General increase in bulk of a part or organ due to CELL ENLARGEMENT and accumulation of FLUIDS AND SECRETIONS, not due to tumor formation, nor to an increase in the number of cells (HYPERPLASIA).
Enlargement of the LEFT VENTRICLE of the heart. This increase in ventricular mass is attributed to sustained abnormal pressure or volume loads and is a contributor to cardiovascular morbidity and mortality.
Enlargement of the HEART, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both HEART VENTRICLES or HEART ATRIA. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of CARDIOMYOPATHIES.
Enlargement of the RIGHT VENTRICLE of the heart. This increase in ventricular mass is often attributed to PULMONARY HYPERTENSION and is a contributor to cardiovascular morbidity and mortality.
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.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
The measurement of an organ in volume, mass, or heaviness.
Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic.
The geometric and structural changes that the HEART VENTRICLES undergo, usually following MYOCARDIAL INFARCTION. It comprises expansion of the infarct and dilatation of the healthy ventricle segments. While most prevalent in the left ventricle, it can also occur in the right ventricle.
The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation.
A form of CARDIAC MUSCLE disease, characterized by left and/or right ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR; HYPERTROPHY, RIGHT VENTRICULAR), frequent asymmetrical involvement of the HEART SEPTUM, and normal or reduced left ventricular volume. Risk factors include HYPERTENSION; AORTIC STENOSIS; and gene MUTATION; (FAMILIAL HYPERTROPHIC CARDIOMYOPATHY).
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
Growth processes that result in an increase in CELL SIZE.
The hollow, muscular organ that maintains the circulation of the blood.
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.
A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight PEPTIDES derived from a common precursor and secreted mainly by the HEART ATRIUM. All these peptides share a sequence of about 20 AMINO ACIDS.
The quantity of volume or surface area of CELLS.
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 octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
A CALCIUM and CALMODULIN-dependent serine/threonine protein phosphatase that is composed of the calcineurin A catalytic subunit and the calcineurin B regulatory subunit. Calcineurin has been shown to dephosphorylate a number of phosphoproteins including HISTONES; MYOSIN LIGHT CHAIN; and the regulatory subunits of CAMP-DEPENDENT PROTEIN KINASES. It is involved in the regulation of signal transduction and is the target of an important class of immunophilin-immunosuppressive drug complexes.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Contractile activity of the MYOCARDIUM.
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
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 collection of lymphoid nodules on the posterior wall and roof of the NASOPHARYNX.
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.
The larger subunits of MYOSINS. The heavy chains have a molecular weight of about 230 kDa and each heavy chain is usually associated with a dissimilar pair of MYOSIN LIGHT CHAINS. The heavy chains possess actin-binding and ATPase activity.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
A pyrrolizidine alkaloid and a toxic plant constituent that poisons livestock and humans through the ingestion of contaminated grains and other foods. The alkaloid causes pulmonary artery hypertension, right ventricular hypertrophy, and pathological changes in the pulmonary vasculature. Significant attenuation of the cardiopulmonary changes are noted after oral magnesium treatment.
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 condition characterized by the thickening of the ventricular ENDOCARDIUM and subendocardium (MYOCARDIUM), seen mostly in children and young adults in the TROPICAL CLIMATE. The fibrous tissue extends from the apex toward and often involves the HEART VALVES causing restrictive blood flow into the respective ventricles (CARDIOMYOPATHY, RESTRICTIVE).
The hemodynamic and electrophysiological action of the left HEART VENTRICLE. Its measurement is an important aspect of the clinical evaluation of patients with heart disease to determine the effects of the disease on cardiac performance.
The pressure within a CARDIAC VENTRICLE. Ventricular pressure waveforms can be measured in the beating heart by catheterization or estimated using imaging techniques (e.g., DOPPLER ECHOCARDIOGRAPHY). The information is useful in evaluating the function of the MYOCARDIUM; CARDIAC VALVES; and PERICARDIUM, particularly with simultaneous measurement of other (e.g., aortic or atrial) pressures.
A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
Refers to animals in the period of time just after birth.
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.
Heart enlargement and other remodeling in cardiac morphology and electrical circutry found in individuals who participate in intense repeated exercises.
A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)
Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
Post-systolic relaxation of the HEART, especially the HEART VENTRICLES.
The act of constricting.
Elements of limited time intervals, contributing to particular results or situations.
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.
A condition in which the LEFT VENTRICLE of the heart was functionally impaired. This condition usually leads to HEART FAILURE; MYOCARDIAL INFARCTION; and other cardiovascular complications. Diagnosis is made by measuring the diminished ejection fraction and a depressed level of motility of the left ventricular wall.
A pathological constriction that can occur above (supravalvular stenosis), below (subvalvular stenosis), or at the AORTIC VALVE. It is characterized by restricted outflow from the LEFT VENTRICLE into the AORTA.
A family of transcription factors characterized by the presence of highly conserved calcineurin- and DNA-binding domains. NFAT proteins are activated in the CYTOPLASM by the calcium-dependent phosphatase CALCINEURIN. They transduce calcium signals to the nucleus where they can interact with TRANSCRIPTION FACTOR AP-1 or NF-KAPPA B and initiate GENETIC TRANSCRIPTION of GENES involved in CELL DIFFERENTIATION and development. NFAT proteins stimulate T-CELL activation through the induction of IMMEDIATE-EARLY GENES such as INTERLEUKIN-2.
Abnormal enlargement or overgrowth of the gingivae brought about by enlargement of existing cells.
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).
Period of contraction of the HEART, especially of the HEART VENTRICLES.
This structure includes the thin muscular atrial septum between the two HEART ATRIA, and the thick muscular ventricular septum between the two HEART VENTRICLES.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The main trunk of the systemic arteries.
Isoforms of MYOSIN TYPE II, specifically found in the ventricular muscle of the HEART. Defects in the genes encoding ventricular myosins result in FAMILIAL HYPERTROPHIC CARDIOMYOPATHY.
A growth differentiation factor that is a potent inhibitor of SKELETAL MUSCLE growth. It may play a role in the regulation of MYOGENESIS and in muscle maintenance during adulthood.
Inbred rats derived from Sprague-Dawley rats and used for the study of salt-dependent hypertension. Salt-sensitive and salt-resistant strains have been selectively bred to show the opposite genetically determined blood pressure responses to excess sodium chloride ingestion.
The non-genetic biological changes of an organism in response to challenges in its ENVIRONMENT.
Diet modification and physical exercise to improve the ability of animals to perform physical activities.
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.
A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.
Calcium-transporting ATPases that catalyze the active transport of CALCIUM into the SARCOPLASMIC RETICULUM vesicles from the CYTOPLASM. They are primarily found in MUSCLE CELLS and play a role in the relaxation of MUSCLES.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
Excision of kidney.
Mature contractile cells, commonly known as myocytes, that form one of three kinds of muscle. The three types of muscle cells are skeletal (MUSCLE FIBERS, SKELETAL), cardiac (MYOCYTES, CARDIAC), and smooth (MYOCYTES, SMOOTH MUSCLE). They are derived from embryonic (precursor) muscle cells called MYOBLASTS.
A GATA transcription factor that is expressed in the MYOCARDIUM of developing heart and has been implicated in the differentiation of CARDIAC MYOCYTES. GATA4 is activated by PHOSPHORYLATION and regulates transcription of cardiac-specific genes.
An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY, the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention.
An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.
A form of CARDIAC MUSCLE disease that is characterized by ventricular dilation, VENTRICULAR DYSFUNCTION, and HEART FAILURE. Risk factors include SMOKING; ALCOHOL DRINKING; HYPERTENSION; INFECTION; PREGNANCY; and mutations in the LMNA gene encoding LAMIN TYPE A, a NUCLEAR LAMINA protein.
The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.
A family of heterotrimeric GTP-binding protein alpha subunits that activate TYPE C PHOSPHOLIPASES dependent signaling pathways. The Gq-G11 part of the name is also spelled Gq/G11.
A direct-acting vasodilator that is used as an antihypertensive agent.
A PEPTIDE that is secreted by the BRAIN and the HEART ATRIA, stored mainly in cardiac ventricular MYOCARDIUM. It can cause NATRIURESIS; DIURESIS; VASODILATION; and inhibits secretion of RENIN and ALDOSTERONE. It improves heart function. It contains 32 AMINO ACIDS.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
A peptidyl-dipeptidase that catalyzes the release of a C-terminal dipeptide, -Xaa-*-Xbb-Xcc, when neither Xaa nor Xbb is Pro. It is a Cl(-)-dependent, zinc glycoprotein that is generally membrane-bound and active at neutral pH. It may also have endopeptidase activity on some substrates. (From Enzyme Nomenclature, 1992) EC
A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH).
A type of stress exerted uniformly in all directions. Its measure is the force exerted per unit area. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.
One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.
Drugs that selectively bind to and activate beta-adrenergic receptors.
Substances which, when ingested, inhaled, or absorbed, or when applied to, injected into, or developed within the body in relatively small amounts may, by their chemical action, cause damage to structure or disturbance of function. (From Dorland, 27th ed)
The repeating contractile units of the MYOFIBRIL, delimited by Z bands along its length.
Application of a ligature to tie a vessel or strangulate a part.
Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.
Myosin type II isoforms found in cardiac muscle.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
An autosomal dominant inherited form of HYPERTROPHIC CARDIOMYOPATHY. It results from any of more than 50 mutations involving genes encoding contractile proteins such as VENTRICULAR MYOSINS; cardiac TROPONIN T; ALPHA-TROPOMYOSIN.
A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC
A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.
A congenital disorder that is characterized by a triad of capillary malformations (HEMANGIOMA), venous malformations (ARTERIOVENOUS FISTULA), and soft tissue or bony hypertrophy of the limb. This syndrome is caused by mutations in the VG5Q gene which encodes a strong angiogenesis stimulator.
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.
Measurement of intracardiac blood flow using an M-mode and/or two-dimensional (2-D) echocardiogram while simultaneously recording the spectrum of the audible Doppler signal (e.g., velocity, direction, amplitude, intensity, timing) reflected from the moving column of red blood cells.
The condition of an anatomical structure's being constricted beyond normal dimensions.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
Hypertension due to RENAL ARTERY OBSTRUCTION or compression.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
The circulation of blood through the CORONARY VESSELS of the HEART.
A non-fibrillar collagen found primarily in terminally differentiated hypertrophic CHONDROCYTES. It is a homotrimer of three identical alpha1(X) subunits.
A serine threonine kinase that controls a wide range of growth-related cellular processes. The protein is referred to as the target of RAPAMYCIN due to the discovery that SIROLIMUS (commonly known as rapamycin) forms an inhibitory complex with TACROLIMUS BINDING PROTEIN 1A that blocks the action of its enzymatic activity.
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.
Pathological conditions involving the HEART including its structural and functional abnormalities.
Polymorphic cells that form cartilage.
The amount of BLOOD pumped out of the HEART per beat, not to be confused with cardiac output (volume/time). It is calculated as the difference between the end-diastolic volume and the end-systolic volume.
Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.
A subclass of alpha-adrenergic receptors that mediate contraction of SMOOTH MUSCLE in a variety of tissues such as ARTERIOLES; VEINS; and the UTERUS. They are usually found on postsynaptic membranes and signal through GQ-G11 G-PROTEINS.
The innermost layer of the heart, comprised of endothelial cells.
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
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 angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.
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 nonstriated involuntary muscle tissue of blood vessels.
A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.
A substituted phenylaminoethanol that has beta-2 adrenomimetic properties at very low doses. It is used as a bronchodilator in asthma.
A family of ribosomal protein S6 kinases that are considered the major physiological kinases for RIBOSOMAL PROTEIN S6. Unlike RIBOSOMAL PROTEIN S6 KINASES, 90KDa the proteins in this family are sensitive to the inhibitory effects of RAPAMYCIN and contain a single kinase domain. They are referred to as 70kDa proteins, however ALTERNATIVE SPLICING of mRNAs for proteins in this class also results in 85kDa variants being formed.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
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.
A state of subnormal or depressed cardiac output at rest or during stress. It is a characteristic of CARDIOVASCULAR DISEASES, including congenital, valvular, rheumatic, hypertensive, coronary, and cardiomyopathic. The serious form of low cardiac output is characterized by marked reduction in STROKE VOLUME, and systemic vasoconstriction resulting in cold, pale, and sometimes cyanotic extremities.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
A round-to-oval mass of lymphoid tissue embedded in the lateral wall of the PHARYNX. There is one on each side of the oropharynx in the fauces between the anterior and posterior pillars of the SOFT PALATE.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).
Relatively complete absence of oxygen in one or more tissues.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
A purely physical condition which exists within any material because of strain or deformation by external forces or by non-uniform thermal expansion; expressed quantitatively in units of force per unit area.
A well-characterized basic peptide believed to be secreted by the liver and to circulate in the blood. It has growth-regulating, insulin-like, and mitogenic activities. This growth factor has a major, but not absolute, dependence on GROWTH HORMONE. It is believed to be mainly active in adults in contrast to INSULIN-LIKE GROWTH FACTOR II, which is a major fetal growth factor.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.
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.
Examinations used to diagnose and treat heart conditions.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
A glycogen synthase kinase that was originally described as a key enzyme involved in glycogen metabolism. It regulates a diverse array of functions such as CELL DIVISION, microtubule function and APOPTOSIS.
A potent direct-acting peripheral vasodilator (VASODILATOR AGENTS) that reduces peripheral resistance and produces a fall in BLOOD PRESSURE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p371)
The aorta from the DIAPHRAGM to the bifurcation into the right and left common iliac arteries.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
A family of non-enveloped viruses infecting mammals (MASTADENOVIRUS) and birds (AVIADENOVIRUS) or both (ATADENOVIRUS). Infections may be asymptomatic or result in a variety of diseases.
KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.
The volume of the HEART, usually relating to the volume of BLOOD contained within it at various periods of the cardiac cycle. The amount of blood ejected from a ventricle at each beat is STROKE VOLUME.
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.
A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects.
A birth defect characterized by the narrowing of the AORTA that can be of varying degree and at any point from the transverse arch to the iliac bifurcation. Aortic coarctation causes arterial HYPERTENSION before the point of narrowing and arterial HYPOTENSION beyond the narrowed portion.
Increase in constituent cells in the PROSTATE, leading to enlargement of the organ (hypertrophy) and adverse impact on the lower urinary tract function. This can be caused by increased rate of cell proliferation, reduced rate of cell death, or both.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
Agents that antagonize ANGIOTENSIN II TYPE 1 RECEPTOR. Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. Some are used as ANTIHYPERTENSIVE AGENTS.
21-Amino-acid peptides produced by vascular endothelial cells and functioning as potent vasoconstrictors. The endothelin family consists of three members, ENDOTHELIN-1; ENDOTHELIN-2; and ENDOTHELIN-3. All three peptides contain 21 amino acids, but vary in amino acid composition. The three peptides produce vasoconstrictor and pressor responses in various parts of the body. However, the quantitative profiles of the pharmacological activities are considerably different among the three isopeptides.
The hemodynamic and electrophysiological action of the HEART VENTRICLES.
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).
A cardioselective beta-1 adrenergic blocker possessing properties and potency similar to PROPRANOLOL, but without a negative inotropic effect.
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.
The area between the EPIPHYSIS and the DIAPHYSIS within which bone growth occurs.
A steroid metabolite that is the 11-deoxy derivative of CORTICOSTERONE and the 21-hydroxy derivative of PROGESTERONE.
A mitogen-activated protein kinase subfamily that regulates a variety of cellular processes including CELL GROWTH PROCESSES; CELL DIFFERENTIATION; APOPTOSIS; and cellular responses to INFLAMMATION. The P38 MAP kinases are regulated by CYTOKINE RECEPTORS and can be activated in response to bacterial pathogens.
Sodium chloride used in foods.
A hydroxylated form of the imino acid proline. A deficiency in ASCORBIC ACID can result in impaired hydroxyproline formation.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
Activities or games, usually involving physical effort or skill. Reasons for engagement in sports include pleasure, competition, and/or financial reward.
An angiotensin receptor subtype that is expressed at high levels in fetal tissues. Many effects of the angiotensin type 2 receptor such as VASODILATION and sodium loss are the opposite of that of the ANGIOTENSIN TYPE 1 RECEPTOR.
An alpha-globulin of about 453 amino acids, depending on the species. It is produced by the liver and secreted into blood circulation. Angiotensinogen is the inactive precursor of natural angiotensins. Upon successive enzyme cleavages, angiotensinogen yields angiotensin I, II, and III with amino acids numbered at 10, 8, and 7, respectively.
Drugs used to cause constriction of the blood vessels.
A condition in which HEART VENTRICLES exhibit impaired function.
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
A sport in which weights are lifted competitively or as an exercise.
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.
Surgical removal of a tonsil or tonsils. (Dorland, 28th ed)
The veins and arteries of the HEART.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
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.
Proteins to which calcium ions are bound. They can act as transport proteins, regulator proteins, or activator proteins. They typically contain EF HAND MOTIFS.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
The hemodynamic and electrophysiological action of the right HEART VENTRICLE.
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.
Excision of the adenoids. (Dorland, 28th ed)
A subtype of transforming growth factor beta that is synthesized by a wide variety of cells. It is synthesized as a precursor molecule that is cleaved to form mature TGF-beta 1 and TGF-beta1 latency-associated peptide. The association of the cleavage products results in the formation a latent protein which must be activated to bind its receptor. Defects in the gene that encodes TGF-beta1 are the cause of CAMURATI-ENGELMANN SYNDROME.
An angiotensin-converting enzyme inhibitor. It is used in patients with hypertension and heart failure.
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)
Cell surface proteins that bind ENDOTHELINS with high affinity and trigger intracellular changes which influence the behavior of cells.
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.
Cation-transporting proteins that utilize the energy of ATP hydrolysis for the transport of CALCIUM. They differ from CALCIUM CHANNELS which allow calcium to pass through a membrane without the use of energy.
The mitochondria of the myocardium.
A polynucleotide consisting essentially of chains with a repeating backbone of phosphate and ribose units to which nitrogenous bases are attached. RNA is unique among biological macromolecules in that it can encode genetic information, serve as an abundant structural component of cells, and also possesses catalytic activity. (Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
A flavoprotein enzyme that catalyzes the univalent reduction of OXYGEN using NADPH as an electron donor to create SUPEROXIDE ANION. The enzyme is dependent on a variety of CYTOCHROMES. Defects in the production of superoxide ions by enzymes such as NADPH oxidase result in GRANULOMATOUS DISEASE, CHRONIC.
Inflammation of the tonsils, especially the PALATINE TONSILS but the ADENOIDS (pharyngeal tonsils) and lingual tonsils may also be involved. Tonsillitis usually is caused by bacterial infection. Tonsillitis may be acute, chronic, or recurrent.
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 .
Cell surface proteins that bind ATRIAL NATRIURETIC FACTOR with high affinity and trigger intracellular changes influencing the behavior of cells. They contain intrinsic guanylyl cyclase activity.

