Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
Mitochondria in hepatocytes. As in all mitochondria, there are an outer membrane and an inner membrane, together creating two separate mitochondrial compartments: the internal matrix space and a much narrower intermembrane space. In the liver mitochondrion, an estimated 67% of the total mitochondrial proteins is located in the matrix. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p343-4)
Contractile tissue that produces movement in animals.
The mitochondria of the myocardium.
Mitochondria of skeletal and smooth muscle. It does not include myocardial mitochondria for which MITOCHONDRIA, HEART is available.
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
A 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.
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)
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.
Proteins encoded by the mitochondrial genome or proteins encoded by the nuclear genome that are imported to and resident in the MITOCHONDRIA.
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.
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.
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.
Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds.
An increase in MITOCHONDRIAL VOLUME due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria.
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)
Non-striated, elongated, spindle-shaped cells found lining the digestive tract, uterus, and blood vessels. They are derived from specialized myoblasts (MYOBLASTS, SMOOTH MUSCLE).
The two lipoprotein layers in the MITOCHONDRION. The outer membrane encloses the entire mitochondrion and contains channels with TRANSPORT PROTEINS to move molecules and ions in and out of the organelle. The inner membrane folds into cristae and contains many ENZYMES important to cell METABOLISM and energy production (MITOCHONDRIAL ATP SYNTHASE).
Thin structures that encapsulate subcellular structures or ORGANELLES in EUKARYOTIC CELLS. They include a variety of membranes associated with the CELL NUCLEUS; the MITOCHONDRIA; the GOLGI APPARATUS; the ENDOPLASMIC RETICULUM; LYSOSOMES; PLASTIDS; and VACUOLES.
The muscles that move the eye. Included in this group are the medial rectus, lateral rectus, superior rectus, inferior rectus, inferior oblique, superior oblique, musculus orbitalis, and levator palpebrae superioris.
The neck muscles consist of the platysma, splenius cervicis, sternocleidomastoid(eus), longus colli, the anterior, medius, and posterior scalenes, digastric(us), stylohyoid(eus), mylohyoid(eus), geniohyoid(eus), sternohyoid(eus), omohyoid(eus), sternothyroid(eus), and thyrohyoid(eus).
One of two types of muscle in the body, characterized by the array of bands observed under microscope. Striated muscles can be divided into two subtypes: the CARDIAC MUSCLE and the SKELETAL MUSCLE.
A 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 metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell.
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.
Double-stranded DNA of MITOCHONDRIA. In eukaryotes, the mitochondrial GENOME is circular and codes for ribosomal RNAs, transfer RNAs, and about 10 proteins.
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.
Conical muscular projections from the walls of the cardiac ventricles, attached to the cusps of the atrioventricular valves by the chordae tendineae.
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)
A multisubunit enzyme complex containing CYTOCHROME A GROUP; CYTOCHROME A3; two copper atoms; and 13 different protein subunits. It is the terminal oxidase complex of the RESPIRATORY CHAIN and collects electrons that are transferred from the reduced CYTOCHROME C GROUP and donates them to molecular OXYGEN, which is then reduced to water. The redox reaction is simultaneously coupled to the transport of PROTONS across the inner mitochondrial membrane.
Chemical agents that uncouple oxidation from phosphorylation in the metabolic cycle so that ATP synthesis does not occur. Included here are those IONOPHORES that disrupt electron transfer by short-circuiting the proton gradient across mitochondrial membranes.
The voltage difference, normally maintained at approximately -180mV, across the INNER MITOCHONDRIAL MEMBRANE, by a net movement of positive charge across the membrane. It is a major component of the PROTON MOTIVE FORCE in MITOCHONDRIA used to drive the synthesis of ATP.
Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.
Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.
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.
Muscles forming the ABDOMINAL WALL including RECTUS ABDOMINIS, external and internal oblique muscles, transversus abdominis, and quadratus abdominis. (from Stedman, 25th ed)
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.
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.
The rate dynamics in chemical or physical systems.
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.
A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
A closely related group of toxic substances elaborated by various strains of Streptomyces. They are 26-membered macrolides with lactone moieties and double bonds and inhibit various ATPases, causing uncoupling of phosphorylation from mitochondrial respiration. Used as tools in cytochemistry. Some specific oligomycins are RUTAMYCIN, peliomycin, and botrycidin (formerly venturicidin X).
A masticatory muscle whose action is closing the jaws.
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.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
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).
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)
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.
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.
Elements of limited time intervals, contributing to particular results or situations.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A group of cytochromes with covalent thioether linkages between either or both of the vinyl side chains of protoheme and the protein. (Enzyme Nomenclature, 1992, p539)
A botanical insecticide that is an inhibitor of mitochondrial electron transport.
A glycoside of a kaurene type diterpene that is found in some plants including Atractylis gummifera (ATRACTYLIS); COFFEE; XANTHIUM, and CALLILEPIS. Toxicity is due to inhibition of ADENINE NUCLEOTIDE TRANSLOCASE.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
Muscular contractions characterized by increase in tension without change in length.
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 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.
An antibiotic substance produced by Streptomyces species. It inhibits mitochondrial respiration and may deplete cellular levels of ATP. Antimycin A1 has been used as a fungicide, insecticide, and miticide. (From Merck Index, 12th ed)
A proton ionophore that is commonly used as an uncoupling agent in biochemical studies.
Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.
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 chemical reactions involved in the production and utilization of various forms of energy in cells.
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.
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.
The process by which ELECTRONS are transported from a reduced substrate to molecular OXYGEN. (From Bennington, Saunders Dictionary and Encyclopedia of Laboratory Medicine and Technology, 1984, p270)
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.
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 class of nucleotide translocases found abundantly in mitochondria that function as integral components of the inner mitochondrial membrane. They facilitate the exchange of ADP and ATP between the cytosol and the mitochondria, thereby linking the subcellular compartments of ATP production to those of ATP utilization.
The process of moving proteins from one cellular compartment (including extracellular) to another by various sorting and transport mechanisms such as gated transport, protein translocation, and vesicular transport.
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.
The various filaments, granules, tubules or other inclusions within mitochondria.
A proton ionophore. It is commonly used as an uncoupling agent and inhibitor of photosynthesis because of its effects on mitochondrial and chloroplast membranes.
Derivatives of SUCCINIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain a 1,4-carboxy terminated aliphatic structure.
A species of the genus SACCHAROMYCES, family Saccharomycetaceae, order Saccharomycetales, known as "baker's" or "brewer's" yeast. The dried form is used as a dietary supplement.
Adenosine 5'-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5'-position.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
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 coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). (Dorland, 27th ed)
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.
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.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Transport proteins that carry specific substances in the blood or across cell membranes.
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.
Property of membranes and other structures to permit passage of light, heat, gases, liquids, metabolites, and mineral ions.
A member of the Bcl-2 protein family and homologous partner of C-BCL-2 PROTO-ONCOGENE PROTEIN. It regulates the release of CYTOCHROME C and APOPTOSIS INDUCING FACTOR from the MITOCHONDRIA. Several isoforms of BCL2-associated X protein occur due to ALTERNATIVE SPLICING of the mRNA for this protein.
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.
A flavoprotein and iron sulfur-containing oxidoreductase complex that catalyzes the conversion of UBIQUINONE to ubiquinol. In MITOCHONDRIA the complex also couples its reaction to the transport of PROTONS across the internal mitochondrial membrane. The NADH DEHYDROGENASE component of the complex can be isolated and is listed as EC 1.6.99.3.
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.
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)
Components of a cell produced by various separation techniques which, though they disrupt the delicate anatomy of a cell, preserve the structure and physiology of its functioning constituents for biochemical and ultrastructural analysis. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p163)
Use of electric potential or currents to elicit biological responses.
A masticatory muscle whose action is closing the jaws; its posterior portion retracts the mandible.
An inorganic dye used in microscopy for differential staining and as a diagnostic reagent. In research this compound is used to study changes in cytoplasmic concentrations of calcium. Ruthenium red inhibits calcium transport through membrane channels.
A flavoprotein containing oxidoreductase that catalyzes the dehydrogenation of SUCCINATE to fumarate. In most eukaryotic organisms this enzyme is a component of mitochondrial electron transport complex II.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
A water-soluble, colorless crystal with an acid taste that is used as a chemical intermediate, in medicine, the manufacture of lacquers, and to make perfume esters. It is also used in foods as a sequestrant, buffer, and a neutralizing agent. (Hawley's Condensed Chemical Dictionary, 12th ed, p1099; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1851)
Techniques to partition various components of the cell into SUBCELLULAR FRACTIONS.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Established cell cultures that have the potential to propagate indefinitely.
A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.
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.
Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
Proton-translocating ATPases responsible for ADENOSINE TRIPHOSPHATE synthesis in the MITOCHONDRIA. They derive energy from the respiratory chain-driven reactions that develop high concentrations of protons within the intermembranous space of the mitochondria.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
A toxic thiol mercury salt formerly used as a diuretic. It inhibits various biochemical functions, especially in mitochondria, and is used to study those functions.
Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.
Neurons which activate MUSCLE CELLS.
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.
Gated, ion-selective glycoproteins that traverse membranes. The stimulus for ION CHANNEL GATING can be due to a variety of stimuli such as LIGANDS, a TRANSMEMBRANE POTENTIAL DIFFERENCE, mechanical deformation or through INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
An element with atomic symbol O, atomic number 8, and atomic weight [15.99903; 15.99977]. It is the most abundant element on earth and essential for respiration.
A constituent of STRIATED MUSCLE and LIVER. It is an amino acid derivative and an essential cofactor for fatty acid metabolism.
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.
The excitable plasma membrane of a muscle cell. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)
A family of voltage-gated eukaryotic porins that form aqueous channels. They play an essential role in mitochondrial CELL MEMBRANE PERMEABILITY, are often regulated by BCL-2 PROTO-ONCOGENE PROTEINS, and have been implicated in APOPTOSIS.
A lipid-soluble benzoquinone which is involved in ELECTRON TRANSPORT in mitochondrial preparations. The compound occurs in the majority of aerobic organisms, from bacteria to higher plants and animals.
A multisubunit enzyme complex that contains CYTOCHROME B GROUP; CYTOCHROME C1; and iron-sulfur centers. It catalyzes the oxidation of ubiquinol to UBIQUINONE, and transfers the electrons to CYTOCHROME C. In MITOCHONDRIA the redox reaction is coupled to the transport of PROTONS across the inner mitochondrial membrane.
A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials.
Acidic phospholipids composed of two molecules of phosphatidic acid covalently linked to a molecule of glycerol. They occur primarily in mitochondrial inner membranes and in bacterial plasma membranes. They are the main antigenic components of the Wassermann-type antigen that is used in nontreponemal SYPHILIS SERODIAGNOSIS.
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 group of enzymes which catalyze the hydrolysis of ATP. The hydrolysis reaction is usually coupled with another function such as transporting Ca(2+) across a membrane. These enzymes may be dependent on Ca(2+), Mg(2+), anions, H+, or DNA.
The synapse between a neuron and a muscle.
The normality of a solution with respect to HYDROGEN ions; H+. It is related to acidity measurements in most cases by pH = log 1/2[1/(H+)], where (H+) is the hydrogen ion concentration in gram equivalents per liter of solution. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
The properties, processes, and behavior of biological systems under the action of mechanical forces.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
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).
Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.
A light microscopic technique in which only a small spot is illuminated and observed at a time. An image is constructed through point-by-point scanning of the field in this manner. Light sources may be conventional or laser, and fluorescence or transmitted observations are possible.
A system of cisternae in the CYTOPLASM of many cells. In places the endoplasmic reticulum is continuous with the plasma membrane (CELL MEMBRANE) or outer membrane of the nuclear envelope. If the outer surfaces of the endoplasmic reticulum membranes are coated with ribosomes, the endoplasmic reticulum is said to be rough-surfaced (ENDOPLASMIC RETICULUM, ROUGH); otherwise it is said to be smooth-surfaced (ENDOPLASMIC RETICULUM, SMOOTH). (King & Stansfield, A Dictionary of Genetics, 4th ed)
A flavoprotein and iron sulfur-containing oxidoreductase that catalyzes the oxidation of NADH to NAD. In eukaryotes the enzyme can be found as a component of mitochondrial electron transport complex I. Under experimental conditions the enzyme can use CYTOCHROME C GROUP as the reducing cofactor. The enzyme was formerly listed as EC 1.6.2.1.
Inorganic salts of phosphoric acid.
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.
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.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
An antibiotic produced by Pseudomonas cocovenenans. It is an inhibitor of MITOCHONDRIAL ADP, ATP TRANSLOCASES. Specifically, it blocks adenine nucleotide efflux from mitochondria by enhancing membrane binding.
Electron microscopy in which the ELECTRONS or their reaction products that pass down through the specimen are imaged below the plane of the specimen.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
The part of a cell that contains the CYTOSOL and small structures excluding the CELL NUCLEUS; MITOCHONDRIA; and large VACUOLES. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)
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.
A family of compounds containing an oxo group with the general structure of 1,5-pentanedioic acid. (From Lehninger, Principles of Biochemistry, 1982, p442)
Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)
The continuous remodeling of MITOCHONDRIA shape by fission and fusion in response to physiological conditions.
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.
Thin layers of tissue which cover parts of the body, separate adjacent cavities, or connect adjacent structures.
Proteolytic breakdown of the MITOCHONDRIA.
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.
Multisubunit enzymes that reversibly synthesize ADENOSINE TRIPHOSPHATE. They are coupled to the transport of protons across a membrane.
An intermediate compound in the metabolism of carbohydrates, proteins, and fats. In thiamine deficiency, its oxidation is retarded and it accumulates in the tissues, especially in nervous structures. (From Stedman, 26th ed)
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)
An electrochemical technique for measuring the current that flows in solution as a function of an applied voltage. The observed polarographic wave, resulting from the electrochemical response, depends on the way voltage is applied (linear sweep or differential pulse) and the type of electrode used. Usually a mercury drop electrode is used.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
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.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
An enzyme that catalyzes reversibly the conversion of palmitoyl-CoA to palmitoylcarnitine in the inner mitochondrial membrane. EC 2.3.1.21.
A metallic element that has the atomic symbol Mg, atomic number 12, and atomic weight 24.31. It is important for the activity of many enzymes, especially those involved in OXIDATIVE PHOSPHORYLATION.
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).
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
An enzyme that catalyzes the conversion of ATP and a D-hexose to ADP and a D-hexose 6-phosphate. D-Glucose, D-mannose, D-fructose, sorbitol, and D-glucosamine can act as acceptors; ITP and dATP can act as donors. The liver isoenzyme has sometimes been called glucokinase. (From Enzyme Nomenclature, 1992) EC 2.7.1.1.
A member of the Bcl-2 protein family that reversibly binds MEMBRANES. It is a pro-apoptotic protein that is activated by caspase cleavage.
Signal transduction mechanisms whereby calcium mobilization (from outside the cell or from intracellular storage pools) to the cytoplasm is triggered by external stimuli. Calcium signals are often seen to propagate as waves, oscillations, spikes, sparks, or puffs. The calcium acts as an intracellular messenger by activating calcium-responsive proteins.
Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the MITOCHONDRIA; the GOLGI APPARATUS; ENDOPLASMIC RETICULUM; LYSOSOMES; PLASTIDS; and VACUOLES.
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.
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.
The repeating contractile units of the MYOFIBRIL, delimited by Z bands along its length.
A metabolic process that converts GLUCOSE into two molecules of PYRUVIC ACID through a series of enzymatic reactions. Energy generated by this process is conserved in two molecules of ATP. Glycolysis is the universal catabolic pathway for glucose, free glucose, or glucose derived from complex CARBOHYDRATES, such as GLYCOGEN and STARCH.
Proteins obtained from the species SACCHAROMYCES CEREVISIAE. The function of specific proteins from this organism are the subject of intense scientific interest and have been used to derive basic understanding of the functioning similar proteins in higher eukaryotes.
The physiological renewal, repair, or replacement of tissue.
Voltage-dependent anion channel 1 is the major pore-forming protein of the mitochondrial outer membrane. It also functions as a ferricyanide reductase in the PLASMA MEMBRANE.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
A species of ascomycetous fungi of the family Sordariaceae, order SORDARIALES, much used in biochemical, genetic, and physiologic studies.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
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 quantity of volume or surface area of MITOCHONDRIA.
A flavoprotein that functions as a powerful antioxidant in the MITOCHONDRIA and promotes APOPTOSIS when released from the mitochondria. In mammalian cells AIF is released in response to pro-apoptotic protein members of the bcl-2 protein family. It translocates to the CELL NUCLEUS and binds DNA to stimulate CASPASE-independent CHROMATIN condensation.
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 fatty acid coenzyme derivative which plays a key role in fatty acid oxidation and biosynthesis.
Agents that emit light after excitation by light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags.
A cyclododecadepsipeptide ionophore antibiotic produced by Streptomyces fulvissimus and related to the enniatins. It is composed of 3 moles each of L-valine, D-alpha-hydroxyisovaleric acid, D-valine, and L-lactic acid linked alternately to form a 36-membered ring. (From Merck Index, 11th ed) Valinomycin is a potassium selective ionophore and is commonly used as a tool in biochemical studies.
The segregation and degradation of damaged or unwanted cytoplasmic constituents by autophagic vacuoles (cytolysosomes) composed of LYSOSOMES containing cellular components in the process of digestion; it plays an important role in BIOLOGICAL METAMORPHOSIS of amphibians, in the removal of bone by osteoclasts, and in the degradation of normal cell components in nutritional deficiency states.
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.
A glycoside obtained from Digitalis purpurea; the aglycone is digitogenin which is bound to five sugars. Digitonin solubilizes lipids, especially in membranes and is used as a tool in cellular biochemistry, and reagent for precipitating cholesterol. It has no cardiac effects.
A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 9. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.

