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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Protein supplementation before and after exercise does not further augment skeletal muscle hypertrophy after resistance training in elderly men. Whats the best protein shake after a workout? Should you take your whey protein shake before or after your workout? It also might help to grab some water to restore lost electrolytes or have a quick snack or protein shake before things really start heating up. (6). Look for a protein blend that has a 2:1:1 BCAA ratio-10 grams of BCAAs per serving, five of which are leucine. Theres no need to reach for a shake after every run. Everyone has their likes and dislikes. There are a handful of reasons for this and you can click on the links in the above paragraph to see exactly how dextrose and creatine may help take your workouts up a notch. This is key because exercise causes the breakdown and oxidation of BCAAs. Determining whether to drink a protein shake before or after a workout seems to come down to personal preference. -, Carbohydrate does not ...
Quickly learn the science behind muscle hypertrophy and how to achieve maximum growth through strategic strength training and supplementation
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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. ...
Persistent overexpression of IGF-I in mice skeletal muscle results in hypertrophy, which is likely mediated via the mTOR/p70S6K pathway, potentially via an Akt-independent signaling pathway.
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...
... of the temporal muscles Athlete's heart Ventricular hypertrophy (including left ventricular hypertrophy and right ... Eccentric hypertrophy is a type of hypertrophy where the walls and chamber of a hollow organ undergo growth in which the ... Muscle hypertrophy List of biological development disorders Hernandez, Richard; Kravitz, Len. "Skeletal muscle hypertrophy". ... a type of concentric hypertrophy, where sarcomeres are added in parallel). Hypertrophy of breast, c. 1870 Forensic post-mortem ...
... is a hypertrophic growth of a hollow organ without overall enlargement, in which the walls of the organ ... These compensatory changes, termed "concentric hypertrophy," reduce the increase in wall tension observed in aortic stenosis.[ ... concentric hypertrophy is related to increased pressure overload of the heart, often due to hypertension and/or aortic stenosis ...
... (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. ...
... can cause a wide spectrum of defects or may involve only muscle or bone. it is usually treated ... Hemifacial hypertrophy (also termed facial hemihypertrophy, facial hemihyperplasia, or Friedreich's disease) abbreviated as ( ... "Comparison between true and partial hemifacial hypertrophy". Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 104 (4): 501-9. ...
... may be divided into two categories: concentric hypertrophy and eccentric hypertrophy. These adaptations ... In individuals with eccentric hypertrophy there may be little or no indication that hypertrophy has occurred as it is generally ... Eccentric hypertrophy is related to volume overload and leads to the addition of sarcomeres in series. Concentric hypertrophy ... Eccentric hypertrophy is generally regarded as healthy, or physiologic hypertrophy and is often termed "athlete's heart." It is ...
... is classified in one of five ways: as either pubertal (virginal hypertrophy), gestational (gravid ... Only 15% of cases of breast hypertrophy are unrelated to puberty or pregnancy. Other types and causes of breast hypertrophy ... Hypertrophy of the breast can affect the breasts equally, but usually affects one breast more than the other, thereby causing ... Breast hypertrophy is a rare medical condition of the breast connective tissues in which the breasts become excessively large. ...
... or muscle building involves a hypertrophy or increase in size of skeletal muscle through a growth in size of ... Sarcoplasmic hypertrophy is greater in the muscles of bodybuilders because studies suggest sarcoplasmic hypertrophy shows a ... During puberty in males, hypertrophy occurs at an increased rate. Natural hypertrophy normally stops at full growth in the late ... Two factors contribute to hypertrophy: sarcoplasmic hypertrophy, which focuses more on increased muscle glycogen storage; and ...
... left-sided ventricular hypertrophy and resulting increased left ventricular mass. While ventricular hypertrophy occurs ... Left ventricular hypertrophy (LVH) is thickening of the heart muscle of the left ventricle of the heart, that is, ... "Lesson VIII - Ventricular Hypertrophy". Retrieved 2009-01-07. Sokolow M, Lyon TP (1949). "The ventricular complex in left ... "Ask the doctor: Left Ventricular Hypertrophy". Retrieved 2007-12-07. Meijs MF, Bots ML, Vonken EJ, et al. (2007). "Rationale ...
A hypertrophy has also been observed in spermatocytes; in general an enlargement of the gametes is observed. Such viruses have ... Viral gametocytic hypertrophy is a pathological condition observed in the Pacific oyster. The condition was first discovered in ... The health of the oysters is not noticeably affected by viral gametocytic hypertrophy. Garcia, Céline; Robert, Maeva; Arzul, ... Cheslett, D; Mc Kiernan, F; Hickey, C; Collins, E (25 February 2009). "Viral gametocytic hypertrophy of the Pacific oyster ...