Central peptidergic neurons are hyperactive during collateral sprouting and inhibition of activity suppresses sprouting. (1/2412)

Little is known regarding the effect of chronic changes in neuronal activity on the extent of collateral sprouting by identified CNS neurons. We have investigated the relationship between activity and sprouting in oxytocin (OT) and vasopressin (VP) neurons of the hypothalamic magnocellular neurosecretory system (MNS). Uninjured MNS neurons undergo a robust collateral-sprouting response that restores the axon population of the neural lobe (NL) after a lesion of the contralateral MNS (). Simultaneously, lesioned rats develop chronic urinary hyperosmolality indicative of heightened neurosecretory activity. We therefore tested the hypothesis that sprouting MNS neurons are hyperactive by measuring changes in cell and nuclear diameters, OT and VP mRNA pools, and axonal cytochrome oxidase activity (COX). Each of these measures was significantly elevated during the period of most rapid axonal growth between 1 and 4 weeks after the lesion, confirming that both OT and VP neurons are hyperactive while undergoing collateral sprouting. In a second study the hypothesis that chronic inhibition of neuronal activity would interfere with the sprouting response was tested. Chronic hyponatremia (CH) was induced 3 d before the hypothalamic lesion and sustained for 4 weeks to suppress neurosecretory activity. CH abolished the lesion-induced increases in OT and VP mRNA pools and virtually eliminated measurable COX activity in MNS terminals. Counts of the total number of axon profiles in the NL revealed that CH also prevented axonal sprouting from occurring. These results are consistent with the hypothesis that increased neuronal activity is required for denervation-induced collateral sprouting to occur in the MNS.  (+info)

Measurement of serum TSH in the investigation of patients presenting with thyroid enlargement. (2/2412)

In otherwise euthyroid patients presenting with thyroid enlargement, reduction in serum thyrotrophin (TSH) concentrations measured in a sensitive assay may be a marker of thyroid autonomy and may therefore indicate a benign underlying pathology. We investigated prospectively a cohort of 467 subjects presenting consecutively to our thyroid clinic with nodular or diffuse enlargement of the thyroid. Subjects were divided into those with normal (0.4-5.5 mU/l), low but detectable (0.1-0.39 mU/l) or undetectable (< 0.1 mU/l) serum TSH concentrations. The final pathological diagnosis was defined by fine-needle aspiration cytology and clinical follow-up of at least 2 years or by fine-needle aspiration cytology and histology following surgical treatment. Serum TSH concentrations below normal were found in 75 patients (16.1%), those with low serum TSH results having higher mean free T4 concentrations, were older and were more likely to be female. In those with undetectable serum TSH, no patient had a diagnosis of thyroid neoplasia and in those with low but detectable TSH, thyroid neoplasms were diagnosed in two patients (3.4%). In those with normal serum TSH, 12.0% had a final diagnosis of thyroid neoplasm (p = 0.013). Overall, thyroid malignancy was found in one patient (1.3%) of those with a serum TSH measurement below the normal range and 6.9% of those with normal serum TSH (p < 0.06). Reduction in serum TSH at presentation may identify a group which requires less intensive investigation and follow-up than those without biochemical evidence of thyroid autonomy.  (+info)

Mycophenolate mofetil prevents the progressive renal failure induced by 5/6 renal ablation in rats. (3/2412)

BACKGROUND: Extensive renal ablation is associated with progressive sclerosis of the remnant kidney. Because lymphocytes and monocytes accumulate in the remnant kidney, it is likely that they play a role in the renal scarring. Therefore, we treated rats with 5/6 nephrectomy (5/6Nx) with mycophenolate mofetil (MMF), a drug that has an antiproliferative effect and that suppresses the expression of intercellular adhesion molecules. METHODS: Sprague-Dawley rats with 5/6Nx received MMF (30 mg. kg-1. day-1 by daily gastric gavage, N = 15) or vehicle (N = 16). Ten additional rats were sham operated. All rats were fed a 30% protein diet. Body weight, serum creatinine, and urinary protein excretion were determined weekly. Lipid peroxidation, as a measure of oxidative stress observed by urinary malondialdehyde determinations, was performed every two weeks. Histologic studies were done in the remnant kidney four weeks (9 rats from the vehicle-treated group, 7 rats from the MMF group, and 5 sham-operated rats) and eight weeks after surgery (the remaining rats). Glomerular volume, sclerosis in glomeruli (segmental and global) and interstitium (semiquantitative scale), infiltrating lymphocytes and macrophages (CD43- and ED1-positive cells), and expression of adhesion molecules (CD54, CD18, and CD11b) were analyzed. RESULTS: MMF treatment prevented the progressive increment in serum creatinine and the proteinuria observed in the 5/6 nephrectomized rats during the eight weeks of observation (P < 0.01). Weight gain was comparable in the MMF-treated and sham-operated rats, whereas weight gain was decreased in untreated 5/6 nephrectomized rats. Excretion of malondialdehyde increased after surgery but returned sooner to control levels in the MMF-treated rats. Increments in glomerular size and mean arterial blood pressure induced by renal ablation were not modified by MMF treatment. Eight weeks after surgery, segmental sclerosis was present in 48.4 +/- 8.35% (+/- sd) glomeruli in the vehicle-treated group versus 25 +/- 10.5% in the MMF-treated group (P < 0.001). Interstitial fibrosis was reduced significantly with MMF treatment (P < 0.001). Infiltration with CD43- and ED1-positive cells in glomeruli and interstitium was two to five times lower in MMF-treated rats (P < 0.01). Expression of adhesion molecules CD18 and CD11b was similarly reduced. CONCLUSION: MMF ameliorates the progressive renal damage in the remnant kidney after 5/6Nx. This effect is associated with a reduction in the infiltration of lymphocytes and monocytes, whereas glomerular hypertrophy and systemic hypertension are unchanged.  (+info)

M2 receptors in genito-urinary smooth muscle pathology. (4/2412)

In vitro bladder contractions in response to cumulative carbachol doses were measured in the presence of selective muscarinic antagonists from rats which had their major pelvic ganglion bilaterally removed (denervation, DEN) or from rats in which the spinal cord was injured (SCI) via compression. DEN induced both hypertrophy (505+/-51 mg bladder weight) and a supersensitivity of the bladders to carbachol (EC50=0.7+/-0.1 uM). Some of the SCI rats regained the ability to void spontaneously (SPV). The bladders of these animals weighed 184+/-17 mg, significantly less than the bladders of non voiding rats (NV, 644+/-92 mg). The potency of carbachol was greater in bladder strips from NV SCI animals (EC50=0.54+/-0.1 uM) than either bladder strips from SPV SCI (EC50=0.93+/-0.3 microM), DEN or control (EC50=1.2+/-0.1 microM) animals. Antagonist affinities in control bladders for antagonism of carbachol induced contractions were consistent with M3 mediated contractions. Antagonist affinities in DEN bladders for 4-diphenlacetoxy-N-methylpiperidine methiodide (4-DAMP, 8.5) and para fluoro hexahydrosilodifenidol (p-F-HHSiD, 6.6); were consistent with M2 mediated contractions, although the methoctramine affinity (6.5) was consistent with M3 mediated contractions. p-F-HHSiD inhibited carbachol induced contraction with an affinity consistent with M2 receptors in bladders from NV SCI (pKb=6.4) animals and M3 receptors in bladders from SPV SCI animals (pKb=7.9). Subtype selective immunoprecipitation of muscarinic receptors revealed an increase in total and an increase in M2 receptor density with no change in M3 receptor density in bladders from DEN and NV SCI animals compared to normal or sham operated controls. M3 receptor density was lower in bladders from SPV SCI animals while the M2 receptor density was not different from control. This increase in M2 receptor density is consistent with the change in affinity of the antagonists for inhibition of carbachol induced contractions and may indicate that M2 receptors or a combination of M2 and M3 receptors directly mediate smooth muscle contraction in bladders from DEN and NV SCI rats.  (+info)

Regulation of chondrocyte differentiation by Cbfa1. (5/2412)

Cbfa1, a developmentally expressed transcription factor of the runt family, was recently shown to be essential for osteoblast differentiation. We have investigated the role of Cbfa1 in endochondral bone formation using Cbfa1-deficient mice. Histology and in situ hybridization with probes for indian hedgehog (Ihh), collagen type X and osteopontin performed at E13.5, E14.5 and E17.5 demonstrated a lack of hypertrophic chondrocytes in the anlagen of the humerus and the phalanges and a delayed onset of hypertrophy in radius/ulna in Cbfa1-/- mice. Detailed analysis of Cbfa1 expression using whole mount in situ hybridization and a lacZ reporter gene reveled strong expression not only in osteoblasts but also in pre-hypertrophic and hypertrophic chondrocytes. Our studies identify Cbfa1 as a major positive regulator of chondrocyte differentiation.  (+info)

Effects of an angiotensin-converting enzyme inhibitor and a beta-blocker on cerebral arterioles in rats. (6/2412)

We examined the effects of an angiotensin-converting enzyme inhibitor, perindopril, and a beta-blocker, propranolol, on cerebral arterioles in stroke-prone spontaneously hypertensive rats (SHRSP). The structure and mechanics of cerebral arterioles were examined in untreated Wistar-Kyoto rats (WKY) and SHRSP that were untreated or treated for 3 months with a high (2 mg/kg per day) or a low (0.3 mg/kg per day) dose of perindopril or propranolol (250 mg/kg per day) alone or in combination with the low dose of perindopril. We measured pressure, external diameter, and cross-sectional area of the vessel wall (CSA) in maximally dilated (with EDTA) cerebral arterioles. Treatment of SHRSP with the high dose of perindopril or the combination of propranolol and the low dose of perindopril normalized cerebral arteriolar mean pressure (50+/-1 [mean+/-SEM] and 43+/-2 mm Hg vs 50+/-1 mm Hg in WKY and 94+/-3 mm Hg in untreated SHRSP; P<0.05), pulse pressure (15+/-1 and 16+/-1 mm Hg vs 13+/-1 mm Hg in WKY and 35+/-1 mm Hg in untreated SHRSP; P<0.05), and CSA (1103+/-53 and 1099+/-51 microm2, respectively, vs 1057+/-49 microm2 in WKY and 1281+/-62 microm2 in untreated SHRSP; P<0.05). In contrast, treatment of SHRSP with the low dose of perindopril or propranolol alone did not normalize arteriolar pulse pressure (24+/-1 and 21+/-1 mm Hg) and failed to prevent increases in CSA (1282+/-77 and 1267+/-94 microm2). Treatment with either dose of perindopril or the combination of propranolol and perindopril significantly increased external diameter in cerebral arterioles of SHRSP (99+/-3, 103+/-2, and 98+/-3 microm vs 87+/-2 microm in untreated SHRSP; P<0.05), whereas propranolol alone did not (94+/-3 microm; P>0.05). These findings suggest that effects of angiotensin-converting enzyme inhibitors on cerebral arteriolar hypertrophy in SHRSP may depend primarily on their effects on arterial pressure, particularly pulse pressure, whereas their effects on cerebral arteriolar remodeling (defined as a reduction in external diameter) may be pressure independent.  (+info)

Functional intestinal obstruction due to deficiency of argyrophil neurones in the myenteric plexus. Familial syndrome presenting with short small bowel, malrotation, and pyloric hypertrophy. (7/2412)

In 3 infants functional intestinal obstruction, associated with a short small intestine, malrotation, and pyloric hypertrophy, was shown to be due to failure of development of the argyrophil myenteric plexus, with the absence of ongoing peristalsis. 4 infants with similar clinical features have been described previously, and there is evidence for an autosomal recessive mode of inheritance of this syndrome.  (+info)

Apparent loss and hypertrophy of interneurons in a mouse model of neuronal ceroid lipofuscinosis: evidence for partial response to insulin-like growth factor-1 treatment. (8/2412)

The neuronal ceroid lipofuscinoses (NCL) are progressive neurodegenerative disorders with onset from infancy to adulthood that are manifested by blindness, seizures, and dementia. In NCL, lysosomes accumulate autofluorescent proteolipid in the brain and other tissues. The mnd/mnd mutant mouse was first characterized as exhibiting adult-onset upper and lower motor neuron degeneration, but closer examination revealed early, widespread pathology similar to that seen in NCL. We used the autofluorescent properties of accumulated storage material to map which CNS neuronal populations in the mnd/mnd mouse show NCL-like pathological changes. Pronounced, early accumulation of autofluorescent lipopigment was found in subpopulations of GABAergic neurons, including interneurons in the cortex and hippocampus. Staining for phenotypic markers normally present in these neurons revealed progressive loss of staining in the cortex and hippocampus of mnd/mnd mice, with pronounced hypertrophy of remaining detectable interneurons. In contrast, even in aged mutant mice, many hippocampal interneurons retained staining for glutamic acid decarboxylase. Treatment with insulin-like growth factor-1 partially restored interneuronal number and reduced hypertrophy in some subregions. These results provide the first evidence for the involvement of interneurons in a mouse model of NCL. Moreover, our findings suggest that at least some populations of these neurons persist in a growth factor-responsive state.  (+info)