Expression of uncoupling protein-3 and mitochondrial activity in the transition from hypothyroid to hyperthyroid state in rat skeletal muscle. (1/1585)

We sought a correlation between rat skeletal muscle triiodothyronine (T3)-mediated regulation of uncoupling protein-3 (UCP3) expression and mitochondrial activity. UCP3 mRNA expression increased strongly during the hypothyroid-hyperthyroid transition. The rank order of mitochondrial State 3 and State 4 respiration rates was hypothyroid < euthyroid < hyperthyroid. The State 4 increase may have been due to the increased UCP3 expression, as the proton leak kinetic was stimulated in the hypothyroid-hyperthyroid transition and a good correlation exists between the State 4 and UCP3 mRNA level. As a significant proportion of an organism's resting oxygen consumption is dedicated to opposing the proton leak, skeletal muscle mitochondrial UCP3 may mediate part of T3's effect on energy metabolism.  (+info)

Reduced cytosolic acidification during exercise suggests defective glycolytic activity in skeletal muscle of patients with Becker muscular dystrophy. An in vivo 31P magnetic resonance spectroscopy study. (2/1585)

Becker muscular dystrophy is an X-linked disorder due to mutations in the dystrophin gene, resulting in reduced size and/or content of dystrophin. The functional role of this subsarcolemma protein and the biochemical mechanisms leading to muscle necrosis in Becker muscular dystrophy are still unknown. In particular, the role of a bioenergetic deficit is still controversial. In this study, we used 31p magnetic resonance spectroscopy (31p-MRS) to investigate skeletal muscle mitochondrial and glycolytic ATP production in vivo in 14 Becker muscular dystrophy patients. Skeletal muscle glycogenolytic ATP production, measured during the first minute of exercise, was similar in patients and controls. On the other hand, during later phases of exercise, skeletal muscle in Becker muscular dystrophy patients was less acidic than in controls, the cytosolic pH at the end of exercise being significantly higher in Becker muscular dystrophy patients. The rate of proton efflux from muscle fibres of Becker muscular dystrophy patients was similar to that of controls, pointing to a deficit in glycolytic lactate production as a cause of higher end-exercise cytosolic pH in patients. The maximum rate of mitochondrial ATP production was similar in muscle of Becker muscular dystrophy patients and controls. The results of this in vivo 31P-MRS study are consistent with reduced glucose availability in dystrophin-deficient muscles.  (+info)

Subcellular adaptation of the human diaphragm in chronic obstructive pulmonary disease. (3/1585)

Pulmonary hyperinflation impairs the function of the diaphragm in patients with chronic obstructive pulmonary disease (COPD). However, it has been recently demonstrated that the muscle can counterbalance this deleterious effect, remodelling its structure (i.e. changing the proportion of different types of fibres). The aim of this study was to investigate whether the functional impairment present in COPD patients can be associated with structural subcellular changes of the diaphragm. Twenty individuals (60+/-9 yrs, 11 COPD patients and 9 subjects with normal spirometry) undergoing thoracotomy were included. Nutritional status and respiratory function were evaluated prior to surgery. Then, small samples of the costal diaphragm were obtained and processed for electron microscopy analysis. COPD patients showed a mean forced expiratory volume in one second (FEV1) of 60+/-9% predicted, a higher concentration of mitochondria (n(mit)) in their diaphragm than controls (0.62+/-0.16 versus 0.46+/-0.16 mitochondrial transections (mt) x microm(-2), p<0.05). On the other hand, subjects with air trapping (residual volume (RV)/total lung capacity (TLC) >37%) disclosed not only a higher n(mit) (0.63+/-0.17 versus 0.43+/-0.07 mt x microm(-2), p<0.05) but shorter sarcomeres (L(sar)) than subjects without this functional abnormality (2.08+/-0.16 to 2.27+/-0.15 microm, p<0.05). Glycogen stores were similar in COPD and controls. The severity of airways obstruction (i.e. FEV1) was associated with n(mit) (r=-0.555, p=0.01), while the amount of air trapping (i.e. RV/TLC) was found to correlate with both n(mit) (r=0.631, p=0.005) and L(sar) (r=-0.526, p<0.05). Finally, maximal inspiratory pressure (PI,max) inversely correlated with n(mit) (r=-0.547, p=0.01). In conclusion, impairment in lung function occurring in patients with chronic obstructive pulmonary disease is associated with subcellular changes in their diaphragm, namely a shortening in the length of sarcomeres and an increase in the concentration of mitochondria. These changes form a part of muscle remodelling, probably contributing to a better functional muscle behaviour.  (+info)

Release of Ca2+ from the sarcoplasmic reticulum increases mitochondrial [Ca2+] in rat pulmonary artery smooth muscle cells. (4/1585)

1. The Ca2+-sensitive fluorescent indicator rhod-2 was used to measure mitochondrial [Ca2+] ([Ca2+]m) in single smooth muscle cells from the rat pulmonary artery, while simultaneously monitoring cytosolic [Ca2+] ([Ca2+]i) with fura-2. 2. Application of caffeine produced an increase in [Ca2+]i and also increased [Ca2+]m. The increase in [Ca2+]m occurred after the increase in [Ca2+]i, and remained elevated for a considerable time after [Ca2+]i had returned to resting values. 3. The protonophore carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP), which causes the mitochondrial membrane potential to collapse, markedly attenuated the increase in [Ca2+]m following caffeine application and also increased the half-time for recovery of [Ca2+]i to resting values. 4. Activation of purinoceptors with ATP also produced increases in both [Ca2+]i and [Ca2+]m in these smooth muscle cells. In some cells, oscillations in [Ca2+]i were observed during ATP application, which produced corresponding oscillations in [Ca2+]m and membrane currents. 5. This study provides direct evidence that Ca2+ release from the sarcoplasmic reticulum, either through ryanodine or inositol 1,4, 5-trisphosphate (InsP3) receptors, increases both cytosolic and mitochondrial [Ca2+] in smooth muscle cells. These results have potential implications both for the role of mitochondria in Ca2+ regulation in smooth muscle, and for understanding how cellular metabolism is regulated.  (+info)

Mitochondrial regulation of the cytosolic Ca2+ concentration and the InsP3-sensitive Ca2+ store in guinea-pig colonic smooth muscle. (5/1585)