... management of right ventricular hypertrophy is about either preventing the development of right ventricular hypertrophy in the ... but what right ventricular hypertrophy represents is. Right ventricular hypertrophy is the intermediate stage between increased ... Hypertrophy can also be caused by mechanical forces, mTOR pathways, nitric oxide and immune cells. Immune cells can cause ... Hypertrophy of individual myocytes results in an increase in right ventricular wall thickness. The worldwide incidence of PH is ...
Gene doping Muscle hypertrophy Myostatin Hysterical strength activin A "Super Strong Kids May Hold Genetic Secrets". ABC News. ... Myostatin-related muscle hypertrophy is a rare genetic condition characterized by reduced body fat and increased skeletal ... Myostatin-related muscle hypertrophy has a pattern of inheritance known as incomplete autosomal dominance. People with a ... Myostatin-related muscle hypertrophy at NIH Genetics Home Reference (Articles lacking in-text citations from February 2014, All ...
... (1919) is a work of art by the German artist Max Ernst who was a pioneer of the Dada movement and ... Help! Help![citation needed] Trophy, Hypertrophied is a part of the collection of the Museum of Modern Art in New York City, ... "Trophy, Hypertrophied by Max Ernst". Retrieved 2022-09-09. "Max Ernst. Hypertrophic Trophy (hypertrophie ...
... is a rare cutaneous condition of unknown pathology that present to ...
Hypertrophy. Biology-Online dictionary. Retrieved 2016-06-08. Medical Definition of pseudohypertrophic. Merriam-Webster Online ...
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 ...
Hinman Jr F (1983). Benign Prostatic Hypertrophy. Springer Science & Business Media. pp. 259, 266, 272. ISBN 978-1-4612-5476-8 ...
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 ...
Left ventricular hypertrophy is thought to be a leading cause of sudden cardiac deaths in the adult population. This is most ... Left ventricular hypertrophy can be demonstrated on an echocardiogram and electrocardiogram (EKG). A 1999 review of sudden ... Katholi RE, Couri DM (2011). "Left ventricular hypertrophy: major risk factor in patients with hypertension: update and ... Previous adverse cardiac events, non-sustained ventricular tachycardia (NSVT), syncope, and left ventricular hypertrophy (LVT) ...
... hypertrophy usually mild; restrictive phenotype may be present; may carry high risk of sudden cardiac death maple syrup urine ...
Burns E, Buttner R (2018-08-01). "Left Ventricular Hypertrophy (LVH)". Life in the Fast Lane • LITFL. Retrieved 2022-01-17. ... Burns E, Buttner R (2018-08-01). "Left Ventricular Hypertrophy (LVH)". Life in the Fast Lane • LITFL. Retrieved 2022-01-17. ... right and left ventricular hypertrophy, or a faulty ECG recording technique. R wave peak time (RWPT) represents the time from ... ventricular hypertrophy, myocardial infarction, electrolyte derangements, and other disease states. High frequency analysis of ...
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 ...
This is in contrast with typical muscle hypertrophy, in which the muscle tissue itself increases in size. Because ... Cros, D; Harnden, P; Pellissier, JF; Serratrice, G (January 1989). "Muscle hypertrophy in Duchenne muscular dystrophy. A ... Walters, J (October 2017). "Muscle hypertrophy and pseudohypertrophy". Practical Neurology. 17 (5): 369-379. doi:10.1136/ ...
Calf hypertrophy can occur. Involvement of the heart occurs in almost all cases, presenting as syncope in second or third ...
"Right Ventricular Hypertrophy (RVH) • LITFL • ECG Library Diagnosis". Life in the Fast Lane. 2018-08-01. Archived from the ... The boot like shape is due to the right ventricular hypertrophy present in TOF. Lung fields are often dark (absence of ... Electrocardiography shows right ventricular hypertrophy (RVH), along with right axis deviation. RVH is noted on EKG as tall R- ... Another common finding associated with ASDs is right ventricular hypertrophy, also known as enlargement of the right ventricle ...
Myostatin-related muscle hypertrophy is a rare condition characterized by reduced body fat and increased muscle size. Explore ... 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 ... Myostatin-related muscle hypertrophy has a pattern of inheritance known as incomplete autosomal dominance. People with a ...
The goal of SPHERES is to understand the dynamics and consequences of adipocyte hypertrophy (enlargement) through investigation ... Multi-level dynamics of adipocyte hypertrophy. Adipocyte hypertrophy is a condition associated with larger than normal lipid ... Adipocyte hypertrophy is irrespective of body fat and causes a wide range of pathological conditions including cardiometabolic ... The work will pave the way for a better understanding of the underlying mechanisms of adipocyte hypertrophy as well as the ...