TY - JOUR. T1 - Role of mammalian target of rapamycin signaling in compensatory renal hypertrophy. AU - Chen, Jiankang. AU - Chen, Jianchun. AU - Neilson, Eric G.. AU - Harris, Raymond C.. PY - 2005/12/9. Y1 - 2005/12/9. N2 - Loss of functioning nephrons stimulates the growth of residual kidney tissue to augment work capacity and maintain normal renal function. This growth largely occurs by hypertrophy rather than from hyperplasia of the remaining nephrons. The signaling mechanisms that increase RNA and protein synthesis during compensatory renal hypertrophy are unknown. This study found that the remaining kidney hypertrophied 42% by 16 d after unilateral nephrectomy (UNX) in DBA/2 mice. Immunoblotting analysis revealed increased phosphorylation of the 40S ribosomal protein S6 (rpS6) and the eukaryotic translation initiation factor (eIF) 4E-binding protein 1 (4E-BP1), the two downstream effectors of the mammalian target of rapamycin (mTOR). The highly specific mTOR inhibitor rapamycin blocked ...
TY - JOUR. T1 - Thromboxane A2 stimulates vascular smooth muscle hypertrophy by up- regulating the synthesis and release of endogenous basic fibroblast growth factor. AU - Ali, S.. AU - Davis, M. G.. AU - Becker, M. W.. AU - Dorn, G. W.. PY - 1993. Y1 - 1993. N2 - We have shown previously that thromboxane A2 stimulates hypertrophy of cultured rat aortic smooth muscle cells defined as protooncogene expression and protein synthesis without DNA synthesis or cellular proliferation (Dorn, G. W., II, Becker, M. W., Davis, M. G. (1992) J. Biol. Chem. 267, 24897- 24905). Since endogenous growth modulators could possibly regulate vascular smooth muscle growth to this vasoconstrictor, we tested the hypothesis that thromboxane-stimulated vascular smooth muscle hypertrophy was due to increased expression of endogenously produced basic fibroblast growth factor (bFGF). The thromboxane mimetic (15S)-hydroxy-11α,9α-(epoxymethano)prosta- 5Z,13E-dienoic acid (U46619) (1 μM) increased cultured rat aorta derived ...
Introduction: The calcium/calmodulin-dependent kinase II (CaMKII) is activated by angiotensin-II, a strong inducer of vascular smooth muscle cell (VSM) hypertrophy. CaMKII activates HDAC4/MEF-2 dependent gene transcription by phosphorylation of HDAC4 S467 and 632. Here, we demonstrate that CaMKII mediates Ang-II-induced VSM hypertrophy in vitro and in vivo by activation of the HDAC4/MEF-2 signal transduction pathway.. Methods and Results: Medial hypertrophy by Ang-II infusion at pressor dose over 10 days was significantly reduced in C57Bl/6 mice when the CaMKII inhibitor KN93 was given daily i.p. (0.070 mm2 vs 0.052 mm2, p,0.05). In vitro, Ang-II increased the 3H-Leucine/3H-Thymidine uptake in control aortic VSM cells by 50% after 24 hr, whereas overexpression of the CaMKII peptide inhibitor CaMKIIN resulted only in 14 % increase (p,0.05). Ang-II induced phosphorylation of HDAC4 that was further increased under overexpression of CaMKIIδ2. CaMKII overexpression resulted in increased ...
It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic si...gnal. ...
Vascular smooth muscle cell hypertrophy is a normal compensatory state that may play a pathogenic role in hypertension. Angiotensin II stimulates a hypertrophic response in cultured vascular smooth muscle cells. As part of the growth response, angiotensin II rapidly activates the Na(+)-H+ exchanger, increasing Na+ influx. Because Na+, K(+)-ATPase is the major cellular mechanism for regulating intracellular Na+, we studied the effects of angiotensin II-induced hypertrophy on Na+, K(+)-ATPase expression and activity. Angiotensin II caused rapid increases in both steady-state Na+, K(+)-ATPase activity (ouabain-sensitive 86Rb uptake) and intracellular [Na+]. Angiotensin II also caused a sustained increase in Na+, K(+)-ATPase at 24 hours with a 73% increase in maximal 86Rb uptake per milligram protein and a fourfold increase in Na+, K(+)-ATPase alpha-1 messenger RNA levels. Thus, angiotensin II hypertrophy was associated with rapid increases in Na+, K(+)-ATPase activity due to increased Na+ entry and ...
The fact that isobaric compliance and distensibility of the radial artery were either unchanged or increased in hypertensive patients21 22 may appear surprising because several studies have demonstrated that sustained hypertension decreases large artery distensibility and compliance. This has been reported for pressure-dimension experiments as well as ring and strip studies of human and animal large arteries both in vivo and in vitro.11 12 24 25 26 Thus, in contrast to large arteries our findings suggest a normal distensibility at the site of medium-sized arteries during sustained hypertension, despite hypertrophy of the arterial wall. A likely explanation for the difference in our findings and those of previous studies is that the arteries examined in these studies were of different sizes. Composition of the arterial wall varies with vessel size,27 and the effect of hypertension on conduit arteries may vary with vessel caliber. For instance, previous studies on forearm arterial distensibility ...
The streptozotocin-induced diabetic rat is a model of mesenteric vascular hypertrophy without physical damage to the vessels; at a cellular level, the hypertrophy is due to both increased smooth muscle cell mass and ECM. We have used this model to demonstrate that the development of the vascular hypertrophy is preceded by activation of NHE in the vascular smooth muscle and that the administration of an inhibitor of NHE activity, cariporide, prevents the development of the hypertrophy. It is important to appreciate that the vascular changes observed in this model do not represent atherosclerosis but may be important as early manifestations of diabetes-associated vascular disease.. In this study, as a prelude to the investigation of NHE activity in the hypertrophying vessels, we confirmed the time course of the development of mesenteric hypertrophy after streptozotocin administration to adult rats. We observed no increase in mesenteric weight by 1 week but a 56% increase at 3 weeks after ...
TY - JOUR. T1 - Evidence-Based Resistance Training Recommendations for Muscular Hypertrophy. AU - Fisher, James. AU - Steele, James. AU - Smith, Dave. PY - 2013. Y1 - 2013. M3 - Article. VL - 17. SP - 217. EP - 235. JO - Medicina Sportiva. JF - Medicina Sportiva. IS - 4. ER - ...
Muscle Hypertrophy is the increase in the size of muscle cells. Hypertrophy for a bodybuilder or general gym goer is the prime goal in the majority of cases, so must be understood properly if you are to achieve it. There are different types of hypertrophy, different ways of achieving it and they will all have different effects on the body. The 2 forms of muscle hypertrophy are myofibrillar hypertrophy and sarcoplasmic hypertrophy. Myofibrillar hypertrophy is the increase in number of the contractile proteins actin and myosin. These proteins join onto the myofibrils (the chains in a muscle cell) and increase the size of the muscle as well as improving the strength of the contraction. Myofibrillar hypertrophy increases strength as well as size. Sarcoplasmic hypertrophy is the increase in volume of sarcoplasmic fluid in the muscle cell. This increase in fluid greatly increases the size of the muscle but doesnt affect strength. The effect on strength that these 2 forms of hypertrophy have shows why a 90kg
050120 Muscular hypertrophy by Daniel Pare CSO, NCCP Daniel Pare CSO, NCCP, prominent strength coach and owner of the St. Thomas Strength and Athletics gym located in St. Thomas, Canada very clearly explains the differences. My appreciation goes out to Daniel for the information he presents in the following paragraphs. Danny Strength training has become…
ALDAI ELKORO-IRIBE, Noelia (2006) Beef fatty acid profile depending on breed and muscular hypertrophy genotype. PhD thesis, UPV/EHU.. Texto completo no está disponible desde este repositorio ...
Im about 2-3 weeks ahead of schedule this year over last in my off-season lifting. I just finished week one of the muscular hypertrophy phase. Im pretty much using the same 1 RM from last year, although I adjusted the squat weights for a 0 pound bar on the Smith Machine. Every time I go to the gym, the free weight bars are in use by somebody - so I am doing the squats on the Smith this season (unless I walk in and find the free weights and rack available which usually never happens ...
Vaughan, M K.; Benson, B; Norris, J T.; and Vaughan, G M., Inhibition of compensatory ovarian hypertrophy in mice by melatonin, 5-hydroxytryptamine and pineal powder. (1971). Subject Strain Bibliography 1971. 573 ...
Endogenous norepinephrine exerts growth factor-like activity, through α1A-ARs on medial SMCs and α1B-ARs on adventitial fibroblasts, that contributes to wall hypertrophy and restenosis of balloon-injured rat aorta and carotid.6,7,10 This adrenergic trophic activity has been confirmed in carotid arteries of mice with genetic deletion of either catecholamine synthesis or α1-AR subtypes.9 Prolonged elevation of wall norepinephrine also causes hypertrophy of uninjured arteries.10,11 Catecholamine-induced growth of medial SMCs and adventitial fibroblasts requires generation of NAD(P)H oxidase-dependent ROS.12 The present study identified additional steps in this pathway in rat aorta studied ex vivo. In media, these steps consist of ROS generation, followed by HB-EGF shedding, EGFR activation, and ERK1/2 activation (online Figure 1 in the online data supplement provides a model of the pathway in SMCs). This trophic pathway differs from that described in cell culture for angiotensin, thrombin, and ...
What are the functions of mTOR? Can mTOR activation lead to hypertrophy? Are there situations where mTOR activation does not lead to gains?
en] Two-dimensional electrophoresis was used to investigate the effects of a QTL for muscle hypertrophy on sarcoplasmic protein expression in ovine muscles. In the Belgian Texel breed, the QTL for muscle hypertrophy is localized in the myostatin-encoding gene. Based on microsatellite markers flanking the myostatin gene, we compared the hypertrophied genotype with the normal genotype. The average age of the sheep was 3 mo. Among the 4 muscles studied, in the hypertrophied genotype only the vastus medialis was normal, whereas the semimembranosus, tensor fasciae latae, and LM were hypertrophied. In the hypertrophied genotype, these muscles showed upregulation of enzymes involved in glycolytic metabolism together with oxidative metabolism in LM. Certain chaperone proteins, including glutathione S-transferase-Pi, heat shock protein-27, and heat shock cognate-70, were also more highly expressed, probably due to increased use of energetic pathways. Expression of the iron transport protein transferrin ...
Muscle Hypertrophy is essentially the increase in size and growth of muscle cells. I like to think of this like a callus. The harder you rub down on your skin, the thicker the callus forms. There are two main components for muscle hypertrophy, the stimulation and the repair of muscle cells. First, when we lift weights, we are stimulating a contraction in our muscles. This contraction is what causes tiny micro tears in our muscle fibers. As we continue to workout, those muscle fibers continue to
OBJECTIVES: The consequences of breast hypertrophy have been described based on the alteration of body mass distribution, leading to an impact on psychological and physical aspects. The principles of motor control suggest that breast hypertrophy can lead to sensorimotor alterations and the impairment of body balance due to postural misalignment. The aim of this study is to evaluate the postural control of women with breast hypertrophy under different sensory information conditions. METHOD: This cross-sectional study included 14 women with breast hypertrophy and 14 without breast hypertrophy, and the mean ages of the groups were 39 ±15 years and 39±16 years, respectively. A force platform was used to assess the sensory systems that contribute to postural control: somatosensory, visual and vestibular. Four postural conditions were sequentially tested: eyes open and fixed platform, eyes closed and fixed platform, eyes open and mobile platform, and eyes closed and mobile platform. The data were ...
There are two types of hypertrophy: sarcoplasmic and myofibrillar.. Sarcoplasmic hypertrophy (i.e., an increase in the volume of sarcoplasmic fluid inside the muscle cell) is more likely to build muscle thickness. This is often referred to as training for size.. Thats in contrast to training for strength, the goal of which is to achieve myofibrillar hypertrophy. This type of hypertrophy involves the growth of muscle fibers.. Hypertrophy training for size typically uses higher rep ranges with a lower weight. This is a training style associated with bodybuilders.. The goal is to get in a good amount of volume before you hit muscle exhaustion. In practice, that may mean using a weight that feels challenging but not exhausting for 12-15 reps for 3-6 sets.. When you increase the load and the number of sets you perform, you are asking the muscle tissue to rebuild bigger and stronger to accommodate for the increased demands, explains Cody Braun, CPT, Assistant Manager of Fitness at ...
The science of muscle hypertrophy can be pretty complex. But in this article we break down the research to tell you in simple terms. Find out more here...
Skeletal muscle mass is a result of the balance between protein breakdown and protein synthesis. It has been shown that multiple conditions of muscle atrophy are characterized by the common regulation of a specific set of genes, termed atrogenes. It is not known whether various models of muscle hypertrophy are similarly regulated by a common transcriptional program. Here, we characterized gene expression changes in 3 different conditions of muscle growth, examining each condition during acute and chronic phases. Specifically, we compared the transcriptome of Extensor Digitorum Longus (EDL) muscles collected 1) during the rapid phase of postnatal growth at 2 and 4 weeks of age 2) 24 hours or three weeks after constitutive activation of AKT, and 3) 24 hours or three weeks after overload hypertrophy caused by tenotomy of the Tibialis Anterior muscle. We observed an important overlap between significantly regulated genes when comparing each single condition at the two different timepoints. Furthermore,
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in Genome Research (2010), 20(12), 1651-62. The callipyge phenotype is a monogenic muscular hypertrophy that is only expressed in heterozygous sheep receiving the CLPG mutation from their sire. The wild-type phenotype of CLPG/CLPG animals is ... [more ▼]. The callipyge phenotype is a monogenic muscular hypertrophy that is only expressed in heterozygous sheep receiving the CLPG mutation from their sire. The wild-type phenotype of CLPG/CLPG animals is thought to result from translational inhibition of paternally expressed DLK1 transcripts by maternally expressed miRNAs. To identify the miRNA responsible for this trans effect, we used high-throughput sequencing to exhaustively catalog miRNAs expressed in skeletal muscle of sheep of the four CLPG genotypes. We have identified 747 miRNA species of which 110 map to the DLK1-GTL2 or callipyge domain. We demonstrate that the latter are imprinted and preferentially expressed from the maternal allele. We show that the CLPG mutation affects their level ...
Urgency. Changes in the right ventricle (RV) under hypertrophic cardiomyopathy (HCVP) are understudied. Aim. To study the condition of RV in this disease. Materials and methods. 86 patients with different forms and variants of HCVP including 69 patients with non-obstructive form of the disease (HNCVP) were evaluated using echoCG. The RV condition was studied by measuring the cavity dimensions and the systolic and diastolic thickness of the anterior wall with estimation of additional parameters reflecting the local diastolic and systolic function. Results. Predominant hypertrophy of the RV anterior wall was found in HCVP including the non-obstructive form. These changes were observed in almost 50% of patients. Anterior wall hypertrophy was associated with disorders of the wall diastolic function. The RV changes were detected primarily in the presence of more advanced and pronounced LV hypertrophy, especially in the apical region ...
Resistance training doesnt play an important role in increasing the muscle fiber numbers. However, it plays an essential role in increasing the cross-sectional area. The levels of hypertrophy can be different in a person based on their age and sex.. The way someones body reacts to a particular exercise is completely different from others. It is often found that a way that helped someone in increasing muscle strength in a person couldnt help others in the same way. So, you must keep all the elements in your mind before you start taking any type of fibers.. The supplements that people take nowadays also play an important role in affecting the muscle hypertrophy. Therefore, you must choose the supplements very careful because wrong supplements damage your muscles badly. You must figure out that what type of exercise, fibers, and supplements are perfect for your body according to your age and sex. ...
Cardiac hypertrophy is a thickening of the heart muscle - characterized by increased cell size rather than number - in response to conditions such as high blood pressure and coronary heart disease, which results in a decrease in size of the chambers of the heart, including the left and right ventricles. Since hypertrophy is associated with heart failure, irregular heart rhythms and an increased risk of angina and heart attack, understanding the mechanisms underlying this abnormal thickening is of great importance. Scientists at the Babraham Institute have now identified a new signalling process in the heart which contributes to cardiac hypertrophy. Rhythmical Ca2+ increases are fundamental to contraction of the heart muscle, but elevated Ca2+ levels also regulate the gene transcription that leads to hypertrophy. The Babraham team found that it is localised increases in Ca2+ concentrations in the cell nucleus that activate the genes responsible for hypertrophy. These nuclear Ca2+ signals, which ...
Gqα signaling continues to be implicated in cardiac hypertrophy. the improved production of superoxide anion NAD(P)H oxidase activity improved manifestation of Gqα phospholipase C (PLC)β1 insulin like growth element-1 receptor (IGF-1R) and epidermal growth element receptor (EGFR) proteins in VSMC from SHR. In addition the enhanced phosphorylation of c-Src PKCδ-Tyr311 IGF-1R EGFR and ERK1/2 exhibited by VSMC from SHR was also attenuated by rottlerin. These results suggest that VSMC from SHR show enhanced activity of PKCδ and that HA14-1 PKCδ is the upstream molecule of reactive oxygen varieties (ROS) and contributes to the enhanced manifestation of Gqα and PLCβ1 proteins and resultant VSMC hypertrophy including c-Src growth element receptor transactivation and MAP kinase signaling. Intro Essential hypertension is definitely associated with vascular redesigning characterized by enhanced press to lumen percentage in arteries [1] and is due to IL12RB2 increased vascular clean muscle mass ...
The term myocardial hypertrophy, say the working group, lacks precision. In cell biology the term hypertrophy describes growth via cell enlargement as opposed to growth by cell division, where hyperplasia is the correct term. Currently in cardiology the term hypertrophy is commonly applied to the situation in the whole heart where myocardial enlargement is accompanied by both hypertrophy and hyperplasia. In addition the term hypertrophy does not take account of the fact that non myocytes in the heart are not passive bystanders and also change in number when the heart remodels. Additionally there may be an invasion of inflammatory cells into the heart, and angiogenesis may occur.. The advantage of the term cardiac remodelling is that it simply defines reorganisation of the different cardiac tissue components, and can be used to describe an increase, or decrease in the size of the left ventricle, as well as a change to the cellular components, explained the first author of the paper, Ralph ...
A recent study looking at fiber type conversions during muscle hypertrophy may have uncovered a possible mechanism for this phenomenon. For
Fisher, James. (2012). Beware the Meta-Analysis: Is Multiple Set Training Really Better than Single-Set Training for Muscle Hypertrophy? Journal of Exercise Physiology Online, December 2012, 15 (6), pp. 23-30 ...
