrophic muscular disorders.

It is important to note that atrophic muscular disorders are a group of rare and complex conditions, and each type has its own unique set of symptoms and characteristics. If you suspect that you or someone you know may be experiencing symptoms of an atrophic muscular disorder, it is important to consult with a healthcare professional for proper evaluation and diagnosis.

1. Complete paralysis: When there is no movement or sensation in a particular area of the body.
2. Incomplete paralysis: When there is some movement or sensation in a particular area of the body.
3. Localized paralysis: When paralysis affects only a specific part of the body, such as a limb or a facial muscle.
4. Generalized paralysis: When paralysis affects multiple parts of the body.
5. Flaccid paralysis: When there is a loss of muscle tone and the affected limbs feel floppy.
6. Spastic paralysis: When there is an increase in muscle tone and the affected limbs feel stiff and rigid.
7. Paralysis due to nerve damage: This can be caused by injuries, diseases such as multiple sclerosis, or birth defects such as spina bifida.
8. Paralysis due to muscle damage: This can be caused by injuries, such as muscular dystrophy, or diseases such as muscular sarcopenia.
9. Paralysis due to brain damage: This can be caused by head injuries, stroke, or other conditions that affect the brain such as cerebral palsy.
10. Paralysis due to spinal cord injury: This can be caused by trauma, such as a car accident, or diseases such as polio.

Paralysis can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, work, and participate in social and recreational activities. Treatment options for paralysis depend on the underlying cause and may include physical therapy, medications, surgery, or assistive technologies such as wheelchairs or prosthetic devices.

Hypotonia is a state of decreased muscle tone, which can be caused by various conditions, such as injury, disease, or disorders that affect the nervous system. It is characterized by a decrease in muscle stiffness and an increase in joint range of motion. Muscle hypotonia can result in difficulty with movement, coordination, and balance.

There are several types of muscle hypotonia, including:

1. Central hypotonia: This type is caused by dysfunction in the central nervous system and results in a decrease in muscle tone throughout the body.
2. Peripheral hypotonia: This type is caused by dysfunction in the peripheral nervous system and results in a selective decrease in muscle tone in specific muscle groups.
3. Mixed hypotonia: This type combines central and peripheral hypotonia.

Muscle hypotonia can be associated with a variety of symptoms, such as fatigue, weakness, poor coordination, and difficulty with speech and swallowing. Treatment options vary depending on the underlying cause of the condition and may include physical therapy, medication, and lifestyle modifications.

Muscle hypotonia is a common condition that can affect people of all ages, from children to adults. Early diagnosis and treatment are important to help manage symptoms and improve quality of life. If you suspect you or your child may have muscle hypotonia, consult with a healthcare professional for proper evaluation and treatment.

The exact cause of cachexia is not fully understood, but it is thought to be related to a combination of factors such as inflammation, hormonal imbalances, and changes in metabolism. Treatment for cachexia often focuses on addressing the underlying cause of the wasting, such as managing cancer or HIV/AIDS, as well as providing nutritional support and addressing any related complications.

In the medical field, cachexia is a serious condition that requires careful management to improve quality of life and outcomes for patients. It is important for healthcare providers to be aware of the signs and symptoms of cachexia and to provide appropriate treatment and support to affected individuals.

The term "decerebrate" comes from the Latin word "cerebrum," which means brain. In this context, the term refers to a state where the brain is significantly damaged or absent, leading to a loss of consciousness and other cognitive functions.

Some common symptoms of the decerebrate state include:

* Loss of consciousness
* Flaccid paralysis (loss of muscle tone)
* Dilated pupils
* Lack of responsiveness to stimuli
* Poor or absent reflexes
* Inability to speak or communicate

The decerebrate state can be caused by a variety of factors, including:

* Severe head injury
* Stroke or cerebral vasculature disorders
* Brain tumors or cysts
* Infections such as meningitis or encephalitis
* Traumatic brain injury

Treatment for the decerebrate state is typically focused on addressing the underlying cause of the condition. This may involve medications to control seizures, antibiotics for infections, or surgery to relieve pressure on the brain. In some cases, the decerebrate state may be a permanent condition, and individuals may require long-term care and support.

There are different types of anoxia, including:

1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.

Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.

Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.

In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.

The exact cause of malignant hyperthermia is not fully understood, but it is believed to be related to a genetic predisposition and exposure to certain anesthetic agents. The condition can be triggered by a variety of factors, including the use of certain anesthetics, stimulation of the sympathetic nervous system, and changes in blood sugar levels.

Symptoms of malignant hyperthermia can include:

* Elevated body temperature (usually above 104°F/40°C)
* Muscle rigidity and stiffness
* Heart arrhythmias and palpitations
* Shivering or tremors
* Confusion, agitation, or other neurological symptoms
* Shortness of breath or respiratory failure

If left untreated, malignant hyperthermia can lead to serious complications such as seizures, brain damage, and even death. Treatment typically involves the immediate discontinuation of any triggering anesthetic agents, cooling measures such as ice packs or cold compresses, and medications to help regulate body temperature and reduce muscle rigidity. In severe cases, mechanical ventilation may be necessary to support breathing.

Overall, malignant hyperthermia is a rare but potentially life-threatening condition that requires prompt recognition and treatment to prevent serious complications and improve outcomes.

There are several types of ischemia, including:

1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.

Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.

The symptoms of myositis, inclusion body can vary in severity and may include:

* Muscle weakness and wasting, particularly in the legs and pelvis
* Muscle pain and stiffness
* Fatigue
* Limited range of motion in affected joints
* Difficulty swallowing or breathing (in severe cases)

The condition typically affects adults over the age of 50, and men are more frequently affected than women. The exact cause of myositis, inclusion body is not known, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy muscle tissue.

There is no cure for myositis, inclusion body, but treatment options are available to manage the symptoms and slow the progression of the condition. These may include:

* Medications such as corticosteroids, immunosuppressive drugs, and anti-inflammatory agents
* Physical therapy to maintain muscle strength and flexibility
* Assistive devices such as canes or walkers to improve mobility
* In severe cases, surgery may be necessary to repair damaged muscles or tendons.

It is important for individuals with myositis, inclusion body to work closely with their healthcare provider to develop a personalized treatment plan and monitor their condition regularly to adjust the treatment as needed. With appropriate management, many people with this condition are able to lead active and fulfilling lives.

There are several subtypes of LGMD, each caused by mutations in different genes that code for proteins involved in muscle function and structure. The most common forms of LGMD include:

1. Muscular dystrophy-dystroglycanopathy type A (MDDGA): This is a severe form of LGMD caused by mutations in the DAG1 gene, which codes for the protein dystroglycan. Symptoms typically appear in infancy and progress rapidly, leading to early death.
2. Limb-girdle muscular dystrophy type 1A (LGMD1A): This is a mild form of LGMD caused by mutations in the LAMA2 gene, which codes for the protein laminin alpha 2 chain. Symptoms typically appear in childhood and progress slowly over time.
3. Limb-girdle muscular dystrophy type 2B (LGMD2B): This is a severe form of LGMD caused by mutations in the CAV3 gene, which codes for the protein caveolin-3. Symptoms typically appear in childhood and progress rapidly, leading to early death.

There is currently no cure for LGMD, but various treatments are available to manage symptoms and slow disease progression. These may include physical therapy, orthotics and assistive devices, pain management medications, and respiratory support as needed. Research into the genetic causes of LGMD is ongoing, with the goal of developing new and more effective treatments for this debilitating group of disorders.

Polymyositis can affect people of all ages, but it most commonly occurs in adults between the ages of 30 and 60. It is more common in women than men, and the symptoms can vary in severity. The disease may be acute or chronic, and it can affect one or more muscle groups.

The symptoms of polymyositis include:

* Muscle weakness and fatigue
* Pain in the affected muscles
* Wasting of the affected muscles
* Difficulty swallowing (in severe cases)
* Shortness of breath (in severe cases)

The diagnosis of polymyositis is based on a combination of clinical findings, laboratory tests, and imaging studies. Laboratory tests may include blood tests to check for muscle enzymes and inflammatory markers, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Imaging studies, such as magnetic resonance imaging (MRI), can help to confirm the diagnosis and assess the extent of the disease.

There is no cure for polymyositis, but treatment can help to manage the symptoms and slow the progression of the disease. Treatment options may include:

* Corticosteroids to reduce inflammation
* Immunosuppressive drugs to suppress the immune system
* Physical therapy to maintain muscle strength and function
* Pain management with analgesics and other medications
* Plasmapheresis to remove antibodies from the blood

The prognosis for polymyositis varies, depending on the severity of the disease and the response to treatment. In general, the prognosis is better for patients who have a mild form of the disease and who respond well to treatment. However, in severe cases, the disease can be life-threatening, and mortality rates are estimated to be as high as 20% to 30%.

The symptoms of dermatomyositis can vary in severity and may include:

* Rashes and lesions on the skin, particularly on the face, neck, and hands
* Muscle weakness and fatigue
* Joint pain and stiffness
* Swelling and redness in the affected areas
* Fever
* Headaches
* Fatigue

Dermatomyositis is often associated with other autoimmune disorders, such as polymyositis, and can be triggered by certain medications or infections. There is no cure for dermatomyositis, but treatment options are available to manage the symptoms and prevent complications. Treatment may include medications such as corticosteroids, immunosuppressive drugs, and physical therapy to maintain muscle strength and flexibility.

The term "dermatomyositis" is derived from the Greek words "derma," meaning skin, "myo," meaning muscle, and "-itis," indicating inflammation. The condition was first described in the medical literature in the early 20th century, and since then has been studied extensively to better understand its causes and develop effective treatments.

In summary, dermatomyositis is a rare autoimmune disease that affects both the skin and muscles, causing inflammation and various symptoms such as rashes, weakness, and joint pain. While there is no cure for the condition, treatment options are available to manage the symptoms and prevent complications.

There are two main types of myotonia:

1. Thomsen's disease: This is an inherited form of myotonia that affects the muscles of the face, neck, and limbs. It is caused by mutations in the CLCN1 gene and can be severe, causing difficulty with speaking, swallowing, and breathing.
2. Becker's muscular dystrophy: This is a form of muscular dystrophy that affects both the skeletal and cardiac muscles. It is caused by mutations in the DMPK gene and can cause myotonia, muscle weakness, and heart problems.

The symptoms of myotonia can vary depending on the severity of the condition and may include:

* Muscle stiffness and rigidity
* Spasms or twitches
* Difficulty with movement and mobility
* Fatigue and weakness
* Cramps
* Muscle wasting

Myotonia can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electromyography (EMG) and muscle biopsy. There is no cure for myotonia, but treatment options may include:

* Physical therapy to improve movement and mobility
* Medications to relax muscles and reduce spasms
* Lifestyle modifications such as avoiding triggers and taking regular breaks to rest
* Surgery in severe cases to release or lengthen affected muscles.

It is important to note that myotonia can be a symptom of other underlying conditions, so proper diagnosis and management by a healthcare professional is essential to determine the best course of treatment.

The term "nemaline" refers to the rod-like structures that are found in the muscle fibers of people with this condition. These structures are composed of abnormally folded myofibrils (the basic units of muscle tissue) and are thought to be caused by faulty protein synthesis or degradation.

Nemaline myopathy can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner, depending on the specific mutations that cause the condition. The disorder is usually diagnosed through muscle biopsy and genetic testing. Treatment options are limited and may include physical therapy, bracing, and medications to manage symptoms such as muscle spasms and weakness.

The progression of nemaline myopathy can vary widely among individuals, with some experiencing mild symptoms while others may have more severe muscle weakness and wasting. In some cases, the disorder may be associated with other medical conditions such as intellectual disability, seizures, or congenital anomalies.

The exact prevalence of nemaline myopathy is not known, but it is estimated to affect approximately 1 in 50,000 to 1 in 100,000 individuals worldwide. The disorder can occur at any age, but most cases are diagnosed in infancy or childhood. With advances in medical technology and ongoing research, there is hope for improved treatment options and management strategies for nemaline myopathy in the future.

Early Postmortem Changes:

1. Cessation of metabolic processes: After death, the body's metabolic processes come to a standstill, leading to a decrease in body temperature, cellular respiration, and other physiological functions.
2. Decline in blood pressure: The heart stops pumping blood, causing a rapid decline in blood pressure.
3. Cardiac arrest: The heart stops beating, leading to a lack of oxygen supply to the body's tissues.
4. Brain death: The brain ceases to function, causing a loss of consciousness and reflexes.
5. Rigor mortis: The muscles become stiff and rigid due to the buildup of lactic acid and other metabolic byproducts.
6. Livor mortis: Blood settles in the dependent parts of the body, causing discoloration and swelling.
7. Algor mortis: The body's temperature cools, causing the skin to feel cool to the touch.

Late Postmortem Changes:

1. Decomposition: Bacteria and other microorganisms begin to break down the body's tissues, leading to putrefaction and decay.
2. Autolysis: Enzymes within the body's cells break down cellular components, causing self-digestion and softening of the tissues.
3. Lipid decomposition: Fats and oils in the body undergo oxidation, leading to the formation of offensive odors.
4. Coagulative necrosis: Blood pools in the body's tissues, causing damage to the cells and tissues.
5. Putrefaction: Bacteria in the gut and other parts of the body cause the breakdown of tissues, leading to the formation of gases and fluids.

It is important to note that postmortem changes can significantly impact the interpretation of autopsy findings and the determination of cause of death. Therefore, it is essential to consider these changes when performing an autopsy and interpreting the results.

Wasting syndrome is characterized by weight loss, muscle wasting, and a decrease in body condition score. It can also lead to a range of other health problems such as dehydration, electrolyte imbalances, and decreased immune function.

To diagnose wasting syndrome in your cat, your veterinarian will need to perform a series of tests to rule out other potential causes of weight loss and muscle wasting. These tests may include blood work, urinalysis, and imaging studies such as X-rays or ultrasound.

Treatment for wasting syndrome will depend on the underlying cause of the condition. For example, if the condition is caused by chronic kidney disease, treatment may involve managing the symptoms of the disease and providing supportive care such as fluid therapy and medication to help slow the progression of the disease.

In addition to medical treatment, there are several things you can do at home to help your cat feel more comfortable and manage their weight loss. These include:

* Providing a high-quality, nutrient-rich diet that is appropriate for your cat's age, health status, and lifestyle.
* Encouraging your cat to drink plenty of water by placing multiple water bowls around the house and making water more appealing through the use of flavored or scented water.
* Providing a safe and comfortable environment for your cat to rest and relax.
* Monitoring your cat's weight and body condition score regularly and working with your veterinarian to adjust their diet and treatment plan as needed.

It is important to work closely with your veterinarian to manage wasting syndrome in your cat, as this condition can have a significant impact on their quality of life and longevity. With proper diagnosis and treatment, many cats are able to recover from wasting syndrome and lead happy, healthy lives.

There are several types of strabismus, including:

* Esotropia: where one eye turns inward toward the nose
* Exotropia: where one eye turns outward away from the face
* Hypertropia: where one eye turns upward
* Hypotropia: where one eye turns downward
* Duane's syndrome: a rare type of strabismus that affects only one eye and is caused by nerve damage.

Strabismus can have both visual and social consequences, including:

* Difficulty with depth perception and binocular vision
* Blurred or double vision
* Difficulty with eye teaming and tracking
* Poor eye-hand coordination
* Social and emotional effects such as low self-esteem, anxiety, and depression.

Treatment options for strabismus include:

* Glasses or contact lenses to correct refractive errors
* Prism lenses to align the eyes
* Eye exercises to strengthen the muscles and improve eye teaming
* Surgery to adjust the position of the muscles that control eye movement.

It is important for individuals with strabismus to receive timely and appropriate treatment to address the underlying cause of the condition and prevent long-term vision loss and social difficulties.

There are different types of hyperplasia, depending on the location and cause of the condition. Some examples include:

1. Benign hyperplasia: This type of hyperplasia is non-cancerous and does not spread to other parts of the body. It can occur in various tissues and organs, such as the uterus (fibroids), breast tissue (fibrocystic changes), or prostate gland (benign prostatic hyperplasia).
2. Malignant hyperplasia: This type of hyperplasia is cancerous and can invade nearby tissues and organs, leading to serious health problems. Examples include skin cancer, breast cancer, and colon cancer.
3. Hyperplastic polyps: These are abnormal growths that occur in the gastrointestinal tract and can be precancerous.
4. Adenomatous hyperplasia: This type of hyperplasia is characterized by an increase in the number of glandular cells in a specific organ, such as the colon or breast. It can be a precursor to cancer.

The symptoms of hyperplasia depend on the location and severity of the condition. In general, they may include:

* Enlargement or swelling of the affected tissue or organ
* Pain or discomfort in the affected area
* Abnormal bleeding or discharge
* Changes in bowel or bladder habits
* Unexplained weight loss or gain

Hyperplasia is diagnosed through a combination of physical examination, imaging tests such as ultrasound or MRI, and biopsy. Treatment options depend on the underlying cause and severity of the condition, and may include medication, surgery, or other interventions.