1. Mitochondrial regulation of the cytosolic Ca2+ concentration ([Ca2+]c) in guinea-pig single colonic myocytes has been examined, using whole-cell recording, flash photolysis of caged InsP3 and microfluorimetry. 2. Depolarization increased [Ca2+]c and triggered contraction. Resting [Ca2+]c was virtually restored some 4 s after the end of depolarization, a time when the muscle had shortened to 50 % of its fully relaxed length. The muscle then slowly relaxed (t = 17 s). 3. The decline in the Ca2+ transient was monophasic but often undershot or overshot resting levels, depending on resting [Ca2+]c. The extent of the overshoot or undershoot increased with increasing peak [Ca2+]c. 4. Carbonyl cyanide m-chlorophenyl hydrazone (CCCP; 5 microM), which dissipates the mitochondrial proton electrochemical gradient and therefore prevents mitochondrial Ca2+ accumulation, slowed Ca2+ removal at high ( > 300 nM) but not at lower [Ca2+]c and abolished [Ca2+]c overshoots. Oligomycin B (5 microM), which prevents mitchondrial ATP production, affected neither the rate of decline nor the magnitude of the overshoot. 5. During depolarization, the global rhod-2 signal (which represents the mitochondrial matrix Ca2+ concentration, [Ca2+]m) rose slowly in a CCCP-sensitive manner during and for about 3 s after depolarization had ended. [Ca2+]m then slowly decreased over tens of seconds. 6. Inhibition of sarcoplasmic reticulum Ca2+ uptake with thapsigargin (100 nM) reduced the undershoot and increased the overshoot. 7. Flash photolysis of caged InsP3 (20 microM) evoked reproducible increases in [Ca2+]c. CCCP (5 microM) reduced the magnitude of the [Ca2+]c transients evoked by flash photolysis of caged InsP3. Oligomycin B (5 microM) did not reduce the inhibition of the InsP3-induced Ca2+ transient by CCCP thus minimizing the possibility that CCCP lowered ATP levels by reversing the mitochondrial ATP synthase and so reducing SR Ca2+ refilling. 8. While CCCP reduced the magnitude of the InsP3-evoked Ca2+ signal, the internal Ca2+ store content, as assessed by the magnitude of ionomycin-evoked Ca2+ release, did not decrease significantly. 9. [Ca2+]c decline in smooth muscle, following depolarization, may involve mitochondrial Ca2+ uptake. Following InsP3-evoked Ca2+ release, mitochondrial uptake of Ca2+ may regulate the local [Ca2+]c near the InsP3 receptor so maintaining the sensitivity of the InsP3 receptor to release Ca2+ from the SR.  (+info)

Contribution of mitochondrial proton leak to respiration rate in working skeletal muscle and liver and to SMR. (6/1585)

Proton pumping across the mitochondrial inner membrane and proton leak back through the natural proton conductance pathway make up a futile cycle that dissipates redox energy. We measured respiration and average mitochondrial membrane potential in perfused rat hindquarter with maximal tetanic contraction of the left gastrocnemius-soleus-plantaris muscle group, and we estimate that the mitochondrial proton cycle accounted for 34% of the respiration rate of the preparation. Similar measurements in rat hepatocytes given substrates to cause a high rate of gluconeogenesis and ureagenesis showed that the proton cycle accounted for 22% of the respiration rate of these cells. Combining these in vitro values with literature values for the contribution of skeletal muscle and liver to standard metabolic rate (SMR), we calculate that the proton cycle in working muscle and liver may account for 15% of SMR in vivo. Although this value is less than the 20% of SMR we calculated previously using data from resting skeletal muscle and hepatocytes, it is still large, and we conclude that the futile proton cycle is a major contributor to SMR.  (+info)

Calcium-dependent regulation of cytochrome c gene expression in skeletal muscle cells. Identification of a protein kinase c-dependent pathway. (7/1585)

Mitochondrial biogenesis can occur rapidly in mammalian skeletal muscle subjected to a variety of physiological conditions. However, the intracellular signal(s) involved in regulating this process remain unknown. Using nuclearly encoded cytochrome c, we show that its expression in muscle cells is increased by changes in cytosolic Ca2+ using the ionophore A23187. Treatment of myotubes with A23187 increased cytochrome c mRNA expression up to 1.7-fold. Transfection experiments using promoter-chloramphenicol acetyltransferase constructs revealed that this increase could be transcriptionally mediated since A23187 increased chloramphenicol acetyltransferase activity by 2.5-fold. This increase was not changed by KN62, an inhibitor of Ca2+/calmodulin-dependent kinases II and IV, and it was not modified by overexpression of protein kinase A and cAMP response element-binding protein, demonstrating that the A23187 effect was not mediated through Ca2+/calmodulin-dependent kinase- or protein kinase A-dependent pathways. However, treatment of myotubes with staurosporine or 12-O-tetradecanoylphorbol-13-acetate reduced the effect of A23187 on cytochrome c transactivation by 40-50%. Coexpression of the Ca2+-sensitive protein kinase C isoforms alpha and betaII, but not the Ca2+-insensitive delta isoform, exaggerated the A23187-mediated response. The short-term effect of A23187 was mediated in part by mitogen-activated protein kinase (extracellular signal-regulated kinases 1 and 2) since its activation peaked 2 h after A23187 treatment, and cytochrome c transactivation was reduced by PD98089, a mitogen-activated protein kinase/extracellular signal-regulated kinase kinase inhibitor. These results demonstrate the existence of a Ca2+-sensitive, protein kinase C-dependent pathway involved in cytochrome c expression and implicate Ca2+ as a signal in the up-regulation of nuclear genes encoding mitochondrial proteins.  (+info)

Sub maximal oxygen uptake related to fat free mass and lean leg volume in trained runners. (8/1585)

The sub maximal oxygen uptake (VO2) of 32 trained male middle and long distance runners aged 19.5-36.0 years was determined at five treadmill speeds. There was a significant linear relationship (p less than 0.01) between VO2 at each of the treadmill speeds and Fat-Free Mass (FFM) and Lean Leg Volume (LLV). To explain the relationship other factors are considered, the most important of which may be the mechanical configuration of muscle and mitochondrial function.  (+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.

Mitochondrial diseases can affect anyone, regardless of age or gender, and they can be caused by mutations in either the mitochondrial DNA (mtDNA) or the nuclear DNA (nDNA). These mutations can be inherited from one's parents or acquired during embryonic development.

Some of the most common symptoms of mitochondrial diseases include:

1. Muscle weakness and wasting
2. Seizures
3. Cognitive impairment
4. Vision loss
5. Hearing loss
6. Heart problems
7. Neurological disorders
8. Gastrointestinal issues
9. Liver and kidney dysfunction

Some examples of mitochondrial diseases include:

1. MELAS syndrome (Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes)
2. Kearns-Sayre syndrome (a rare progressive disorder that affects the nervous system and other organs)
3. Chronic progressive external ophthalmoplegia (CPEO), which is characterized by weakness of the extraocular muscles and vision loss
4. Mitochondrial DNA depletion syndrome, which can cause a wide range of symptoms including seizures, developmental delays, and muscle weakness.
5. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
6. Leigh syndrome, which is a rare genetic disorder that affects the brain and spinal cord.
7. LHON (Leber's Hereditary Optic Neuropathy), which is a rare form of vision loss that can lead to blindness in one or both eyes.
8. Mitochondrial DNA mutation, which can cause a wide range of symptoms including seizures, developmental delays, and muscle weakness.
9. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
10. Kearns-Sayre syndrome, which is a rare progressive disorder that affects the nervous system and other organs.

It's important to note that this is not an exhaustive list and there are many more mitochondrial diseases and disorders that can affect individuals. Additionally, while these diseases are rare, they can have a significant impact on the quality of life of those affected and their families.

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.

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 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 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 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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Some common examples of neurodegenerative diseases include:

1. Alzheimer's disease: A progressive loss of cognitive function, memory, and thinking skills that is the most common form of dementia.
2. Parkinson's disease: A disorder that affects movement, balance, and coordination, causing tremors, rigidity, and difficulty with walking.
3. Huntington's disease: An inherited condition that causes progressive loss of cognitive, motor, and psychiatric functions.
4. Amyotrophic lateral sclerosis (ALS): A disease that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness, paralysis, and eventually death.
5. Prion diseases: A group of rare and fatal disorders caused by misfolded proteins in the brain, leading to neurodegeneration and death.
6. Creutzfeldt-Jakob disease: A rare, degenerative, and fatal brain disorder caused by an abnormal form of a protein called a prion.
7. Frontotemporal dementia: A group of diseases that affect the front and temporal lobes of the brain, leading to changes in personality, behavior, and language.

Neurodegenerative diseases can be caused by a variety of factors, including genetics, age, lifestyle, and environmental factors. They are typically diagnosed through a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment options for neurodegenerative diseases vary depending on the specific condition and its underlying causes, but may include medications, therapy, and lifestyle changes.

Preventing or slowing the progression of neurodegenerative diseases is a major focus of current research, with various potential therapeutic strategies being explored, such as:

1. Stem cell therapies: Using stem cells to replace damaged neurons and restore brain function.
2. Gene therapies: Replacing or editing genes that are linked to neurodegenerative diseases.
3. Small molecule therapies: Developing small molecules that can slow or prevent the progression of neurodegenerative diseases.
4. Immunotherapies: Harnessing the immune system to combat neurodegenerative diseases.
5. Lifestyle interventions: Promoting healthy lifestyle choices, such as regular exercise and a balanced diet, to reduce the risk of developing neurodegenerative diseases.

In conclusion, neurodegenerative diseases are a complex and diverse group of disorders that can have a profound impact on individuals and society. While there is currently no cure for these conditions, research is providing new insights into their causes and potential treatments. By continuing to invest in research and developing innovative therapeutic strategies, we can work towards improving the lives of those affected by neurodegenerative diseases and ultimately finding a cure.

MRI can occur in various cardiovascular conditions, such as myocardial infarction (heart attack), cardiac arrest, and cardiac surgery. The severity of MRI can range from mild to severe, depending on the extent and duration of the ischemic event.

The pathophysiology of MRI involves a complex interplay of various cellular and molecular mechanisms. During ischemia, the heart muscle cells undergo changes in energy metabolism, electrolyte balance, and cell membrane function. When blood flow is restored, these changes can lead to an influx of calcium ions into the cells, activation of enzymes, and production of reactive oxygen species (ROS), which can damage the cells and their membranes.

The clinical presentation of MRI can vary depending on the severity of the injury. Some patients may experience chest pain, shortness of breath, and fatigue. Others may have more severe symptoms, such as cardiogenic shock or ventricular arrhythmias. The diagnosis of MRI is based on a combination of clinical findings, electrocardiography (ECG), echocardiography, and cardiac biomarkers.

The treatment of MRI is focused on addressing the underlying cause of the injury and managing its symptoms. For example, in patients with myocardial infarction, thrombolysis or percutaneous coronary intervention may be used to restore blood flow to the affected area. In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) and other life-saving interventions may be necessary.

Prevention of MRI is crucial in reducing its incidence and severity. This involves aggressive risk factor management, such as controlling hypertension, diabetes, and dyslipidemia, as well as smoking cessation and stress reduction. Additionally, patients with a history of MI should adhere to their medication regimen, which may include beta blockers, ACE inhibitors or ARBs, statins, and aspirin.

In conclusion, myocardial injury with ST-segment elevation (MRI) is a life-threatening condition that requires prompt recognition and treatment. While the clinical presentation can vary depending on the severity of the injury, early diagnosis and management are crucial in reducing morbidity and mortality. Prevention through aggressive risk factor management and adherence to medication regimens is also essential in preventing MRI.

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.