Download Science and Development of Muscle Hypertrophy, 2nd Edition Torrent for free, Direct Downloads via Magnet Link and FREE Movies Online to Watch Also available, Hash : F9A197DEB8EE1047A38055EE589EA3282B66FC11.
There is a But, when youre not doing this program, feel free to use varying rep ranges if you feel you can handle it. Hypertrophy vs Strength Training: Sets, Reps and Rest Intervals. No muscle group should be trained twice in the same three days. Hypertrophy in strength training is both a natural and sought out characteristic of strength training. Figure 2: Specificity requirements for hypertrophy But these additional days will not look the same as your primary training days - far from it. And by heavy, Im talking about sets of somewhere between 1 and 8 reps. Training for hypertrophy, on the other hand, can involve a variety of loads, ranging from light to medium to heavy. The 5 x 5 program could also be considered a full-body workout program to a degree, since you work almost all the major muscle groups with the three exercises you choose. Breaking Down The Total Package. HST is also known to create fast strength gains so this is an added bonus. A good program for that is the Texas Method ...
The word toned has gotten a bad rep which I dont think is fully warranted. Toned accurately describes the look some people are going for, and training for hypertrophy is an important strategy toward that goal. Tone is an actual term. Resting muscle tone, also called tonus, is a state of partial contraction that is characteristic of normal muscle, maintained at least in part by a continuous bombardment of motor impulses originating reflexly, and serves to maintain body posture.4. Good posture is not only the starting point for strength, it is a starting point for developing a toned appearance from hypertrophy training. The stronger you are, the better tone your muscles can hold.. Hypertrophy training also builds up tendons, ligaments, and small stabilizer muscles and allow you to address specific muscle groups more directly. Tendons and ligaments adapt more slowly than muscles (which is why joint issues are often a concern in heavy lifting). Lighter hypertrophy training gives your joints and ...
Hypertrophy - What is element hypertrophy? Hypertropphy. Just means that something is increased in size. For example lots of weight lifting leads to muscle hypertrophy.
Hypertrophy is the process of muscle tissue growth and it can occur in two ways known as sarcoplasmic and myofibrillar hypertrophy which are very different.
Dive into the basics of hypertrophy vs. strength. We explain the differences of each, and how aiming for either hypertrophy or strength will impact your training.
For myself, a shake work best because liquid is absorbed faster and can be guzzled down as you walk out the gym doors. Once again nutrition is a critical component of results.. Hypertrophy also emphasizes the importance of recovery and the common idea of training different body parts on different days in order to experience hypertrophy in the designated areas.. Stereotypes would say that men embrace the gain while women fear the bulk. The truth is that the benefits of strength training for both genders are vital to our neuromuscular, cardiovascular, and skeletal systems.. Whether or not hypertrophy is the goal, lifting weights is a highly recommended component of an exercise program.. The Lifestyle of the FIT and Healthy includes strength training and in turn when we LIFT ourselves up through better health, we influence the lives of others to do the same.. Megan Johnson McCullough is an NASM Master Trainer and Instructor who owns a fitness studio in Oceanside CA called Every BODYs Fit. She ...
Overtraining is probably the most ignored factor by exercise enthusiasts. In order to build muscle, the body has to receive a stimulus ‑‑ a reason ‑‑ to grow bigger, or hypertrophy. Its really very simple: the body only does what it needs to do ‑‑ what it is required to do. It isnt going to suddenly expand its muscle mass because it anticipates needing more muscles. But if it is challenged to move weights around, it will respond by growing. Another way to look at it is if you take ANY body-builder and put him in bed for weeks at a time, hell begin to rapidly lose muscle mass ‑‑ because the body will sense it doesnt need the extra muscle any more! So, one needs to deliver the STIMULUS to stimulate muscular hypertrophy (growth) in the body ‑‑ and thats what lifting weights does. BUT - overdoing that, overtraining, overstresses the body and initiates the process of actually breaking down muscle mass as the body begins to burn its own muscles to use for fuel! This is why so ...
Overtraining is probably the most ignored factor by exercise enthusiasts. In order to build muscle, the body has to receive a stimulus ‑‑ a reason ‑‑ to grow bigger, or hypertrophy. Its really very simple: the body only does what it needs to do ‑‑ what it is required to do. It isnt going to suddenly expand its muscle mass because it anticipates needing more muscles. But if it is challenged to move weights around, it will respond by growing. Another way to look at it is if you take ANY body-builder and put him in bed for weeks at a time, hell begin to rapidly lose muscle mass ‑‑ because the body will sense it doesnt need the extra muscle any more! So, one needs to deliver the STIMULUS to stimulate muscular hypertrophy (growth) in the body ‑‑ and thats what lifting weights does. BUT - overdoing that, overtraining, overstresses the body and initiates the process of actually breaking down muscle mass as the body begins to burn its own muscles to use for fuel! This is why so ...
While much of the hypertrophy signaling cascade has been identified, the initiating, resistance exercise-induced and hypertrophy-stimulating stimuli have remained elusive. For the purpose of this review, we define an initiating, resistance exercise-induced and hypertrophy-stimulating signal as hypertrophy stimulus, and the sensor of such a signal as hypertrophy sensor ...
As the leading cause of mortality in the United States, heart failure (HF) represents a disease state affected by a complex interplay between genetic, physiological, and environmental factors. Understanding the molecular mechanisms underlying the progression from normal cardiac function to ventricular dysfunction and overt HF will facilitate the identification of new therapeutic targets. Specifics of the underlying ultrastructural and molecular determinants of the progression to ventricular dysfunction and HF are still incompletely elucidated. The early adaptive response to increasing myocardial load and functional demand is characterized by cell hypertrophy and angiogenesis before pathological hypertrophy develops. A balance between compensatory hypertrophy and apoptotic pathways exists in the early stages of ventricular dysfunction, whereas upregulation of apoptotic pathways leading to myocyte damage and apoptosis as well as subsequent myocardial fibrosis is indicative of the progression to ...
Memory is a process in which information is encoded, stored, and retrieved. For vertebrates, the modern view has been that it occurs only in the brain. This review describes a cellular memory in skeletal muscle in which hypertrophy is remembered such that a fibre that has previously .... ...
Pik3ip1 silencing-induced cardiomyocyte hypertrophy is dependent on PI3K activity.NRCMs were transfected with siNegative and siPik3ip1 for 24 h and subsequently
Fingerprint Dive into the research topics of S6 kinase 1 knockout inhibits uninephrectomy- or diabetes-induced renal hypertrophy. Together they form a unique fingerprint. ...
When it comes to the intention of progressive overload, training for Strength and for Hypertrophy are two different avenues which can lend into one another: Hypertrophy Training to target and overload specific areas and muscle groups. Strength Lifting an object from point A to point B and building this up to the heaviest weight possible…
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Quickly learn the science behind muscle hypertrophy and how to achieve maximum growth through strategic strength training and supplementation
In neo formed myotubes, RSV looks to maintain hypertrophy procedure, rising myotubes size and regulating nuclei arrangement. Importantly, the current in vitro finding might have a probable impact in in vivo Inhibitors,Modulators,Libraries regulation of protein metab olism. In actual fact, provided RSV action on MRFs and muscle precise skeletal proteins synthesis joined to the control of AMPK, IGF 1 R, AKT and ERK proteins, we may speculate a hypothetical clinical use of this organic polyphenol in situations of muscle mass harm hypo trophy. To accomplish this aim it is actually crucial to more clarify the connection amongst used RSV doses and ob served results. Actually, many authors indicated that RSV, utilized in other various doses, displays controversial anti irritation and insulin resistance results.. Conclusions In summary, our data demonstrate that Resveratrol could control proliferation, start selleck inhibitor myogenesis procedure and induce hypertrophy. RSV appears to be ready to manage ...
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Myostatin-related muscle hypertrophy (or myotonic hypertrophy) is a rare genetic condition characterized by reduced body fat and increased skeletal muscle size. Affected individuals have up to twice the usual amount of muscle mass in their bodies. They also tend to have increased muscle strength. Myostatin-related muscle hypertrophy is not known to cause medical problems, and affected individuals are intellectually normal. The prevalence of this condition is unknown. Mutations in the MSTN gene cause myostatin-related muscle hypertrophy. The MSTN gene provides instructions for making a protein called myostatin, which is active in muscles used for movement (skeletal muscles) both before and after birth. This protein normally restrains muscle growth, ensuring that muscles do not grow too large. Mutations that reduce the production of functional myostatin lead to an overgrowth of muscle tissue. Myostatin-related muscle hypertrophy has a pattern of inheritance known as incomplete autosomal dominance. ...
Heat shock protein 60 (HSP60) is a mitochondrial chaperone. Advanced glycation end products (AGEs) have been shown to interfere with the β-cell function. We hypothesized that AGEs induced β-cell hypertrophy and dysfunction through a HSP60 dysregulation pathway during the stage of islet/β-cell hypertrophy of type-2-diabetes. We investigated the role of HSP60 in AGEs-induced β-cell hypertrophy and dysfunction using the models of diabetic mice and cultured β-cells. Hypertrophy, increased levels of p27Kip1, AGEs, and receptor for AGEs (RAGE), and decreased levels of HSP60, insulin, and ATP content were obviously observed in pancreatic islets of 12-week-old db/db diabetic mice. Low-concentration AGEs significantly induced the cell hypertrophy, increased the p27Kip1 expression, and decreased the HSP60 expression, insulin secretion, and ATP content in cultured β-cells, which could be reversed by RAGE neutralizing antibody. HSP60 overexpression significantly reversed AGEs-induced hypertrophy, ...
Enlarged adenoids can become nearly the size of a ping pong ball and completely block airflow through the nasal passages. Even if enlarged adenoids are not substantial enough to physically block the back of the nose, they can obstruct airflow enough so that nasal breathing requires an uncomfortable amount of work, and inhalation occurs instead through mouth breathing. Adenoids can also obstruct the nasal airway enough to affect the voice without actually stopping nasal airflow altogether.[1] Nasal blockage is determined by at least two factors: 1) the size of the adenoids, and 2) the size of the nasal pharynx passageway. The adenoid usually reaches its greatest size by about age 5 years or so, and then fades away (atrophies) by late childhood - generally by the age of 7 years. The lymphoid tissue remains under the mucosa of the nasopharynx, and could be seen under a microscope if the area was biopsied, but the mass is so reduced in size that the roof of the nasopharynx becomes flat rather than ...
During longitudinal development of the long bone cartilage, periarticular chondrocyte differentiation, which adds cells to the columnar region, is followed by chondrocyte hypertrophy, which reduces cells in the columnar region. Therefore, the length of the columnar chondrocyte region is determined by three parameters: the pace of periarticular chondrocyte differentiation, the pace of chondrocyte hypertrophy and the rate of columnar chondrocyte proliferation (Fig. 7). As upregulated Ihh signaling promotes periarticular chondrocyte differentiation and increases the rate of columnar chondrocyte proliferation (Kobayashi et al., 2005b), the proliferating columnar chondrocyte region would be increased if chondrocyte hypertrophy were not altered. Our observation that the columnar chondrocyte region was shorter in the PTHrP-/-;Ptch1c/-; Col2a1-Cre double mutant than in the PTHrP-/- single mutant (Fig. 2B, Fig. 3A) demonstrates that Hh signaling also acts to promote chondrocyte hypertrophy in the absence ...
Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your hearts main pumping chamber (left ventricle).. Left ventricular hypertrophy can develop in response to some factor - such as high blood pressure or a heart condition - that causes the left ventricle to work harder. As the workload increases, the muscle tissue in the chamber wall thickens, and sometimes the size of the chamber itself also increases. The enlarged heart muscle loses elasticity and eventually may fail to pump with as much force as needed.. Left ventricular hypertrophy is more common in people who have uncontrolled high blood pressure. But no matter what your blood pressure is, developing left ventricular hypertrophy puts you at higher risk for a heart attack and stroke.. Treating high blood pressure can help ease your symptoms and may reverse left ventricular hypertrophy.. Left ventricular hypertrophy usually develops gradually. You may experience no signs or symptoms, especially during ...
After reduction mammaplasty, patients typically experience soreness, swelling and bruising for several days. Bandages are removed after 2 days, and replaced with a surgical bra. Physical activity should be limited for 1 to 2 weeks, while exercise and other strenuous activity should be avoided for at least 4 weeks. Stitches are removed after 2 to 3 weeks, at which point most patients return to work and other regular activities.. The results of reduction mammaplasty are noticeable immediately after surgery. As swelling and bruising subside, the breasts appearance improves. Scars fade with time, and usually cannot be seen when a patient wears a bathing suit or low-cut top.. ...
Skeletal muscle exhibits remarkable plasticity in its ability to modulate its mass in response to the physiologic changes associated with functional use, systemic disease, and aging. Although a gradual loss of muscle mass normally occurs with advancing age, its increasingly rapid progression results in sarcopenia in a subset of individuals. The identities of muscle-enriched, long noncoding RNAs that regulate this process are unknown. Here, we identify a long noncoding RNA, named Chronos, whose expression in muscle is positively regulated with advancing age and negatively regulated during Akt1-mediated growth. Inhibition of Chronos induces myofiber hypertrophy both in vitro and in vivo, in part, through the epigenetic modulation of Bmp7 signaling. ...
The exploration of tridimensional (3D) technology of computational tomography and the development of valid 3D printed models may improve the assessment of adenoid obstruction. The identification of an enlarged adenoid in childhood would streamline the referral of appropriately selected cases to an otolaryngologist, leading to early treatment of affected children when indicated. The objective of this study is to validate the use of a 3D printed model depicting adenoid hypertrophy based on the pediatric otolaryngologist, head and neck surgeon (OHNS) participants assessment. A cross-sectional study was performed to develop and validate 3D depictions, including print-outs, of the nasopharynx including different degrees of Adenoidal Hypertrophy (AH). The print-outs were obtained from 14 Cone-beam computed tomography (CBCT) scans of 14 children (12 boys, 2 girls; mean age of 10.61 years) representing grades 1, 2, 3, and 4 nasopharyngeal adenoidal obstructions, according to a previously Nasoendoscopy-graded
Ok, so its well established that a level of mechanical tension is needed in order to maximise the hypertrophic responses to resistance training. But what about metabolic stress? Well, it has been suggested that metabolic stress might play an additive role by enhancing the post exercise hypertrophic response (Schoenfeld, 2013). As highlighted by Schoenfeld (2010), the effects of metabolic stress are likely to arise through metabolite build up as a result of what is called anaerobic glycolysis. Anaerobic glycolysis is simply the production of energy using glucose in the absence of oxygen. It is likely that the products of anaerobic glycolysis (e.g. lactate, hydrogen ions, creatine) initiates a series of processes (fibre recruitment, enhanced hormone release, cellular swelling, production of ROS, altered myokine production), which contribute to the hypertrophy process (Schoenfeld, 2013).. Interestingly, bodybuilding-type resistance training programs are likely to induce significant amounts of ...
Previous work has revealed important roles for HIRA in myogenesis. It is important for the differentiation of C2C12 myoblasts into myotubes (Song et al., 2012). HIRA facilitates expression of Myod1 through incorporation of histone H3.3 into its promoter and enhancer regions (Yang et al., 2011b). Histone H3.3 itself epigenetically maintains expression of the Myod1 gene after cell division (Ng and Gurdon, 2008). HIRA cooperates with MEF2 transcription factors to drive expression of MEF2 target genes, like Myog (Yang et al., 2011a). HIRA is also a substrate for AKT proteins. HIRA phosphorylation by AKT proteins in myoblasts preserves the proliferative state. Dephosphorylation occurs as myoblasts differentiate towards myotubes (Yang et al., 2016). Thus, HIRA-mediated chromatin assembly is critical during myogenesis. In this study, we expanded our understanding of the function of HIRA in skeletal muscle by determining the consequence of its loss after myogenesis in the homeostasis and function of ...
Background: Adenoid hypertrophy treatment for children is generally planned in accordance with the degree of airway obstruction and related morbidity. If surgical treatment is indicated, the individual risk/benefit analysis of patients should be assessed in terms of anesthetic and postoperative complications. Although there are few alternative treatment options, these may be considered as a nonsurgical approach in less serious cases. Accordingly, studies about intranasal steroid applications under various protocols have been presented. ...
In previous studies, we have shown the exclusive expression of the Xtr gene in germ line cells of Xenopus and the occurrence of Xtr in germ line cells as well as early embryonic cells as a maternal factor (Ikema et al. 2002; Hiyoshi et al. 2005). Loss-of-function of Xtr in fertilized eggs using anti-Xtr antibody caused the lack of chromosome condensation and microtubule assembly, resulting in cleavage arrest (Hiyoshi et al. 2005). Since Xtr is a member of mRNP complex associated with mRNAs encoding the proteins such as XL-INCENP and RCC1 (Mostafa et al. 2009), which play an important role in karyokinesis (Ohtsubo et al. 1989; Mackay et al. 1998; Adams et al. 2001), the inhibition of karyokinesis progression induced by ablation of Xtr function was expected to be ascribable to translational suppression of these mRNAs. In Xenopus spermatogenesis, the amount of Xtr increases immediately after spermatogenic cells enter into meiotic phase (Hiyoshi et al. 2005). Therefore, Xtr was also thought to be ...
Originally published on Muscle hypertrophy, the process of increasing muscle size, requires a combination of strength training and nutrition. Too often, people