There are several types of atrophy that can occur in different parts of the body. For example:

1. Muscular atrophy: This occurs when muscles weaken and shrink due to disuse or injury.
2. Neuronal atrophy: This occurs when nerve cells degenerate, leading to a loss of cognitive function and memory.
3. Cardiac atrophy: This occurs when the heart muscle weakens and becomes less efficient, leading to decreased cardiac output.
4. Atrophic gastritis: This is a type of stomach inflammation that can lead to the wasting away of the stomach lining.
5. Atrophy of the testes: This occurs when the testes shrink due to a lack of use or disorder, leading to decreased fertility.

Atrophy can be diagnosed through various medical tests and imaging studies, such as MRI or CT scans. Treatment for atrophy depends on the underlying cause and may involve physical therapy, medication, or surgery. In some cases, atrophy can be prevented or reversed with proper treatment and care.

In summary, atrophy is a degenerative process that can occur in various parts of the body due to injury, disease, or disuse. It can lead to a loss of function and decreased quality of life, but with proper diagnosis and treatment, it may be possible to prevent or reverse some forms of atrophy.

There are several types of carotid artery injuries, including:

1. Carotid artery dissection: This is a tear in the inner lining of the artery that can lead to bleeding and inflammation.
2. Carotid artery thrombosis: This is the formation of a blood clot within the artery that can block blood flow to the brain.
3. Carotid artery occlusion: This is the complete blockage of the artery, which can cause a stroke or transient ischemic attack (TIA).
4. Carotid artery injury due to trauma: This type of injury can occur as a result of a blow to the neck or head.
5. Carotid artery injury due to surgery: This type of injury can occur during surgical procedures that involve the carotid arteries, such as endarterectomy or stenting.

The symptoms of carotid artery injuries can vary depending on the severity of the injury and the location of the damage. Some common symptoms include:

* Sudden weakness or numbness in the face, arm, or leg
* Sudden confusion or trouble speaking
* Sudden vision loss or double vision
* Sudden difficulty walking or maintaining balance
* Sudden severe headache

The diagnosis of carotid artery injuries is typically made using imaging tests such as ultrasound, computed tomography (CT) scans, or magnetic resonance imaging (MRI). Treatment options for carotid artery injuries depend on the severity and location of the injury, and may include medications, endovascular procedures, or surgery.

Prevention of carotid artery injuries is key to reducing the risk of complications. This can be achieved through:

* Maintaining a healthy lifestyle, including regular exercise and a balanced diet
* Avoiding smoking and limiting alcohol consumption
* Managing underlying medical conditions such as high blood pressure or diabetes
* Properly managing medications that may increase the risk of bleeding or injury
* Using appropriate precautions during surgical procedures, such as using sterile equipment and monitoring for signs of bleeding or injury.

In conclusion, carotid artery injuries can have serious consequences if left untreated. It is important to be aware of the causes, symptoms, diagnosis, and treatment options for these injuries in order to provide appropriate care and prevent complications. Proper precautions during surgical procedures and a healthy lifestyle can also help reduce the risk of carotid artery injuries.

Example sentences:

1. The patient experienced a spasm in their leg while running, causing them to stumble and fall.
2. The doctor diagnosed the patient with muscle spasms caused by dehydration and recommended increased fluids and stretching exercises.
3. The athlete suffered from frequent leg spasms during their training, which affected their performance and required regular massage therapy to relieve the discomfort.

Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.

There are many different types of fibrosis, including:

* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.

Fibrosis can be diagnosed through a variety of methods, including:

* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.

There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:

* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.

It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.

There are several different types of obesity, including:

1. Central obesity: This type of obesity is characterized by excess fat around the waistline, which can increase the risk of health problems such as type 2 diabetes and cardiovascular disease.
2. Peripheral obesity: This type of obesity is characterized by excess fat in the hips, thighs, and arms.
3. Visceral obesity: This type of obesity is characterized by excess fat around the internal organs in the abdominal cavity.
4. Mixed obesity: This type of obesity is characterized by both central and peripheral obesity.

Obesity can be caused by a variety of factors, including genetics, lack of physical activity, poor diet, sleep deprivation, and certain medications. Treatment for obesity typically involves a combination of lifestyle changes, such as increased physical activity and a healthy diet, and in some cases, medication or surgery may be necessary to achieve weight loss.

Preventing obesity is important for overall health and well-being, and can be achieved through a variety of strategies, including:

1. Eating a healthy, balanced diet that is low in added sugars, saturated fats, and refined carbohydrates.
2. Engaging in regular physical activity, such as walking, jogging, or swimming.
3. Getting enough sleep each night.
4. Managing stress levels through relaxation techniques, such as meditation or deep breathing.
5. Avoiding excessive alcohol consumption and quitting smoking.
6. Monitoring weight and body mass index (BMI) on a regular basis to identify any changes or potential health risks.
7. Seeking professional help from a healthcare provider or registered dietitian for personalized guidance on weight management and healthy lifestyle choices.

There are several types of ophthalmoplegia, including:

1. External ophthalmoplegia: This type affects the muscles that control lateral and vertical movements of the eyes.
2. Internal ophthalmoplegia: This type affects the muscles that control rotational movements of the eyes.
3. Superior oblique paresis: This type affects the superior oblique muscle, which controls downward and outward movements of the eye.
4. Inferior oblique paresis: This type affects the inferior oblique muscle, which controls upward and outward movements of the eye.

Symptoms of ophthalmoplegia may include difficulty moving the eyes, double vision, droopy eyelids, and blurred vision. Treatment options depend on the underlying cause of the condition and may include physical therapy, prism lenses, or surgery.

Arteriosclerosis can affect any artery in the body, but it is most commonly seen in the arteries of the heart, brain, and legs. It is a common condition that affects millions of people worldwide and is often associated with aging and other factors such as high blood pressure, high cholesterol, diabetes, and smoking.

There are several types of arteriosclerosis, including:

1. Atherosclerosis: This is the most common type of arteriosclerosis and occurs when plaque builds up inside the arteries.
2. Arteriolosclerosis: This type affects the small arteries in the body and can cause decreased blood flow to organs such as the kidneys and brain.
3. Medial sclerosis: This type affects the middle layer of the artery wall and can cause stiffness and narrowing of the arteries.
4. Intimal sclerosis: This type occurs when plaque builds up inside the innermost layer of the artery wall, causing it to become thick and less flexible.

Symptoms of arteriosclerosis can include chest pain, shortness of breath, leg pain or cramping during exercise, and numbness or weakness in the limbs. Treatment for arteriosclerosis may include lifestyle changes such as a healthy diet and regular exercise, as well as medications to lower blood pressure and cholesterol levels. In severe cases, surgery may be necessary to open up or bypass blocked arteries.

Neoplasms can be classified as benign (non-cancerous) or malignant (cancerous). Malignant neoplasms can further be divided into primary neoplasms, which originate in the muscle tissue itself, and secondary neoplasms, which spread to the muscle from another part of the body.

Examples of malignant muscle neoplasms include rhabdomyosarcoma (a type of cancer that arises in immature muscle cells) and adult-type fibromyxoma (a rare, slow-growing tumor that usually affects the extremities).

In contrast, benign muscle neoplasms are non-cancerous growths that do not spread to other parts of the body. Examples include benign fibrous histiocytomas and benign pleomorphic adipose tumors.

Neoplasms, Muscle Tissue Symptoms The symptoms of muscle neoplasms vary depending on their size, location, and malignant potential. In general, patients may experience painless lumps or masses, muscle weakness or wasting, and localized swelling or redness.

Diagnosis The diagnosis of muscle neoplasms is based on a combination of clinical findings, imaging studies (such as MRI or CT scans), and biopsy results. Imaging studies can help to identify the size, location, and extent of the tumor, while biopsy can provide a definitive diagnosis by examining the tissue under a microscope.

Treatment Treatment options for muscle neoplasms depend on the type, size, location, and malignant potential of the tumor, as well as the patient's overall health. Surgery is often the primary treatment modality for both benign and malignant muscle neoplasms. In some cases, radiation therapy or chemotherapy may be added to the treatment regimen.

Prognosis The prognosis for patients with muscle neoplasms varies depending on the type and malignant potential of the tumor. In general, benign muscle neoplasms have a good prognosis and do not spread to other parts of the body, while malignant muscle neoplasms can be aggressive and may have a poorer prognosis if left untreated.

Differential Diagnosis The differential diagnosis for muscle neoplasms includes other soft tissue tumors such as lipomas, hemangiomas, and synovial sarcomas, as well as non-tumorous conditions such as inflammatory myopathies and fibromatoses.

There are two main types of myotonic dystrophy:

1. Type 1 (also known as DM1): This is the most common form of the disorder and affects about 90% of all cases. It is caused by a mutation in the DMPK gene on chromosome 19.
2. Type 2 (also known as DM2): This form of the disorder is less common and affects about 10% of all cases. It is caused by a mutation in the CNBP gene on chromosome 3.

Symptoms of myotonic dystrophy typically appear in adults between the ages of 20 and 40, but can sometimes be present at birth. They may include:

* Muscle stiffness and rigidity
* Weakness of the face, neck, and limbs
* Difficulty swallowing (dysphagia)
* Difficulty speaking or slurred speech (dysarthria)
* Eye problems, such as cataracts or muscle imbalance in the eyelids
* Cramps and muscle spasms
* Fatigue and weakness
* Slowed muscle relaxation after contraction (myotonia)

Myotonic dystrophy is diagnosed through a combination of physical examination, medical history, and genetic testing. There is currently no cure for the disorder, but various treatments can help manage symptoms and slow its progression. These may include:

* Physical therapy to improve muscle strength and function
* Medications to relax muscles and reduce spasms
* Speech therapy to improve communication and swallowing difficulties
* Occupational therapy to assist with daily activities and independence
* Orthotics and assistive devices to help with mobility and other challenges

It is important for individuals with myotonic dystrophy to work closely with their healthcare providers to manage their symptoms and maintain a good quality of life. With appropriate treatment and support, many people with the disorder are able to lead active and fulfilling lives.

There are several types of mitochondrial myopathies, each with different clinical features and inheritance patterns. Some of the most common forms include:

1. Kearns-Sayre syndrome: This is a rare progressive disorder that affects the nervous system, muscles, and other organs. It is characterized by weakness and paralysis, seizures, and vision loss.
2. MELAS syndrome (mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes): This condition is characterized by recurring stroke-like episodes, seizures, muscle weakness, and cognitive decline.
3. MERRF (myoclonic epilepsy with ragged red fibers): This disorder is characterized by myoclonus (muscle jerks), seizures, and progressive muscle weakness.
4. LHON (Leber's hereditary optic neuropathy): This condition affects the optic nerve and can lead to sudden vision loss.

The symptoms of mitochondrial myopathies can vary widely, depending on the specific disorder and the severity of the mutation. They may include muscle weakness, muscle cramps, muscle wasting, seizures, vision loss, and cognitive decline.

There is no cure for mitochondrial myopathies, but various treatments can help manage the symptoms. These may include physical therapy, medications to control seizures or muscle spasms, and nutritional supplements to support energy production. In some cases, a lung or heart-lung transplant may be necessary.

The diagnosis of a mitochondrial myopathy is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include blood tests to measure the levels of certain enzymes and other molecules in the body, as well as muscle biopsy to examine the muscle tissue under a microscope. Genetic testing can help identify the specific mutation responsible for the condition.

The prognosis for mitochondrial myopathies varies depending on the specific disorder and the severity of the symptoms. Some forms of the disease are slowly progressive, while others may be more rapidly debilitating. In general, the earlier the diagnosis and treatment, the better the outcome.

There is currently no cure for mitochondrial myopathies, but research is ongoing to develop new treatments and therapies. In addition, there are several organizations and support groups that provide information and resources for individuals with these conditions and their families.

Smooth muscle tumors can be benign or malignant. Benign smooth muscle tumors are not cancerous and do not spread to other parts of the body. Malignant smooth muscle tumors are cancerous and can invade nearby tissues and organs, and can also spread to other parts of the body through the bloodstream or lymphatic system.

There are several types of smooth muscle tumors, including:

* Leiomyoma: A benign smooth muscle tumor that is common in the uterus and is often referred to as a fibroid.
* Leiomyosarcoma: A malignant smooth muscle tumor that can occur in any part of the body, but is most common in the abdomen or retroperitoneum.
* Schwannoma: A benign smooth muscle tumor that originates from the covering of nerves.
* Neurofibroma: A benign smooth muscle tumor that occurs in the peripheral nervous system.

Smooth muscle tumors can cause a variety of symptoms depending on their location and size, such as abdominal pain, bloating, constipation, or difficulty swallowing. They are often diagnosed through imaging tests such as ultrasound, CT scan, or MRI, and may also require a biopsy to confirm the diagnosis.

Treatment for smooth muscle tumors depends on the type and location of the tumor, as well as the patient's overall health. Benign smooth muscle tumors may not require treatment, while malignant tumors may be treated with surgery, radiation therapy, or chemotherapy.

Rhabdomyolysis can be caused by a variety of factors, including:

1. Physical trauma or injury to the muscles
2. Overuse or strain of muscles
3. Poor physical conditioning or training
4. Infections such as viral or bacterial infections that affect the muscles
5. Certain medications or drugs, such as statins and antibiotics
6. Alcohol or drug poisoning
7. Heat stroke or other forms of extreme heat exposure
8. Hypothyroidism (underactive thyroid)
9. Genetic disorders that affect muscle function.

Symptoms of rhabdomyolysis can include:

1. Muscle weakness or paralysis
2. Muscle pain or cramping
3. Confusion or disorientation
4. Dark urine or decreased urine output
5. Fever, nausea, and vomiting
6. Shortness of breath or difficulty breathing
7. Abnormal heart rhythms or cardiac arrest.

If you suspect that someone has rhabdomyolysis, it is important to seek medical attention immediately. Treatment typically involves supportive care, such as fluids and electrolyte replacement, as well as addressing any underlying causes of the condition. In severe cases, hospitalization may be necessary to monitor and treat complications such as kidney failure or cardiac problems.

Types of Experimental Diabetes Mellitus include:

1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.

Experimental Diabetes Mellitus has several applications in research, including:

1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.

In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.

Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.

There are several types of necrosis, including:

1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.

The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.

What is a Chronic Disease?

A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:

1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke

Impact of Chronic Diseases

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.

Addressing Chronic Diseases

Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:

1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.

Conclusion

Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.

Starvation is a condition where an individual's body does not receive enough nutrients to maintain proper bodily functions and growth. It can be caused by a lack of access to food, poverty, poor nutrition, or other factors that prevent the intake of sufficient calories and essential nutrients. Starvation can lead to severe health consequences, including weight loss, weakness, fatigue, and even death.

Types of Starvation:

There are several types of starvation, each with different causes and effects. These include:

1. Acute starvation: This occurs when an individual suddenly stops eating or has a limited access to food for a short period of time.
2. Chronic starvation: This occurs when an individual consistently does not consume enough calories and nutrients over a longer period of time, leading to gradual weight loss and other health problems.
3. Malnutrition starvation: This occurs when an individual's diet is deficient in essential nutrients, leading to malnutrition and other health problems.
4. Marasmus: This is a severe form of starvation that occurs in children, characterized by extreme weight loss, weakness, and wasting of muscles and organs.
5. Kwashiorkor: This is a form of malnutrition caused by a diet lacking in protein, leading to edema, diarrhea, and other health problems.

Effects of Starvation on the Body:

Starvation can have severe effects on the body, including:

1. Weight loss: Starvation causes weight loss, which can lead to a decrease in muscle mass and a loss of essential nutrients.
2. Fatigue: Starvation can cause fatigue, weakness, and a lack of energy, making it difficult to perform daily activities.
3. Weakened immune system: Starvation can weaken the immune system, making an individual more susceptible to illnesses and infections.
4. Nutrient deficiencies: Starvation can lead to a deficiency of essential nutrients, including vitamins and minerals, which can cause a range of health problems.
5. Increased risk of disease: Starvation can increase the risk of diseases such as tuberculosis, pellagra, and other infections.
6. Mental health issues: Starvation can lead to mental health issues such as depression, anxiety, and irritability.
7. Reproductive problems: Starvation can cause reproductive problems, including infertility and miscarriage.
8. Hair loss: Starvation can cause hair loss, which can be a sign of malnutrition.
9. Skin problems: Starvation can cause skin problems, such as dryness, irritation, and infections.
10. Increased risk of death: Starvation can lead to increased risk of death, especially in children and the elderly.

It is important to note that these effects can be reversed with proper nutrition and care. If you or someone you know is experiencing starvation, it is essential to seek medical attention immediately.

Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.

Common symptoms of type 2 diabetes include:

* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections

If left untreated, type 2 diabetes can lead to a range of complications, including:

* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation

The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:

* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.

There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.

In medicine, cadavers are used for a variety of purposes, such as:

1. Anatomy education: Medical students and residents learn about the human body by studying and dissecting cadavers. This helps them develop a deeper understanding of human anatomy and improves their surgical skills.
2. Research: Cadavers are used in scientific research to study the effects of diseases, injuries, and treatments on the human body. This helps scientists develop new medical techniques and therapies.
3. Forensic analysis: Cadavers can be used to aid in the investigation of crimes and accidents. By examining the body and its injuries, forensic experts can determine cause of death, identify suspects, and reconstruct events.
4. Organ donation: After death, cadavers can be used to harvest organs and tissues for transplantation into living patients. This can improve the quality of life for those with organ failure or other medical conditions.
5. Medical training simulations: Cadavers can be used to simulate real-life medical scenarios, allowing healthcare professionals to practice their skills in a controlled environment.

In summary, the term "cadaver" refers to the body of a deceased person and is used in the medical field for various purposes, including anatomy education, research, forensic analysis, organ donation, and medical training simulations.

There are different types of contractures, including:

1. Scar contracture: This type of contracture occurs when a scar tissue forms and tightens, causing a loss of movement in the affected area.
2. Neurogenic contracture: This type of contracture is caused by nerve damage and can occur after an injury or surgery.
3. Post-burn contracture: This type of contracture occurs after a burn injury and is caused by scarring and tightening of the skin and underlying tissues.
4. Congenital contracture: This type of contracture is present at birth and can be caused by genetic or environmental factors.

Signs and symptoms of contractures may include:

1. Limited range of motion
2. Pain or stiffness in the affected area
3. Skin tightening or shrinkage
4. Deformity of the affected area

Treatment options for contractures depend on the severity and cause of the condition, and may include:

1. Physical therapy to improve range of motion and strength
2. Bracing to support the affected area and prevent further tightening
3. Surgery to release or lengthen the scar tissue or tendons
4. Injections of botulinum toxin or other medications to relax the muscle and improve range of motion.

There are several different types of spinal cord injuries that can occur, depending on the location and severity of the damage. These include:

1. Complete spinal cord injuries: In these cases, the spinal cord is completely severed, resulting in a loss of all sensation and function below the level of the injury.
2. Incomplete spinal cord injuries: In these cases, the spinal cord is only partially damaged, resulting in some remaining sensation and function below the level of the injury.
3. Brown-Sequard syndrome: This is a specific type of incomplete spinal cord injury that affects one side of the spinal cord, resulting in weakness or paralysis on one side of the body.
4. Conus medullaris syndrome: This is a type of incomplete spinal cord injury that affects the lower part of the spinal cord, resulting in weakness or paralysis in the legs and bladder dysfunction.

The symptoms of spinal cord injuries can vary depending on the location and severity of the injury. They may include:

* Loss of sensation in the arms, legs, or other parts of the body
* Weakness or paralysis in the arms, legs, or other parts of the body
* Difficulty walking or standing
* Difficulty with bowel and bladder function
* Numbness or tingling sensations
* Pain or pressure in the neck or back

Treatment for spinal cord injuries typically involves a combination of medical and rehabilitative therapies. Medical treatments may include:

* Immobilization of the spine to prevent further injury
* Medications to manage pain and inflammation
* Surgery to relieve compression or stabilize the spine

Rehabilitative therapies may include:

* Physical therapy to improve strength and mobility
* Occupational therapy to learn new ways of performing daily activities
* Speech therapy to improve communication skills
* Psychological counseling to cope with the emotional effects of the injury.

Overall, the prognosis for spinal cord injuries depends on the severity and location of the injury, as well as the age and overall health of the individual. While some individuals may experience significant recovery, others may experience long-term or permanent impairment. It is important to seek medical attention immediately if symptoms of a spinal cord injury are present.

The symptoms of myotonia congenita can vary in severity and may include:

* Muscle stiffness and rigidity, especially in the legs, arms, and neck
* Difficulty relaxing muscles after contraction, leading to prolonged muscle tensing
* Muscle cramps and spasms
* Weakness and fatigue of the muscles
* Delayed or absent deep tendon reflexes
* Abnormal posture or gait
* Difficulty with speech and swallowing in severe cases

Myotonia congenita can be diagnosed through a combination of clinical evaluation, electromyography (EMG), and genetic testing. Treatment for the condition typically involves physical therapy, massage, and relaxation techniques to help manage muscle stiffness and improve mobility. In severe cases, medications such as sodium channel blockers or chloride channel activators may be prescribed to help regulate muscle contraction and relaxation.

Myotonia congenita is a rare condition, and its prevalence is not well established. However, it is estimated to affect approximately 1 in 100,000 to 1 in 200,000 individuals worldwide. The condition can be inherited in an autosomal dominant manner, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be sporadic, meaning they are not inherited from either parent.

Overall, myotonia congenita is a rare and complex genetic disorder that affects the muscles and can significantly impact an individual's quality of life. With proper diagnosis and management, individuals with myotonia congenita can lead fulfilling lives despite the challenges posed by the condition.

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

The symptoms of myasthenia gravis can vary in severity and may include:

* Weakness in the arms and legs
* Fatigue and muscle tiredness
* Difficulty swallowing (dysphagia)
* Difficulty speaking or slurred speech (dysarthria)
* Drooping eyelids (ptosis)
* Double vision (diplopia)
* Weakness in the muscles of the face, arms, and legs

The exact cause of myasthenia gravis is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissues. It can also be caused by other medical conditions such as thyroid disease, vitamin deficiencies, or infections.

There is no cure for myasthenia gravis, but there are various treatments available to manage the symptoms and improve quality of life. These include:

* Medications such as corticosteroids, immunosuppressants, and cholinesterase inhibitors
* Plasmapheresis, a procedure that removes harmful antibodies from the blood
* Intravenous immunoglobulin (IVIG), which contains antibodies that can help block the immune system's attack on the nerve-muscle junction
* Surgery to remove the thymus gland, which is believed to play a role in the development of myasthenia gravis

It is important for individuals with myasthenia gravis to work closely with their healthcare provider to manage their symptoms and prevent complications. With proper treatment and self-care, many people with myasthenia gravis are able to lead active and fulfilling lives.

Myalgia refers to muscle pain or soreness, which can be caused by a variety of factors such as injury, overuse, infection, or inflammation. It is a common symptom of many medical conditions and can range from mild to severe. Myalgia can affect any part of the body, but it is most commonly experienced in the back, neck, arms, and legs.

The symptoms of myalgia can vary depending on the underlying cause, but they typically include:

* Muscle aches and pains
* Tenderness or sensitivity to touch
* Stiffness or limited range of motion
* Fatigue or weakness
* Swelling or redness in the affected area

Myalgia can be caused by a variety of factors, including:

* Overuse or strain: This is one of the most common causes of myalgia, particularly in athletes or individuals who engage in strenuous physical activity.
* Injury or trauma: Myalgia can occur as a result of a direct blow to the muscle or a sudden twisting or bending motion that causes muscle strain.
* Infection: Certain infections, such as flu or cold, can cause myalgia as a symptom.
* Inflammatory conditions: Conditions such as arthritis, fibromyalgia, and polymyositis can cause myalgia.
* Medication side effects: Certain medications, such as statins and corticosteroids, can cause myalgia as a side effect.

Myalgia is typically diagnosed through a physical examination and medical history. Imaging tests such as X-rays or MRI may be ordered to rule out other conditions and determine the extent of the injury or inflammation. Treatment for myalgia depends on the underlying cause, but it can include rest, physical therapy, medication, and in some cases, surgery.

In conclusion, myalgia is a common symptom of many medical conditions that can cause muscle pain and stiffness. It is important to seek medical attention if the symptoms persist or worsen over time, as early diagnosis and treatment can help alleviate the discomfort and prevent further complications.

Symptoms of myofascial pain syndrome include:

* Pain in specific areas of the body, such as the neck, back, or limbs
* Pain that is worse with movement or activity
* Muscle stiffness and limited range of motion
* Trigger points, which are areas of hypersensitivity within the muscle that can cause pain when stimulated
* Poor posture or gait
* Fatigue
* Decreased strength and endurance

Treatment for myofascial pain syndrome typically involves a combination of physical therapy, pain management strategies, and self-care techniques. Physical therapy may include stretching exercises, myofascial release techniques, and other modalities to help relieve pain and improve range of motion. Pain management strategies may include medication, injections, or alternative therapies such as acupuncture or massage. Self-care techniques can also be helpful, such as heat or cold applications, relaxation techniques, and good posture.

The prognosis for myofascial pain syndrome varies depending on the severity of the condition and the effectiveness of treatment. In general, with appropriate treatment and self-care, many people are able to manage their symptoms and improve their quality of life. However, in some cases, the condition can be challenging to treat and may require ongoing management.

Overall, myofascial pain syndrome is a common and often misunderstood condition that can cause significant pain and disability. With proper diagnosis and treatment, however, many people are able to find relief and improve their quality of life.

In hyperinsulinism, the body produces too much insulin, leading to a range of symptoms including:

1. Hypoglycemia (low blood sugar): Excessive insulin can cause blood sugar levels to drop too low, leading to hypoglycemic symptoms such as shakiness, dizziness, confusion, and rapid heartbeat.
2. Weight gain: Hyperinsulinism can lead to weight gain due to the body's inability to effectively use glucose for energy production.
3. Fatigue: Excessive insulin can cause fatigue, as the body's cells are not able to effectively use glucose for energy production.
4. Mood changes: Hyperinsulinism can lead to mood changes such as irritability, anxiety, and depression.
5. Polycystic ovary syndrome (PCOS): Women with PCOS are at a higher risk of developing hyperinsulinism due to insulin resistance.
6. Gestational diabetes: Hyperinsulinism can occur during pregnancy, leading to gestational diabetes.
7. Acanthosis nigricans: A condition characterized by dark, velvety patches on the skin, often found in the armpits, neck, and groin area.
8. Cancer: Hyperinsulinism has been linked to an increased risk of certain types of cancer, such as breast, colon, and pancreatic cancer.
9. Cardiovascular disease: Excessive insulin can increase the risk of cardiovascular disease, including high blood pressure, heart disease, and stroke.
10. Cognitive impairment: Hyperinsulinism has been linked to cognitive impairment and an increased risk of dementia.

There are several causes of hyperinsulinism, including:

1. Insulin-producing tumors: Tumors that produce excessive amounts of insulin can lead to hyperinsulinism.
2. Familial hyperinsulinism: A genetic disorder that affects the regulation of insulin secretion and action.
3. Pancreatic beta-cell dysfunction: Dysfunction in the pancreatic beta cells, which produce insulin, can lead to hyperinsulinism.
4. Medications: Certain medications such as steroids and certain psychiatric drugs can cause hyperinsulinism.
5. Pituitary tumors: Tumors in the pituitary gland can lead to excessive secretion of growth hormone, which can stimulate insulin production.
6. Maternal diabetes during pregnancy: Women with diabetes during pregnancy may experience hyperinsulinism due to increased insulin resistance and higher insulin levels.
7. Gestational diabetes: High blood sugar during pregnancy can lead to hyperinsulinism.
8. Polycystic ovary syndrome (PCOS): Women with PCOS may experience hyperinsulinism due to insulin resistance and high insulin levels.
9. Cushing's syndrome: An endocrine disorder caused by excessive cortisol production can lead to hyperinsulinism.
10. Other medical conditions: Certain medical conditions such as thyroid disorders, adrenal gland disorders, and pituitary gland disorders can also cause hyperinsulinism.

It's important to note that some individuals with hyperinsulinism may not experience any symptoms, while others may experience a range of symptoms, including:

1. Weight gain
2. Fatigue
3. Headaches
4. Numbness or tingling in the hands and feet
5. Memory loss and difficulty concentrating
6. Mood changes, such as anxiety and depression
7. Skin problems, such as acne and thinning skin
8. Increased risk of heart disease and stroke
9. Growth retardation in children
10. Increased risk of developing type 2 diabetes

If you suspect that you or your child may have hyperinsulinism, it's important to consult with a healthcare professional for proper diagnosis and treatment. A doctor may perform a physical examination, take a medical history, and order blood tests to determine if hyperinsulinism is present and what may be causing it. Treatment options for hyperinsulinism will depend on the underlying cause of the condition. In some cases, medications such as metformin or other anti-diabetic drugs may be prescribed to help regulate blood sugar levels and reduce insulin production. In other cases, surgery or lifestyle changes may be necessary. With proper diagnosis and treatment, it is possible to manage hyperinsulinism and prevent or manage related health complications.

Examples of abnormal reflexes include:

1. Overactive reflexes: Reflexes that are too strong or exaggerated, such as an oversensitive knee jerk reflex.
2. Underactive reflexes: Reflexes that are too weak or diminished, such as a decreased tendon reflex in the arm.
3. Delayed reflexes: Reflexes that take longer than expected to occur, such as a delayed deep tendon reflex.
4. Abnormal reflex arc: A reflex arc that is not normal or expected for the situation, such as a spastic reflex arc.
5. Reflexes that are out of proportion to the stimulus: Such as an excessive or exaggerated reflex response to a mild stimulus.
6. Reflexes that occur in the absence of a stimulus: Such as a spontaneous reflex.
7. Reflexes that do not resolve: Such as a persistent reflex.
8. Reflexes that are painful or uncomfortable: Such as an abnormal rectal reflex.

It's important to note that not all abnormal reflexes are necessarily indicative of a serious medical condition, but they should be evaluated by a healthcare professional to determine the underlying cause and appropriate treatment.

A sprain is a stretch or tear of a ligament, which is a fibrous connective tissue that connects bones to other bones and provides stability to joints. Sprains often occur when the joint is subjected to excessive stress or movement, such as during a fall or sudden twisting motion. The most common sprains are those that affect the wrist, knee, and ankle joints.

A strain, on the other hand, is a stretch or tear of a muscle or a tendon, which is a fibrous cord that connects muscles to bones. Strains can occur due to overuse, sudden movement, or injury. The most common strains are those that affect the hamstring, calf, and back muscles.

The main difference between sprains and strains is the location of the injury. Sprains affect the ligaments, while strains affect the muscles or tendons. Additionally, sprains often cause joint instability and swelling, while strains may cause pain, bruising, and limited mobility.

Treatment for sprains and strains is similar and may include rest, ice, compression, and elevation (RICE) to reduce inflammation and relieve pain. Physical therapy exercises may also be recommended to improve strength and range of motion. In severe cases, surgery may be required to repair the damaged tissue.

Prevention is key in avoiding sprains and strains. This can be achieved by maintaining proper posture, warming up before physical activity, wearing appropriate protective gear during sports, and gradually increasing exercise intensity and duration. Proper training and technique can also help reduce the risk of injury.

Overall, while sprains and strains share some similarities, they are distinct injuries that require different approaches to treatment and prevention. Understanding the differences between these two conditions is essential for proper diagnosis, treatment, and recovery.

The exact cause of leiomyosarcoma is not known, but it is believed to be linked to genetic mutations that occur in the smooth muscle cells. It can occur at any age, but it is more common in women, especially after menopause.

Symptoms of leiomyosarcoma may include:

* Abnormal bleeding or discharge from the uterus or cervix
* Pelvic pain or discomfort
* A mass or lump in the abdomen or pelvis
* Weakness, fatigue, or fever

If leiomyosarcoma is suspected, a healthcare provider may perform a variety of tests to confirm the diagnosis, including:

* Pelvic examination and imaging tests, such as ultrasound, computed tomography (CT) scan, or magnetic resonance imaging (MRI) to visualize the tumor.
* Biopsy, where a sample of tissue is removed from the suspected tumor and examined under a microscope for cancer cells.

Treatment options for leiomyosarcoma depend on the location, size, and stage of the cancer, as well as the patient's age and overall health. Surgery is often the primary treatment, and may involve removing the uterus, cervix, or other affected organs. Radiation therapy and chemotherapy may also be used to kill any remaining cancer cells.

Overall, leiomyosarcoma is a rare and aggressive form of cancer that requires prompt medical attention if symptoms persist or worsen over time. With proper treatment, many people with leiomyosarcoma can achieve long-term survival and a good quality of life.

In some cases, hyperemia can be a sign of a more serious underlying condition that requires medical attention. For example, if hyperemia is caused by an inflammatory or infectious process, it may lead to tissue damage or organ dysfunction if left untreated.

Hyperemia can occur in various parts of the body, including the skin, muscles, organs, and other tissues. It is often diagnosed through physical examination and imaging tests such as ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI). Treatment for hyperemia depends on its underlying cause, and may include antibiotics, anti-inflammatory medications, or surgery.