... a diuretic to ACE inhibitor therapy is more effective than ACE inhibitor monotherapy in reducing left ventricular hypertrophy, ... One of the largest ever studies in the reversal of left ventricular hypertrophy (LVH) has provided new evidence for the ... Dahlof B. The PICXEL study: benefits of a low dose combination on left ventricular hypertrophy reduction. Presented at the ... The results of the Perindopril/Indapamide in a double-blind Controlled study versus Enalapril in Left ventricular hypertrophy ( ...
New guidance has been released today by the National Institute for Health and Care Excellence (NICE) recommending Olympus Medicals transurethral resection in saline (TURis) system for use in surgery to reduce the size of enlarged prostate glands in men. NICE published the guidance in light of the potential it offers NHS hospitals to realise substantial cost savings of £285-£375 per patient whilst also improving patient outcomes.. ...
Compared with those without left ventricular hypertrophy (n=51) and left ventricular hypertrophy without ECG strain (n=30), ... Left ventricular hypertrophy with strain and aortic stenosis Circulation. 2014 Oct 28;130(18):1607-16. doi: 10.1161/ ... Background: ECG left ventricular hypertrophy with strain is associated with an adverse prognosis in aortic stenosis. We ...
Lipomatous hypertrophy is an uncommon benign lesion of the atrium, generally asymptomatic, characterized by unencapsulated ... Lipomatous Hypertrophy: An Accidental Finding in Heart. F. Petrelli. ,1,2L. Spagnoli. ,1,2S. Aversa. ,1,2S. Tripodi. ,2and C. ... M. Bolognesi, "Lipomatous hypertrophy of the interatrial septum and arrhythmia: A case report," Journal of Integrative ... Lipoma, unlike lipomatous hypertrophy, is an encapsulated lesion composed of only mature adipocytes and few, if any, myocytes. ...
Alvin S Chen, Rachel E Bent, Matthew Wheeler, Joshua W Knowles, Francois Haddad, Victor Froelicher, Euan Ashley, Marco V Perez ...
... , Tonsillar Hypertrophy, Adenotonsillar Hypertrophy. ... Tonsillar Hypertrophy Grading Scale Aka: Tonsillar Hypertrophy Grading Scale, Tonsillar Hypertrophy, Adenotonsillar Hypertrophy ... These images are a random sampling from a Bing search on the term "Tonsillar Hypertrophy Grading Scale." Click on the image (or ... Tonsillar Hypertrophy Grading Scale Tuning Fork Test Tympanometry Whispered Voice Testing ...
Tag: labial hypertrophy. One side of my outer labia is much larger than the other. There is an obvious difference in size, and ... I think I have labial hypertrophy. Do I have to have surgery? Updated 22 January 2014 under Ask Us. No, you dont have to have ... Labial hypertrophy (pronounced: lay-bee-al hi-per-tro-fee) is a long name that means the enlargement of the labia (sometimes ... Labial hypertrophy (pronounced: lay-bee-al hi-per-tro-fee) is a long name that means the enlargement of the labia (sometimes ...
... hypertrophy in adipocytes is the main cause of energy metabolic system dysfunction, obesity and its afflictions such as T2D. ... Hypertrophy of adipocytes is the main cause of obesity7,8,9. These results from the excessive storage of energy in the form of ... Lipid droplets hypertrophy: a crucial determining factor in insulin regulation by adipocytes. *Bahram Sanjabi1 na1, ... Sanjabi, B., Dashty, M., Özcan, B. et al. Lipid droplets hypertrophy: a crucial determining factor in insulin regulation by ...
Tonsillar hypertrophy, or enlarged tonsils, can happen due to an ongoing (chronic) condition or a temporary effect of an ... Tonsillar hypertrophy, or enlarged tonsils, can be caused by an ongoing (chronic) condition or be a temporary effect of an ...
The Mammalian Phenotype (MP) Ontology is a community effort to provide standard terms for annotating phenotypic data. You can use this browser to view terms, definitions, and term relationships in a hierarchical display. Links to summary annotated phenotype data at MGI are provided in Term Detail reports.
Left ventricular hypertrophy (LVH) is a common cardiovascular complication and an independent risk factor for cardiovascular ... Fibroblast Growth Factor 23 and Left Ventricular Hypertrophy in Hemodialysis Patients () Ayaka Saito1,2, Takako Onuki2, ... Silberberg, J.S., Barre, P.E., Prichard, S.S. and Sniderman, A.D. (1989) Impact of Left Ventricular Hypertrophy on Survival in ... Background: Left ventricular hypertrophy (LVH) is a common cardiovascular complication and an independent risk factor for ...