... mitochondrion and endoplasmic reticulum cisternae. C. High resolution image illustrating in detail multiple mitochondria, ... Rat striated skeletal muscle (diaphargm). A typical TC (blue) with two convoluted Tp is shown, by transmission electron ... Mitochondria represent only 2% of cell body volume and the Golgi complex is small in TC. Fibroblasts Golgi complex is prominent ... A blue telopode of 14.2 µm in the section plane is illustrated around a nerve ending (green) between smooth muscle cells (brown ...
... has more mitochondria than smooth muscle. Both smooth muscle cells and cardiac muscle cells have a ... There are two types of striated muscle: Cardiac muscle (heart muscle) Skeletal muscle (muscle attached to the skeleton) ... They contain many mitochondria and myoglobin. Unlike skeletal muscle, cardiac muscle cells are unicellular. These cells are ... "Muscle Physiology - Introduction to Muscle". muscle.ucsd.edu. Retrieved 2015-11-24. Uygur, Aysu; Lee, Richard T. (February 22, ...
Muscle fibers also have multiple mitochondria to meet energy needs. Muscle fibers are in turn composed of myofibrils. The ... The muscle cells of skeletal muscles are much longer than in the other types of muscle tissue, and are often known as muscle ... Deep muscles, superficial muscles, muscles of the face and internal muscles all correspond with dedicated regions in the ... out of the muscles in order to not impair muscle function. Once moved out of muscles, lactic acid can be used by other muscles ...
Estabrook RW, Sacktor B (October 1958). "alpha-Glycerophosphate oxidase of flight muscle mitochondria". The Journal of ... "Pathways of hydrogen transport in the oxidation of extramitochondrial reduced diphosphopyridine nucleotide in flight muscle". ... glycerol phosphate shuttle was first characterized as a major route of mitochondrial hydride transport in the flight muscles of ...
The mitochondria can be found nestled between myofibrils of muscle or wrapped around the sperm flagellum. Often, they form a ... Mitochondria Atlas at University of Mainz Mitochondria Research Portal at mitochondrial.net Mitochondria: Architecture dictates ... This ratio is variable and mitochondria from cells that have a greater demand for ATP, such as muscle cells, contain even more ... They were discovered by Albert von Kölliker in 1857 in the voluntary muscles of insects. The term mitochondrion was coined by ...
Meanwhile, the first 12 amino acids of the highly hydrophobic N-terminal serve to bind the enzyme to the mitochondria, while ... In particular, HK2 is ubiquitously expressed in tissues, though it is majorly found in muscle and adipose tissue. In cardiac ... It localizes to the outer membrane of mitochondria. Expression of this gene is insulin-responsive, and studies in rat suggest ... Shulga N, Wilson-Smith R, Pastorino JG (Oct 2009). "Hexokinase II detachment from the mitochondria potentiates cisplatin ...
Some calcium is also taken up by the mitochondria. An enzyme, phospholamban, serves as a brake for SERCA. At low heart rates, ... muscle contraction does not necessarily mean muscle shortening because muscle tension can be produced without changes in muscle ... Muscle tension is the force exerted by the muscle on an object whereas a load is the force exerted by an object on the muscle. ... The termination of muscle contraction is followed by muscle relaxation, which is a return of the muscle fibers to their low ...
Brooks GA, Brown MA, Butz CE, Sicurello JP, Dubouchaud H (Nov 1999). "Cardiac and skeletal muscle mitochondria have a ... Bonen A (Nov 2001). "The expression of lactate transporters (MCT1 and MCT4) in heart and muscle". European Journal of Applied ... Muscle & Nerve. 23 (1): 90-7. doi:10.1002/(SICI)1097-4598(200001)23:1. 3.0.CO;2-M. PMID 10590411. S2CID 36707820. Kirk P, ...
Along with muscle strength weakness associated with the muscles involved from loss of filament interaction. Dehydration is a ... Calcium ions build up in the mitochondria, impairing cellular respiration. The mitochondria are unable to produce enough ATP to ... A high concentration of calcium activates muscle cells, causing the muscle to contract while inhibiting its ability to relax. ... The increase of sustained muscle contraction leads to oxygen and ATP depletion with prolonged exposure to calcium. The muscle ...
It is believed low levels of citrate in the cytosol and high levels of citrate in the mitochondria caused by the impaired ... Lower or no levels are present in the brain, heart, skeletal muscle, placenta and lung. The tricarboxylate transport protein is ... located within the inner mitochondria membrane. It provides a link between the mitochondrial matrix and cytosol by transporting ...
"Mitochondria control functional CaV1.2 expression in smooth muscle cells of cerebral arteries". Circulation Research. 107 (5): ... In the arteries of the brain, high levels of calcium in mitochondria elevates activity of nuclear factor kappa B NF-κB and ... It depolarizes at -30mV and helps define the shape of the action potential in cardiac and smooth muscle. The protein encoded by ... Cav1.2 is widely expressed in the smooth muscle, pancreatic cells, fibroblasts, and neurons. However, it is particularly ...
Additionally, he examined the function of mitochondria in muscle and liver tissue. With his research group, he is contributing ... Dynamic changes of muscle insulin sensitivity after metabolic surgery. Nat. Commun., Bd. 10, S. 4179. DOI: 10.1038/s41467-019- ... Role of diacylglycerol activation of PKCθ in lipid-induced muscle insulin resistance in humans. Proceedings of the National ... Rapid impairment of skeletal muscle glucose transport/phosphorylation by free fatty acids in humans. Diabetes. 48, Nr. 2, ISSN ...
Acid fuchsine may be used to stain collagen, smooth muscle, or mitochondria. Acid fuchsin is used as the nuclear and ... Most recipes produce red keratin and muscle fibers, blue or green staining of collagen and bone, light red or pink staining of ... In a skillfully made H&E preparation the red blood cells are almost orange, and collagen and cytoplasm (especially muscle) ... Acid fuchsin is also a traditional stain for mitochondria (Altmann's method). Haematoxylin (hematoxylin in North America) is a ...
... for muscle. Furthermore, he discovered that exercise and resveratrol synergistically increase mitochondria in muscles. "Faculty ... He was the first to determine that thyroid hormone modifies mitochondria in heart and muscle during growth and development, and ... Hood is credited with making significant research advances in understanding of the biology of exercise, mitochondria and muscle ... Wicks, K. L.; Hood, D. A. (1991). "Mitochondrial adaptations in denervated muscle: relationship to muscle performance". ...
"Association of mitochondria with plectin and desmin intermediate filaments in striated muscle". Experimental Cell Research. 252 ... In cardiac muscle and skeletal muscle, plectin is localized to specialized entities known as Z-discs. Plectin binds several ... In muscle, plectin binds to the periphery of Z-discs, and along with the intermediate filament protein desmin, may form lateral ... Skeletal and cardiac muscle tissues were also significantly affected. Cardiac intercalated discs were disintegrated and ...
... levels are highest in liver, heart, skeletal muscle, and erythrocytes. NMNAT3 is localized in mitochondria or cytoplasm ...
The proteins Twinkle and Twinky are both found in the mitochondria. Each mitochondrion contains a small amount of DNA which is ... The gene is expressed at high levels in skeletal muscles. The gene encodes for a protein that has a full length of 684 units of ... The symptoms of this disease include ataxia, muscle hypertonia, loss of deep-tendon reflexes, and athetosis and later on in the ... A homolog (B5X582) is found in Arabidopsis thaliana chloroplast and mitochondria. In 2001, a team was able to identify the ...
T and X showed no contractile effects on the rat arterio smooth muscle. There was only a relaxing effect on the muscle. In ... Norbormide has a strong effect on the mitochondria in the cell. Therefore, norbormide transfer through the outer mitochondrial ... In all animals tested and also in the rat aorta and extravascular smooth muscle tissue, NRB exhibits vasorelaxant properties in ... has shown that in respiratory, urinary and gastrointestinal smooth muscle there was no contraction by norbormide. The symptoms ...
Its high oxygen consumption is noted by the many mitochondria and capillaries present; more than in any other skeletal muscle. ... involves the internal intercostal muscles used in conjunction with the abdominal muscles, which act as an antagonist paired ... The muscle fibres from these attachments converge in a central tendon, which forms the crest of the dome. Its peripheral part ... The muscle fibres of the diaphragm emerge from many surrounding structures and can be divided into vertebral, costal, sternal, ...
As a result, muscle cells cannot produce enough energy, leading to the muscle problems that affect infants with infantile ... The tRNAGlu molecule is localized to the mitochondria, and is involved in the assembly of oxidative phosphorylation proteins. ... The myopathy is characterized by clinical manifestations such as severe muscle weakness, hypotonia (poor muscle tone), and ... It is unknown why only muscles are involved or how affected infants recover from the condition. Specific mutations of 14674T>G ...
"Investigation of glycosylation processes in mitochondria and microsomal membranes from human skeletal muscle". Clinica Chimica ...
This in turn reduces lysosomal degradative ability and blocks autophagy.[citation needed] The muscle fibers are rarely necrotic ... The vacuoles may contain remains of mitochondria, membrane whorls and calcium apatite crystals.[citation needed] The diagnosis ... a new hereditary muscle disease. Ann Neurol 23(3):258-265 (Articles with short description, Short description is different from ... is a rare childhood onset disease characterized by slow progressive vacuolation and atrophy of skeletal muscle. There is no ...
CTL2s occur especially in the mitochondria in the tongue, kidneys, muscles and heart. They are associated with the ... Severe deficiency causes muscle damage and non-alcoholic fatty liver disease, which may develop into cirrhosis. Besides humans ... This is a neurotransmitter which plays a necessary role in muscle contraction, memory and neural development, for example. ... In humans, choline is oxidized irreversibly in liver mitochondria to glycine betaine aldehyde by choline oxidases. This is ...
... destroying the sarcomere connections in the muscle fibers and reducing the mitochondria and sarcoplasmic reticular. The ant is ... A deficit in leucine results in the prevention of muscle regeneration because the amino acid is a nutrient regulator of muscle ... A decrease in mitochondria ultimately results in a reduction of energy and calcium levels due to the lack of ATP and ... This is possibly a result of the atrophy of the ant's mandibular muscles caused by the secretion of fungal compounds. In ...
Neurological effects include muscle twitching and seizures; consciousness becomes progressively impaired after a few hours ... Alternatively, fluorocitrate interferes with citrate transport in the mitochondria. In humans, the symptoms of poisoning ... use of muscle relaxants, anti-convulsants, mechanical ventilation, and other supportive measures may all be required. Few ... only traces were detectable in sheep muscle after 72-96 h Brent, J. (2005). Critical Care Toxicology. St. Louis: Mosby. p. 970 ...
Cardiac muscle (like skeletal muscle) is characterized by striations - the stripes of dark and light bands resulting from the ... Lipids, and glycogen are also stored within the sarcoplasm and these are broken down by mitochondria to release ATP. The cells ... In cardiac muscle the T-tubules are only found at the Z-lines. When an action potential causes cells to contract, calcium is ... Initially, as the muscles in the ventricle contract, the pressure of the blood within the chamber rises, but it is not yet high ...
... while mutant SOD1 has been observed to promote apoptosis in spinal cord mitochondria, but not in liver mitochondria, though it ... Mice lacking SOD1 have increased age-related muscle mass loss (sarcopenia), early development of cataracts, macular ... Although a large burst of ROS is known to lead to cell damage, a moderate release of ROS from the mitochondria, which occurs ... 8-OHdG accumulates in the mitochondria of spinal motor neurons of persons with ALS. In transgenic ALS mice harboring a mutant ...
UCP2 in hippocampus cells and UCP3 in muscle cells stimulate production of mitochondria. The larger number of mitochondria ... Mitochondria respiration is coupled to ATP synthesis (ADP phosphorylation) but is regulated by UCPs. UCPs belong to the ... Mitochondria are a major site of calcium storage in neurons, and the storage capacity increases with potential across ... Thus, cancer cells may increase the production of UCP2 in mitochondria. This theory is supported by independent studies which ...
PTAH is ideal for demonstrating striated muscle fibers and mitochondria, often without a counterstain. As such, it is used to ... It is used to show gliosis in the central nervous system, tumours of skeletal muscles, and fibrin deposits in lesions. Muscle ... This lake stains the muscle cross striations, fibrin, nuclei, and other tissue elements blue. The rest of the phosphotungstic ...