In the context of dermatology, hyperemia is often used to describe a condition called erythema, which is characterized by redness and swelling of the skin due to increased blood flow. Erythema can be caused by various factors, such as sun exposure, allergic reactions, or skin infections. Treatment for erythema may include topical medications, oral medications, or other therapies depending on its underlying cause.

There are two forms of Pompe disease, infantile-onset and late-onset. Infantile-onset Pompe disease is the most severe form and is usually diagnosed in the first few months of life. Children with this form of the disorder may experience difficulty breathing, weakness, and floppiness. Late-onset Pompe disease, on the other hand, typically affects adults and may cause muscle weakness, fatigue, and shortness of breath.

Pompe disease is caused by mutations in the GAA gene, which is inherited in an autosomal recessive pattern. This means that a person must inherit two copies of the mutated gene, one from each parent, to develop the disorder. Pompe disease is rare, affecting approximately 1 in 40,000 people worldwide.

Treatment for Pompe disease typically involves enzyme replacement therapy (ERT), which involves replacing the missing GAA enzyme with a synthetic version given through a vein. This can help reduce glycogen accumulation and improve symptoms. In some cases, a bone marrow transplant may also be performed to help restore normal GAA enzyme activity.

In summary, glycogen storage disease type II (Pompe disease) is a rare genetic disorder caused by a deficiency of the GAA enzyme, leading to glycogen accumulation in cells and a range of symptoms including muscle weakness, respiratory problems, and cardiac issues. Treatment typically involves enzyme replacement therapy and may also include bone marrow transplantation.

Neointima can be observed in various cardiovascular conditions such as atherosclerosis, stenosis, and graft stenosis. The thickness of the neointima is an important predictor of cardiovascular events such as restenosis after angioplasty or stenting.

Neointima can be characterized using various imaging techniques such as intravascular ultrasound (IVUS) and optical coherence tomography (OCT), which provide detailed information on the morphology and composition of the neointima.

Understanding the mechanisms of neointima formation and its role in cardiovascular disease can help to develop new therapeutic strategies for preventing or treating these conditions.

Here are some possible causes of myoglobinuria:

1. Muscle injury or trauma: This can cause myoglobin to leak into the bloodstream and then into the urine.
2. Muscle disease: Certain muscle diseases, such as muscular dystrophy, can cause myoglobinuria.
3. Kidney damage: Myoglobin can accumulate in the kidneys and cause damage if the kidneys are not functioning properly.
4. Sepsis: Sepsis is a systemic infection that can cause muscle breakdown and myoglobinuria.
5. Burns: Severe burns can cause muscle damage and lead to myoglobinuria.
6. Heart attack: A heart attack can cause muscle damage and myoglobinuria.
7. Rhabdomyolysis: This is a condition where the muscles break down and release myoglobin into the bloodstream. It can be caused by various factors such as medication, infection, or injury.

Symptoms of myoglobinuria may include dark urine, proteinuria (excess protein in the urine), and kidney damage. Treatment depends on the underlying cause and may involve supportive care, medication, or dialysis to remove waste products from the blood.

The disorder is caused by a defect in one copy of the D4Z4 repeat on chromosome 4, which leads to the degeneration of muscle fibers and a loss of motor neurons. The age of onset and progression of the disease vary widely, with some individuals experiencing symptoms in childhood while others may not develop them until adulthood.

There is no cure for FSHD, but various treatments can help manage the symptoms and slow its progression. These include physical therapy, bracing and orthotics, medications to reduce inflammation and pain, and in some cases, surgery. Research into the genetic causes of the disorder is ongoing, with the goal of developing new and more effective treatments.

The term "cumulative" refers to the gradual buildup of damage over time, as opposed to a single traumatic event that causes immediate harm. The damage can result from repetitive motions, vibrations, compressive forces, or other forms of stress that accumulate and lead to tissue injury and inflammation.

Some common examples of CTDs include:

1. Carpal tunnel syndrome: A condition that affects the wrist and hand, caused by repetitive motion and compression of the median nerve.
2. Tendinitis: Inflammation of a tendon, often caused by repetitive motion or overuse.
3. Bursitis: Inflammation of a bursa, a fluid-filled sac that cushions joints and reduces friction between tissues.
4. Tennis elbow: A condition characterized by inflammation of the tendons on the outside of the elbow, caused by repetitive gripping or twisting motions.
5. Plantar fasciitis: Inflammation of the plantar fascia, a band of tissue that runs along the bottom of the foot, caused by repetitive strain and overuse.
6. Repetitive stress injuries: A broad category of injuries caused by repetitive motion, such as typing or using a computer mouse.
7. Occupational asthma: A condition caused by inhaling allergens or irritants in the workplace, leading to inflammation and narrowing of the airways.
8. Hearing loss: Damage to the inner ear or auditory nerve caused by exposure to loud noises over time.
9. Vibration white finger: A condition that affects the hands, causing whiteness or loss of blood flow in the fingers due to exposure to vibrating tools.
10. Carpal tunnel syndrome: Compression of the median nerve in the wrist, leading to numbness, tingling, and weakness in the hand and arm.

It's important to note that these conditions can have a significant impact on an individual's quality of life, ability to work, and overall well-being. If you are experiencing any of these conditions, it is important to seek medical attention to receive proper diagnosis and treatment.

In the medical field, fatigue is often evaluated using a combination of physical examination, medical history, and laboratory tests to determine its underlying cause. Treatment for fatigue depends on the underlying cause, but may include rest, exercise, stress management techniques, and medication.

Some common causes of fatigue in the medical field include:

1. Sleep disorders, such as insomnia or sleep apnea
2. Chronic illnesses, such as diabetes, heart disease, or arthritis
3. Infections, such as the flu or a urinary tract infection
4. Medication side effects
5. Poor nutrition or hydration
6. Substance abuse
7. Chronic stress
8. Depression or anxiety
9. Hormonal imbalances
10. Autoimmune disorders, such as thyroiditis or lupus.

Fatigue can also be a symptom of other medical conditions, such as:

1. Anemia
2. Hypoglycemia (low blood sugar)
3. Hypothyroidism (underactive thyroid)
4. Hyperthyroidism (overactive thyroid)
5. Chronic fatigue syndrome
6. Fibromyalgia
7. Vasculitis
8. Cancer
9. Heart failure
10. Liver or kidney disease.

It is important to seek medical attention if fatigue is severe, persistent, or accompanied by other symptoms such as fever, pain, or difficulty breathing. A healthcare professional can diagnose and treat the underlying cause of fatigue, improving overall quality of life.

There are several different types of pain, including:

1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.

The medical field uses a range of methods to assess and manage pain, including:

1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.

It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.

There are two main types of heart failure:

1. Left-sided heart failure: This occurs when the left ventricle, which is the main pumping chamber of the heart, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the lungs and other organs.
2. Right-sided heart failure: This occurs when the right ventricle, which pumps blood to the lungs, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the body's tissues and organs.

Symptoms of heart failure may include:

* Shortness of breath
* Fatigue
* Swelling in the legs, ankles, and feet
* Swelling in the abdomen
* Weight gain
* Coughing up pink, frothy fluid
* Rapid or irregular heartbeat
* Dizziness or lightheadedness

Treatment for heart failure typically involves a combination of medications and lifestyle changes. Medications may include diuretics to remove excess fluid from the body, ACE inhibitors or beta blockers to reduce blood pressure and improve blood flow, and aldosterone antagonists to reduce the amount of fluid in the body. Lifestyle changes may include a healthy diet, regular exercise, and stress reduction techniques. In severe cases, heart failure may require hospitalization or implantation of a device such as an implantable cardioverter-defibrillator (ICD) or a left ventricular assist device (LVAD).

It is important to note that heart failure is a chronic condition, and it requires ongoing management and monitoring to prevent complications and improve quality of life. With proper treatment and lifestyle changes, many people with heart failure are able to manage their symptoms and lead active lives.

Causes:

1. Brain injury during fetal development or birth
2. Hypoxia (oxygen deficiency) to the brain, often due to complications during labor and delivery
3. Infections such as meningitis or encephalitis
4. Stroke or bleeding in the brain
5. Traumatic head injury
6. Genetic disorders
7. Premature birth
8. Low birth weight
9. Multiples (twins, triplets)
10. Maternal infections during pregnancy.

Symptoms:

1. Weakness or paralysis of muscles on one side of the body
2. Lack of coordination and balance
3. Difficulty with movement, posture, and gait
4. Spasticity (stiffness) or hypotonia (looseness) of muscles
5. Intellectual disability or learning disabilities
6. Seizures
7. Vision, hearing, or speech problems
8. Swallowing difficulties
9. Increased risk of infections and bone fractures
10. Delays in reaching developmental milestones.

Diagnosis:

1. Physical examination and medical history
2. Imaging tests, such as CT or MRI scans
3. Electromyography (EMG) to test muscle activity
4. Developmental assessments to evaluate cognitive and motor skills
5. Genetic testing to identify underlying causes.

Treatment:

1. Physical therapy to improve movement, balance, and strength
2. Occupational therapy to develop daily living skills and fine motor activities
3. Speech therapy for communication and swallowing difficulties
4. Medications to control seizures, spasticity, or pain
5. Surgery to correct anatomical abnormalities or release contracted muscles
6. Assistive devices, such as braces, walkers, or wheelchairs, to aid mobility and independence.

It's important to note that each individual with Cerebral Palsy may have a unique combination of symptoms and require a personalized treatment plan. With appropriate medical care and support, many individuals with Cerebral Palsy can lead fulfilling lives and achieve their goals despite the challenges they face.

There are two types of hypertension:

1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.

Some common causes of secondary hypertension include:

* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use

There are also several risk factors for hypertension, including:

* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress

Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:

* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease

Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.

Rigor mortis typically sets in within a few hours of death and can last for up to 72 hours. During this time, the body will feel stiff and unyielding, making it difficult to move or manipulate. The speed at which rigor mortis sets in and the duration of the condition can vary depending on factors such as the age of the individual, the cause of death, and the temperature of the environment.

Rigor mortis is often used as an indicator of time since death, as it can provide a rough estimate of how long ago the person died. It is also an important consideration for pathologists and coroners who perform autopsies, as they must take care to avoid damaging the body during the procedure.

In addition to its use in forensic science, rigor mortis has other practical applications in medicine as well. For example, it can be used to assess the effectiveness of certain medications or therapies that are designed to reduce muscle stiffness. It is also an important consideration for surgeons who perform procedures on the muscles and joints, as they must take care to avoid causing damage to the already-stiff tissues.

Overall, rigor mortis is a fascinating phenomenon that has many practical applications in medicine and forensic science. While it may seem morbid or unsettling to some people, it is an important aspect of human physiology and can provide valuable insights into the nature of life and death.

Example sentences:

1. The patient was diagnosed with piriformis muscle syndrome after complaining of pain in her legs and difficulty walking.
2. The doctor recommended physical therapy to treat the piriformis muscle syndrome and relieve the compression on the sciatic nerve.
3. After a few weeks of stretching exercises and massage therapy, the patient experienced significant improvement in her symptoms and was able to resume normal activities.

Leiomyomas are the most common type of gynecologic tumor and affect up to 80% of women at some point in their lifetime. They are more common in women who have a family history of leiomyomas or who are obese.

There are several different types of leiomyomas, including:

1. Submucosal leiomyomas: These tumors grow into the uterine cavity and can cause bleeding and other symptoms.
2. Intramural leiomyomas: These tumors grow within the muscle of the uterus and can cause pelvic pain and heavy menstrual bleeding.
3. Pedunculated leiomyomas: These tumors are attached to the uterine wall by a stalk-like structure and can be felt during a pelvic exam.
4. Broad ligament leiomyomas: These tumors grow on the broad ligament, which is a band of tissue that connects the uterus to the pelvis.

Leiomyomas are typically diagnosed through a combination of pelvic examination, ultrasound, and hysteroscopy (a procedure in which a small camera is inserted into the uterus to examine the inside of the organ). Treatment options for leiomyomas depend on the size and location of the tumors, as well as the severity of symptoms. Treatment may include watchful waiting, medications to regulate hormones or shrink the tumors, or surgery to remove the tumors.

In some cases, leiomyomas can be associated with other conditions such as endometriosis or adenomyosis, and it is important for women with these tumors to receive ongoing care from a healthcare provider to monitor for any changes in their condition.

There are several types of acidosis, including:

1. Respiratory acidosis: This occurs when the lung's ability to remove carbon dioxide from the blood is impaired, leading to an increase in blood acidity.
2. Metabolic acidosis: This type of acidosis occurs when there is an excessive production of acid in the body due to factors such as diabetes, starvation, or kidney disease.
3. Mixed acidosis: This type of acidosis is a combination of respiratory and metabolic acidosis.
4. Severe acute respiratory acidosis (SARA): This is a life-threatening condition that occurs suddenly, usually due to a severe lung injury or aspiration of a corrosive substance.

The symptoms of acidosis can vary depending on the type and severity of the condition. Common symptoms include:

1. Fatigue
2. Weakness
3. Confusion
4. Headaches
5. Nausea and vomiting
6. Abdominal pain
7. Difficulty breathing
8. Rapid heart rate
9. Muscle twitching

If left untreated, acidosis can lead to complications such as:

1. Kidney damage
2. Seizures
3. Coma
4. Heart arrhythmias
5. Respiratory failure

Treatment of acidosis depends on the underlying cause and the severity of the condition. Some common treatments include:

1. Oxygen therapy
2. Medications to help regulate breathing and heart rate
3. Fluid and electrolyte replacement
4. Dietary changes
5. Surgery, in severe cases.

In conclusion, acidosis is a serious medical condition that can have severe consequences if left untreated. It is important to seek medical attention immediately if you suspect that you or someone else may have acidosis. With prompt and appropriate treatment, it is possible to effectively manage the condition and prevent complications.

There are several types of cardiomyopathies, each with distinct characteristics and symptoms. Some of the most common forms of cardiomyopathy include:

1. Hypertrophic cardiomyopathy (HCM): This is the most common form of cardiomyopathy and is characterized by an abnormal thickening of the heart muscle, particularly in the left ventricle. HCM can lead to obstruction of the left ventricular outflow tract and can increase the risk of sudden death.
2. Dilated cardiomyopathy: This type of cardiomyopathy is characterized by a decrease in the heart's ability to pump blood effectively, leading to enlargement of the heart and potentially life-threatening complications such as congestive heart failure.
3. Restrictive cardiomyopathy: This type of cardiomyopathy is characterized by stiffness of the heart muscle, which makes it difficult for the heart to fill with blood. This can lead to shortness of breath and fatigue.
4. Left ventricular non-compaction (LVNC): This is a rare type of cardiomyopathy that occurs when the left ventricle does not properly compact, leading to reduced cardiac function and potentially life-threatening complications.
5. Cardiac amyloidosis: This is a condition in which abnormal proteins accumulate in the heart tissue, leading to stiffness and impaired cardiac function.
6. Right ventricular cardiomyopathy (RVCM): This type of cardiomyopathy is characterized by impaired function of the right ventricle, which can lead to complications such as pulmonary hypertension and heart failure.
7. Endocardial fibroelastoma: This is a rare type of cardiomyopathy that occurs when abnormal tissue grows on the inner lining of the heart, leading to reduced cardiac function and potentially life-threatening complications.
8. Cardiac sarcoidosis: This is a condition in which inflammatory cells accumulate in the heart, leading to impaired cardiac function and potentially life-threatening complications.
9. Hypertrophic cardiomyopathy (HCM): This is a condition in which the heart muscle thickens, leading to reduced cardiac function and potentially life-threatening complications such as arrhythmias and sudden death.
10. Hypokinetic left ventricular cardiomyopathy: This type of cardiomyopathy is characterized by decreased contraction of the left ventricle, leading to reduced cardiac function and potentially life-threatening complications such as heart failure.

It's important to note that some of these types of cardiomyopathy are more common in certain populations, such as hypertrophic cardiomyopathy being more common in young athletes. Additionally, some types of cardiomyopathy may have overlapping symptoms or co-occurring conditions, so it's important to work with a healthcare provider for an accurate diagnosis and appropriate treatment.

There are several different types of weight gain, including:

1. Clinical obesity: This is defined as a BMI of 30 or higher, and is typically associated with a range of serious health problems, such as heart disease, type 2 diabetes, and certain types of cancer.
2. Central obesity: This refers to excess fat around the waistline, which can increase the risk of health problems such as heart disease and type 2 diabetes.
3. Muscle gain: This occurs when an individual gains weight due to an increase in muscle mass, rather than fat. This type of weight gain is generally considered healthy and can improve overall fitness and athletic performance.
4. Fat gain: This occurs when an individual gains weight due to an increase in body fat, rather than muscle or bone density. Fat gain can increase the risk of health problems such as heart disease and type 2 diabetes.