List of causes of Muscle hypertrophy and Musculoskeletal symptoms, alternative diagnoses, rare causes, misdiagnoses, patient stories, and much more.
This pathway shows the role of microRNAs in the process of cardiac hypertrophy. MicroRNA targets were predicted by the TargetScan algorithm, and the predicted interactions are shown in pink. MicroRNAs are shown as purple rounded rectangles. It is not sure which WNT and frizzled proteins influence cardiac hypertrophy. Though there are strong indications that WNT3A, WNT5A, frizzled1 and frizzled2 play a role in cardiac hypertrophy. Thus these have been added to the pathway instead of all the WNT and frizzled proteins. Experiments which will shed light on this are still being done ...
Serotonin, in addition to its fundamental role as a neurotransmitter, plays a critical role in the cardiovascular system, where it is thought to be involved in the development of cardiac hypertrophy and failure. Indeed, we recently found that mice with deletion of monoamine oxidase A had enhanced levels of blood and cardiac 5-HT, which contributed to exacerbation of hypertrophy in a model of experimental pressure overload. 5-HT2A receptors are expressed in the heart and mediate a hypertrophic response to 5-HT in cardiac cells. However, their role in cardiac remodeling in vivo and the signaling pathways associated are not well understood. In the present study, we evaluated the effect of a selective 5-HT2A receptor antagonist, M100907, on the development of cardiac hypertrophy induced by transverse aortic constriction (TAC). Cardiac 5-HT2A receptor expression was transiently increased after TAC, and was recapitulated in cardiomyocytes, as observed with 5-HT2A in situ labeling by immunohistochemistry.
Q: Ive been following the current bodybuilding training trend of hitting each muscle once a week with lots of sets. Growth has been slow, but youd think that with so much volume and intensity at one workout, it should take a full week for that muscle to completely recover, right?. Well, training each muscle with lots of volume once a week will produce some growth-if intensity is high enough to produce significant damage. The question is how much is enough?. Less volume for each muscle but with more frequent body part hits has proven a better, more sure-fire method for optimal hypertrophy in most cases and works as a sort of anabolic phasing…. In Anabolic Reload we discuss a recent study by hypertrophy researcher Brad Schoenfeld, Ph.D. He compared a workout program that trained each target muscle once a week and the less popular full-body workout performed on Monday, Wednesday, and Friday.. He made sure that the trainees were doing the SAME VOLUME of work for each muscle…. In other words, ...
The researchers put resistance-trained men on a six-week very-high-volume lifting program and then performed biopsies on the subjects vastus lateralis. The results showed a substantial increase in muscle fiber size (greater than 20 percent) that was accompanied by a roughly 30 percent reduction in the proportion of myofibrillar proteins. Those findings suggest that the hypertrophy was due to an increase in sarcoplasmic components (likely a combination of fluid and proteins related to metabolic stress).. Whats really interesting is that follow-up work from the same lab found that a heavier-load, lower-volume protocol resulted in type 2 fiber hypertrophy, but the changes occurred without significant increases in sarcoplasmic proteins and fluid.[5] Collectively, these studies suggest that bodybuilding-type training routines, with higher volume and moderate loads, produce greater increases in sarcoplasmic growth, whereas powerlifting-type programs, with lower volume and heavier loads, may generate ...
The researchers put resistance-trained men on a six-week very-high-volume lifting program and then performed biopsies on the subjects vastus lateralis. The results showed a substantial increase in muscle fiber size (greater than 20 percent) that was accompanied by a roughly 30 percent reduction in the proportion of myofibrillar proteins. Those findings suggest that the hypertrophy was due to an increase in sarcoplasmic components (likely a combination of fluid and proteins related to metabolic stress).. Whats really interesting is that follow-up work from the same lab found that a heavier-load, lower-volume protocol resulted in type 2 fiber hypertrophy, but the changes occurred without significant increases in sarcoplasmic proteins and fluid.[5] Collectively, these studies suggest that bodybuilding-type training routines, with higher volume and moderate loads, produce greater increases in sarcoplasmic growth, whereas powerlifting-type programs, with lower volume and heavier loads, may generate ...
Increased cytosolic [Na] despite increased sodium potassium pump activity during early development of heart failure in beta1 adrenergic receptor overexpressing mice. Schoenleitner, P.; Antoons, G.; Khan, S.; Unterer, G. J.; Wakula, P.; Engelhardt, S.; Pieske, B.; Heinzel, F. R. // Proceedings of the Physiological Society;2013, p274P Chronic stimulation of the β1-adrenergic pathway leads to cardiac hypertrophy and heart failure (HF). In mice overexpressing the β1-adrenergic receptor (β1), changes in Ca2+ handling precede the development of structural hypertrophy at an early stage of remodelling (8-12w). The Na+/K+... ...
Asthma is a chronic inflammatory disorder of the airways characterized by airway hyperresponsiveness and airflow limitation. Despite respiratory symptoms may be episodic, progressive changes occur in the structure of the airway, leading to its irreversible remodeling. Changes include mucus hypersecretion, injury to epithelial cells, smooth muscle hypertrophy, sub-basement membrane fibrosis and angiogenesis. The risk factors for developing asthma are a combination of genetic predisposition along with environmental exposure to inhaled substances and particles that may provoke allergic reactions or irritate the airways, such as in- and out-door allergens, tobacco smoke, chemical irritants in the workplace and air pollution. Asthma is a clinically heterogeneous entity due to the complexity of its pathogenetic substrate. Recent evidence suggests asthma to be associated with a sort of immunodeficiency accounting for an increased susceptibility to infection in asthmatic patients. The role of infections ...
Citation: Freking, B.A., Murphy, S., Wylie, A., Jirtle, R.L., Rhodes, S., Keele, J.W., Leymaster, K.A., Smith, T.P. 2002. Identification of the single base change causing the callipyge muscle hypertrophy phenotype, the only known example of polar overdominance in animals. Genome Research. 12:1496-1506. Interpretive Summary: A mutation in sheep, named callipyge, with large effects on lean and fat development as well as eating quality of meat was uncovered. Expression of muscle hypertrophy is inherited in a unique parent-of-origin manner referred to as polar overdominance. Specifically, animals exhibiting characteristic muscle hypertrophy must inherit the mutated allele from the sire, and not from the dam, making callipyge a unique phenomenon. We identified the specific causative mutation by sequencing key inbred animals identical-by-descent for a 210-Kb region known to contain the gene. A single base change was revealed as the only variable position in the sequenced region within these two rams ...
This course is a set of videos taken from these live hangouts -. Hypertrophy will run online and live at - 1pm MST, 7pm GMT, 7am EST on 8,15,22 and 29th January. All the powerpoints used will be downloadable and also fully referenced.. If you thought that squatting at a certain tempo and for a certain amount of reps and sets is all you need to know in order to get bigger, then this is a course you need to look at. Covering all the latest research on muscle growth, rest and recovery, fatigue management, periodisation and even touching on nutrition. This course will look at creating symmetry, analysing movements and exercises for growth as well as covering how to program most effectively.. Scroll down to see the titles of each meet up / pre-recorded lecture.. Obsessed about Hypertrophy Training. Week 1 - Introduction about Hypertrophy Training and how it has been mis-interpreted by most Personal Trainers. Week 2 - How do muscles grow? Type 1, Type 2, Rest, Recovery, Work Load and other ...
Ventricular hypertrophy following chronic overload results from the hypertrophy of cardiomyocytes and the hyperplasia of non muscle cells in the
In an earlier post (Click here to view the related post mentioned) the question was asked, who is giving away the biggest bonuses when obtaining Hypertrophy Max? The bonuses mentioned here are exclusive bonuses that associates of Vince Delmonte and Ben Pakulski are giving away when obtaining Hypertrophy Max from the link they provide. This has become a great competition among associates as the public will always be interested to get great value for money, which in turn is lucrative for the associate. Yes, you are right. It is true that it is much more lucrative to buy from Vince and Bens associates than it is to buy from them personally. What is the reasoning behind it. Simple. The associates as already mentioned usually give away all the bonuses Vince and Ben offers, but also their own exclusive gifts that you will find no where else when obtaining Hypertrophy Max.. I have done my own little research on the internet browsing all the big sites or at least those sites that rank well for ...
Training a muscle to lactic failure is a great way to signal many hypertrophy pathways - be tough & embrace the burn! Expect to see noticeable changes in body composition during this program as you will be stressing your total lactic tolerance... one of the key ways to increase growth hormone secretion similar to that seen from HIIT! Keep your head down, work hard, & get ready to get results over the next 6 weeks!
When a heart responds to increased workload it does so by hypertrophy. This is characterized by an increase in cell size in the absence of cell division, and is accompanied by distinct qualitative and quantitative changes in gene expression. The use
One of the most overlooked forms of treating muscle soreness is a top quality massage! Massage therapy has been around for many thousands of years and is perhaps the most effective way of healing muscle soreness, injuries and also accelerating the rate of recovery in the muscle tissue. This article aims to outline the benefits of a good massage and why you should consider having one done on the regular.So to begin with how can having massage therapy regularly increase the rate at which you heal? Well what a massage does is instantly increase the blood flow into your muscle tissue, thus increasing the amount of nutrients available to your muscle cells to assimilate. As a result the muscle tissue is able to recover an awful lot quicker. Working on the same principles of increased blood flow, consistently having massage therapy can indeed improve your muscle tone and the rate at which muscular hypertrophy occurs within. Massage therapy can also improve the rate of recovery by removing the toxins which are
Poster: ECR 2018 / C-2133 / Hypertrophic olivary degeneration: a review of literature and presentation of cases by: M. Lopez-Arroyave, M. Vega, F. Restrepo, L. Garcia, A. Arbelaez; Medellin/CO
Muscle mass is the main goal of a large part of the gym population. Whether youre looking to get stronger, have a sleeker physique or lose body fat, gaining muscle mass the right way is the best path to success.. It might be because of its popularity that this topic is the source of so many myths and misconceptions. In order to gain the most muscle mass, you have to know what to do, how to do it, and also what not to do.. It is for this specific reason that Christian Thibaudeau designed this course. He will divulge everything you need to know on all the topics related to training for hypertrophy.. In this course, you will learn:. - The science of hypertrophy and the key concepts necessary for successfully gaining muscle mass. - What types of training, methods and techniques works, and for what type of people. - How to structure your mass-gaining effort; how to build an effective workout plan and how to optimize your periodization in order to keep making gains.. You will discover the very ...
The present study aimed to identify sex-differently expressed miRNAs in a late stage of hypertrophy (9 weeks) and the possible role of ERs in the regulation of these differences. Our previous studies identified ERbeta as an important determinant factor of the observed sex differences in pressure overload, playing different roles in males and females. This report identified a total of 30 miRNAs with sex and/or sex*surgery interaction effect 9 weeks after TAC in WT mice. The same effects were not observed in ERbeta-/- animals partially due to the higher expression of these miRNAs in ERbeta-/- females than in their WT counterparts. This study reveals a repression of a number of miRNAs by estradiol and its receptors alpha and beta in female cardiomyocytes, confirming the in vivo results and accentuating the important protective role of oestrogen and ERbeta in the female heart. Six of the miRNAs with sex differences in WT but not in ERbeta-/- hypertrophy models were found to be possible fibrosis ...
I thought this was a really good article. Ive been interested in the whole size vs. strength debate. Lately, Ive really been looking for a physiological explanation for the different types of muscle building. With a quick google search, you can find that muscular growth is called hypertrophy and that the two primary types are myofibrillar and sarcoplasmic. Some facts are that myofibrillar hypertrophy means an increase in the number of muscle fibers and that sarcoplasmic hypertrophy means an increase in the size of muscle fibers because of an increase in sarcoplasm in the fibers themselves. The myth is that you can actually train your muscles for one type of hypertrophy over the other. The fact is that there is that there is no research that suggests that different types of training result in any difference in the relative amount of each type of hypertrophy. They simply happen together. Unfortunately, the myth that you can make your muscles larger (sarcoplasmic hypertrophy) with no effect on ...
Dr. Kaji is a clinician-scientist interested in the molecular mechanisms underlying cardiac hypertrophy and failure. Kaji has developed transgenic and knockout murine models of heart failure and hypertrophy. Using mouse models, Kaji tests the function of nuclear and cytoplasmic proteins in loss-of-function and gain-of-function models.. To make an appointment with Dr. Kaji call (608) 768-3900 ...
Focused hypertrophy training is often overlooked by coaches and athletes in competitive CrossFit. Perhaps this is because hypertrophy is generally considered to be within the purview of bodybuilding, and old school CrossFit was generally juxtapositioned to this style of training (along with excessive low intensity steady state endurance training.) I am of the opinion that … Continued
There are various causes of breast hypertrophy which include overproduction of estrogens, patients genetics and being overweight. The weight of the breasts is the major consequence of hypertrophy; others are pain in the upper back, shoulders, neck, poor posture.
In the first scripture course I ever took, when I was nineteen years old and didnt know applesauce from sin, professor Hanker gave us an examination on Jeremiah. The essay question asked, Do you think that Jeremiah suffered from a hypertrophy of sympathy for God? Why or why not? Since none of us knew what hypertrophy meant, it was a hard question to answer. I wish I knew what ever happened to Eddie Hanker. He was an important influence on me in learning how to relate to the Word with reverence. Whenever anyone was saying anything without critical foundation he would start yelling, rega, rega!, which I think means something like hold on or wait a minute in Hebrew ...
RESUMO: Physical exercise with resistance application is usually employed, aiming at gaining strength and muscle hypertrophy, in addition to improving the other neuromuscular components. In this perspective, several training protocols appear as possibilities for greater muscular gains, among which the training with repetition to failure and training with variation of 70-85% of the 1RM (Maximum Repetition) stand out. In addition, training with vascular occlusion, which consists of a training with low load, many repetitions and restriction of blood flow, appears to potentiate the training with light loads. In view of the above, it is important to evaluate the best form of resistance training, considering the differences and conflicts found in the literature regarding the protocols. Thus, the present study aims to compare different protocols of resistance training in young and sedentary women, with the purpose of gaining strength and muscle hypertrophy. This is a randomized clinical trial in which ...
Fredrik Tonstad Vårvik is from Norway and has a MSc. degree in exercise physiology. He works as a research assistant at
Abel is a writer, podcaster, video creator and coach at Sustainable Self Development, helping people to get into their best shape, while also...
The purpose of this study was to examine the effect of isokinetic eccentric (ECC) and concentric (CON) training at two velocities [fast, 180° s&#
Hypertrophy is increase in muscle size from an increase in size of individual muscle cells. This usually occurs as a result of ...
Effect on cardiac hypertrophy[edit]. Trx1 has been shown to downregulate cardiac hypertrophy, the thickening of the walls of ... Trx 1 also controls microRNA levels in the heart and has been found to inhibit cardiac hypertrophy by upregulating miR-98/let-7 ... "A redox-dependent pathway for regulating class II HDACs and cardiac hypertrophy". Cell. 133 (6): 978-93. doi:10.1016/j.cell. ... reduced HDAC4 downregulates the activity of transcription factors such as NFAT that mediate cardiac hypertrophy.[18] ...
Benign prostatic hypertrophy[edit]. A meta‐analysis found that tadalafil 5 mg once‐daily is an effective treatment for lower ... Tadalafil 10 mg is FDA-approved for men as a once-daily therapy to treat and prevent symptoms of benign prostatic hypertrophy ( ...
Papillitis/hypertrophy[edit]. Papillitis refers to inflammation of the papillae, and sometimes the term hypertrophy is used ...
... which can then cause ventricular hypertrophy. Left ventricular hypertrophy, for example, increases an individual's chance of ... 3.3 Current research on REST/NRSF and ventricular hypertrophy in mammals. *3.4 Mutations in polycomb-group response elements ( ... Current research on REST/NRSF and ventricular hypertrophy in mammals[edit]. See also: Atrial natriuretic peptide ... Thus, an abnormal induction of the ANP gene can lead to ventricular hypertrophy and severe cardiac consequences. In order to ...
7 (2). "Cardiac hypertrophy". Macmillan Publishers Limited. Retrieved 10 April 2018. Zhao, Yong; Ransom, Joshua F ... Previously, histone tail acetylation has been linked to cardiac hypertrophy or abnormal heart muscle thickening that is usually ... Some studies have shown that inhibiting HDAC activity can attenuate cardiac hypertrophy. trichostatin A and sodium butyrate are ... "MicroRNA-1 negatively regulates expression of the hypertrophy-associated calmodulin and Mef2a genes". Molecular and Cellular ...
Benign Prostatic Hypertrophy. Springer Science & Business Media. 6 December 2012. pp. 277-. ISBN 978-1-4612-5476-8. John David ... Lebech PE, Nordentoft EL (1967). "A study of endocrine function in the treatment of benign prostatic hypertrophy with megestrol ... "Megestrol acetate in treatment of benign prostatic hypertrophy". Urology. 6 (5): 580-7. doi:10.1016/0090-4295(75)90506-3. PMID ...
Benign Prostatic Hypertrophy. Springer Science & Business Media. 6 December 2012. pp. 266-. ISBN 978-1-4612-5476-8. Ablin RJ, ... Geller J, Bora R, Roberts T, Newman H, Lin A, Silva R (July 1965). "Treatment of benign prostatic hypertrophy with ... LH P < 0.05, LH/FSH P < 0.01). Benign Prostatic Hypertrophy. Springer Science & Business Media. 6 December 2012. pp. 266-. ISBN ... 128-. ISBN 978-94-009-8887-3. Castro JE (9 March 2013). The Treatment of Prostatic Hypertrophy and Neoplasia. Springer Science ...
1983). Benign Prostatic Hypertrophy. Springer Science & Business Media. pp. 259, 266, 272. ISBN 978-1-4612-5476-8. Wein AJ, ...