... during muscle contraction. Some products of these transcriptions release H2 into the muscles. This can cause calcium ions to ... and can diffuse out of the mitochondria and out of the cell. In prokaryotes, which have no mitochondria, this reaction is ... Calcium ions have a role in regulation of PDC in muscle tissue, because it activates PDP, stimulating glycolysis on its release ... This irreversible reaction traps the acetyl-CoA within the mitochondria (the acetyl-CoA can only be transported out of the ...
For example, muscle contraction depends upon the movement of calcium, sodium and potassium through ion channels in the cell ... This is done in eukaryotes by a series of proteins in the membranes of mitochondria called the electron transport chain. In ... Ions are also critical for nerve and muscle function, as action potentials in these tissues are produced by the exchange of ... This force drives protons back into the mitochondrion through the base of an enzyme called ATP synthase. The flow of protons ...
TTC39B is well expressed in muscles, internal organs, secretory organs, reproductive organs, the immune system, and the nervous ... mitochondria, and Golgi apparatus. The TTC39B protein folds into an alpha-alpha super helix. 40% of its structure matches with ...
The reasons mitochondria have retained some genes are debated. The existence in some species of mitochondrion-derived ... and muscle movements. Some evidence suggests that they might be major contributors to the aging process and age-associated ... In sexual reproduction, mitochondria are normally inherited exclusively from the mother; the mitochondria in mammalian sperm ... Also, mitochondria are only in the sperm tail, which is used for propelling the sperm cells and sometimes the tail is lost ...
Muscle weakness can be found with either presentation. In countries with expanded newborn screening, SPCD can be identified ... Carnitine is needed to transport long chain fatty acids into the mitochondria, where they can be broken down to produce acetyl- ... Later cases were reported with cardiomyopathy and muscle weakness. Newborn screening expanded the potential phenotypes ... leading to a variety of symptoms such as chronic muscle weakness, cardiomyopathy, hypoglycemia and liver dysfunction. The ...
The process in which they move into the mitochondria is called the carnitine shuttle. Long chain FA are first activated via ... and was rather used by athletes to prevent damage to the heart and muscles caused by lack of oxygen during high-intensity ... In the mitochondria themselves, meldonium also competitively inhibits the carnitine shuttle protein SLC22A5. This results in ... Carnitine transports long-chain fatty acids (FA) from the cytosol of the cell into the mitochondrion and is therefore essential ...
H-FABP is 20 times more specific to cardiac muscle than myoglobin, it is found at 10-fold lower levels in skeletal muscle than ... H-FABP is involved in active fatty acid metabolism where it transports fatty acids from the cell membrane to mitochondria for ... Peeters RA, Veerkamp JH, Geurts van Kessel A, Kanda T, Ono T (May 1991). "Cloning of the cDNA encoding human skeletal-muscle ... Young AC, Scapin G, Kromminga A, Patel SB, Veerkamp JH, Sacchettini JC (Jun 1994). "Structural studies on human muscle fatty ...
Li LY, Luo X, Wang X (Jul 2001). "Endonuclease G is an apoptotic DNase when released from mitochondria". Nature. 412 (6842): 95 ... Similarly, myonuclear localization of EndoG is correlated with atrophied aging skeletal muscle, leading to increased apoptotic ... In some apoptotic pathways, EndoG is released from the mitochondrion and migrates to the nucleus, where it degrades chromatin ... that how BNIP3 interacts with mitochondria. It has been shown that BNIP3 interacts with the voltage-dependent anion channel ( ...
... on mitochondrial function after 9 days of spaceflight in which no reduction in the capacity of skeletal muscle mitochondria to ... The collective observations clearly show that these types of muscle undergo significant reductions in muscle mass (muscle ... of the muscle mass can be lost in antigravity muscles of the lower extremity such as the soleus (Sol; a calf muscle) and vastus ... isokinetic muscle strength, and fatigability. Similar losses in muscle volume, paralleled by decreases in muscle strength and ...
Protein Synthesis, skeletal muscle regeneration, and skeletal muscle proteolysis have all been noted to change when ɑ-KIC is ... whereas the dehydrogenase enzyme is found exclusively in the mitochondrion (Sabourin and Bieber 1981, 1983). Importantly, this ... participants reported delayed onset of muscle soreness, as well as other positive effects such as increased muscle girth. It is ... Studies have shown that taking ɑ-KIC and its derivatives before acute physical activity led to an increase in muscle work by 10 ...
... muscle - muscle protein - mutagen - mutation - myc gene - mycology - myelin basic protein - myeloma protein - myosin N- ... mitochondrion - mitogen receptor - mitosis - mitotic spindle - mixture - modern evolutionary synthesis - molar volume - mole ( ...
In mice, when catalase expression is increased specifically in mitochondria, oxidative DNA damage (8-OHdG) in skeletal muscle ... Muscle strength, and stamina for sustained physical effort, decline in function with age in humans and other species. Skeletal ... reported that the oxidative DNA damage 8-OHdG accumulates in heart and skeletal muscle (as well as in brain, kidney and liver) ... Accumulation of DNA damage with age in mammalian muscle has been reported in at least 18 studies since 1971. Hamilton et al. ...
Levels of β-hydroxybutyric acid increase in the liver, heart, muscle, brain, and other tissues with exercise, calorie ... and hence effectively out of the mitochondria) via carnitine-acylcarnitine translocase (39). 3HIA-carnitine is thought to be ...
Its protective effect is probably caused primarily by impaired mitochondria metabolism, particularly decreased reactive oxygen ... "Metformin selectively attenuates mitochondrial H2O2 emission without affecting respiratory capacity in skeletal muscle of obese ... functionally impaired mitochondria produce ROS excessively presence of T cell-specific biomarkers of senescence (circular ...
... and mitochondria in fresh frozen muscle sections, among other applications. It helps in identifying increases in collagenous ... Smooth muscle tissue, for example, is hard to differentiate from collagen. A trichrome stain can colour the muscle tissue red, ... One of the oldest single-step approaches to trichrome staining is van Gieson's method, which stains muscle and cytoplasm yellow ... Trichrome methods are now used for differentiating muscle from collagen, pituitary alpha cells from beta cells, fibrin from ...
Caughey WS, York JL (1962). "Isolation and some properties of the green heme of cytochrome oxidase from beef heart muscle". J. ... Due to its lipophilic properties, it impairs lipid bilayers in organelles such as mitochondria and nuclei. These properties of ... which are caused by dissolved CO2 in working muscles, etc.), releasing oxygen from the heme group. There are several ... of ALAs by heme or hemin is by decreasing stability of mRNA synthesis and by decreasing the intake of mRNA in the mitochondria ...
Kölliker's contributions to histology were widespread; smooth muscle, striated muscle, skin, bone, teeth, blood vessels and ... These sarcosomes have come to be known as the mitochondria-the power houses of the cell. In the words of Lehninger, "Kölliker ... In 1888 he teased these granules from insect muscle, in which they are very profuse, found them to swell in water, and showed ... A few years before this, there was doubt whether arteries had muscle in their walls - in addition, no solid histological basis ...
Trevisson E, DiMauro S, Navas P, Salviati L. (2011). "Coenzyme Q deficiency in muscle". Curr Opin Neurol. 24 (5): 449-456. doi: ... and the mitochondria. Professor Navas earned his Master of Science degree in biology in 1976 and his Ph.D. in cell biology in ... to the levels of known bio-markers for muscle damage (creatine kinase), kidney damage (uric acid), and stress damage (cortisol ... Their findings suggested that high levels of plasma Coenzyme Q10 can prevent muscle damage, improve kidney function, and ...
The mitochondrion is the powerhouse of the cell. Every muscle cell has mitochondria, and if the muscle cell's mitochondria have ... On biopsy, the muscle tissue of patients with these diseases usually demonstrate "ragged red" muscle fibers. These ragged-red ... Progressive myoclonic epilepsy Clumps of diseased mitochondria accumulate in muscle fibers and appear as "ragged-red fibers" ... Muscle biopsy: ragged red fibers in Gömöri trichrome stain. Although no cure currently exists, there is hope in treatment for ...
However, BMI does not account for whether the excess weight is fat or muscle, and is not a measure of body composition. For ... These fatty acids can create oxidative stress, disrupting the functions of mitochondria and endoplasmic reticula, leading to ...
This is the case in human erythrocytes, which have no mitochondria, and in oxygen-depleted muscle. Adenosine triphosphate is a ... In working skeletal muscles and the brain, Phosphocreatine is stored as a readily available high-energy phosphate supply, and ... ATP can be generated by substrate-level phosphorylation in mitochondria in a pathway that is independent from the proton motive ... Substrate-level phosphorylation occurs in the cytoplasm of cells during glycolysis and in mitochondria either during the Krebs ...
... is found in the developing embryo and is produced in even greater amounts in adult muscle. Aldolase A expression is ... ALDOA has also been found in mitochondria. ALDOA is regulated by the energy metabolism substrates glucose, lactate, and ... Aldolase A deficiency is a rare, autosomal recessive disorder that is linked to hemolysis and accompanied by weakness, muscle ... ALDOA is ubiquitously expressed in most tissues, though it is predominantly expressed in developing embryo and adult muscle. In ...
Depending on the tissue type, each cell contains hundreds to thousands of mitochondria. There are 2-10 mtDNA molecules in each ... muscle and neurologic impairment, and, frequently, early death. It is usually fatal in infancy. The few patients who survive ... Autologous cd34+ Cells Enriched With Blood Derived Mitochondria) in Pediatric Patients With Pearson Syndrome". {{cite journal ... An mtDNA is genetic material contained in the cellular organelle called the mitochondria. ...
It has been observed that MCD mRNA is most abundant in cardiac and skeletal muscles, tissues in which cytoplasmic malonyl-CoA ... MCD presents two isoforms which can be transcribed form one gene: a long isoform (54kDa), distributed in mitochondria, and a ... The long isoform includes a sequence of signaling towards mitochondria in the N-terminus; whereas the short one only contains ... Malonyl-CoA also plays an important role inside the mitochondria, where it is an intermediary between fatty acids and acetyl- ...
... in mitochondria-associated membranes and has a mitochondrial targeting signal that promotes its association with mitochondria ... muscle". Am. J. Physiol. Endocrinol. Metab. 293 (6): E1772-81. doi:10.1152/ajpendo.00158.2007. PMID 17940217. Yen CL, Stone SJ ...
Mitochondrion. 9 (5): 299-305. doi:10.1016/j.mito.2009.04.001. PMID 19389488. Blázquez A, Gil-Borlado MC, Morán M, Verdú A, ... muscle weakness, exercise intolerance, lactic acidosis, hypotonia, seizures, and optic atrophy. Pathogenic mutations have ... a novel mechanism of import into mitochondria". The EMBO Journal. 15 (3): 479-87. doi:10.1002/j.1460-2075.1996.tb00380.x. PMC ... does not contain a mitochondrial targeting sequence but experimental studies confirm that it is imported into mitochondria. A ...
"Estrogen receptor beta is involved in skeletal muscle hypertrophy induced by the phytoecdysteroid ecdysterone". Molecular ... and mitochondria. Upon binding to 17-β-estradiol, estriol or related ligands, the encoded protein forms homo-dimers or hetero- ...
Research done on endothelial and smooth muscle cells is consistent to the hypothesis that S1P has a crucial role in regulating ... in the mitochondria-associated membranes (MAMs) and the perinuclear membranes. Being located in the metabolic hub, ceramide ... which then diffuses into the smooth muscle tissue and causes relaxation. DAG remains bound to the membrane by its fatty acid " ...
Common symptoms in infants include lack of motor skills, weak muscle tone, and macrocephaly. It may also be accompanied by ... Recent animal studies have shown the chronic oxidative stress may cause dysfunction in mitochondria, rendering the brain more ... As the disease progresses, patients may have decreased muscle tone and inactivation of Moro reflex, also known as startle ... where swollen astrocytes with distorted and elongated mitochondria can be seen in patients. Urine examinations are used to ...
The findings could provide new insights into diseases linked to energy use in muscle. ... Mitochondria within mouse muscle cells can quickly distribute energy through a grid-like network. ... Muscle Mitochondria May Form Energy Power Grid. At a Glance. *Researchers found that mitochondria in mouse muscles not only ... This high-resolution 3-D microscopic image shows a network of interconnected mitochondria within a mouse muscle cell.Brian ...
ERα36, a variant of estrogen receptor α, is predominantly localized in mitochondria of human uterine smooth muscle and ... ERα36, a variant of estrogen receptor α, is predominantly localized in mitochondria of human uterine smooth muscle and ... Fig 3. Colocalization analysis of ERα36 with mitochondria, F-actin or endoplasmic reticulum in ht-UtLM cells. Top row: A. ERα36 ... Fig 2. Colocalization analysis of ERα36 with mitochondria, F-actin or endoplasmic reticulum in ht-UtSMC cells. Top row: A. ER ...