Weight gain can be measured using a variety of methods, including:

1. Body mass index (BMI): This is a widely used measure of weight gain that compares an individual's weight to their height. A BMI of 18.5-24.9 is considered normal, while a BMI of 25-29.9 is considered overweight, and a BMI of 30 or higher is considered obese.
2. Waist circumference: This measures the distance around an individual's waistline and can be used to assess central obesity.
3. Skinfold measurements: These involve measuring the thickness of fat at specific points on the body, such as the abdomen or thighs.
4. Dual-energy X-ray absorptiometry (DXA): This is a non-invasive test that uses X-rays to measure bone density and body composition.
5. Bioelectrical impedance analysis (BIA): This is a non-invasive test that uses electrical impulses to measure body fat percentage and other physiological parameters.

Causes of weight gain:

1. Poor diet: Consuming high amounts of processed foods, sugar, and saturated fats can lead to weight gain.
2. Lack of physical activity: Engaging in regular exercise can help burn calories and maintain a healthy weight.
3. Genetics: An individual's genetic makeup can affect their metabolism and body composition, making them more prone to weight gain.
4. Hormonal imbalances: Imbalances in hormones such as insulin, thyroid, and cortisol can contribute to weight gain.
5. Medications: Certain medications, such as steroids and antidepressants, can cause weight gain as a side effect.
6. Sleep deprivation: Lack of sleep can disrupt hormones that regulate appetite and metabolism, leading to weight gain.
7. Stress: Chronic stress can lead to emotional eating and weight gain.
8. Age: Metabolism slows down with age, making it more difficult to maintain a healthy weight.
9. Medical conditions: Certain medical conditions such as hypothyroidism, Cushing's syndrome, and polycystic ovary syndrome (PCOS) can also contribute to weight gain.

Treatment options for obesity:

1. Lifestyle modifications: A combination of diet, exercise, and stress management techniques can help individuals achieve and maintain a healthy weight.
2. Medications: Prescription medications such as orlistat, phentermine-topiramate, and liraglutide can aid in weight loss.
3. Bariatric surgery: Surgical procedures such as gastric bypass surgery and sleeve gastrectomy can be effective for severe obesity.
4. Behavioral therapy: Cognitive-behavioral therapy (CBT) and other forms of counseling can help individuals develop healthy eating habits and improve their physical activity levels.
5. Meal replacement plans: Meal replacement plans such as Medifast can provide individuals with a structured diet that is high in protein, fiber, and vitamins, and low in calories and sugar.
6. Weight loss supplements: Supplements such as green tea extract, garcinia cambogia, and forskolin can help boost weight loss efforts.
7. Portion control: Using smaller plates and measuring cups can help individuals regulate their portion sizes and maintain a healthy weight.
8. Mindful eating: Paying attention to hunger and fullness cues, eating slowly, and savoring food can help individuals develop healthy eating habits.
9. Physical activity: Engaging in regular physical activity such as walking, running, swimming, or cycling can help individuals burn calories and maintain a healthy weight.

It's important to note that there is no one-size-fits-all approach to treating obesity, and the most effective treatment plan will depend on the individual's specific needs and circumstances. Consulting with a healthcare professional such as a registered dietitian or a physician can help individuals develop a personalized treatment plan that is safe and effective.

Hemiplegia can cause a range of symptoms including weakness, paralysis, loss of sensation, and difficulty with movement and coordination on one side of the body. The affected side may also experience muscle spasticity or rigidity, causing stiffness and limited mobility.

Depending on the severity and location of the damage, hemiplegia can be classified into different types:

1. Left hemiplegia: This type affects the left side of the body and is caused by damage to the left hemisphere of the brain.
2. Right hemiplegia: This type affects the right side of the body and is caused by damage to the right hemisphere of the brain.
3. Mixed hemiplegia: This type affects both sides of the body and is caused by damage to both hemispheres of the brain or other areas of the brainstem.
4. Progressive hemiplegia: This type progressively worsens over time and is often associated with neurodegenerative disorders such as Parkinson's disease or multiple sclerosis.

Treatment for hemiplegia typically focuses on physical therapy, occupational therapy, and rehabilitation to improve mobility, strength, and function. Medications such as anticonvulsants, muscle relaxants, and pain relievers may also be prescribed to manage symptoms. In severe cases, surgery may be necessary to relieve pressure on the brain or spinal cord.

In summary, hemiplegia is a condition characterized by paralysis or weakness on one side of the body, often caused by damage to the brain or spinal cord. Treatment options vary depending on the severity and underlying cause of the condition.

1. Chronic bronchitis: This condition causes inflammation of the bronchial tubes (the airways that lead to the lungs), which can cause coughing and excessive mucus production.
2. Emphysema: This condition damages the air sacs in the lungs, making it difficult for the body to take in oxygen and release carbon dioxide.

The main causes of COPD are smoking and long-term exposure to air pollution, although genetics can also play a role. Symptoms of COPD can include shortness of breath, wheezing, and coughing, particularly during exercise or exertion. The disease can be diagnosed through pulmonary function tests, chest X-rays, and blood tests.

There is no cure for COPD, but there are several treatment options available to manage the symptoms and slow the progression of the disease. These include medications such as bronchodilators and corticosteroids, pulmonary rehabilitation programs, and lifestyle changes such as quitting smoking and increasing physical activity. In severe cases, oxygen therapy may be necessary to help the patient breathe.

Prevention is key in avoiding the development of COPD, and this includes not smoking and avoiding exposure to air pollution. Early detection and treatment can also help manage the symptoms and slow the progression of the disease. With proper management, many people with COPD are able to lead active and productive lives.

* Type 1: Hypokalemic Periodic Paralysis (Hyperkalemia-induced muscle weakness)
* Type 2: Hyperkalemic Periodic Paralysis (K+ channels dysfunction, leading to muscle weakness)
* Type 3: Peripheral nerve damage causing FPPA
* Type 4: Central nervous system damage causing FPPA

Slide 3: Causes of Familial Periodic Paralysis (FPPA)

* Genetic mutations in SCN4A, KCNA1, and other genes involved in ion channel function
* Abnormalities in the expression and function of ion channels
* Autosomal dominant or recessive inheritance pattern

Slide 4: Symptoms of Familial Periodic Paralysis (FPPA)

* Muscle weakness or paralysis, often triggered by changes in diet, physical activity, or other environmental factors
* Weakness of the lower extremities more pronounced than the upper extremities
* Muscle cramps and twitching
* Abdominal pain
* Nausea and vomiting

Slide 5: Diagnosis of Familial Periodal Paralysis (FPPA)

* Clinical evaluation, including patient history and physical examination
* Electromyography (EMG) to assess muscle activity and diagnose FPPA
* Genetic testing to identify genetic mutations associated with FPPA
* Blood tests to measure potassium levels and rule out other conditions

Slide 6: Treatment of Familial Periodic Paralysis (FPPA)

* Potassium supplements to maintain normal potassium levels
* Avoiding triggers such as stress, cold temperature, and certain medications
* Physical therapy to improve muscle strength and function
* Pain management with analgesics and other medications as needed

Slide 7: Prognosis of Familial Periodic Paralysis (FPPA)

* FPPA is a chronic condition with no cure, but with proper management, patients can lead relatively normal lives
* The prognosis varies depending on the severity and frequency of attacks, as well as the presence of any complications
* Early diagnosis and treatment can improve the quality of life for patients with FPPA

Slide 8: Current Research in Familial Periodic Paralysis (FPPA)

* Genetic research to better understand the underlying causes of FPPA and develop new treatments
* Studies on the effectiveness of new medications and therapies for FPPA
* Investigation into the potential use of stem cells for treating FPPA

Slide 9: Current Challenges in Familial Periodic Paralysis (FPPA)

* Limited awareness and understanding of FPPA among healthcare professionals and the general public
* Lack of effective treatments for severe cases of FPPA
* Limited availability of specialized care and support for patients with FPPA

Slide 10: Conclusion

* Familial periodic paralysis (FPPA) is a rare and complex condition that affects both children and adults
* Early diagnosis and proper management are critical to improving the quality of life for patients with FPPA
* Ongoing research offers hope for new treatments and therapies, but more work needs to be done to increase awareness and understanding of this condition.

The symptoms of hypokalemic periodic paralysis can vary in severity and may include:

* Muscle weakness or paralysis, typically affecting the legs but sometimes affecting the arms or face as well
* Muscle cramps and twitching
* Abnormal heart rhythms
* Weakness or paralysis of the respiratory muscles, which can lead to breathing difficulties
* Vision problems, such as blurred vision or double vision
* Dizziness and fainting

The exact cause of hypokalemic periodic paralysis is not known, but it is thought to be related to mutations in certain genes that affect the way potassium ions are regulated in the body. The disorder is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis.

There is no cure for hypokalemic periodic paralysis, but treatment options may include:

* Potassium supplements to maintain normal potassium levels in the blood
* Medications to regulate heart rhythms and prevent abnormal heartbeats
* Physical therapy to improve muscle strength and function
* Avoiding triggers such as stress, certain medications, or changes in potassium levels
* In severe cases, a pacemaker may be implanted to regulate the heartbeat.

It is important to note that hypokalemic periodic paralysis can be a challenging disorder to manage and may have a significant impact on quality of life. However, with proper treatment and management, many individuals with this condition are able to lead active and fulfilling lives.

Distal myopathies can be caused by a variety of factors, including genetic mutations, autoimmune disorders, and nutritional deficiencies. Some common forms of distal myopathy include:

1. Limb-girdle muscular dystrophy: This is a group of inherited disorders that affect the muscles around the shoulders and hips.
2. Facioscapulohumeral muscular dystrophy (FSHD): This is a genetic disorder that affects the muscles of the face, shoulder blades, and upper arms.
3. Myotonic dystrophy: This is the most common form of adult-onset muscular dystrophy, which causes muscle stiffness and spasms.
4. Inflammatory myopathies: These are autoimmune disorders that cause muscle inflammation and damage.
5. Nutritional deficiencies: Deficiencies in certain nutrients, such as vitamin D and calcium, can cause distal myopathy.

Symptoms of distal myopathies can vary depending on the specific disorder and the severity of the condition. Common symptoms include:

1. Muscle weakness and wasting in the arms and legs
2. Muscle cramps and spasms
3. Difficulty walking or standing
4. Weak grip strength
5. Difficulty swallowing or speaking (in some cases)

Diagnosis of distal myopathies typically involves a combination of physical examination, medical history, and laboratory tests such as muscle biopsy and genetic analysis. Treatment options vary depending on the specific disorder and can include physical therapy, medications, and in some cases, surgery.

In summary, distal myopathies are a group of muscle disorders that affect the distal muscles of the arms and legs, causing weakness and wasting. The specific causes and symptoms can vary depending on the disorder, but early diagnosis and treatment can help manage symptoms and improve quality of life.

The disease begins with endothelial dysfunction, which allows lipid accumulation in the artery wall. Macrophages take up oxidized lipids and become foam cells, which die and release their contents, including inflammatory cytokines, leading to further inflammation and recruitment of more immune cells.

The atherosclerotic plaque can rupture or ulcerate, leading to the formation of a thrombus that can occlude the blood vessel, causing ischemia or infarction of downstream tissues. This can lead to various cardiovascular diseases such as myocardial infarction (heart attack), stroke, and peripheral artery disease.

Atherosclerosis is a multifactorial disease that is influenced by genetic and environmental factors such as smoking, hypertension, diabetes, high cholesterol levels, and obesity. It is diagnosed by imaging techniques such as angiography, ultrasound, or computed tomography (CT) scans.

Treatment options for atherosclerosis include lifestyle modifications such as smoking cessation, dietary changes, and exercise, as well as medications such as statins, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. In severe cases, surgical interventions such as bypass surgery or angioplasty may be necessary.

In conclusion, atherosclerosis is a complex and multifactorial disease that affects the arteries and can lead to various cardiovascular diseases. Early detection and treatment can help prevent or slow down its progression, reducing the risk of complications and improving patient outcomes.

Example Sentence: The patient was diagnosed with pulmonary hypertension and began treatment with medication to lower her blood pressure and improve her symptoms.