Thus, myostatin, LIF, IL-6 and IL-7 are involved in muscle hypertrophy and myogenesis, whereas BDNF and IL-6 are involved in ... Likewise, the heart has two potential responses to either stress: cardiac hypertrophy, which is a normal, physiologic, adaptive ... Hill JA (May 2015). "Braking bad hypertrophy". The New England Journal of Medicine. 372 (22): 2160-2. doi:10.1056/ ... hypertrophy). Brain-derived neurotrophic factor (BDNF) is also a myokine, though BDNF produced by contracting muscle is not ...
Benign Prostatic Hypertrophy. New York: Springer-Verlag. pp. 51-54. ISBN 978-1-4612-54768. "Official Register of the National ...
Benign Prostatic Hypertrophy. Springer Science & Business Media. 6 December 2012. pp. 266-. ISBN 978-1-4612-5476-8. ... Rangno RE, McLeod PJ, Ruedy J, Ogilvie RI (1971). "Treatment of benign prostatic hypertrophy with medrogestone". Clinical ...
Benign Prostatic Hypertrophy. Spring. pp. 45-58. ISBN 978-1-4612-5478-2. Anonymous (1890). "Obituary: A. F. McGill FRCS". Br ...
... hypertrophy usually mild; restrictive phenotype may be present; may carry high risk of sudden cardiac death maple syrup urine ...
Jadassohn-Pellizzari anetoderma is a benign condition with focal loss of dermal elastic tissue.[3] Jadassohn-Pellizzari is one of two major classifications of primary anetoderma, the other being Schweninger-Buzzi anetoderma. The difference between the two is that Jadassohn-Pellizzari anetoderma is preceded by inflammatory lesions.[1] ...
Normally, a callus will form on any part of the skin exposed to excess friction over a long period of time. For example, people often develop calluses on the middle finger or ring finger of their dominant hand due to writing with a pen or pencil. Another cause is from playing string instruments like the guitar or the violin; calluses will develop on the four fingers of the hand used in holding the strings down to the fingerboard, and sometimes on the fingers of the hand used for pizzicato or strumming. Weightlifters commonly experience callus on the upper-palm area due to repeated friction. Calluses are also very common on the fingers of rock climbers on almost all of their fingers. There are many activities that can result in the formation of a callus, which may even be viewed as a badge of experience and commitment to the activity. Activities that are notorious for causing calluses include (but are not limited to) construction work, many sports, wood carving, playing musical instruments, use ...
I42.1) Obstructive hypertrophy cardiomyopathy. *(I42.2) Other hypertrophic cardiomyopathy. *(I42.3) Endomyocardial ( ...
It is typically believed that lupus is influenced by multiple genes. Lupus is usually influenced by gene polymorphisms, 30 of which have now been linked with the disorder. Some of these polymorphisms have been linked very tentatively however, as the role that they play or the degree to which they influence the disease is unknown. Other genes that are commonly thought to be associated with lupus are those in the human leukocyte antigen (HLA) family. There have been several cases where a single gene influence appears to be present, but this is rare. When a single gene deficiency does cause lupus, it is usually attributed to the complement protein genes C1, C2, or C4. The influence of sex chromosomes and environmental factors are also noteworthy. Usually, these factors contribute to lupus by influencing the immune system.[4] Several studies also indicate a potential association of lupus with mutations in DNA repair genes [5] ...
... is a group of autoimmune diseases that may result in changes to the skin, blood vessels, muscles, and internal organs.[2][6][8] The disease can be either localized to the skin or involve other organs, as well.[2] Symptoms may include areas of thickened skin, stiffness, feeling tired, and poor blood flow to the fingers or toes with cold exposure.[1] One form of the condition, known as CREST syndrome, classically results in calcium deposits, Raynaud's syndrome, esophageal problems, thickening of the skin of the fingers and toes, and areas of small, dilated blood vessels.[1] The cause is unknown, but it may be due to an abnormal immune response.[2] Risk factors include family history, certain genetic factors, and exposure to silica.[3][4][5] The underlying mechanism involves the abnormal growth of connective tissue, which is believed to be the result of the immune system attacking healthy tissues.[6] Diagnosis is based on symptoms, supported by a skin biopsy or blood tests.[6] While no ...
The best treatment is prevention in patients with a known predisposition. This includes preventing unnecessary trauma or surgery (including ear piercing, elective mole removal), whenever possible. Any skin problems in predisposed individuals (e.g., acne, infections) should be treated as early as possible to minimize areas of inflammation. Treatment of a keloid scar is age dependent. Radiotherapy, anti-metabolites and corticoids would not be recommended to be used in children, in order to avoid harmful side effects, like growth abnormalities.[9] In adults, corticosteriods combined with 5-FU and PDL in a triple therapy, enhance results and diminish side effects.[9] Further prophylactic and therapeutic strategies include pressure therapy, silicone gel sheeting, intra-lesional triamcinolone acetonide (TAC), cryosurgery, radiation, laser therapy, IFN, 5-FU and surgical excision as well as a multitude of extracts and topical agents.[10] Surgical excision is currently still the most common treatment ...
Hypertrophy. Main article: Muscle hypertrophy. Independent of strength and performance measures, muscles can be induced to grow ... Biological factors such as age and hormone levels can affect muscle hypertrophy. During puberty in males, hypertrophy occurs at ... Natural hypertrophy normally stops at full growth in the late teens. As testosterone is one of the body's major growth hormones ... Taking additional testosterone or other anabolic steroids will increase muscular hypertrophy.. Muscular, spinal and neural ...
Zone of cell hypertrophy. Next, the chondrocytes cease to divide and begin to hypertrophy (enlarge), much like they do in the ...
... hypertrophy of long bones; and thickened skin and subcutaneous tissues, particularly of the hands and feet, including plantar ...
"Right Ventricular Hypertrophy (RVH) • LITFL • ECG Library Diagnosis". Life in the Fast Lane. 2018-08-01. Retrieved 2019-01-21. ... The boot like shape is due to the right ventricular hypertrophy present in TOF. Lung fields are often dark (absence of ... Right ventricular hypertrophy develops progressively from resistance to blood flow through the right ventricular outflow tract ... Electrocardiography shows right ventricular hypertrophy (RVH), along with right axis deviation. RVH is noted on EKG as tall R- ...
"Myostatin-related muscle hypertrophy". Retrieved 8 December 2014. "Types of Muscular Dystrophy and Neuromuscular ...
"Regulation of Cardiac Hypertrophy , Molkentin Lab". Retrieved 2021-01-03. "Cincinnati Children's ...
Trophy, Hypertrophied (1919). *Little Machine Constructed by Minimax Dadamax in Person (1919-20) ...
Calf muscular hypertrophy may occur. Type 5 is due to mutations in the AKT2 gene. It has been reported in four patients all ...
"A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure". Proceedings of the ... "MicroRNA-133 controls cardiac hypertrophy". Nature Medicine. 13 (5): 613-8. doi:10.1038/nm1582. PMID 17468766. S2CID 10097893. ... "Expression of microRNAs is dynamically regulated during cardiomyocyte hypertrophy". Journal of Molecular and Cellular ...
Rosendorff, C (1996). "The renin-angiotensin system and vascular hypertrophy". Journal of the American College of Cardiology. ... "Moexipril and left ventricular hypertrophy." Vascular Health Risk Management. 3.1 (2007): 23-30. Cawello, W; Boekens, H; ...
Adenoid hypertrophy (enlarged adenoids) is the unusual growth (hypertrophy) of the adenoid (pharyngeal tonsil) first described ... He described a long term adenoid hypertrophy that will cause an obstruction of the nasal airways. These will lead to a ... "Systematic review and meta-analysis of randomized controlled trials on the role of mometasone in adenoid hypertrophy in ... some low-quality evidence suggesting that mometasone may lead to symptomatic improvement in children with adenoid hypertrophy.[ ...
Right ventricular hypertrophy (RVH) is a form of ventricular hypertrophy affecting the right ventricle. ... An ECG with right ventricular hypertrophy may or may not show a right axis deviation on the graph.[1] ... This can lead to right ventricular hypertrophy. It can affect electrocardiography (ECG) findings. ... Retrieved from "" ...
... during the early adaptations of skeletal muscle hypertrophy. Long-term changes in hypertrophy show increases in nuclei (see C ... Skeletal Muscle Hypertrophy. Len Kravitz, Ph.D.. Introduction. Determining the optimal resistance training program for the ... With hypertrophy, recent research shows that muscle fibers tend to increase the myonuclear domain (note fluid increase from A ... This is a major research finding (alas, at the molecular level of muscle) which shows that skeletal muscle fiber hypertrophy ...
hypertrophy increase in the volume of an organ or tissue due to the enlargement of its component cells ... Hypertrophy with ulceration of the neck of the uterus Wellcome L0062129.jpg 5,448 × 3,804; 3.21 MB. ... Media in category "Hypertrophy". The following 10 files are in this category, out of 10 total. ... Hands and feet from a case of partial hypertrophy of the foot Wellcome L0061375.jpg 3,708 × 5,077; 2.62 MB. ...
... including left ventricular hypertrophy and right ventricular hypertrophy) Muscle hypertrophy List of biological development ... Eccentric hypertrophy is a type of hypertrophy where the walls and chamber of a hollow organ undergo growth in which the ... showing thickening of the cardiac muscle Kidney hypertrophy Wellcome L0005308 Athletes heart Ventricular hypertrophy ( ... Although hypertrophy and hyperplasia are two distinct processes, they frequently occur together, such as in the case of the ...
... also known as muscle hypertrophy. Hypertrophy of muscle occurs in type I (slow-twitch) and type II (fast-twitch) muscle fibres ... Manipulation of volume and intensity of resistance training will cause more or less hypertrophy to those respective muscle ... Other articles where Muscle hypertrophy is discussed: resistance training: Muscular: …muscle fibres, ... muscle fibres, also known as muscle hypertrophy. Hypertrophy of muscle occurs in type I (slow-twitch) and type II (fast-twitch ...
Concentric hypertrophy is a hypertrophic growth of a hollow organ without overall enlargement, in which the walls of the organ ... In the heart, concentric hypertrophy is related to increased pressure overload of the heart, often due to hypertension and/or ... These compensatory changes, termed "concentric hypertrophy," reduce the increase in wall tension observed in aortic stenosis. v ...
Myostatin-related muscle hypertrophy is a rare condition characterized by reduced body fat and increased muscle size. Explore ... Mutations in the MSTN gene cause myostatin-related muscle hypertrophy. The MSTN gene provides instructions for making a protein ... Myostatin-related muscle hypertrophy is a rare condition characterized by reduced body fat and increased muscle size. Affected ... Myostatin-related muscle hypertrophy is not known to cause any medical problems, and affected individuals are intellectually ...
Grounded in the principles and hallmarks of urology, Management of Benign Prostatic Hypertrophy satisfies the needs of ... In Management of Benign Prostatic Hypertrophy, a panel of internationally recognized expert clinicians and investigators in ... α-Adrenergic Antagonists in the Treatment of Benign Prostatic Hypertrophy-Associated Lower Urinary Tract Symptoms ...
Castration for Prostatic Hypertrophy. Br Med J 1895; 1 doi: (Published 19 January 1895 ...
The most notable change in the metabolic profile of hypertrophied hearts is an increased reliance on glucose with an overall ... Glucose metabolism and cardiac hypertrophy Cardiovasc Res. 2011 May 1;90(2):194-201. doi: 10.1093/cvr/cvr071. ... The most notable change in the metabolic profile of hypertrophied hearts is an increased reliance on glucose with an overall ... Impaired myocardial energetics in cardiac hypertrophy also triggers AMP-activated protein kinase (AMPK), leading to increased ...
Create healthcare diagrams like this example called Benign Prostatic Hypertrophy in minutes with SmartDraw. SmartDraw includes ... Benign Prostatic Hypertrophy. Create healthcare diagrams like this example called Benign Prostatic Hypertrophy in minutes with ... Benign Prostatic Hypertrophy. Sagittal section of male pelvis showing a prostate with benign prostatic hypertrophy (enlarged) ...
... benign prostatic hypertrophy (bph): the prostate grows naturally under the stimulation of testosterone. for ma ... Benign prostatic hypertrophy (BPH): The prostate grows naturally under the stimulation of testosterone. For many men, their ... Can testosterone therapy worsen benign prostatic hypertrophy (BPH)?. ANSWER There are a few health conditions that experts ... This condition, benign prostatic hypertrophy, can be made worse by testosterone therapy. ...
Adaptive hypertrophy definition at, a free online dictionary with pronunciation, synonyms and translation. Look ...
Cardiac hypertrophy happens when the muscles of the heart thicken, according to the University of Southern California Keck ... Cardiac hypertrophy is often caused by high blood pressure and a narrowing of the valves of the heart, claims the University of ... Cardiac hypertrophy happens when the muscles of the heart thicken, according to the University of Southern California Keck ... Symptoms of cardiac hypertrophy include chest pain or pressure after exercise or after meals, shortness of breath, tiredness, ...
... results came back as Mild septal hypertrophy with obstruction at rest, lv was hyperdynamic possibly due to sinus tach ( I was ... Im 28, Doc heard a murmur and sent for an echo, results came back as Mild septal hypertrophy with obstruction at rest, lv was ... My echo says mild hypertrophy of the septum originally it said it was obstructed, but when I got the original hospital echo it ... My echo says mild hypertrophy of the septum originally it said it was obstructed, but when I got the original hospital echo it ...
Learn what causes labial hypertrophy, when it needs treatment, and tips for managing the condition. ... Labial hypertrophy is the medical term for enlarged labia. This condition may cause discomfort in your vaginal region. In some ... What are the symptoms of labial hypertrophy?. If you have mild labial hypertrophy, you may not notice it. Labia minora, however ... The term "labia majora hypertrophy" refers to labia majora that are enlarged. Likewise, the term "labia minora hypertrophy" ...
Right Ventricular Hypertrophy. I. Correlation of Isolated Right Ventricular Hypertrophy at Autopsy with the ... The electrocardiograms of 22 cases showing isolated right ventricular hypertrophy at autopsy were examined for changes ... Factors contributing to the development of electrocardiographic changes of right ventricular hypertrophy are discussed. ... at least one of the criteria of Sokolow and Lyon and only three could be diagnosed as having right ventricular hypertrophy by ...
Shoulder shrugs are the most common exercise used to target the upper trapezius area. If youre unsure as to which muscles the upper "traps" are, just picture a really muscular guy with large muscles around his neck. Large traps almost make for a "no neck... Read , ...
Vicarious hypertrophy definition at, a free online dictionary with pronunciation, synonyms and translation. Look ... vicarious hypertrophy. vicariance, vicariant, vicariate, vicariate apostolic, vicarious, vicarious hypertrophy, vicarious ...
Cricopharyngeal hypertrophy, GERD Julianne W.M. I am a 30 year old woman who has had GERD for 15 years, I was also diagnosed ...
Tonsillar hypertrophy is another term for enlarged tonsils. While theyre sometimes a sign of an infection, they dont always ... What is tonsillar hypertrophy?. Tonsillar hypertrophy is the medical term for persistently enlarged tonsils. The tonsils are ... What causes tonsillar hypertrophy?. Tonsillar hypertrophy tends to affect children, but experts arent sure why. Some children ... When tonsillar hypertrophy leads to sleep apnea and trouble sleeping, it can cause a range of complications if left untreated, ...
Enlarged Heart (mild hypertrophy ellie35 Can a pacemaker, after three years, cause an increase in the size of the heart muscle ... Enlarged Heart (mild hypertrophy. Can a pacemaker, after three years, cause an increase in the size of the heart muscle. I had ...
Overall, we identify an important epigenetic role for a number of largely unstudied genes in muscle hypertrophy/memory. ... followed by later hypertrophy (reloading). We discovered increased frequency of hypomethylation across the genome after ... indicating a memory of these genes methylation signatures following earlier hypertrophy. Further, UBR5, RPL35a, HEG1, PLA2G16, ... and gene expression analysis after muscle hypertrophy (loading), return of muscle mass to baseline (unloading), ...
asymmetric septal hypertrophy Also called hypertrophic cardiomyopathy, asymmetric septal hypertrophy is a condition that occurs ... Children with asymmetric septal hypertrophy are not allowed to play competitive sports because of the possibility of a sudden ...
Breast hypertrophy has various different causes including a patients genetics, oversensitivity to or overproduction of ... it is helpful to consider breast hypertrophy in terms of how large and heavy the breasts are and whether the breast hypertrophy ... Breast hypertrophy is more common in overweight women but there is a very real association between a patients body mass index ... Although, breast hypertrophy, which really just means overgrowth of breast tissue, can be divided into macromastia and ...
Testicular Hypertrophy. Compensatory Hypertrophy. *Observed in monorchidism, cryptorchidism, and after testicular injury. ... Hypertrophy occurs prior to or during puberty, but thereafter the hypertrophic testis returns to normal or remains only ...
Ventricular Hypertrophy, Left, Hypertrophy, Left Ventricular, Hypertrophies, Left Ventricular, Left Ventricular Hypertrophies, ... hypertrophy of left ventricle (diagnosis), left ventricular hypertrophy, LVH (left ventricular hypertrophy), Hypertrophy, Left ... LEFT VENTRICULAR HYPERTROPHY, LV hypertrophy, LVH - Left ventricular hypertrophy, Left ventricular hypertrophy, LV+ - Left ... hypertrophy left ventricular, lv hypertrophy, Ventricular hypertrophy (& [left]), Ventricular hypertrophy (& [left]) (disorder) ...
... , Right Ventricular Enlargement, Right Ventricular Hypertrophy Related EKG Changes. ... RV hypertrophy, RVH - Right ventricular hypertrophy, Right ventricular hypertrophy, Right ventricular hypertrophy (disorder). ... Right Ventricular Hypertrophies, Ventricular Hypertrophies, Right, RVH - Right ventr hypertrophy, Right Ventricular Hypertrophy ... Right Ventricular Hypertrophy. Right Ventricular Hypertrophy Aka: Right Ventricular Hypertrophy, Right Ventricular Enlargement ...
Read about the different classifications of cardiac hypertrophy, including the developmental, physiological and pathological ... 3. Molecular regulators of cardiac hypertrophy. 3.1 Contractile molecules. Cardiac hypertrophy is associated with increased ... 2. Pathological and physiological hypertrophy. 3. Molecular regulators of cardiac hypertrophy. 4. Class selective HDAC ... 2. Pathological and physiological hypertrophy. Hypertrophy can be dissected into three distinct classifications:. * ...
  • Right ventricular hypertrophy (RVH) is a form of ventricular hypertrophy affecting the right ventricle . (
  • This can lead to right ventricular hypertrophy. (
  • An ECG with right ventricular hypertrophy may or may not show a right axis deviation on the graph. (
  • The electrocardiograms of 22 cases showing isolated right ventricular hypertrophy at autopsy were examined for changes suggestive of right ventricular hypertrophy. (
  • Only 5 of 22 cases fulfilled at least one of the criteria of Sokolow and Lyon and only three could be diagnosed as having right ventricular hypertrophy by the criteria of Myers, Klein and Stofer. (
  • Factors contributing to the development of electrocardiographic changes of right ventricular hypertrophy are discussed. (