Quadriceps Muscle, Sedentary behavior, Young Adult. Abstract. INTRODUCTION: Skeletal muscle mitochondria have dynamic shifts in ... Adult, Cell Respiration, Exercise, Female, Humans, Hydrogen Peroxide, Male, Mitochondria, Muscle, Oxidative Phosphorylation, ... 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.. ...
Here the authors report that that loss of LONP1-dependent mitochondrial proteolysis in muscle causes reduced muscle mass and ... In humans and mice, disuse-related muscle loss is associated with decreased mitochondrial LONP1 protein. Skeletal muscle- ... in skeletal muscle induces mitochondrial dysfunction, autophagy activation, and cause muscle loss and weakness. Thus, these ... plays a role in controlling mitochondrial function as well as skeletal muscle mass and strength in response to muscle disuse. ...
... DI MEO, SERGIO;IOSSA, SUSANNA;VENDITTI, PAOLA ... Skeletal muscle insulin resistance: role of mitochondria and other ROS sources / DI MEO, Sergio; Iossa, Susanna; Venditti, ... Skeletal muscle insulin resistance: role of mitochondria and other ROS sources / DI MEO, Sergio; Iossa, Susanna; Venditti, ... dealing with the mitochondria-centered mechanisms proposed to explain the onset of obesity-linked IR in skeletal muscle. We ...
... and muscle [PCr] (an index of metabolic perturbation, measured by (31)P-MRS) in hypoxia would be accelerated after dietary ... Mitochondria, Muscle / drug effects * Mitochondria, Muscle / metabolism * Muscle Contraction / drug effects* * Muscle, Skeletal ... Dietary nitrate accelerates postexercise muscle metabolic recovery and O2 delivery in hypoxia J Appl Physiol (1985). 2014 Dec ... and muscle [PCr] (an index of metabolic perturbation, measured by (31)P-MRS) in hypoxia would be accelerated after dietary ...
Glycolytic processes in liver mitochondria MITOCHONDRIA, LIVER /*metab *GLYCOLYSIS /enzymology Used with organs, tissues and ... Calcium content of fast twitch muscle fibers MUSCLE FIBERS, FAST-TWITCH/*chem. CALCIUM /*anal ... Metalloprotease activity in liver mitochondria MITOCHONDRIA, LIVER /*enzymol METALLOPROTEASES /*metab /chemistry Used for the ...
Autophagy, apoptosis, and mitochondria: molecular integration and physiological relevance in skeletal muscle. Author: Darin ... Keywords: apoptosis; autophagy; mitochondria; mitophagy; skeletal muscle; aging; metabolism; cancer. PMID: 31017800 PMCID: ... Although both autophagic and apoptotic signaling are active in skeletal muscle during various diseases and atrophy, their ...
ERα36, a Variant of Estrogen Receptor α, is Predominantly Localized in Mitochondria of Human Uterine Smooth Muscle and ... is Predominantly Localized in Mitochondria of Human Uterine Smooth Muscle and Leiomyoma Cells ... The distinctive colocalization pattern of ERα36 with mitochondria in ht-UtSMC and ht-UtLM cells, and the association of ERα36 ... Colocalization analysis of ERα36 with mitochondria, F-actin or endoplasmic reticulum in ht-UtLM cells. Top row: A. ERα36 signal ...
ERα36, a Variant of Estrogen Receptor α, is Predominantly Localized in Mitochondria of Human Uterine Smooth Muscle and ... is Predominantly Localized in Mitochondria of Human Uterine Smooth Muscle and Leiomyoma Cells ... The distinctive colocalization pattern of ERα36 with mitochondria in ht-UtSMC and ht-UtLM cells, and the association of ERα36 ... Colocalization analysis of ERα36 with mitochondria, F-actin or endoplasmic reticulum in ht-UtLM cells. Top row: A. ERα36 signal ...
Eventually, the brain becomes unable to control muscle movement.. Some gene variants appear to disturb the cell machinery that ... Other variants may affect the function of mitochondria. , the energy-producing structures within cells. As a byproduct of ... When these dopamine-producing neurons are damaged or die, communication between the brain and muscles weakens. ... energy production, mitochondria make unstable molecules called free radicals that can damage cells. Cells normally counteract ...
Mitochondria at work: Regulation of skeletal muscle mitochondria function during exercise. Jorgen Jensen, School of Clinical ... The mitochondrias role in autophagy and cell cycle control. Professor Jennifer Lippincott-Schwartz, National Institutes of ... Mitochondria in cell fate reprogramming: from mechanisms to disease investigation. Dr Alessandro Prigione, Max Delbrueck ... Exploitation of host mitochondria by human pathogenic Neisseria. Professor Thomas Rudel, Biozentrum, University of Wuerzburg, ...
... scientists found evidence that chronic heavy alcohol use affects a gene involved in mitochondrial repair and muscle ... Muscle weakness from long-term alcoholism may stem from an inability of mitochondria, the powerhouses of cells, to self-repair ... Skeletal muscle constantly relies on mitochondria for power. When mitochondria become damaged, they can repair themselves ... Muscle weakness from long-term alcoholism may stem from an inability of mitochondria, the powerhouses of cells, to self-repair ...
Nitric oxide; Metabolism; Proteins; Fatty acids; Oxidative phosphorylation; Skeletal system; Muscles; Citrates; Oxygen; ... Mitochondria; Nitric oxide ... and oxidative phosphorylation with reference to skeletal muscle ...
Knowledge of the fundamentals of muscle biopsy pathology is useful to promote understanding of the pathogenesis of many types ... Muscle biopsy often contributes significantly to the evaluation of patients with neuromuscular disease. ... These mitochondria are larger than entire sarcomeres. Normal mitochondria are much smaller than sarcomeres. View Media Gallery ... Neurogenic Changes in Muscle Biopsy. Skeletal muscle can show neurogenic changes in disorders that affect any part of motor ...
acts_upstream_of_or_within positive regulation of cardiac muscle hypertrophy IMP Inferred from Mutant Phenotype. more info ... involved_in autophagy of mitochondrion IMP Inferred from Mutant Phenotype. more info ... involved_in autophagy of mitochondrion ISO Inferred from Sequence Orthology. more info ... Involved in several processes, including autophagy of mitochondrion; cellular response to glucose starvation; and engulfment of ...
Mitochondria, Electricity and My Recovery From Secondary Progressive MS 3 hours ago Linda P. Faulks ... Muscle Meals 2 Go. 2 min read 1 year ago Linda P. Faulks ... Tags: meals muscle Continue Reading. Previous The Influence Of ... As a basic rule of thumb, it is best not to eat immediately before a exercise as a result of while your muscle tissue are ...
MeSH Terms: Animals; Heart; Mice; Mitochondria; Muscle Proteins/chemistry*; Oligopeptides*/pharmacology; Oxidation-Reduction; ... shotgun proteomics to assess the effects of aging on these post-translational modifications and the ability of the mitochondria ...
Brian Glancy, is to determine how mitochondria are optimized within muscle cells to help maintain ener ... The focus of the Muscle Energetics Laboratory, led by Dr. ... Muscle Energetics. The focus of the Muscle Energetics ... Leg muscle (upper left), jump muscle (upper right), direct flight muscle (bottom right), and indirect flight muscle (bottom ... 3D rendering of mitochondria (various colors) and the sarcotubular network (green) in an oxidative mouse skeletal muscle. ...
Acetyl-CoA production from fatty acid and glucose metabolism in muscle mitochondria. Fatty acids enter the cells by fatty acid ... Acetyl-CoA production from fatty acid and glucose metabolism in muscle mitochondria. Fatty acids… ... Carnitine in Human Muscle Bioenergetics: Can Carnitine Supplementation Improve Physical Exercise? Antonio Gnoni 1 , Serena ... Carnitine in Human Muscle Bioenergetics: Can Carnitine Supplementation Improve Physical Exercise? Antonio Gnoni et al. ...
Phosphine interferes with enzymes and protein synthesis, primarily in the mitochondria of heart and lung cells. As a result, ... Metabolic changes in heart muscle cause cation disturbances that alter transmembrane potentials. Ultimately, cardiac arrest, ... Phosphine interferes with enzymes and protein synthesis, primarily in the mitochondria of heart and lung cells. ...
"When you exercise you get more mitochondria growing in your muscle. If you dont exercise, the number of mitochondria goes down ... The researchers found the mice without the muscle AMPK genes had lower levels of mitochondria and an impaired ability for their ... the base level of fitness in the population is going down and that is reducing the mitochondria in peoples muscles. This in ... "While the normal mice could run for miles, those without the genes in their muscle could only run the same distance as down the ...
Seminar Title: Fibroids: Why is uterine muscle so vulnerable to benign tumor development? Host: Franco DeMayo ... Seminar Title: Metabolic regulation of germ cells and their mitochondria Host: Humphrey Yao ... Seminar Title: "Alternative Splicing Regulation of Membrane Trafficking Genes Impacts Cardiac and Skeletal Muscle Biology". ...
You can lose weight, sleep better, fight stress and high blood pressure, improve your mood, plus strengthen bones and muscles. ... where the muscle disposes of damaged mitochondria, making the muscle and cells healthier. Credit: University of Virginia ... where the muscle disposes of the damaged or dysfunctional mitochondria, making the muscle healthier. Yan compares exercise- ... How Exercise Removes Mitochondria Clunkers. For this study, Yan and colleagues assessed the skeletal muscle of a mouse model ...
3. The NADH oxidase system (external) of muscle mitochondria and its role in the oxidation of cytoplasmic NADH.. Rasmussen UF; ... 2. Oxidation of NADH via an "external" pathway in skeletal-muscle mitochondria and its possible role in the repayment of ... 4. L-lactate oxidation by skeletal muscle mitochondria.. Szczesna-Kaczmarek A. Int J Biochem; 1990; 22(6):617-20. PubMed ID: ... Effect of fatty acids and ketones on the activity of pyruvate dehydrogenase in skeletal-muscle mitochondria.. Ashour B; ...
... fitness is a measure of your bodys ability to take oxygen from the atmosphere and use it to produce energy for your muscle ... Aerobic energy is produced in the mitochondria of your muscle cells, using carbohydrates and fats for fuel. Mitochondria are ... The central component involves the ability of your lungs, heart and vascular system to deliver oxygen to your muscles via your ... The secondary component involves the ability of your muscle cells to extract oxygen from your blood and use it to make ...
A group of fats called long-chain fatty acids must be attached to a substance known as carnitine to enter mitochondria. Once ... Fatty acids are a major source of energy for the heart and muscles. During periods of fasting, fatty acids are also an ... Without enough functional CACT protein, long-chain fatty acids cannot be transported into mitochondria. As a result, these ... Fatty acid oxidation takes place within mitochondria. , which are the energy-producing centers in cells. ...
A new study finds the mechanism that underpins this protection, and mitochondria are key. ... The role of mitochondria. In earlier experiments, the authors of the new study found that caffeine levels equivalent to around ... Once within these organelles, it triggered tasks vital for the repair of heart muscle following a heart attack. ... Mitochondria are often called the powerhouses of the cell. We explain how they got this title, and outline other important ...
  • Skeletal muscle mitochondria have dynamic shifts in oxidative metabolism to meet energy demands of aerobic exercise. (oregonstate.edu)
  • It is unclear if aerobic exercise stimulates intrinsic oxidative metabolism of mitochondria or varies between substrates. (oregonstate.edu)
  • In this review we have summarized the effects of NO on glycolysis, fatty acid metabolism, the TCA cycle, and oxidative phosphorylation with reference to skeletal muscle. (cdc.gov)
  • Mitochondrial fatty acid oxidation represents an important energy source for muscle metabolism particularly during physical exercise. (nih.gov)
  • Mitochondria are microscopic organelles that function as energy factories for aerobic metabolism. (livestrong.com)
  • Mechanistically, aberrant accumulation of mitochondrial-retained protein in muscle upon loss of LONP1 induces the activation of autophagy-lysosome degradation program of muscle loss. (nature.com)
  • Overexpressing a mitochondrial-retained mutant ornithine transcarbamylase (ΔOTC), a known protein degraded by LONP1, in skeletal muscle induces mitochondrial dysfunction, autophagy activation, and cause muscle loss and weakness. (nature.com)
  • 4. Denervation-induced mitochondrial dysfunction and autophagy in skeletal muscle of apoptosis-deficient animals. (nih.gov)
  • 19. Time-dependent changes in autophagy, mitophagy and lysosomes in skeletal muscle during denervation-induced disuse. (nih.gov)
  • 11. Increased production of reactive oxygen species by rat liver mitochondria after chronic ethanol treatment. (nih.gov)
  • 12. The redox state of free nicotinamide-adenine dinucleotide in the cytoplasm and mitochondria of rat liver. (nih.gov)
  • 15. An electron-transport system associated with the outer membrane of liver mitochondria. (nih.gov)
  • 16. [Intermembrane electron transport in the dynamics of high-amplitude swelling of rat liver mitochondria]. (nih.gov)
  • People with CACT deficiency also usually have excess ammonia in the blood (hyperammonemia), an enlarged liver (hepatomegaly), and a weakened heart muscle (cardiomyopathy). (nih.gov)
  • Fatty acids and long-chain acylcarnitines (fatty acids still attached to carnitine) may also build up in cells and damage the liver, heart, and muscles. (nih.gov)
  • Hardest hit are organs and tissues that need a lot of energy, like muscles, brain, heart, kidneys and liver. (nih.gov)