Word class: Noun phrase / medical condition

The muscle cells of skeletal muscles are much longer than in the other types of muscle tissue, and are often known as muscle ... Skeletal Muscle Architecture, Effect of Muscle Architecture on Muscle Function "9.6 Forces and Torques in Muscles and Joints - ... A single muscle such as the biceps in a young adult male contains around 253,000 muscle fibers. Skeletal muscle fibers are the ... Skeletal muscles are voluntary muscles under the control of the somatic nervous system. The other types of muscle are cardiac ...
The skeletal-muscle pump is a collection of skeletal muscles that aid the heart in the circulation of blood. It is especially ... Experiments have shown that a strong muscle contraction can occur without a corresponding increase in skeletal muscle blood ... "Muscle pump does not enhance blood flow in exercising skeletal muscle". Journal of Applied Physiology. 94 (1): 6-10. doi: ... it would seem impossible for a muscle contraction and skeletal muscle hyperemia to be uncoupled. Another experiment recently ...
"Differential expression of slow and fast skeletal muscle troponin C. Slow skeletal muscle troponin C is expressed in human ... Troponin C, skeletal muscle is a protein that in humans is encoded by the TNNC2 gene. Troponin (Tn), is a key protein complex ... Townsend PJ, Yacoub MH, Barton PJ (1998). "Assignment of the human fast skeletal muscle troponin C gene (TNNC2) between D20S721 ... "Entrez Gene: TNNC2 troponin C type 2 (fast)". Romero-Herrera AE, Castillo O, Lehmann H (1977). "Human skeletal muscle proteins ...
"Entrez Gene: ACTA1 actin, alpha 1, skeletal muscle". Bandman E (December 1992). "Contractile protein isoforms in muscle ... alpha skeletal muscle is a protein that in humans is encoded by the ACTA1 gene. Actin alpha 1 which is expressed in skeletal ... "Alpha-skeletal actin induces a subset of muscle genes independently of muscle differentiation and withdrawal from the cell ... Skeletal alpha actin expression is induced by stimuli and conditions known to cause muscle formation. Such conditions result in ...
A key component in lateral force transmission in skeletal muscle is the extracellular matrix (ECM). Skeletal muscle is a ... The mechanical properties of skeletal muscle depend on both the properties of muscle fibers and the ECM, and the interaction ... The structure of the endomysium is generally equivalent for all skeletal muscle from different muscles and species. Many of the ... variations with muscle length, J Muscle Res Cell Motil 15, 299-304. Huijing, P.A. (1999). Muscle as a collagen fiber reinforced ...
This is a table of skeletal muscles of the human anatomy. There are around 650 skeletal muscles within the typical human body. ... These muscles are described using anatomical terminology. The term "muscle" is omitted from muscle names (except when a muscle ... John., Stewart, Gregory (2009). "Chapter 8: Skeletal muscles". The skeletal and muscular systems. New York: Chelsea House. ISBN ... Muscle Tables for the Human Body Lower Extremity Muscle Atlas Tutorial and quizzes on skeletal muscular anatomy Muscles of ...
"The teres minor muscle in rotator cuff tendon tears". Skeletal Radiology. 40 (10): 1335-1344. doi:10.1007/s00256-011-1178-3. ... Teres minor muscle Accessory muscles of the scapula This article incorporates text in the public domain from page 441 of the ... The teres minor (Latin teres meaning 'rounded') is a narrow, elongated muscle of the rotator cuff. The muscle originates from ... one of which separates it from the infraspinatus muscle, the other from the teres major muscle. Its fibers run obliquely ...
In particular, Wnt10b is a Wnt protein that increases this sensitivity in skeletal muscle cells. Since its initial discovery, ... Skeletal Muscle. 3 (1): 5. doi:10.1186/2044-5040-3-5. PMC 3602004. PMID 23497616. Malinauskas T, Jones EY (December 2014). " ... catenin signaling increases insulin sensitivity through a reciprocal regulation of Wnt10b and SREBP-1c in skeletal muscle cells ... These processes are necessary for proper formation of important tissues including bone, heart and muscle. Its role in embryonic ...
For musculo-skeletal aspects THI has not been used that much, although this method features some useful potential. For example ... Subscapularis muscle (shown in red). Animation. Same as the left, but the bones around the muscle are shown as semi-transparent ... The tendon of the muscle is separated from the neck of the scapula by a large bursa, which communicates with the cavity of the ... And it really turned out to ease a detailed examination of the muscle which just abuts to the scapula. However, the tendon of ...
Alpha-dystroglycan in skeletal muscles helps to prevent the breakdown of muscle fibers through stabilization and protection. ... FCMD mainly affects the brain, eyes, and muscles, in particular, the disorder affects development of the skeletal muscles ... Use of the destabilized muscle fibers over time causes them to break down and a gradual decline in muscle tone and atrophy of ... Skeletal Muscle. 1: 22. doi:10.1186/2044-5040-1-22. ISSN 2044-5040. PMC 3156645. Fukuyama type muscular dystrophy at NIH's ...
Skeletal Muscle. 3 (1): 1. doi:10.1186/2044-5040-3-1. PMC 3599653. PMID 23282144. Crosbie RH, Heighway J, Venzke DP, Lee JC, ... is a 25-kDa transmembrane protein located in the dystrophin-associated protein complex of skeletal muscle cells, where it is ... Without SSPN, Akt signaling pathways will be hindered and muscle regeneration will not occur. The loss of dystrophin results in ... "Sarcospan-dependent Akt activation is required for utrophin expression and muscle regeneration". The Journal of Cell Biology. ...
Skeletal muscles make up 58.8% of the lion's body weight. Today, P. l. leo occurs in West and Central Africa and India. It is ... Calder, W. A. (1996). "Skeletal muscle". Size, Function, and Life History. New York: Courier Corporation. p. 17-21. ISBN 978-0- ...
... skeletal muscle > pancreas. Data from Human Protein Atlas and RNA-Seq based suggest TRPV6 mRNA is low in most tissues except ... Exome sequencing of an infant with severe antenatal onset thoracic insufficiency with accompanying fetal skeletal abnormalities ... skeletal deformities, osteoarthritis, male sterility, Pendred syndrome, and certain sub-types of Cancer. Peng et al identified ... the insufficient maternal-fetal transport caused by pathogenic genomic variants of TRPV6 is thought to be a cause for skeletal ...
Skeletal muscles make up 58.8% of the lion's body weight. The largest known lion measured 3.35 m (11.0 ft) in length and ... Calder, W. A. (1996). "Skeletal muscle". Size, Function, and Life History. New York: Courier Corporation. p. 17-21. ISBN 978-0- ...
Only skeletal and smooth muscles are part of the musculoskeletal system and only the muscles can move the body. Cardiac muscles ... Skeletal muscles of the human body Skeletal muscle Muscular system Musculoskeletal+System at the US National Library of ... Skeletal muscles are attached to bones and arranged in opposing groups around joints. Muscles are innervated, to communicate ... There are three types of muscles-cardiac, skeletal, and smooth. Smooth muscles are used to control the flow of substances ...
Skeletal muscles of the lion make up 58.8% of its body weight and represents the highest percentage of muscles among mammals. ... doi:10.1111/j.1558-5646.1962.tb03240.x. Calder, W. A. (1996). "Skeletal muscle". Size, Function, and Life History. Courier ... Differentiation and species determination of muscle-cysticerci in East African game animals]". Zeitschrift für Tropenmedizin ...
November 2019). "Two functional variants at 6p21.1 were associated with lean mass". Skeletal Muscle. 9 (1): 28. doi:10.1186/ ... A SNP found within TMEM151B is associated with the development of lean muscle. GRCh38: Ensembl release 89: ENSG00000178233 - ...
Skeletal Muscle. 2 (1): 11. doi:10.1186/2044-5040-2-11. PMC 3514131. PMID 22676848. Colker, Carlon. "New Muscle Drugs Could Be ... Some breeds of cattle do not possess the myostatin gene that helps regulate muscle growth. This causes them to have more muscle ... Backfat is generally found to be less in double-muscled cattle than in cattle with normal muscling. Animals that are double- ... muscled have a higher carcass yield but this does come with new problems for the cattle. The meat from double muscled cattle is ...
Skeletal Muscle. 2 (1): 26. doi:10.1186/2044-5040-2-26. ISSN 2044-5040. PMC 3534636. PMID 23216833. Mull, Aaron J.; Berhanu, ... displays a resistance to muscle dystrophy, and is resistant to experiencing hyperglycemia from a diet high in fats. Clark, Lise ...
Muscle hypertrophy List of biological development disorders Hernandez, Richard; Kravitz, Len. "Skeletal muscle hypertrophy". ... 20-22, ISBN 978-1-59377-189-8 University of California Muscle Physiology Home Page: Hypertrophy Archived 2021-04-21 at the ... showing thickening of the cardiac muscle Kidney hypertrophy Hypertrophy of the ear (macrotia) Hypertrophy of the temporal ... muscles Athlete's heart Ventricular hypertrophy (including left ventricular hypertrophy and right ventricular hypertrophy) ...
Myoglobinuria may result from the breakdown of skeletal muscle known as rhabdomyolysis, a condition in which muscle cells ... As skeletal muscle relies predominantly on glycogenolysis for the first few minutes as it transitions from rest to activity, as ... McArdle accurately concluded that the patient had a disorder of glycogen breakdown that specifically affected skeletal muscle. ... Valberg, Stephanie J. (2008). "Skeletal Muscle Function". Clinical Biochemistry of Domestic Animals. pp. 459-484. doi:10.1016/ ...
A muscle relaxant is a drug that affects skeletal muscle function and decreases the muscle tone. It may be used to alleviate ... It reduces skeletal muscle strength by inhibiting the excitation-contraction coupling in the muscle fiber. In normal muscle ... "Muscle relaxants." WebMD. Last Updated: February 15, 2006. Retrieved on September 19, 2007. "Skeletal Muscle Relaxant (Oral ... Muscle that contracts more rapidly is more sensitive to dantrolene than muscle that contracts slowly, although cardiac muscle ...
... is a congenital neuromuscular channelopathy that affects skeletal muscles (muscles used for movement). It is ... But once the muscles are warmed up, they can once again function normally. This can happen in various muscles, even in muscles ... In skeletal muscle fibers the equilibrium potential for Cl− is around -80 mV, equal to that of K+ at rest. Cl− moves towards ... In skeletal muscle fibers, a large transverse tubule system with a high surface-area to volume ratio exists. The onset of ...
Gherardi, Romain; Amato, Anthony A.; Lidov, Hart G.; Girolami, Umberto De (Nov 2018). "Pathology of Skeletal Muscle". In Gray, ... This dysregulated RNA splicing is particularly toxic to skeletal, cardiac, and smooth muscle.[citation needed] One example in ... DMPK codes for myotonic dystrophy protein kinase, a protein expressed predominantly in skeletal muscle. Between 5 and 37 ... Muscle biopsy can reveal damage of the muscle, but findings are generally nonspecific and do not greatly aid in diagnosis. ...
Caldwell JE (1995). "New skeletal muscle relaxants". Int Anesthesiol Clin. 33 (1): 39-60. doi:10.1097/00004311-199500000-00003 ... used adjunctively in anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery ... Serra C, Oliveira A (2006). "Cisatracurium: myographical and electrophysiological studies in the isolated rat muscle". Fundam ... Hull CJ (1995). "Pharmacokinetics and pharmacodynamics of the benzylisoquinolinium muscle relaxants". Acta Anaesthesiol Scand. ...
Burkholder, TJ (2007). "Mechanotransduction in skeletal muscle". Frontiers in Bioscience. 12: 174-91. doi:10.2741/2057. PMC ... When a deformation is imposed on a muscle, changes in cellular and molecular conformations link the mechanical forces with ...
The fusion of myoblasts is specific to skeletal muscle, and not cardiac muscle or smooth muscle. Myoblasts in skeletal muscle ... A skeletal muscle cell is long and threadlike with many nuclei and is called a muscle fiber. Muscle cells (including myocytes ... A single muscle such as the biceps brachii in a young adult human male contains around 253,000 muscle fibers. Skeletal muscle ... Skeletal muscle cells are the individual contractile cells within a muscle, and are more usually known as muscle fibers because ...
"Tone of skeletal muscles / A.K. Jamil". catalogue.nla.gov.au. National Library of Australia. Archived from the original on 10 ... Tone of skeletal muscles. Magnetic vacuum and magnetic high pressure Information on patient due for anaesthesia Non-Kink ...
ISBN 978-0-443-06952-9. Stone, Robert & Judith (2000). Atlas of skeletal muscles. McGraw-Hill. p. 26. ISBN 978-0-07-290332-4. " ... The occipitofrontalis muscle (epicranius muscle) is a muscle which covers parts of the skull. It consists of two parts or ... However, Terminologia Anatomica currently classifies it as a single muscle, and also includes the temporoparietalis muscle as ... The occipitofrontalis muscle consists of two parts or bellies: the occipital belly, near the occipital bone. It originates on ...
The toxin or toxins paralyze muscle tissue; in particular: Skeletal muscles. This results in the overt paralysis for which the ... Heart muscle. This results in congestive heart failure and pulmonary oedema, seen also as labored breathing. Spring is the peak ... Respiratory muscles. Initially this results in rapid, shallow breathing with an inability to cough. In advanced stages it is ... Laryngeal muscles. This results in an altered 'voice' and an increased risk of aspiration pneumonia (inhalation of food, saliva ...
Close to the midline are the motor efferent nuclei, such as the oculomotor nucleus, which control skeletal muscle. Just lateral ...
... is primarily expressed in skeletal muscle and is transcriptionally regulated by thyroid hormone. Mutations in this gene ...
Lohuis, T. D.; Harlow, H. J.; Beck, T. D. I. (2007). "Hibernating black bears (Ursus americanus) experience skeletal muscle ... They also increase the availability of certain essential amino acids in the muscle, as well as regulate the transcription of a ... allowing them to stop urinating for months and to avoid muscle atrophy. They stay hydrated with the metabolic fat that is ... A new approach for muscle wasting therapy?". Clinical Nutrition. 26 (5): 658-661. doi:10.1016/j.clnu.2007.07.003. PMID 17904252 ...
The tongue muscle is anchored to the chin, and translation of the mandible forward pulls the tongue forward as well. If the ... The first involves surgery of the soft tissue (tonsillectomy, uvulopalatopharyngoplasty) and the second involves skeletal ...
Less common features include an atrial septal defect, increased muscle tone or skeletal abnormalities. Physical features may ... as well as reduced heart muscle tissue (myocardium) and abnormally small heart muscle cells (cardiomyocytes). One affected ... A few of those affected have had increased muscle tone. One individual had cortical heterotopia, which is a sign of impaired ... skeletal, brain and intestinal malformations in others. The variable severity is usually due to the presence or absence in each ...
Fernando P, Kelly JF, Balazsi K, Slack RS, Megeney LA (August 2002). "Caspase 3 activity is required for skeletal muscle ... such as skeletal muscle cell. Targeting of p21 promoter is responsible for inducing cell differentiation, which is promoted by ... Referring to the example of skeletal cells, their differentiation is associated to cleavage of the kinase MST1. Moreover, it ... Caspase-3 activation is a cell requirement during early stages of the skeletal myoblast differentiation. Its catalytic site ...
Koseki T, Inohara N, Chen S, Núñez G (Jun 1998). "ARC, an inhibitor of apoptosis expressed in skeletal muscle and heart that ...
... "alpha-Glucosidase isoenzymes in normal and acid maltase-deficient human skeletal muscles". Muscle & Nerve. 11 (4): 365-71. doi: ...
... sarcoglycan in smooth muscle and its interaction with the smooth muscle sarcoglycan-sarcospan complex". The Journal of ... and dystrophin molecules in normal skeletal myofiber: triple immunogold labeling electron microscopy". Microscopy Research and ... The dystrophin-glycoprotein complex (DGC) comprises a group of proteins that are critical to the stability of muscle fiber ... Roberds SL, Anderson RD, Ibraghimov-Beskrovnaya O, Campbell KP (Nov 1993). "Primary structure and muscle-specific expression of ...
A muscle is made up of several muscle bundles, which in turn are made up of muscle fibers. Muscle fibers have myofibrils, which ... though it is not the same skeletal structure as an ankle in humans; known to anatomists as the metacarpophalangeal (front) or ... extensor muscle). Therefore, one muscle of the pair must be relaxed in order for the other muscle in the pair to contract and ... When a muscle contracts, it pulls a tendon, which acts on the horse's bones to move them. Muscles are commonly arranged in ...
When they attempt to touch her, she transforms into a much larger and more frightening skeletal form and causes the trio to ... Abby hires Kevin Beckman because she needs a muscle-strong person to carry heavy equipment. Unlike Erin and maybe Jillian, she ... but includes skeletal protrusions and spikes, with energy surging throughout its body (due to Jason Reitman's desire to use ...
Moreover, reductions in skeletal muscle NOX4 in aging and obesity was shown to contribute to the development of insulin ... "Skeletal muscle NOX4 is required for adaptive responses that prevent insulin resistance". Science Advances. 7 (51): eabl4988. ... 2005). "Human urotensin II is a novel activator of NADPH oxidase in human pulmonary artery smooth muscle cells". Arterioscler. ... 2002). "Cytochrome b558-dependent NAD(P)H oxidase-phox units in smooth muscle and macrophages of atherosclerotic lesions". ...
Staining of skeletal muscle samples with hematoxylin and eosin may reveal the ragged red fibers sign indicating disrupted ... Patients suffer from exercise intolerance and may also have neuromuscular symptoms such as ataxia, dysarthia and muscle ...
It possesses hypnotic, anxiolytic, anticonvulsant, sedative, and skeletal muscle relaxant properties. It was patented in 1961 ... Side effects of lormetazepam include: Somnolence Paradoxical increase in aggression Lightheadedness Confusion Muscle weakness ... and pain Muscle pain, weakness, tension, painful tremor, shaking attacks, jerks, blepharospasm Excitability, jumpiness, and ...
... can be asymptomatic and may go undetected until a significant amount of muscle is lost. Skeletal muscle serves ... Muscle atrophy is the loss of skeletal muscle mass. It can be caused by immobility, aging, malnutrition, medications, or a wide ... Muscle atrophy leads to muscle weakness and causes disability. Disuse causes rapid muscle atrophy and often occurs during ... in which the muscle is compromised primarily by declines in muscle protein synthesis rates rather than changes in muscle ...