  • Although the electrocardiogram is commonly obtained in the evaluation of patients with pulmonary hypertension, its value as a screening test for right ventricular hypertrophy or pulmonary hypertension is unclear. (
  • Therefore, we sought to determine the value of an electrocardiogram in the diagnosis of right ventricular hypertrophy using echocardiography as the gold standard. (
  • Despite a statistically significant relationship between an electrocardiogram and echocardiography in the diagnosis of right ventricular hypertrophy, an electrocardiogram has limited value as a screening tool for right ventricular hypertrophy because of its relatively low sensitivity and positive predictive value. (
  • However, soon after birth, cardiac myocytes withdraw irreversibly from the cell cycle and subsequent growth of the heart occurs predominantly through hypertrophy rather than myocyte hyperplasia. (
  • Not to be confused with hyperplasia, the process of increasing the number of cells, hypertrophy is the process of increasing the size of the cells that are already there. (
  • Benign prostatic hypertrophy (BPH), or cystic hyperplasia, is an age related change of the prostate where the prostate increases in size. (
  • MF Hypertrophy or Hyperplasia? (
  • Although hypertrophy and hyperplasia are two distinct processes, they frequently occur together, such as in the case of the hormonally-induced proliferation and enlargement of the cells of the uterus during pregnancy. (
  • Significantly, some anabolic (muscle growth-promoting) hormones-including insulin-like growth factor, testosterone and growth hormone-play a primary role in promoting hypertrophy (Schoenfeld 2010). (
  • Hypertrophy occurs prior to or during puberty, but thereafter the hypertrophic testis returns to normal or remains only slightly enlarged. (
  • ROS scavenger) and fisetin did not have synergistic inhibitory effects on PE-induced cardiomyocyte hypertrophy, indicating that the anti-hypertrophic effects of fisetin are mainly associated with the blockade of oxidative stress. (
  • Left ventricular hypertrophy due to hypertrophic cardiomyopathy may be treated with medication, a nonsurgical procedure, surgery, implanted devices and lifestyle changes. (
  • Other causes include athletic hypertrophy (a condition related to exercise), valve disease , hypertrophic cardiomyopathy (HOCM) , and congenital heart disease . (
  • However, there is no information about the possible role of H(2)S in cardiomyocyte hypertrophy (CH). Our results showed that pretreatment with NaHS, an H(2)S donor, significantly reduced [(3)H]-leucine incorporation, cell surface area, mRNA expression of brain natriuretic peptide (BNP), intracellular reactive oxygen species (ROS), miR-21 and increased atrial natriuretic peptide (ANP) and miR-133a expression in hypertrophic cardiomyocytes. (
  • Sarcomeres are added in series, as for example in dilated cardiomyopathy (in contrast to hypertrophic cardiomyopathy, a type of concentric hypertrophy, where sarcomeres are added in parallel). (
  • Concentric hypertrophy is a hypertrophic growth of a hollow organ without overall enlargement, in which the walls of the organ are thickened and its capacity or volume is diminished. (
  • Determining the optimal resistance training program for the development of skeletal muscle hypertrophy (size) is of great interest to many personal trainers working with clients who seek increases in muscularity. (
  • 2016) summarize current recommendations suggesting loads of 70% to 85% of a person's one-repetition maximum (1RM) are traditionally considered a criterion for maximizing skeletal muscle hypertrophy from resistance training. (
  • Unpredictably, the HR and LR were equally effective in stimulating skeletal muscle hypertrophy (as measured with muscle biopsy techniques) in this resistance-trained group of males. (
  • The researchers concluded that training to volitional failure is the most important variable for skeletal muscle hypertrophy gains in males. (
  • They summarized that trained males exercising to volitional failure between 30-90% 1RM will sufficiently activate skeletal muscle motor units, which is the driving mechanism for skeletal muscle hypertrophy. (
  • Skeletal muscle - Hypertrophy in a male Harlan Sprague-Dawley rat from a subchronic study. (
  • Transcriptome wide changes in human skeletal muscle after acute (anabolic) and chronic resistance exercise (RE) induced hypertrophy have been extensively determined in the literature. (
  • We have also recently undertaken DNA methylome analysis (850,000 + CpG sites) in human skeletal muscle after acute and chronic RE, detraining and retraining, where we identified an association between DNA methylation and epigenetic memory of exercise induced skeletal muscle hypertrophy. (
  • Importantly, these 5 genes demonstrated retained hypomethylation even during detraining (following training induced hypertrophy) when exercise was ceased and lean mass returned to baseline (pre-training) levels, identifying them as genes associated with epigenetic memory in skeletal muscle. (
  • Importantly, for the first time across the transcriptome and epigenome combined, this study identifies novel differentially methylated genes associated with human skeletal muscle anabolism, hypertrophy and epigenetic memory. (
  • Skeletal muscle tissue demonstrates extensive plasticity, responding dynamically to sustained mechanical loading and contraction with muscle hypertrophy. (
  • Scientifically speaking, hypertrophy is the physiological response that increases skeletal muscle mass and the cross-sectional area of muscle when work is done against a form of resistance. (
  • There isn't an exact measurement that defines whether the labia are hypertrophied or not, as the diagnosis is generally made based on a physical exam and individual's symptoms. (
  • There is no specific lab test for breast hypertrophy, and the diagnosis is made by most women themselves and confirmed by clinical assessment. (
  • More than one-third of people show evidence of left ventricular hypertrophy at the time of their diagnosis with hypertension. (
  • What is labial hypertrophy? (
  • Either way, labial hypertrophy doesn't mean that you have a medical issue. (
  • What are the symptoms of labial hypertrophy? (
  • If you have mild labial hypertrophy, you may not notice it. (
  • Labial hypertrophy can cause a noticeable bulge in your clothing, especially when you're wearing a bathing suit. (
  • In some cases, labial hypertrophy may occur due to infection or trauma to the area. (
  • There's no special test to determine if you have labial hypertrophy. (
  • If your labia minora extend beyond your labia majora, your doctor may diagnose it as labial hypertrophy upon physical examination. (
  • When labial hypertrophy isn't causing a problem, you don't need treatment. (
  • If labial hypertrophy interferes with your life and your ability to enjoy physical activities or sexual relations, see your OB-GYN. (
  • Your doctor may recommend a surgery called a labioplasty for severe labial hypertrophy. (
  • The surgery can provide relief for women who experience pain and discomfort from labial hypertrophy. (
  • Labial hypertrophy is a harmless condition in which one or both sides of the labia grow to larger sizes. (
  • The cause of labial hypertrophy is unclear. (
  • Women with labial hypertrophy have normal sexual function because the clitoris, clitoral hood and vagina are normal. (
  • At Children's Center for Congenital Anomalies of the Reproductive Tract , an interdisciplinary team of pediatricians, gynecologists, urogynecologists and colorectal surgeons will work with your daughter to find the best approach to her labial hypertrophy. (
  • Labial hypertrophy (pronounced: lay-bee-al hi-per-tro-fee) is a long name that means the enlargement of the labia (sometimes called the vaginal lips). (
  • It is unclear what causes labial hypertrophy. (
  • I have labial hypertrophy (enlarged labia) and haven't gotten my period yet although my mother and sister got it when they were 13 years old. (
  • I think I have labial hypertrophy. (
  • Adenoid hypertrophy ( enlarged adenoids ) is the unusual growth ( hypertrophy ) of the adenoid (pharyngeal tonsil) first described in 1868 by the Danish physician Wilhelm Meyer (1824-1895) in Copenhagen . (
  • He described a long term adenoid hypertrophy that will cause an obstruction of the nasal airways. (
  • There is some low-quality evidence suggesting that mometasone may lead to symptomatic improvement in children with adenoid hypertrophy. (
  • When the adenoids themselves are infected, they become inflamed and enlarged in a condition known as adenoid hypertrophy. (
  • Adults and children who experience multiple sinus infections, chronic snoring, and worsening breathing problems should be evaluated by physicians to check for adenoid hypertrophy and discuss treatment options. (
  • Adenoid hypertrophy is a natural part of early airway development. (
  • Since adenoid hypertrophy is often accompanied by tonsil swelling, a tonsillectomy may be performed as well. (
  • tolleranza - In addition to adenoid hypertrophy, adenoids can become inflamed just as I'm sure your husband's tonsils did. (
  • Homeopathy for Adenoid Hypertrophy. (
  • Adenoid's symptoms, treatment, adenoids in children, homeopathic treatment and homeopathic medicine for adenoid hypertrophy. (
  • Are you looking for a homeopathic cure for adenoid hypertrophy? (
  • This article discusses the homeopathy treatment of adenoid hypertrophy along with the best homeopathic medicine for adenoid hypertrophy treatment. (
  • Other problems caused by chronic adenoid hypertrophy include blockage of the eustachian tubes and chronic ear disease and hearing loss. (
  • The selection of homeopathic medicine for adenoid hypertrophy is based upon the theory of individualization and symptoms similarity by using holistic approach. (
  • The aim of homeopathic medicine for adenoid hypertrophy is not only to treat enlarged/infected adenoid but to address its underlying cause and individual susceptibility. (
  • Tuberculinum -homeopathic medicine for adenoid hypertrophy in weak children with the history of tuberculosis in the family. (
  • These images are a random sampling from a Bing search on the term "Left Ventricular Hypertrophy. (
  • Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart's main pumping chamber (left ventricle). (
  • Left ventricular hypertrophy can develop in response to some factor - such as high blood pressure or a heart condition - that causes the left ventricle to work harder. (
  • Left ventricular hypertrophy is more common in people who have uncontrolled high blood pressure. (
  • But no matter what your blood pressure is, developing left ventricular hypertrophy puts you at higher risk for a heart attack and stroke. (
  • Treating high blood pressure can help ease your symptoms and may reverse left ventricular hypertrophy. (
  • Left ventricular hypertrophy usually develops gradually. (
  • If you have high blood pressure or another condition that increases your risk of left ventricular hypertrophy, your doctor is likely to recommend regular appointments to monitor your heart. (
  • Left ventricular hypertrophy can occur when some factor makes your heart work harder than normal to pump blood to your body. (
  • This is the most common cause of left ventricular hypertrophy. (
  • Left ventricular hypertrophy is more common in older people. (
  • Being overweight increases your risk of high blood pressure and left ventricular hypertrophy. (
  • African-Americans are at higher risk of left ventricular hypertrophy than are white people with similar blood pressure measurements. (
  • Women with hypertension are at higher risk of left ventricular hypertrophy than are men with similar blood pressure measurements. (
  • Left ventricular hypertrophy changes the structure and working of the heart. (
  • Echocardiogram can reveal thickened muscle tissue in the left ventricle, blood flow through the heart with each beat, and heart abnormalities related to left ventricular hypertrophy, such as aortic valve stenosis. (
  • Images of your heart can be used to diagnose left ventricular hypertrophy. (
  • Treatment for left ventricular hypertrophy depends on the underlying cause and may involve medication or surgery. (
  • Left ventricular hypertrophy that is caused by aortic valve stenosis might require surgery to repair the narrow valve or to replace it with an artificial or tissue valve. (
  • If you've already been diagnosed with sleep apnea, treating this sleep disorder can lower your blood pressure and help reverse left ventricular hypertrophy if it's caused by high blood pressure. (
  • Lifestyle changes can help lower your blood pressure, improve your heart health and improve left ventricular hypertrophy signs if the left ventricular hypertrophy is caused by high blood pressure. (
  • Left ventricular hypertrophy (LVH) has a significant impact on increasing the morbidity of coronary disease and stroke. (
  • This study combined the random forest and ECG data to develop an ECG left ventricular hypertrophy classifier. (
  • Kannel, W.B.: Left ventricular hypertrophy as a risk factor: the Framingham experience. (
  • Left ventricular hypertrophy dangerous?Please help? (
  • Hello, in the summer I was diagnosed with MVP and Left Ventricular hypertrophy.I also had a big anxiety.Actually everything started after big panic attack which I thought that it was a heart attack. (
  • Objective: The aims of this study were to estimate the frequency of left ventricular hypertrophy and to identify variables associated with this condition in under 25-year-old patients with sickle cell anemia. (
  • The patients were divided into two groups according to the presence or absence of left ventricular hypertrophy and compared according to clinical, echocardiographic and laboratory variables. (
  • Results: A total of 37.6% of the patients had left ventricular hypertrophy in this sample. (
  • There was no difference between the groups of patients with and without hypertrophy according to pathological history or clinical characteristics, except possibly for the use of hydroxyurea, more often used in the group without left ventricular hypertrophy. (
  • Patients with left ventricular hypertrophy presented larger left atria and lower hemoglobin and hematocrit levels, reticulocyte index and a higher albumin:creatinine ratio in urine. (
  • Conclusion: Left ventricular hypertrophy was observed in more than one-third of the young patients with sickle cell anemia with this finding being inversely correlated to the hemoglobin and hematocrit levels, and reticulocyte index and directly associated to a higher albumin/creatinine ratio. (
  • It is possible that hydroxyurea had had a protective effect on the development of left ventricular hypertrophy. (
  • What Is Mild Concentric Left Ventricular Hypertrophy? (
  • Mild concentric left ventricular hypertrophy is the mild enlargement of the muscles of the sinistral cardiac ventricle, which includes an augmented cavity size and thickened walls, according to Mayo Clinic. (
  • Left ventricular hypertrophy is generally associated with accretion in the left pumping chamber of the heart. (
  • Hereditary factors may also play a role in left ventricular hypertrophy. (
  • NEW YORK, Nov. 1 -- Regression or prevention of left-ventricular hypertrophy in hypertension patients may reduce their risk of developing new-onset diabetes, according to a study. (
  • The LIFE study, conducted from 1995 through 2001, of losartan versus atenolol-based therapy for hypertensive patients with left- ventricular hypertrophy, found losartan therapy associated with a lower incidence of diabetes and greater regression of hypertrophy. (
  • In contrast, higher values of left-ventricular hypertrophy were associated with higher rates of new diabetes, they said. (
  • These results and previous findings with ACE-inhibitor and angiotensin-receptor-blocker therapy, they added, suggest that antihypertensive therapies that independently reduce the occurrence of diabetes and also produce left-ventricular hypertrophy regression may provide long-term benefits by reducing cardiovascular morbidity and mortality, at least in part by preventing new-onset diabetes. (
  • Left ventricular hypertrophy (LVH), also known as an enlarged heart, is a condition in which the muscle wall of heart's left pumping chamber (ventricle) becomes thickened (hypertrophy). (
  • Left ventricular hypertrophy in nondiabetic predialysis CKD. (
  • BACKGROUND: Although left ventricular hypertrophy (LVH) is a strong predictor of mortality in patients with end-stage renal disease, few studies are available before the start of dialysis treatment. (
  • Objective Cardiac changes of hypertensive pregnancy include left ventricular hypertrophy (LVH) and diastolic dysfunction. (
  • A new study by researchers at Wake Forest Baptist Medical Center has shown that aggressive lowering of blood pressure in people with hypertension reduced the risk of left ventricular hypertrophy (LVH). (
  • 130mm Hg is associated with a reduction in left ventricular hypertrophy (LVH), according to Italian researchers. (
  • The team found that the overexpression of CnAβ1 in the hearts of mice prevented the development of cardiac hypertrophy and fibrosis, resulting in improved contractility. (
  • The papers presented describe fundamental mechanisms underlying changes in the cellular machinery during the development of cardiac hypertrophy and heart failure. (
  • It has been proposed that several neurohumoral factors may be involved in the genesis of vascular structural changes (remodeling or hypertrophy) frequently observed in essential hypertension. (
  • 5 6 The study of patients with secondary hypertension may help in the evaluation of the possible role of some neurohumoral factors in the development of vascular hypertrophy or remodeling. (
  • In the heart, concentric hypertrophy is related to increased pressure overload of the heart, often due to hypertension and/or aortic stenosis. (
  • Pressure and volume overload results in concentric and eccentric hypertrophy of cardiac ventricular chambers with, respectively, parallel and series replication of sarcomeres. (
  • Schematic overview of the development of concentric hypertrophy with the parallel addition of sarcomeres in pressure overload and of eccentric hypertrophy with a series addition of sarcomeres in volume overload. (
  • Wall thickening induces concentric hypertrophy in pressure overload and contributes to eccentric hypertrophy in volume overload (blue arrow). (
  • Concentric hypertrophy reduces systolic wall stress in pressure overload, and eccentric hypertrophy reduces diastolic wall stress in volume overload (dashed red lines indicate negative feedback). (
  • These compensatory changes, termed "concentric hypertrophy," reduce the increase in wall tension observed in aortic stenosis. (
  • However, a net increased intracellular viscosity limits the efficiency of this effort leading to cardiac myocyte hypertrophy (11, 12) . (
  • Signaling pathways in cardiac myocyte hypertrophy. (
  • The use of cardiomyocytes in cell culture has identified, besides mechanical loading, a range of substances, such as cytokines, growth factors, catecholamines, vasoactive peptides and hormones, involved in mediating cardiac myocyte hypertrophy, and has enabled the molecular dissection of the pathways involved in signal transduction. (
  • Fisetin inhibits cardiac hypertrophy by suppressing oxidative stress. (
  • It's unclear whether this athletic type of left ventricle hypertrophy can lead to stiffening of the heart muscle and disease. (
  • The cellular mechanisms of cardiac hypertrophy remain unclear despite tantalizing clues gleaned from a variety of experimental approaches. (
  • however, the effect of NXT on the cardiac hypertrophy is still unclear. (
  • But whether treatment resolution or continued absence of hypertrophy is independently associated with a decreased incidence of diabetes remained unclear, Dr. Okin said. (
  • Hypertrophy can be thought of as a thickening of muscle fibers, which occurs when the body has been stressed just the right amount to indicate that it must create larger, stronger muscles that can tolerate this new, increased load. (