  • Feeding chickens with oral contraceptive steroids at the dose used by some poultry growers in Egypt has led to the formation of high estrogen residues in the muscles and the liver compared with controls. (who.int)
  • The purpose of this study is to assess the formation of residues in the muscle and liver of chickens of contraceptive steroids applied orally at the same dose used by poultry growers and the resultant level of estrogen in chickens. (who.int)
  • Three duplicate samples of muscles and liver were separately analysed for estrogen (17-estradiol) content by using high pressure liquid chromatography (HPLC) as described earlier [3]. (who.int)
  • A group of fats called long-chain fatty acids must be attached to a substance known as carnitine to enter mitochondria. (nih.gov)
  • Without enough functional CACT protein, long-chain fatty acids cannot be transported into mitochondria. (nih.gov)
  • It is what transports long-chain fatty acids into the mitochondria (thereby increasing energy production via beta-oxidation). (timesofisrael.com)
  • Colocalization ERα36 with mitochondria, F-actin or endoplasmic reticulum (ht-UtSMC). (nih.gov)
  • The vesicles (upper), mitochondria (middle), and endoplasmic reticulum (lower) within each cell are shown. (nih.gov)
  • In this process-known as cellular respiration or oxidative phosphorylation-the mitochondria act like small cellular batteries, using an electrical voltage across their membranes as an intermediate energy source to produce ATP. (nih.gov)
  • Mitochondrial reticulum for cellular energy distribution in muscle. (nih.gov)
  • Mitochondria are cellular structures that generate most of the energy needed by cells. (nih.gov)
  • They found that one important benefit involves the cellular power plant - the mitochondria - which creates the fuel so the body can function properly. (medicalxpress.com)
  • For example, researchers in NICHD's Division of Intramural Research (DIR) study MD at the cellular level to determine whether membrane composition can be improved to stabilize muscle cells. (nih.gov)
  • Within the DIR, the Section on Cellular and Membrane Biophysics focuses on understanding how membrane dynamics affect the structure and function of muscle cells and ways to alter those effects. (nih.gov)
  • A new study shows that exercise triggers a process called mitophagy, where the muscle disposes of damaged mitochondria, making the muscle and cells healthier. (medicalxpress.com)
  • They discovered that this "stress test" induced by aerobic exercise triggers a process called mitophagy, where the muscle disposes of the damaged or dysfunctional mitochondria, making the muscle healthier. (medicalxpress.com)
  • Yan's lab also deleted the Ulk1 gene in mouse skeletal muscle and found that, without the gene, the removal of damaged or dysfunctional mitochondria is dramatically inhibited, suggesting a new role for the Ulk1 gene in exercise and mitophagy. (medicalxpress.com)
  • Ampk phosphorylation of Ulk1 is required for targeting of mitochondria to lysosomes in exercise-induced mitophagy, Nature Communications (2017). (medicalxpress.com)
  • 13. PGC-1α overexpression via local transfection attenuates mitophagy pathway in muscle disuse atrophy. (nih.gov)
  • SIRT3) in skeletal muscle, both of which are regulators of mitochondria biogenesis. (nih.gov)
  • 9. Expression of nuclear-encoded genes involved in mitochondrial biogenesis and dynamics in experimentally denervated muscle. (nih.gov)
  • 10. Role of p53 in mitochondrial biogenesis and apoptosis in skeletal muscle. (nih.gov)
  • The findings reveal a major mechanism for energy distribution in skeletal muscle cells, and could provide new insights into diseases linked to energy use in muscle. (nih.gov)
  • Skeletal muscles are made of long, thin cells that are packed with highly organized proteins and organelles. (nih.gov)
  • To meet this energy demand, muscle cells contain mitochondria. (nih.gov)
  • Scientists have long believed that the energy produced by mitochondria is distributed through muscle cells by some type of diffusion mechanism. (nih.gov)
  • A team led by Drs. Robert S. Balaban and Sriram Subramaniam from NIH's National Heart, Lung, and Blood Institute (NHLBI) and National Cancer Institute (NCI), respectively, hypothesized that some other faster, more efficient energy pathway must spread energy throughout muscle cells. (nih.gov)
  • With isolated mitochondrial preparations, we confirmed that a known mitochondrial protein, prohibitin, was present in mitochondria, and by co-immunoprecipitation analysis that ERα36 was associated with prohibitin in ht-UtLM cells. (nih.gov)
  • The distinctive colocalization pattern of ERα36 with mitochondria in ht-UtSMC and ht-UtLM cells, and the association of ERα36 with a mitochondrial-specific protein suggest that ERα36 is localized primarily in mitochondria and may play a pivotal role in non-genomic signaling and mitochondrial functions. (nih.gov)
  • Comparison of ERα36 and ERα66 domain structures and subcellular ERα36 staining patterns in human uterine smooth muscle (ht-UtSMC) and leiomyoma cells (ht-UtLM). (nih.gov)
  • As a byproduct of energy production, mitochondria make unstable molecules called free radicals that can damage cells. (medlineplus.gov)
  • Muscle weakness from long-term alcoholism may stem from an inability of mitochondria, the powerhouses of cells, to self-repair, according to a study funded by the National Institutes of Health. (nih.gov)
  • It had been thought that this type of mitochondrial self-repair was unlikely in the packed fibers of the skeletal muscle cells, as mitochondria have little opportunity to interact in the narrow space between the thread-like structures called myofilaments that make up muscle. (nih.gov)
  • By tagging mitochondria in the skeletal tissue of rats with different colors, the researchers were able to observe the process in action and confirm that mitochondrial fusion occurs in muscle cells. (nih.gov)
  • The focus of the Muscle Energetics Laboratory, led by Dr. Brian Glancy, is to determine how mitochondria are optimized within muscle cells to help maintain energy homeostasis during the large change in energy demand caused by muscle contraction. (nih.gov)
  • 3D rendering of red blood cells (various colors) within a skeletal muscle capillary of a newborn mouse. (nih.gov)
  • There's a malfunction in the tiny capsule-shaped structures-called mitochondria Known as the cell's "powerhouse," they convert food molecules into a form of energy your cells can use. (nih.gov)
  • Depending on which cells are affected, people with mitochondrial diseases may have muscle weakness and pain, digestive problems, heart disease, seizures and many other symptoms. (nih.gov)
  • Mitochondria produce about 90% of the energy that cells need to function. (nih.gov)
  • These tasks include promoting migration of endothelial cells and protecting heart muscle cells from cell death, also known as apoptosis. (medicalnewstoday.com)
  • The aerobic fitness definition is a measure of your body's ability to take oxygen from the atmosphere and use it to produce energy for your muscle cells. (livestrong.com)
  • The secondary component involves the ability of your muscle cells to extract oxygen from your blood and use it to make adenosine triphosphate, or ATP, the fundamental carrier of energy in cells. (livestrong.com)
  • Regardless of how efficiently your heart pumps blood, aerobic fitness is also dependent on the ability of your muscle cells to extract oxygen from your blood and use it to make energy. (livestrong.com)
  • Aerobic energy is produced in the mitochondria of your muscle cells, using carbohydrates and fats for fuel. (livestrong.com)
  • By borrowing a tool from bacteria that infect plants, scientists have developed a new approach to eliminate mutated DNA inside mitochondria-the energy factories within cells. (nih.gov)
  • Mitochondria convert fuel from food into a form of energy that cells can use. (nih.gov)
  • Researchers created a mouse model with tissues that appear similar to and function similarly to those of MD patients, as well as an inability to exercise or repair muscle cells. (nih.gov)
  • Older muscles lose their mitochondria, the power engines of the cells. (ucdavis.edu)
  • If people use 3 grams of Korean ginseng daily, the number of mitochondria in their cells increases. (ergo-log.com)
  • Supplementation with ginseng caused a sharp increase in the number of mitochondria in the cells of the test subjects. (ergo-log.com)
  • It can help maintain the health of the mitochondria of the cells. (keine-ruhe.org)
  • It may also help keep mitochondria in cells healthy. (keine-ruhe.org)
  • Carnitine in Human Muscle Bioenergetics: Can Carnitine Supplementation Improve Physical Exercise? (nih.gov)
  • Considering the important role of fatty acids in muscle bioenergetics, and the limiting effect of free carnitine in fatty acid oxidation during endurance exercise, l-carnitine supplementation has been hypothesized to improve exercise performance. (nih.gov)
  • The group analyzed high-resolution 3-D images of mouse skeletal muscle. (nih.gov)
  • A fly-through rendering of the mitochondrial network within an oxidative mouse skeletal muscle cell. (nih.gov)
  • Fly-through rendering of the interior structures of a newborn mouse skeletal muscle highlighting cell and organelle membrane as well as myosin filaments. (nih.gov)
  • 3D rendering of the branching contractile structures within a newborn mouse skeletal muscle. (nih.gov)
  • 3D rendering of the interior of a mouse skeletal muscle mitochondrion. (nih.gov)
  • 3D rendering of mitochondria (various colors) and the sarcotubular network (green) in an oxidative mouse skeletal muscle. (nih.gov)
  • and positive regulation of cardiac muscle hypertrophy. (nih.gov)
  • 1. Effect of denervation on mitochondrially mediated apoptosis in skeletal muscle. (nih.gov)
  • 18. Cell death in denervated skeletal muscle is distinct from classical apoptosis. (nih.gov)
  • We will collect muscle specimens from the vastus lateralis and blood at baseline and 90 days for biochemical analyses, as well as monitor blood chemistries and adverse events at monthly clinic visits. (nih.gov)
  • More recent reports suggest that mitochondrial dysfunction is not an early event in the development of insulin resistance, but rather a complication of the hyperlipidemia-induced reactive oxygen species (ROS) production in skeletal muscle, which might promote mitochondrial alterations, lipid accumulation and inhibition of insulin action. (unina.it)
  • Mitochondria have diverse functions and are essential organelles that require continuous surveillance to maintain their function. (nature.com)
  • Once within these organelles, it triggered tasks vital for the repair of heart muscle following a heart attack . (medicalnewstoday.com)
  • During strenuous exercise, the rate of energy use in skeletal muscles can increase by more than 100-fold almost instantly. (nih.gov)
  • 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)
  • These findings suggest that the NO3 (-)-NO2 (-)-NO pathway is a significant modulator of muscle energetics and O2 delivery during hypoxic exercise and subsequent recovery. (nih.gov)
  • As a basic rule of thumb, it is best not to eat immediately before a exercise as a result of while your muscle tissue are trying to do their "thing," your stomach is making an attempt to concurrently digest the meals in your abdomen. (samsungsummerkrush.com)
  • The researchers made their unexpected finding while working with healthy, specially-bred mice, some of which had two genes in muscle essential for exercise removed. (mcmaster.ca)
  • The researchers found the mice without the muscle AMPK genes had lower levels of mitochondria and an impaired ability for their muscles to take up glucose while they exercise. (mcmaster.ca)
  • When you exercise you get more mitochondria growing in your muscle. (mcmaster.ca)
  • If you don't exercise, the number of mitochondria goes down. (mcmaster.ca)
  • And exercise capacity, mainly determined by muscle size and function, is the best predictor of mortality in the general population. (medicalxpress.com)
  • Yan and colleagues have completed a study in mice that, for the first time, shows that just one bout of moderate-to-intense exercise acts as a "stress test" on mitochondria in muscles. (medicalxpress.com)
  • Aerobic exercise removes damaged mitochondria in skeletal muscle," Yan said. (medicalxpress.com)
  • Aerobic exercise training increases your total blood volume, heart muscle size and contractility, resulting in a greater volume of blood being injected per heart beat. (livestrong.com)
  • In response to repeated bouts of aerobic exercise, the density and number of mitochondria increase. (livestrong.com)
  • High-intensity exercise that challenges your aerobic limit has a more profound effect on mitochondria adaptations and oxygen extraction than low- to moderate-intensity activity. (livestrong.com)
  • Both exercise and a keto diet can increase the number of mitochondria in muscles. (ucdavis.edu)
  • Supplementation with Panax ginseng may protect muscles against breakdown caused by intensive exercise. (ergo-log.com)
  • He also suggested that identifying the proteins involved in mitochondrial fusion may aid in drug development for alcohol-related muscle weakness. (nih.gov)
  • Simply writing, "R/O polymyositis" or "weakness", or worse, "muscle weakness" (we would not be concerned about weakness of character here, so using the term muscle weakness in this context seems oddly redundant) does not provide the pathologist with any useful clinical information and is a disservice to the patient. (medscape.com)
  • These abnormal mitochondria cause extreme fatigue and weakness in his legs, trouble breathing and a host of other problems. (nih.gov)