... is most highly expressed in the skeletal muscle and brain tissues.The structure in which it is highly concentrated is ...
"Inhibition of glycogenolysis prolongs action potential repriming period and impairs muscle function in rat skeletal muscle". ... Recently, glycolysis has also been shown to be of particular importance for Na⁺/K⁺-ATPases in skeletal muscles, where ... Dutka TL, Lamb GD (September 2007). "Na+-K+ pumps in the transverse tubular system of skeletal muscle fibers preferentially use ... release from the muscle cells' sarcoplasmic reticulum. Immediately after muscle contraction, intracellular Ca²⁺ is quickly ...
... is a myosin whose expression is restricted primarily to the extrinsic eye muscles which are specialized for function in ... 1999). "Organization of human and mouse skeletal myosin heavy chain gene clusters is highly conserved". Proc. Natl. Acad. Sci. ... Winters LM, Briggs MM, Schachat F (November 1998). "The human extraocular muscle myosin heavy chain gene (MYH13) maps to the ... Schachat F, Briggs MM (2002). "Phylogenetic implications of the superfast myosin in extraocular muscles". J. Exp. Biol. 205 (Pt ...
Camptocormism Camptodactyly fibrous tissue hyperplasia skeletal dysplasia Camptodactyly joint contractures facial skeletal ... photocontact Continuous muscle fiber activity hereditary Continuous spike-wave during slow sleep syndrome Contractural ... ventricle neoplasms Cerebro facio articular syndrome Cerebro facio thoracic dysplasia Cerebro oculo dento auriculo skeletal ... Cerebro reno digital syndrome Cerebroarthrodigital syndrome Cerebro-costo-mandibular syndrome Cerebro-oculo-facio-skeletal ...
... such as visualizing an object moving in a specific direction along various muscle groups throughout the body, while lying ... "based on the idea that imagery can improve skeletal alignment and posture through the re-patterning of neuromuscular pathways ... all without moving a muscle", Yoga Journal (139): 79-87, ISSN 0191-0965 Batson, G (2004), "Motor imagery for stroke ...
... in certain genes give rise to structural abnormalities in nervous system networks responsible for voluntary skeletal muscle ... Patients also often experience discomfort or pain in the upper limbs due to prolonged use of the same muscles. Therefore, ...
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 ... Skeletal system). ... Additionally, lower motor neurons are characterized by muscle ... Overall, spontaneous embryonic activity has been shown to play a role in neuron and muscle development but is probably not ... The VM lower motor neurons control the large, postural muscles of the axial skeleton. These lower motor neurons, unlike those ...
Further, the size of the sagittal crest (and the gluteus muscles) in male western lowland gorillas has been correlated with ... boisei skeletal remains, save for the presumed male OH 80. Based on an approximation of 400 mm (1.3 ft) for the femur before it ... Because skeletal elements are so limited in these species, their affinities with each other and to other australopithecines is ... it is also possible that male gorillas and orangutans require larger temporalis muscles to achieve a wider gape to better ...
In human anatomy, the extensor pollicis longus muscle (EPL) is a skeletal muscle located dorsally on the forearm. It is much ... Superficial muscles. Posterior surface of the forearm. Deep muscles. Transverse section across the wrist and digits. Arteries ... Extensor pollicis longus visible at center right.) Muscle of the hand . Posterior view. This article incorporates text in the ... The extensor pollicis longus muscle receives innervation from the posterior interosseous nerve (C7 and C8) which is the ...
The effective forces felt by the operator are dramatically diminished reducing the risk of muscular/skeletal injuries. The HULC ... the project was a failure as it hindered certain movements and actually increased strain on muscles, going directly against ...
Billow BW, Martorella FJ, Paley SS (January 1960). "Clinical experiences with styramate, a nonsedative skeletal muscle relaxant ... Styramate is a muscle relaxant and anticonvulsant drug. At therapeutic doses, it does not produce significant sedative effects ...
It is abundantly expressed in the human brain, heart tissue, and skeletal muscle, as well as in the kidneys. It is relatively ...
... (INN; EXP 338) is an extremely stable 3-imidazoline derivative with central skeletal muscle relaxant and sedative ...
Skeletal muscle includes skeletal muscle fibers, blood vessels, nerve fibers, and connective tissue. Skeletal muscle is wrapped ... There are two types of striated muscle: Cardiac muscle (heart muscle) Skeletal muscle (muscle attached to the skeleton) ... Both smooth muscle cells and cardiac muscle cells have a single nucleus, and skeletal muscle cells have many nuclei. The main ... Unlike skeletal and cardiac muscle tissue, smooth muscle tissue is not striated since there are no sarcomeres present. Skeletal ...
These studies suggest that mouse Lect2 suppresses insulin signaling in skeletal muscle but not adipose or liver tissues of ... Studies conducted on cultured myocytes, a form of muscle cell, indicates that LECT2 impairs insulin signaling by activating a c ... LECT2 protein is widely expressed in vascular tissues, smooth muscle cells, adipocytes, cerebral neurons, apical squamous ... Several cell types or tissues, e.g. osteoblasts, chondrocytes, cardiac tissue, gastrointestinal smooth muscle cells, and ...
... everything you need for studying or teaching Skeletal muscle. ... Immediately download the Skeletal muscle summary, chapter-by- ... Skeletal Muscle Skeletal muscle is also known as striated muscle because of its striped appearance under the microscope and as ... Skeletal muscle Summary. Everything you need to understand or teach Skeletal muscle. ... Skeletal Muscle System, Embryonic Development The skeletal and muscular systems are taught as individual subjects in ...
Muscle genes are regulated by combinatorial interactions between numerous transcription factors bound to enhancers and ... The mechanisms by which muscle gene expression is initiated and maintained are not fully understood. ... Analysis of muscle gene transcription in cultured skeletal muscle cells Methods Mol Biol. 2012;798:425-43. doi: 10.1007/978-1- ... Using Muscle creatine kinase as a model, we outline the key steps involved in identifying muscle gene control elements, their ...
... the authors show that changes in the mitochondrial interactome of the skeletal muscle contribute to mitochondrial functional ... By making use of quantitative chemical cross-linking technologies, we show that changes in the muscle mitochondrial interactome ... Skeletal muscle transcriptome in healthy aging. Nat. Commun. 12, 2014 (2021).. Article CAS PubMed PubMed Central Google Scholar ... Decline in skeletal muscle mitochondrial function with aging in humans. Proc. Natl Acad. Sci. 102, 5618-5623 (2005). ...
Modulating fast skeletal muscle contraction protects skeletal muscle in animal models of Duchenne muscular dystrophy. ... Modulating fast skeletal muscle contraction protects skeletal muscle in animal models of Duchenne muscular dystrophy. ... We explored the role of fast skeletal muscle contraction in DMD with a potentially novel, selective, orally active inhibitor of ... Selective inhibition of active contraction in fast skeletal muscle decreases CK and increases habitual activity in DMD dogs. ...
Specialized stem cells known as satellite cells reside in skeletal muscle in an inactive state. When muscle injury occurs, a ... Mechanism That May Inhibit Skeletal Muscle Repair Discovered. Dec 30, 2015 , Muscular Dystrophy , 0 , ... They believe this is because TRAF6 is upstream from Pax7 in the signaling process involved in muscle repair and orchestrates ... resulting in reduced muscle regeneration in both normal and Duchenne muscular dystrophy (DMD) mouse models. ...
Skeletal Muscle Relaxants (Direct Acting). Class Summary. Direct-acting skeletal muscle relaxants inhibit muscle contraction by ... Skeletal Muscle Relaxants (Centrally Acting). Class Summary. Centrally acting skeletal muscle relaxants inhibit reflexes at the ... Dantrolene stimulates muscle relaxation by modulating the skeletal muscle contractions at a site beyond the myoneural junction ... The muscle flap in the treatment of chronic lower extremity osteomyelitis: results in patients over 5 years after treatment. ...
Behavioral and Locomotor Measurements Using an Open Field Activity Monitoring System for Skeletal Muscle Diseases. ... Behavioral and Locomotor Measurements Using an Open Field Activity Monitoring System for Skeletal Muscle Diseases ...
Figure 1. Pyrene Muscle Actin Protein Purity Determination. A 100 µg sample of pyrene muscle actin (molecular weight approx. 43 ... Pyrene labeled rabbit muscle actin has an approximate molecular weight of 43 kDa, and is supplied as a white lyophilized powder ... Pyrene muscle actin was polymerized in duplicate wells of a 96-well plate by the addition of Actin Polymerization Buffer (Cat ... Purified rabbit muscle actin (Cat. # AKL99) has been modified to contain covalently linked pyrene at the cysteine 374 residue. ...
Cardiac and skeletal muscle development and maintenance require complex interactions between DNA-binding proteins and chromatin ... Cardiac and skeletal muscle development and maintenance require complex interactions between DNA-binding proteins and chromatin ... skNAC, a Smyd1-interacting transcription factor, is involved in cardiac development and skeletal muscle growth and regeneration ... skNAC, a Smyd1-interacting transcription factor, is involved in cardiac development and skeletal muscle growth and regeneration ...
Transverse tubule remodeling enhances Orai1-dependent Ca2+ entry in skeletal muscle. ... Transverse tubule remodeling enhances Orai1-dependent Ca2+ entry in skeletal muscle ... Transverse tubule remodeling enhances Orai1-dependent Ca2+ entry in skeletal muscle ... A-D) Representative EM images of cross sections (in proximity of I band) of EDL muscle fibers from control mice (A) and from ...
Identification of a 97-kDa Mastoparan-Binding Protein Involving in Ca2+ Release from Skeletal Muscle Sarcoplasmic Reticulum. ... Identification of a 97-kDa Mastoparan-Binding Protein Involving in Ca2+ Release from Skeletal Muscle Sarcoplasmic Reticulum. ... Identification of a 97-kDa Mastoparan-Binding Protein Involving in Ca2+ Release from Skeletal Muscle Sarcoplasmic Reticulum. ... Identification of a 97-kDa Mastoparan-Binding Protein Involving in Ca2+ Release from Skeletal Muscle Sarcoplasmic Reticulum ...
... the treatment of CKD-related muscle injury.The objective is to identify potential compounds for treating ferroptosis and muscle ... Muscle wasting increases morbidity and mortality and is related to chronic kidney disease (CKD) and dialysis. It is still ... In NPM mice, skeletal muscle dysfunction, lipogenesis, reduced GSH/GSSG ratio, decreased GSH content, increased MDA production ... Lobetyolin Alleviates Ferroptosis of Skeletal Muscle in 5/6 Nephrectomized Mice via Activation of Hedgehog-GLI1 Signaling.. May ...
Leonardo mechanography systems and pQCT scanners for the analysis of muscle and bone. ... Metabolic milieu associates with impaired skeletal characteristics in obesity.. PLoS One, 2017; 12(6): e0179660, PMID: 28640843 ... Metabolic milieu associates with impaired skeletal characteristics in obesity.. Year: 2017. Viljakainen HT, Koistinen HA, ...
The Fast Skeletal Troponin Activator, CK-1909178, Increases Skeletal Muscle Force in-vitro and in-situ. ...
Low skeletal muscle index (SMI) has been associated with increased surgical complications and poor quality of life. Aim: To ... P170 Point-of-care ultrasound accurately quantifies skeletal muscle index in patients with Inflammatory Bowel Disease Nguyen, A ... Sonographic muscle thickness of the dominant arm and bilateral thighs (Figure 1) were multiplied by respective bone lengths ( ... Sonographic measurement of the dominant arm ± bilateral thigh muscle thickness accurately assesses DXA-derived SMI at the point ...
GSIS (C-pep/Glc tAUC0-120min) and ß-cell function (Disposition Index [DI: GSIS/IR]) relative to skeletal muscle (InsulintAUC x ... Collectively, short-term INT and CONT training improves ß-cell function relative to skeletal muscle, but not hepatic or adipose ... Short-Term Interval and Continuous Training Improves Pancreatic ß-Cell Function Adjusted for Skeletal Muscle Insulin Resistance ... Short-term training improved skeletal muscle DI by ∼24% (P,0.05), but there was no effect on hepatic or adipose DI. ...
... View/. Open Dissertation Final ... Thus in the presence of unchanged (or "matched") convective O2 delivery with arterial hypoxemia, skeletal muscle V•O2 on- ... to the muscle was held constant by elevating muscle blood flow via a perfusion pump. Blood flow was recorded with an ultrasonic ... Canine gastrocnemius muscles (n=7) were surgically isolated and then electrically stimulated via the sciatic nerve (8 V, 0.2-ms ...
... which is the predominant actin isoform in the sarcomeric thin filaments of adult skeletal muscle, and essential, along with ... myosin, for muscle contraction. ACTA1 disease-causing mutations were first described in 1999, when a total of 15 mutations were ... The ACTA1 gene encodes skeletal muscle alpha-actin, ... skeletal muscle alpha-actin ACTA1 congenital myopathies locus- ... The ACTA1 gene encodes skeletal muscle alpha-actin, which is the predominant actin isoform in the sarcomeric thin filaments of ...
Concerted regulation of skeletal muscle contractility by oxygen tension and endogenous nitric oxide. ... Concerted regulation of skeletal muscle contractility by oxygen tension and endogenous nitric oxide. Journal Article (Journal ... These results reveal a fundamental role for the concerted action of NO and O2 in physiological regulation of skeletal muscle ... contractility of skeletal muscle. However, standard assessments of contractility are carried out at a nonphysiological oxygen ...
INTRODUCTION: Skeletal muscle mitochondria have dynamic shifts in oxidative metabolism to meet energy demands of aerobic ... Substrate-Specific Respiration of Isolated Skeletal Muscle Mitochondria after 1 h of Moderate Cycling in Sedentary Adults. ... Substrate-Specific Respiration of Isolated Skeletal Muscle Mitochondria after 1 h of Moderate Cycling in Sedentary Adults.. ... Adult, Cell Respiration, Exercise, Female, Humans, Hydrogen Peroxide, Male, Mitochondria, Muscle, Oxidative Phosphorylation, ...
Gorski, P, Turner, D, Iraki, J, Morton, J, Sharples, A and Areta, J (2023) Human skeletal muscle methylome after low ... We aimed to investigate the human skeletal muscle (SkM) DNA methylome after exercise in low carbohydrate (CHO) energy balance ( ... with skeletal muscle biopsies collected 30 minutes and 3.5 hours post exercise. Discovery of genome-wide DNA methylation was ... The sleep-low conditions included 9 males that cycled to deplete muscle glycogen while reaching a set energy expenditure. Post- ...
title = "Muscle creatine kinase-deficient mice. II. Cardiac and skeletal muscles exhibit tissue-specific adaptation of the ... T1 - Muscle creatine kinase-deficient mice. II. Cardiac and skeletal muscles exhibit tissue-specific adaptation of the ... Muscle creatine kinase-deficient mice. II. Cardiac and skeletal muscles exhibit tissue-specific adaptation of the mitochondrial ... Muscle creatine kinase-deficient mice. II. Cardiac and skeletal muscles exhibit tissue-specific adaptation of the mitochondrial ...
... Drugs used in nocturnal leg cramps not listed here:. *Quinine sulphate, see 5.4 Antiprotozoal ... 10.2.2 Skeletal muscle relaxants. 10. Musculoskeletal & joint diseases. *Management of gout and cytotoxic-induced ... Musculoskeletal & joint diseases , 10.2 Drugs used in neuromuscular disorders , 10.2.2 Skeletal muscle relaxants ...
They are called skeletal muscles because most of them are attached to bones. A skeletal muscle is… ... Skeletal muscles are the organs of the muscular system. ... Structure of Skeletal Muscle. Skeletal muscles are the organs ... They are called skeletal muscles because most of them are attached to bones. A skeletal muscle is composed mainly of skeletal ... Skeletal Muscle Fibers. The internal structure of skeletal muscle tissue is so highly specialized that specific terminology is ...
Skeletal Muscle Relaxation. IM. Maximum total dose 150 mg.. Adults. Skeletal Muscle Relaxation. IM. Maximum total dose 150 mg. ... Skeletal Muscle Relaxation. Production of skeletal muscle relaxation during procedures of short duration (e.g., endotracheal ... resulting in transient twitching or fasciculation of skeletal muscles, followed by muscle paralysis (phase I block). ... Skeletal Muscle Relaxation. Test Dose. IV To evaluate sensitivity to succinylcholine in patients with reduced plasma ...
van Putten, M., Lloyd, E. M., de Greef, J. C., Raz, V., Willmann, R. & Grounds, M. D., 21 Feb 2020, In: Disease models & mechanisms. 13, 2, dmm043562.. Research output: Contribution to journal › Review article › peer-review ...
Carisoprodol is a muscle relaxant used to relieve the pain and stiffness of muscle spasms and discomfort due to strain and ...
Mechanisms Modulating Skeletal Muscle Phenotype. Mechanisms of Muscle Injury, Repair, and Regeneration. Contact Editor. Submit ... During skeletal muscle regeneration, miR‐26a expression was increased following muscle injury and downregulation of miR‐26a ... During skeletal muscle regeneration, miR‐26a expression was increased following muscle injury and downregulation of miR‐26a ... Diminished skeletal muscle microRNA expression with aging is associated with attenuated muscle plasticity and inhibition of IGF ...
Unlike in other metabolic myopathies, skeletal muscle substrate use during exercise is normal in Pompe disease rendering ... Considering the health benefits of exercise, it is important in Pompe disease to acquire more information about muscle ... Conclusion Reflecting muscle weakness and wasting, Pompe disease is associated with markedly reduced maximal exercise capacity ... Glycogen is an essential source of energy for skeletal muscle during exercise (6). Exercise may increase skeletal muscle energy ...
Adv Skelet Muscle Funct Assess, Official publication of International Society of Tensiomyography,Slovenia ... Effects of active recovery on muscle function following high-intensity training sessions in elite olympic weightlifters. Raeder ...
  • By making use of quantitative chemical cross-linking technologies, we show that changes in the muscle mitochondrial interactome contribute to mitochondrial functional decline in aging in female mice. (nature.com)
  • 15%) were sufficient to protect skeletal muscles in dystrophic mdx mice from stress injury. (jci.org)
  • Viable skNAC(-/-) adult mice had reduced postnatal skeletal muscle growth and impaired regenerative capacity after cardiotoxin-induced injury. (ca.gov)
  • Our results indicate that skNAC plays a critical role in ventricular cardiomyocyte expansion and regulates postnatal skeletal muscle growth and regeneration in mice. (ca.gov)