  • New muscle fibers are not created during hypertrophy in humans, although Paul and Rosenthal (2002) note new-fiber creation has been observed in some animal studies, owing to unique structural differences in muscle anatomy between species. (
  • Myofibrillar hypertrophy - an increase in the size and number of myofibrils (threadlike cellular structures) in the muscle fibers. (
  • With muscle hypertrophy at the cellular level in humans, the actin and myosin contractile proteins increase in size and number (Schoenfeld 2010). (
  • Short rest periods may cause a significant amount of metabolic stress, which is now believed to be a potent stimulator for hypertrophy (Schoenfeld 2011). (
  • In Management of Benign Prostatic Hypertrophy, a panel of internationally recognized expert clinicians and investigators in urology review the new treatments in the light of established urologic principles and tradition. (
  • Grounded in the principles and hallmarks of urology, Management of Benign Prostatic Hypertrophy satisfies the needs of practicing urologists seeking a concise up-to-date interpretation and analysis of the many new therapies available for the treatment of BPH. (
  • Create healthcare diagrams like this example called Benign Prostatic Hypertrophy in minutes with SmartDraw. (
  • Sagittal section of male pelvis showing a prostate with benign prostatic hypertrophy (enlarged) and how the urinary tract, (heavily outlined) is affected. (
  • Can testosterone therapy worsen benign prostatic hypertrophy (BPH)? (
  • Benign prostatic hypertrophy (BPH): The prostate grows naturally under the stimulation of testosterone. (
  • This condition, benign prostatic hypertrophy, can be made worse by testosterone therapy. (
  • This is the case with Benign Prostatic Hypertrophy and Prostate Cancer . (
  • I request a reproduction of the book Benign Prostatic Hypertrophy and Prostate Cancer . (
  • I declare that, after reasonable investigation, I am satisfied that a reproduction (not being a second-hand reproduction) of Benign Prostatic Hypertrophy and Prostate Cancer cannot be obtained within a reasonable time at an ordinary commercial price. (
  • Benign prostatic hypertrophy (BPH) is a very common disease among men aged 50 and its economic burden on health services continues to grow. (
  • With this type of hypertrophy training, one might do a max set of squats once per week or every 10 days. (
  • This type of hypertrophy training spans over 3-4 days depending on your personal preferences and recovery ability. (
  • Eccentric hypertrophy is a type of hypertrophy where the walls and chamber of a hollow organ undergo growth in which the overall size and volume are enlarged. (
  • Hypertrophy is, by definition, the enlargement of an organ or tissue from the increase in size of its cells. (
  • Muscle hypertrophy, or muscle cell enlargement, is a topic of great debate and interest in all fields of health, fitness and sports. (
  • Hypertrophy (from Greek ὑπέρ "excess" + τροφή "nourishment") is the increase in the volume of an organ or tissue due to the enlargement of its component cells. (
  • In conclusion, our study revealed that fisetin protects against cardiac hypertrophy and that oxidative stress inhibition may be one of the pivotal mechanisms involved. (
  • The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training. (
  • Symptoms of cardiac hypertrophy include chest pain or pressure after exercise or after meals, shortness of breath, tiredness, fainting, and palpitations, says WebMD. (
  • If you've been having symptoms such as trouble sleeping or loud snoring, your doctor might also suggest doing a sleep study to check for sleep apnea caused by tonsillar hypertrophy. (
  • What Are the Signs and Symptoms of Turbinate Hypertrophy? (
  • Areas of retinal pigment epithelial (RPE) hypertrophy usually do not cause symptoms. (
  • Almost all patients with retinal pigment epithelial hypertrophy do not have symptoms. (
  • There has been one training principle that has been shown to greatly affect hypertrophy. (
  • Please join this discussion about how to achieve hypertrophy within the Weight Training & Weight Lifting category. (
  • Theres more than one way to skin a cat and there are many tools to achieve hypertrophy. (
  • Is it possible to achieve hypertrophy without going to failure? (
  • The growth seen with developmental and physiological hypertrophy is morphologically distinguishable from that seen in pathological hypertrophy. (
  • Whereas in developmental and physiological hypertrophy, the growth of the cardiac myocytes and hence the ventricular wall and septum is comparable with an increase in chamber dimension, in pathological hypertrophy, the ventricular wall and septum thicken but with a concomitant decrease in ventricular chamber dimension. (
  • Pathological hypertrophy frequently progresses to dilated cardiomyopathy, which may be due, at least in part, to activation of apoptotic pathways (7) . (
  • Epinephrine, norepinephrine, angiotensin II, and aldosterone have been identified as the most important neurohormones stimulating stress-mediated or reactive cardiac hypertrophy, i.e., pathological hypertrophy, and contributing to its progression to heart failure. (
  • Attempts to further define the signaling pathways for cardiac eutrophy, physiological hypertrophy, and pathological hypertrophy have employed a reductionist approach, delineating downstream signaling effectors of each receptor-hormone system and their specific manipulation in tissue culture or in physiologically stressed and genetically modified animal models. (
  • We make this happen is by focusing on training the nervous system and creating what's called Myofibrillar Hypertrophy. (
  • The 2 forms of muscle hypertrophy are myofibrillar hypertrophy and sarcoplasmic hypertrophy. (
  • Myofibrillar hypertrophy is the increase in number of the contractile proteins actin and myosin. (
  • Myofibrillar hypertrophy increases strength as well as size. (
  • Training for myofibrillar hypertrophy involves low reps and heavy weight. (
  • Training for predominantly sarcoplasmic hypertrophy involves higher rep ranges than myofibrillar hypertrophy. (
  • In our present study, we showed that fisetin inhibited pressure overload-induced cardiac hypertrophy, improved cardiac function in vivo and suppressed phenylephrine (PE)-induced cardiomyocyte hypertrophy in vitro. (
  • Tempo lifting is appropriate for hypertrophy, strength, and endurance, but each one of those goals yields different eccentric tempos. (
  • It therefore seems plausible that [Ca2+]i constitutes the crucial link between the initial stimulus for hypertensive hypertrophy (elevated perfusion pressure) and the secondary alterations in gene expression. (
  • Accordingly, the present study evaluated hypertrophy in 7,998 hypertensive patients without diabetes at baseline in the LIFE study who were treated with losartan-based or atenolol-based regimens and followed with serial electrocardiograms and blood pressure determinations. (
  • Further study will be necessary to determine whether regression of hypertrophy will become a valid independent target for therapeutic intervention in hypertensive patients to prevent development of diabetes and other adverse cardiovascular outcomes, the researchers concluded. (
  • Sarcoplasmic hypertrophy - an increase in the volume of the sarcoplasm, a fluid, non-contractile part of the muscle. (
  • Sarcoplasmic hypertrophy is the increase in volume of sarcoplasmic fluid in the muscle cell. (
  • Studies using transgenic mouse models and pharmacological compounds to mimic or counter the switch of substrate preference in cardiac hypertrophy have demonstrated that increased glucose metabolism in adult heart is not harmful and can be beneficial when it provides sufficient fuel for oxidative metabolism. (
  • Cardiac hypertrophy happens when the muscles of the heart thicken, according to the University of Southern California Keck School of Medicine. (
  • Cardiac hypertrophy is often caused by high blood pressure and a narrowing of the valves of the heart, claims the University of Southern California Keck School of Medicine. (
  • Following the stimulus, there is normally a phase of cardiac hypertrophy whereby individual cardiac myocytes increase in size as a means of compensating for damaged heart tissue in order to increase cardiac pump function. (
  • In the long term however, such cardiac hypertrophy can predispose towards heart failure (4, 5, 6) . (
  • Cardiac hypertrophy is a pathophysiological response to various pathological stresses and ultimately leads to heart failure. (
  • Cardiac hypertrophy results from an increase in protein synthesis, cell size, and thickening of the heart muscle. (
  • Cardiac hypertrophy can cause heart failure and arrhythmia. (
  • When a heart responds to increased workload it does so by hypertrophy. (
  • Scientists at the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) have identified a variant of the enzyme calcineurin, called CnAβ1, whose action reduces cardiac hypertrophy and improves heart function. (
  • This increase in heart size, called cardiac hypertrophy, is effective initially, but over time problems arise. (
  • Pathological cardiac hypertrophy is to a large extent mediated by the enzyme calcineurin, which induces a program leading to the production of increased muscle mass in the heart. (
  • The process that allows the python's heart to expand is called hypertrophy . (
  • In a paper in the current issue of Science , they report that a gorging python expands its heart by enlarging existing cells - a process called hypertrophy - and not by creating new ones. (
  • Heart Hypertrophy and Failure brings together leading basic scientists and clinicians, presenting improved knowledge of the pathophysiology and treatment of the condition. (
  • Audience: Students, scientists, clinical and experimental cardiologists who seek to understand and manage the perplexing problems of hypertrophy and heart failure. (
  • Investigators at Beth Israel Deaconess Medical Center (BIDMC) have identified a developmental cause of adult-onset cardiac hypertrophy, a dangerous thickening of the heart muscle that can lead to heart failure and death. (
  • In cardiac hypertrophy, metabolic energy reserves in the heart are depleted, which is thought to contribute to the subsequent development of heart failure. (
  • 2016). Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men. (
  • You might have seen your favorite Instagram trainer mention hypertrophy on her strength training posts. (
  • In general, there are three types of resistance training styles-strength ( heavy weight/low reps ), hypertrophy, and muscular endurance ( low weight/high reps ). (
  • While there's crossover (meaning you'll still build strength when working on hypertrophy and vice versa), you can maximize growth gains by staying within a certain window of reps, sets, and weight. (
  • b) Type IIa and IIb/x Muscle Fiber must be worked to increase Strength and Size (Hypertrophy). (
  • d) Increased Muscle Acidity increases Hypertrophy and Strength. (
  • WHAT, WHEN, HOW and WHY to consider tempo training with the expressed goal of increasing hypertrophy, endurance, and/or strength. (
  • As we gaze upon the masters of bodybuilding, powerlifting, Olympic weightlifting and the popular sports such as American football that require an athlete to be very strong, it's easy to see that maximal strength usually means an increase in muscle hypertrophy. (
  • While it's obvious when looking at their programming that Tommy and Layne are focused on hypertrophy training, Dave Gulledge's focus is primarily strength-oriented and Martin's training preference seems to be fairly low volume (rarely looked upon as hypertrophy training). (
  • This program is primarily focused on producing muscle hypertrophy via strength gains on any given movement. (
  • The effect on strength that these 2 forms of hypertrophy have shows why a 90kg power lifter can lift more weight than a 120kg bodybuilder. (
  • Hypertrophy with Blood Flow Restriction occurs via Metabolic Stress rather than Mechanotransduction. (
  • Growth factors help stimulate muscle hypertrophy while testosterone increases protein synthesis. (
  • Although, breast hypertrophy, which really just means overgrowth of breast tissue, can be divided into macromastia and gigantomastia, the cut offs are fairly arbitrary with the latter defined as breast tissue over that expected by the patient's body type of more than 5.5lb, or breasts weighing more than 3% of total body weight. (
  • It is also important for patients to know that surgery for breast hypertrophy involves the milk producing tissue of the breast and, although many women can breast feed following this type of surgery, a proportion cannot. (
  • Turbinate hypertrophy, inferior turbinate hypertrophy, and nasal turbinate hypertrophy are all descriptions of a similar condition where the tissue on the lateral (outside) walls of the nose are too large, causing nasal obstruction. (
  • The increase in volume of tissue (a phenomenon known as hypertrophy ) is believed to be less prominent in ototoxically deafened cats due to the treatment. (
  • Once satellite cells are stimulated by muscular overload, they fuse to the muscle fiber and facilitate muscle hypertrophy by forming a new nucleus. (
  • TGF-β signaling through the mTOR pathway is critical to glucose-induced cellular hypertrophy. (
  • The exercise-induced stimulus from resistance exercise activates a complex response of cellular messaging pathways, cytokines and hormones that set muscle hypertrophy in motion (see Figure 2). (
  • In the 20 years since Paul Simpson initially demonstrated that neurohormonal stimulation of cultured neonatal cardiomyocytes results in cellular hypertrophy, characteristic changes in cardiac gene expression, and activation of specific kinase signaling pathways ( 1 - 3 ), protein kinases have attracted attention as candidate mediators of the cardiac biomechanical stress and trophic responses. (
  • Are exercises that include a stretch of the targeted muscles and have the sticking point in a more stretched position generally more effective for hypertrophy? (
  • Muscle hypertrophy is the clinical name for the body's process for making muscles larger. (
  • The fast twitch muscles are the ones that grow larger, which is why intense exercise methods like weight lifting are the main activities used to cause muscle hypertrophy. (
  • By week 12, you should be lifting significantly more weight than week 1 due to hypertrophy of the muscles. (
  • The burn you feel [when doing hypertrophy training] is a mechanical stress on the muscles, and the by-product of that is lactic acid," Miranda explains. (
  • Other components of your workout can also be changed to overload the muscles and prompt the hypertrophy, such as frequency, volume, tempo, and so on. (
  • Exercises like squats, deadlifts, military press, and bench press have been noted as highly effective for targeting several muscles at once and prompting hypertrophy. (
  • These observations are relevant to clinical practice, as they relate to the excessive hypertrophy and contractile dysfunction regularly observed in patients with aortic stenosis. (
  • Tonsillar hypertrophy, or enlarged tonsils, can be caused by an ongoing (chronic) condition or be a temporary effect of an infection. (
  • Zymbal's gland - Hypertrophy in a male F344/N rat from a chronic study. (
  • Aside from increased reliance on glucose as an energy source, changes in other glucose metabolism pathways, e.g. the pentose phosphate pathway, the glucosamine biosynthesis pathway, and anaplerosis, are also noted in the hypertrophied hearts. (
  • In recent years, the identification and characterization of the molecular pathways leading to cardiac hypertrophy has highlighted a number of potential therapeutic targets. (
  • Likewise, the molecular events that signal hypertrophy are more complex than initially anticipated, with many parallel and redundant transducer and effector pathways. (
  • After the six weeks i aim to move onto a hypertrophy routine (below) and really nail my diet etc. (
  • My goals for the following routine are to continue building muscle mass but focus on the hypertrophy/aesthetics also. (
  • Obviously diet plays a huge role in hypertrophy but we will leave that for now and look at the simple principle of progressive overload training. (
  • When tonsillar hypertrophy leads to sleep apnea and trouble sleeping, it can cause a range of complications if left untreated, especially in children. (
  • Breast hypertrophy is more common in overweight women but there is a very real association between a patient's body mass index (BMI), a measure of weight compared corrected for the height of the patient, and complications following surgery for breast hypertrophy. (
  • What is tonsillar hypertrophy? (
  • Tonsillar hypertrophy is the medical term for persistently enlarged tonsils . (
  • Tonsillar hypertrophy is particularly common in children, though it can also affect adults. (
  • Tonsillar hypertrophy tends to affect children, but experts aren't sure why. (
  • There might also be a genetic link, as tonsillar hypertrophy often runs in families. (
  • Tonsillar hypertrophy usually only requires treatment if it's interfering you're your ability to sleep, eat, or breathe. (
  • Depending on the underlying cause and whether tonsillar hypertrophy interferes with your breathing, you may need antibiotics or surgery to remove your tonsils. (
  • In a few patients, one symptom of cardiac hypertrophy is sudden death. (
  • Data from patients with adenoidal hypertrophy, who reported starting treatments within the last 5 years. (
  • Congenital retinal pigment epithelial hypertrophy (CHRPE) is usually found before patients reach 30 years of age. (
  • Patients with gastric mucosal hypertrophy may be at a higher risk of stomach cancer. (
  • My echo says mild hypertrophy of the septum originally it said it was obstructed, but when I got the original hospital echo it says septu. (
  • Adenoidal hypertrophy, or enlarged adenoids, can be normal or related to infections. (
  • Motor learning induces astrocytic hypertrophy in the cerebellar cortex. (
  • 1997). B. Motor learning induces hypertrophy of astrocytes in the cerebellar cortex. (
  • These findings demonstrate that learning triggers the hypertrophy of astrocytic processes and furthermore that, unlike learning-induced synaptogenesis, astrocytic growth is reduced in the absence of continued training. (
  • These findings suggest that the extract of NXT inhibited H9c2 cardiomyocyte cell hypertrophy via PPAR γ -mediated cell autophagy. (
  • As a result, they said, these findings reflect a potentially important association but do not establish causality between resolution of hypertrophy and diabetes. (
  • These findings show that glucocorticoids, rather than androgens, undergo adaptive changes in the circulation and in muscle during the development of exercise-induced cardiac hypertrophy. (
  • We report, for the first time in humans, genome-wide DNA methylation (850,000 CpGs) and gene expression analysis after muscle hypertrophy (loading), return of muscle mass to baseline (unloading), followed by later hypertrophy (reloading). (
  • Consequently, hypertrophy of cultured cardiomyocytes cannot simply be characterized as the reversal to the fetal gene expression program. (
  • Many people seek to increase muscle hypertrophy through weight-lifting exercise for cosmetic and athletic reasons. (
  • Muscle hypertrophy is an increase in muscle fiber size, observed when the muscle achieves a larger diameter or thickness. (
  • The term hypertrophy may serve as a general one to comprise all the instances of excessive growth and increased size of organs, whether the increase be general or in one direction merely. (
  • b) Increase Motor Units, greater Muscle Fiber Activation (Type I, IIa, IIb/X). c) Load of 60-85% necessary for Hypertrophy. (
  • Muscle Hypertrophy is the increase in the size of muscle cells. (
  • Fluorescein angiography of RPE hypertrophy typically demonstrates blockage of fluorescence (except in the areas of atrophy which are hyperfluorescent). (
  • These divergent patterns of hypertrophy were related 40 years ago to disparate wall stresses in both conditions, with systolic wall stress eliciting parallel replication of sarcomeres and diastolic wall stress, series replication. (
  • Eye tumor specialists can typically differentiate between retinal pigment epithelial hypertrophy and melanoma by clinical examination (without a biopsy). (