  • Mitochondrial gene mutations can lead to a variety of health problems including muscle weakness, heart disease, and blindness in the case of LHON. (nih.gov)
  • Therefore, a deficiency in this vitamin might explain why some people experience weakness or muscle aching. (timesofisrael.com)
  • Here, we review the literature dealing with the mitochondria-centered mechanisms proposed to explain the onset of obesity-linked IR in skeletal muscle. (unina.it)
  • Mitochondria affect cell membrane repair mechanisms in Duchenne muscular dystrophy. (nih.gov)
  • Here, we demonstrate that LONP1, a major mitochondrial protease resides in the matrix, plays a role in controlling mitochondrial function as well as skeletal muscle mass and strength in response to muscle disuse. (nature.com)
  • In humans and mice, disuse-related muscle loss is associated with decreased mitochondrial LONP1 protein. (nature.com)
  • Thus, these findings reveal a role of LONP1-dependent mitochondrial protein quality-control in safeguarding mitochondrial function and preserving skeletal muscle mass and strength, and unravel a link between mitochondrial protein quality and muscle mass maintenance during muscle disuse. (nature.com)
  • 8. Effect of denervation-induced muscle disuse on mitochondrial protein import. (nih.gov)
  • 16. Muscle apoptotic response to denervation, disuse, and aging. (nih.gov)
  • The working hypothesis in the lab is that mitochondrial function within a muscle cell is dictated not only by the amount and composition of mitochondria but also by spatial relationships between mitochondria and the sites of energy storage, utilization, and signaling. (nih.gov)
  • 70 years), whether 90 days of resveratrol supplementation is associated with (i) increases in muscle mitochondrial function (State 3 & 4 respiration), (ii) increases in levels of PGC-1a, AMP-activated protein kinase (AMPK), and Sirtuins (i.e. (nih.gov)
  • If our hypotheses are supported, this study will be the first to show that resveratrol improves mitochondrial function in muscle, and that these changes are associated with increased levels of physical function in moderate to low functioning older adults ¿ the population who is at greatest risk of functional decline and physical disability. (nih.gov)
  • 2. Effect of prior chronic contractile activity on mitochondrial function and apoptotic protein expression in denervated muscle. (nih.gov)
  • 6. Mitochondrial function and apoptotic susceptibility in aging skeletal muscle. (nih.gov)
  • 11. The role of PGC-1alpha on mitochondrial function and apoptotic susceptibility in muscle. (nih.gov)
  • However, studies have shown that these diffusion pathways alone are not sufficient to support normal muscle contraction. (nih.gov)
  • Initiating and maintaining muscle contraction requires rapid, coordinated movement of signals and material within and among various structures located throughout the relatively large muscle cell. (nih.gov)
  • The Muscle Energetics Laboratory focuses on the energy distribution aspect of continued muscle contraction, deficits in which have been implicated in many pathologies including diabetes and muscular dystrophy as well as aging. (nih.gov)
  • In particular, we aim to determine how mitochondria are optimized as part of the integrated muscle cell to maintain energy homeostasis during the large change in energy demand caused by the onset of muscle contraction. (nih.gov)
  • The mitochondria fluoresce green when they are healthy and turn red when damaged and broken down by the cell's waste-disposal system, the lysosomes. (medicalxpress.com)
  • This high-resolution 3-D microscopic image shows a network of interconnected mitochondria within a mouse muscle cell. (nih.gov)
  • Healthy mitochondria can help convert fat into energy quickly. (keine-ruhe.org)
  • Researchers found that mitochondria in mouse muscles not only produce energy, but can quickly distribute it across the muscle cell through a grid-like network. (nih.gov)
  • The mitochondria were electrically coupled and able to rapidly distribute the mitochondrial membrane voltage-the primary energy for ATP production-throughout the cell. (nih.gov)
  • The discovery of this mechanism for rapid distribution of energy throughout the muscle cell will change the way scientists think about muscle function and will open up a whole new area to explore in health and disease," Balaban says. (nih.gov)
  • Ongoing efforts are centered around the structure, function, composition, and developmental regulation of mitochondrial networks with the goal of gaining better control of and understanding the functional consequences of altering spatial relationships within the muscle energy distribution system. (nih.gov)
  • Fatty acids are a major source of energy for the heart and muscles. (nih.gov)
  • Scientists have learned that among the genes in mtDNA are instructions for making 13 proteins that mitochondria need to produce energy. (nih.gov)
  • Mitochondria won their title because, within their membranes, adenosine triphosphate - which is the energy currency of life - is produced. (medicalnewstoday.com)
  • Mitochondria not only produce energy, they also help the body break down harmful metabolites known as kynurenines . (ucdavis.edu)
  • The more fit we are, the more muscle mitochondria we have, and the more energy our muscles can make from fat, the better we are at breaking down potential neurotoxins . (ucdavis.edu)
  • Myoglobin transports oxygen to the mitochondria in your muscles, which in turn produce ATP to give your muscles energy. (runkeeper.com)
  • So, as you increase your myoglobin, you improve your body's ability to quickly transport oxygen to the muscles for energy, making you able to run faster. (runkeeper.com)
  • Human muscle contains high amounts of carnitine but it depends on the uptake of this compound from the bloodstream, due to muscle inability to synthesize carnitine. (nih.gov)
  • Skeletal muscle-specific ablation of LONP1 in mice resulted in impaired mitochondrial protein turnover, leading to mitochondrial dysfunction. (nature.com)
  • Once these fatty acids are joined with carnitine, the CACT protein transports them into mitochondria. (nih.gov)
  • Using exon skipping, researchers restored up to 90% of dystrophin protein throughout the skeletal and heart muscles in a mouse model of DMD. (nih.gov)
  • Speed workouts also increase your production of myoglobin, which is a protein found in your muscles. (runkeeper.com)
  • Although both autophagic and apoptotic signaling are active in skeletal muscle during various diseases and atrophy, their specific roles here are somewhat unique. (qigonginstitute.org)
  • 3. Effect of chronic contractile activity on SS and IMF mitochondrial apoptotic susceptibility in skeletal muscle. (nih.gov)
  • 5. Differential susceptibility of subsarcolemmal and intermyofibrillar mitochondria to apoptotic stimuli. (nih.gov)
  • 7. Mitochondria-associated apoptotic signalling in denervated rat skeletal muscle. (nih.gov)
  • 14. Decreased DNA fragmentation and apoptotic signaling in soleus muscle of hypertensive rats following 6 weeks of treadmill training. (nih.gov)
  • 20. Mitochondria in skeletal muscle: adaptable rheostats of apoptotic susceptibility. (nih.gov)
  • By removing these genes we identified the key regulator of the mitochondria is the enzyme AMPK," said Steinberg. (mcmaster.ca)
  • During speed workouts, you maximally activate your slow-twitch muscles and intermediate muscle fibers, which increases your aerobic capacity. (runkeeper.com)
  • 1. Regulating effect of mitochondrial lactate dehydrogenase on oxidation of cytoplasmic NADH via an "external" pathway in skeletal muscle mitochondria. (nih.gov)
  • 2. Oxidation of NADH via an "external" pathway in skeletal-muscle mitochondria and its possible role in the repayment of lactacid oxygen debt. (nih.gov)
  • 6. Oxidation of NADH by a rotenone and antimycin-sensitive pathway in the mitochondrion of procyclic Trypanosoma brucei brucei. (nih.gov)
  • 18. [Activation of the external pathway of NADH oxidation in mitochondria at decreased pH]. (nih.gov)
  • Electron microscopy image of a mitochondrion with a donut hole (cyan) as well as sarcoplasmic reticulum (magenta), transverse tubules (orange), and contractile A-bands (green), I-bands (red), and Z-disks (blue) from a mouse glycolytic skeletal muscle. (nih.gov)
  • Substrate-Specific Respiration of Isolated Skeletal Muscle Mitochondria after 1 h of Moderate Cycling in Sedentary Adults. (oregonstate.edu)
  • Skeletal muscle insulin resistance: role of mitochondria and other ROS sources. (unina.it)
  • 3. The NADH oxidase system (external) of muscle mitochondria and its role in the oxidation of cytoplasmic NADH. (nih.gov)
  • Although the etiology of age-related physical disability is complex and multi-factorial, emerging evidence implicates the mitochondria as playing a key role in the initial onset and progression of functional decline in many older adults. (nih.gov)
  • that lead to flawed proteins or other molecules in the mitochondria. (nih.gov)
  • The central component involves the ability of your lungs, heart and vascular system to deliver oxygen to your muscles via your blood stream. (livestrong.com)
  • The researchers traced the paths of mitochondria and found that they formed a network, or reticulum. (nih.gov)
  • Even in healthy people, researchers have found, mitochondria can gradually deteriorate as we grow older. (nih.gov)
  • Over the last decades, though, researchers have learned a lot about mitochondria. (nih.gov)
  • The researchers - led by Judith Haendeler and Joachim Altschmied - found that caffeine caused p27 to move into mitochondria. (medicalnewstoday.com)
  • Your body will become more efficient at recruiting your fast-twitch muscles. (runkeeper.com)
  • 19. Effect of fatty acids and ketones on the activity of pyruvate dehydrogenase in skeletal-muscle mitochondria. (nih.gov)
  • This is due to capsaicin, which is found in the peppers and increases uncoupling proteins found in the muscle. (self.com)
  • Knowledge of the fundamentals of muscle biopsy pathology is useful to promote understanding of the pathogenesis of many types of neuromuscular disorders and assists the non-pathologist clinician to understand reports that he or she receives for the muscle biopsies from his or her patients. (medscape.com)
  • The remainder of this article addresses the key clinical characteristics and pathologic findings on muscle biopsy of selected examples of disorders from 4 different categories of muscle disease: immune-mediated (inflammatory) myopathies, muscular dystrophies, metabolic myopathies, and congenital myopathies. (medscape.com)
  • The article Muscle Biopsy and Clinical and Laboratory Features of Neuromuscular Disease provides information about the procedure of muscle biopsy and background about the general features of the clinical presentations of neuromuscular disorders. (medscape.com)
  • 17. Lactate dehydrogenase is not a mitochondrial enzyme in human and mouse vastus lateralis muscle. (nih.gov)
  • 17. Pyrroloquinoline Quinone Resists Denervation-Induced Skeletal Muscle Atrophy by Activating PGC-1α and Integrating Mitochondrial Electron Transport Chain Complexes. (nih.gov)
  • The safeguard of a functional mitochondrial system is particularly important for skeletal muscle, the largest metabolically active and highly structured tissue that is often affected in diseases of mitochondrial dysfunction. (nature.com)
  • 14. Physical and functional association of lactate dehydrogenase (LDH) with skeletal muscle mitochondria. (nih.gov)
  • Skeletal muscle is the most abundant tissue in humans and faces near instantaneous changes in demand for force production lasting from seconds to minutes to hours. (nih.gov)
  • By supporting and conducting research, NICHD aims to improve our understanding of MD as a way to develop targeted treatments and therapies to slow or stop muscle degeneration, improve muscle strength and function, and optimize overall health for people with MD. (nih.gov)
  • Several DER components support research on MD, muscle development, and muscle function. (nih.gov)
  • Some of this work includes simulators that help model muscle function in people with MD, to allow providers to fine-tune general rehabilitation techniques for the needs to individuals with MD. Other NCMRR-led activities focus on improving assistive technology to help people with MD function better in their surroundings. (nih.gov)
  • A new UC Davis Health study found that a ketogenic (keto) diet improves muscle function in older animals by preventing muscle mass loss due to age ( sarcopenia ). (ucdavis.edu)
  • A keto diet therefore prevents muscle deterioration and even restores muscle function. (ucdavis.edu)
  • But mitochondria have importance beyond rare diseases. (nih.gov)
  • In research conducted with rats, scientists found evidence that chronic heavy alcohol use affects a gene involved in mitochondrial repair and muscle regeneration. (nih.gov)
  • In this Q&A, he shares his latest research on the keto diet, its effect on muscle growth and brain health, and its potential side effects. (ucdavis.edu)
  • They found that the mitochondrial "wires" were electrically conductive and that most of the mitochondria were in direct electrical communication through the interconnecting network. (nih.gov)
  • Mitochondria are colored according to their location relative to the adjacent contractile structures. (nih.gov)
  • New mouse model for muscular dystrophies shows defects in repairing muscles. (nih.gov)
  • When its turned on, Ulk1 activates other components in the cell to execute the removal of dysfunctional mitochondria," Yan said. (medicalxpress.com)
  • Each cell in the body contains dozens or even hundreds of mitochondria. (nih.gov)