  • Lobetyolin Alleviates Ferroptosis of Skeletal Muscle in 5/6 Nephrectomized Mice via Activation of Hedgehog-GLI1 Signaling. (physiciansweekly.com)
  • Initially, we explored whether ferroptosis is present in the skeletal muscle of 5/6 nephrectomized (NPM) mice via RNA-Seq analysis, TUNEL staining, Oil red O staining, MDA/GSH/GSSG level detection and real-time quantitative PCR (qPCR). (physiciansweekly.com)
  • In NPM mice, skeletal muscle dysfunction, lipogenesis, reduced GSH/GSSG ratio, decreased GSH content, increased MDA production and and higher levels of ferroptosis markers were observed. (physiciansweekly.com)
  • We therefore examined, in normal and neuronal NOS (nNOS)-deficient mice, the influence of pO2 on whole-muscle contractility and on myocyte calcium flux and sarcomere shortening. (duke.edu)
  • Muscle creatine kinase-deficient mice. (elsevier.com)
  • Dive into the research topics of 'Muscle creatine kinase-deficient mice. (elsevier.com)
  • Discovery proteomics in aging human skeletal muscle finds change in spliceosome, immunity, proteostasis and mitochondria. (nature.com)
  • We aimed to investigate the human skeletal muscle (SkM) DNA methylome after exercise in low carbohydrate (CHO) energy balance (with high fat) compared with exercise in low-CHO energy deficit (with low fat) conditions. (ljmu.ac.uk)
  • Physical activity has been defined as 'any bodily movement produced by skeletal muscles that results in energy expenditure. (cdc.gov)
  • Physical activity is any bodily movement produced by the skeletal muscles that uses energy. (who.int)
  • WHO defines physical activity as any bodily movement produced by skeletal muscles that requires energy expenditure - including activities undertaken while working, playing, carrying out household chores, travelling, and engaging in recreational pursuits. (who.int)
  • A major contributor to this injury is muscle contraction, controlled by the motor protein myosin. (jci.org)
  • However, how muscle contraction and fast muscle fiber damage contribute to the pathophysiology of DMD has not been well characterized. (jci.org)
  • We explored the role of fast skeletal muscle contraction in DMD with a potentially novel, selective, orally active inhibitor of fast skeletal muscle myosin, EDG-5506. (jci.org)
  • Selective inhibition of active contraction in fast skeletal muscle decreases CK and increases habitual activity in DMD dogs. (jci.org)
  • Direct-acting skeletal muscle relaxants inhibit muscle contraction by decreasing calcium release from the sarcoplasmic reticulum in muscle cells. (medscape.com)
  • These results suggest that the 97-kDa MP-binding protein may have an important role in the excitation-contraction coupling of skeletal muscle. (aspetjournals.org)
  • Blood flow was recorded with an ultrasonic flowmeter while venous O2 saturation was monitored continuously in order to allow measurement of contraction-by-contraction muscle VO2. (auburn.edu)
  • The ACTA1 gene encodes skeletal muscle alpha-actin, which is the predominant actin isoform in the sarcomeric thin filaments of adult skeletal muscle, and essential, along with myosin, for muscle contraction. (inserm.fr)
  • Two additional proteins, troponin and tropomyosin, are present in thin myofilaments and play a role in muscle contraction. (earthslab.com)
  • A sarcomere is a functional unit of skeletal muscle-that is, it is the smallest portion of a myofibril capable of contraction. (earthslab.com)
  • Decline in skeletal muscle mitochondrial function with aging in humans. (nature.com)
  • Cross-linking data have been uploaded to the XLinkdb online database ( http://xlinkdb.gs.washington.edu/xlinkdb/Interactome_of_aged_muscle_mitochondria.php ). (nature.com)
  • Substrate-Specific Respiration of Isolated Skeletal Muscle Mitochondria after 1 h of Moderate Cycling in Sedentary Adults. (oregonstate.edu)
  • Skeletal muscle mitochondria have dynamic shifts in oxidative metabolism to meet energy demands of aerobic exercise. (oregonstate.edu)
  • As compared to control, in situ mitochondria in transgenic ventricular and slow- twitch muscles showed two times lower K(m) values for ADP, and the presence of creatine only slightly decreased the K(m) values. (elsevier.com)
  • The medications most commonly employed for this purpose are muscle relaxants. (medscape.com)
  • Centrally acting skeletal muscle relaxants inhibit reflexes at the spinal level. (medscape.com)
  • Dantrolene stimulates muscle relaxation by modulating the skeletal muscle contractions at a site beyond the myoneural junction and by acting directly on the muscle itself. (medscape.com)
  • They consist of two kinds of myofilaments that interact to produce muscle contractions: (1) thin myofilaments composed mostly of the protein actin and (2) thick myofilaments composed of the protein myosin (table 7.2). (earthslab.com)
  • range of motion, 1.22 rad) and the recovery of isometric force following concentric contractions at different velocities were determined for electrically stimulated plantar flexor muscles in intact rats. (cdc.gov)
  • It is concluded that pre-loaded slow concentric contractions of the plantar flexor muscles in intact rats do not follow the same relationship as that of isometric force and ankle position. (cdc.gov)
  • O2) on-kinetics under hypoxic conditions while holding convective O2 delivery constant in isolated canine muscles in situ. (auburn.edu)
  • Our results in intact rats show that the force output of electrically stimulated ankle plantar flexor muscles measured under the sole of the foot can be used to study the physiological properties of skeletal muscle working in situ. (cdc.gov)
  • Expression of muscle-specific genes varies among different anatomical muscles and in fast- vs. slow-twitch fiber types, suggesting different mechanisms of regulation in response to diverse physiological cues. (nih.gov)
  • Here, we demonstrate a significant enhancement of these measures of muscle performance at low physiological pO2 and an inhibitory influence at higher physiological pO2, which depend on endogenous nNOS. (duke.edu)
  • These results reveal a fundamental role for the concerted action of NO and O2 in physiological regulation of skeletal muscle contractility, and suggest novel molecular aspects of myopathic disease. (duke.edu)
  • Skeletal muscles are the organs of the muscular system. (earthslab.com)
  • In this study of 403 men (33-96 years), we investigated associations between the fatty liver index (FLI) and muscle density, as markers of fat accumulation in these organs. (bvsalud.org)
  • Biopsies were collected from the vastus lateralis muscle on separate study days at rest or 15 min after exercise (1 h cycling at 65% peak aerobic capacity). (oregonstate.edu)
  • The following morning resting baseline biopsies were taken and the participants then undertook 75 minutes of cycling exercise, with skeletal muscle biopsies collected 30 minutes and 3.5 hours post exercise. (ljmu.ac.uk)
  • Furthermore, in these muscles, relatively low oxidative capacity was considerably elevated. (elsevier.com)
  • E ) Percentage of muscle fibers exhibiting SR-stacks. (elifesciences.org)
  • Individual skeletal muscle cells, called muscle fibers due to their long skinny shape, are wrapped in areolar connective tissue. (earthslab.com)
  • Muscle fibers extend most of the length of a whole muscle and are arranged in small bundles called muscle fascicles (fah'-si-kuls) that are each surrounded by a layer of dense irregular connective tissue. (earthslab.com)
  • The organization of thin and thick myofilaments within a muscle fiber produces ttriations-the light and dark cross bands that are characteristic of skeletal muscle fibers when viewed microscopically. (earthslab.com)
  • Metabolic milieu associates with impaired skeletal characteristics in obesity. (galileo-training.com)
  • Accumulation of fat in the liver and skeletal muscle is associated with obesity and poor health outcomes. (bvsalud.org)
  • Longer-term treatment also decreased muscle fibrosis in key disease-implicated tissues. (jci.org)
  • When Pax7 is missing or reduced, the satellite cells undergo premature differentiation, or lose their stem properties and their ability to regenerate injured muscles, the release explains. (rehabpub.com)
  • In their study, Sajedah M. Hindi, PhD and Ashok Kumar, PhD, discovered that removing TRAF6 depletes Pax7, resulting in reduced muscle regeneration in both normal and Duchenne muscular dystrophy (DMD) mouse models. (rehabpub.com)
  • They believe this is because TRAF6 is upstream from Pax7 in the signaling process involved in muscle repair and orchestrates multiple signals controlling the muscle-regeneration process, the release continues. (rehabpub.com)
  • Expression pattern analysis showed that the adrenal glands ' glucocorticoid receptor (NR3C1/GR) had a potential regulatory relationship with the skeletal muscle -related genes (Pax7, mTOR, FBXO32, FOXO3, and FOXO4).5. (bvsalud.org)
  • Fig. 6: Interactome remodeling associated with changes in muscle metabolism with aging. (nature.com)
  • In skeletal muscle protein metabolism , expression levels of the catabolic gene atrogin1/MAFbx and the anabolic gene eEF2 were significantly higher, with concomitant increases after castration . (bvsalud.org)
  • The data showed that castration affected muscle protein metabolism , adrenal steroid and testosterone synthesis. (bvsalud.org)
  • In addition, it was speculated that, after castration , steroid hormones produced by the adrenal gland could have a compensatory effect, which might mediate the changes in skeletal muscle protein metabolism and development. (bvsalud.org)
  • Purified rabbit muscle actin (Cat. (cytoskeleton.com)
  • Pyrene labeled rabbit muscle actin has an approximate molecular weight of 43 kDa, and is supplied as a white lyophilized powder. (cytoskeleton.com)
  • Pyrene Muscle Actin Protein Purity Determination. (cytoskeleton.com)
  • A 100 µg sample of pyrene muscle actin (molecular weight approx. (cytoskeleton.com)
  • Pyrene muscle actin was polymerized in duplicate wells of a 96-well plate by the addition of Actin Polymerization Buffer (Cat. (cytoskeleton.com)
  • Mutations and polymorphisms of the skeletal muscle alpha-actin gene (ACTA1). (inserm.fr)
  • Muscle genes are regulated by combinatorial interactions between numerous transcription factors bound to enhancers and promoters, and their associated protein complexes. (nih.gov)
  • Duchenne muscular dystrophy (DMD) is a lethal muscle disease caused by absence of the protein dystrophin, which acts as a structural link between the basal lamina and contractile machinery to stabilize muscle membranes in response to mechanical stress. (jci.org)
  • University of Louisville (UofL) scientists note that TNF receptor-associated factor 6 (TRAF6) may have a role in ensuring the vitality of stem cells that regenerate muscle tissue. (rehabpub.com)
  • A skeletal muscle is composed mainly of skeletal muscle tissue bound together and electrically insulated by connective tissue layers. (earthslab.com)
  • A muscle is formed when many muscle fascicles are packaged and held together by an external layer of dense irregular connective tissue. (earthslab.com)
  • Groups of whole muscles with similar functions are connected by a superficial layer of dense irregular connective tissue called fascia (fash'-e-ah). (earthslab.com)
  • The fascia is deep and connected to the subcutaneous tissue, which is how the muscles can produce skin movement. (earthslab.com)
  • The internal structure of skeletal muscle tissue is so highly specialized that specific terminology is used to describe some muscle fiber structures. (earthslab.com)
  • In control animals, apparent K(m) values of mitochondrial respiration for ADP in cardiac (ventricular) and slow-twitch (soleus) muscles (137 ± 16 μM and 209 ± 10 μM, respectively) were manyfold higher than that in fast-twitch (gastrocnemius) muscle (7.5 ± 0.5 μM). (elsevier.com)
  • Creatine substantially decreased the K(m) values only in cardiac and slow-twitch muscles (73 ± 11 μM and 131 ± 21 μM, respectively). (elsevier.com)
  • The mechanisms by which muscle gene expression is initiated and maintained are not fully understood. (nih.gov)
  • Using Muscle creatine kinase as a model, we outline the key steps involved in identifying muscle gene control elements, their binding factors, and mechanisms of transcriptional activation and repression. (nih.gov)
  • Effects of testis testosterone deficiency on gene expression in the adrenal gland and skeletal muscle of ducks. (bvsalud.org)
  • To reveal the effects of testis testosterone deficiency on adrenal steroid hormones synthesis and skeletal muscle development, gene expression related to adrenal steroid hormones synthesis and skeletal muscle development were determined by RNA-seq .3. (bvsalud.org)
  • LBT treatment (30 mg/kg or 50 mg/kg) significantly alleviates skeletal muscle injury by inhibiting ferroptosis. (physiciansweekly.com)
  • In addition, responsivity to pO2 is altered significantly in nNOS mutant muscle. (duke.edu)
  • Quantitative proteome analysis of age-related changes in mouse gastrocnemius muscle using mTRAQ. (nature.com)
  • The muscle length and distal fibre length of gastrocnemius medialis at ankle positions between 0.79 rad and 2.01 rad were increased by 12.6 % and 20.3 %, respectively. (cdc.gov)
  • Isometric and concentric performance of electrically stimulated ankle plantar flexor muscles in intact rat. (cdc.gov)
  • skNAC, a Smyd1-interacting transcription factor, is involved in cardiac development and skeletal muscle growth and regeneration. (ca.gov)
  • Home › About CIRM › Our Publications › Grantee publications › skNAC, a Smyd1-interacting transcription factor, is involved in cardiac development and skeletal muscle growth and regeneration. (ca.gov)
  • Risk of acute rhabdomyolysis with hyperkalemia followed by ventricular arrhythmias, cardiac arrest, and death in apparently healthy children and adolescents who subsequently were found to have undiagnosed skeletal muscle myopathy (e.g. (drugs.com)
  • The relationship of the sacro- plasmic reticulum and transverse (T) tubules to myofibrils in a muscle fiber. (earthslab.com)
  • There are reduce muscle spasm, improve range of motion and however a number of limitations to the use of PP muscle strength, correct postural abnormalities and including high cost of the TUS machine, the ultimately improve functional status and QoL complexity of operation due to the wide variables in (Philadelphia panel, 2001). (who.int)
  • Integrated genomic and proteomic analyses identify stimulus-dependent molecular changes associated with distinct modes of skeletal muscle atrophy. (nature.com)
  • Subsequently, utilizing our established molecular phenotyping strategy, we screened potential traditional Chinese herb-derived compounds for alleviation of muscle wasting and ferroptosis. (physiciansweekly.com)
  • The sarcoplasmic reticulum is the name given to the smooth endoplasmic reticulum in a muscle fiber. (earthslab.com)
  • Vitamin D and calcium supplements may be needed to help reduce skeletal deformities resulting from osteomalacia. (medlineplus.gov)
  • They are called skeletal muscles because most of them are attached to bones. (earthslab.com)
  • A few muscles attach to other muscles, dermis, and ligaments, in addition to bones. (earthslab.com)
  • Muscle wasting increases morbidity and mortality and is related to chronic kidney disease (CKD) and dialysis. (physiciansweekly.com)
  • We previously reported that Smyd1, a muscle-restricted histone methyltransferase, is essential for cardiogenesis and functions with a network of cardiac regulatory proteins. (ca.gov)
  • Skeletal Muscle Skeletal muscle is also known as striated muscle because of its striped appearance under the microscope and as voluntary muscle because it can be controlled at will. (bookrags.com)
  • GSIS (C-pep/Glc tAUC 0-120min ) and ß-cell function (Disposition Index [DI: GSIS/IR]) relative to skeletal muscle (Insulin tAUC x Glc tAUC ), hepatic (HOMA-IR) and adipose (Adipose-IR fasting ) IR were calculated. (diabetesjournals.org)
  • Collectively, short-term INT and CONT training improves ß-cell function relative to skeletal muscle, but not hepatic or adipose, IR. (diabetesjournals.org)
  • Sonographic muscle thickness of the dominant arm and bilateral thighs (Figure 1) were multiplied by respective bone lengths (humerus or femur) and described in cm 2 . (ecco-ibd.eu)
  • Should include activities that strengthen muscle and bone, at least 3 times per week. (who.int)
  • The sarcoplasm contains many threadlike myofibrils, which extend the length of the muscle fiber. (earthslab.com)
  • Myofibrils are the contractile elements of a muscle fiber. (earthslab.com)
  • Fatty Liver Index and Skeletal Muscle Density. (bvsalud.org)
  • Muscle density was measured using pQCT at the radius and tibia . (bvsalud.org)
  • There was a pattern of decreasing muscle density across increasing quartiles of FLI. (bvsalud.org)
  • After adjusting for age and lifestyle , mean radial muscle density in Q4 was 2.1% lower than Q1 (p muscle density was 1.8% lower in Q3 and 3.0% lower in Q4, compared to Q1 (p = 0.022 and (bvsalud.org)
  • The results showed that castrating male ducks had significant effects on their body weight but no significant impact on cross-sectional area (CSA) or density of pectoral muscle fibres. (bvsalud.org)
  • Convective O2 delivery [blood flow (Qm) x arterial O2 content (CaO2)] to the muscle was held constant by elevating muscle blood flow via a perfusion pump. (auburn.edu)
  • In mutant fast-twitch muscle, a decrease rather than increase in mitochondrial sensitivity to ADP occurred, but creatine still had no effect. (elsevier.com)
  • Cardiac and skeletal muscle development and maintenance require complex interactions between DNA-binding proteins and chromatin remodeling factors. (ca.gov)
  • The sleep-low conditions included 9 males that cycled to deplete muscle glycogen while reaching a set energy expenditure. (ljmu.ac.uk)
  • Specialized stem cells known as satellite cells reside in skeletal muscle in an inactive state. (rehabpub.com)
  • When muscle injury occurs, a complex chain of signals prompts the satellite cells to awaken and generate new muscle cells to repair the injury. (rehabpub.com)
  • Here we show that the muscle-specific transcription factor skNAC is the major binding partner for Smyd1 in the developing heart. (ca.gov)
  • The objective is to identify potential compounds for treating ferroptosis and muscle wasting and explore the potential mechanisms in vivo/in vitro. (physiciansweekly.com)
  • Skeletal Muscle System, Embryonic Development The skeletal and muscular systems are taught as individual subjects in traditional anatomy courses. (bookrags.com)
  • Low skeletal muscle index (SMI) has been associated with increased surgical complications and poor quality of life. (ecco-ibd.eu)
  • muscle core pO2 approximately 400 mmHg), force production is enhanced but control of contractility by NO/nitrosylation is greatly attenuated. (duke.edu)