Employing negative lifting to bolster strength and hypertrophy training is an excellent progressive overload approach to help ... Negative Lifting For Strength and Hypertrophy: Creative Progressive Overload. Posted September 17th, 2019 by Theresa Perales ... Home , NFPT Blog , Negative Lifting For Strength and Hypertrophy: Creative Progressive Overload ...
... and follicular cell adenoma in the rat. ... At the microscopic level, thyroid hypertrophy was observed in all phenobarbital-treated rats and to a lesser degree in most ... Studies on the mechanism of simvastatin-induced thyroid hypertrophy and follicular cell adenoma in the rat. - GreenMedInfo ... Studies on the mechanism of simvastatin-induced thyroid hypertrophy and follicular cell adenoma in the rat. ...
... Q: I got the Power-Density Mass Workout 2.0 and was motivated by [Mr. America] Doug ... High-End Hypertrophy Progression: Your Muscles Will Blow Up Big Time ==========================================. Q: I got the ... Ezine #902: Heavy/Light, X-centric Sets and Muscle Hypertrophy I really like X-centric sets . Great muscle feel and pump. Im ... Ezine #905: Rhythm Method for More Muscle Hypertrophy Ive been doing mostly compound exercises with X-centric on the first set ...
Chapter 9 - Ab Training during a Stubborn Muscle Hypertrophy Routine. *Chapter 10 - Cardio during a Stubborn Muscle Hypertrophy ...
Five Principles of Hypertrophy. 1 Train More Often. Drop the notion that a muscle group can only be trained once a week. ... The Anti-Bodybuilding Hypertrophy Program. Break the by Chad Waterbury , January 17, 2003. June 9, 2022. ... If maximum hypertrophy is your goal, eat plenty and use advanced workout nutrition. Follow the details of this program and ... Hypertrophy, Like Youve Never Heard it Before. Never has there been a subject with more misinformation. Common sense and ...
Left ventricular hypertrophy is thickening of the walls of the lower left heart chamber. The lower left heart chamber is called ... Left ventricular hypertrophy. Left ventricular hypertrophy is a thickening of the wall of the hearts main pumping chamber. ... Things that increase the risk of left ventricular hypertrophy include:. *Age. Left ventricular hypertrophy is more common in ... Left ventricular hypertrophy is thickening of the walls of the lower left heart chamber. The lower left heart chamber is called ...
What is mild facet hypertrophy?. Facet Hypertrophy. Facet Hypertrophy is a condition in which there is a swelling, or ... What causes mild facet hypertrophy?. Hypertrophy in your facet joints is related to spinal arthritis, and like spinal arthritis ... Is mild facet hypertrophy serious?. This swelling in the facet joint can increase to the point where nerves in the spine come ... Facet Hypertrophy is the term used to describe a degeneration and enlargement of the facet joints. The facet joints, which are ...
A 12-Lead ECG-Based System With Physiological Parameters and Machine Learning to Identify Right Ventricular Hypertrophy in ... A 12-Lead ECG-Based System With Physiological Parameters and Machine Learning to Identify Right Ventricular Hypertrophy in ... The presence of right ventricular hypertrophy (RVH) accounts for approximately 5-10% in young adults. The sensitivity estimated ...
Home , E. Pathology by systems , Cardiovascular system , Heart , myocardial hypertrophy. myocardial hypertrophy. Wednesday 16 ... Cardiac hypertrophy, however, is associated with reinduction of ANF gene expression. ANF is a peptide hormone that causes salt ... What are the triggers for hypertrophy and for these changes in gene expression? In the heart, there are at least two groups of ... The mechanisms of cardiac muscle hypertrophy involve many signal transduction pathways, leading to the induction of a number of ...
In this early inflammatory phase of LV hypertrophy Ly6Chigh monocytes infiltrated the heart in response to a C-C chemokine ... CX3CR1 expression impacts the immune response in the development of LV hypertrophy and its absence has clear cardioprotective ... Here, the authors demonstrate that Fraktalkine-receptor CX3CR1 is a prerequisite for the development of cardiac hypertrophy and ... The comparison of C57BL/6 mice with CX3CR1 deficient mice displayed reduced LV hypertrophy and preserved cardiac function in ...
Return to Article Details Adenoid hypertrophy and open bite Download Download PDF ...
Acquisition of cardiac hypertrophy gene dataset. Target genes associated with cardiac hypertrophy were downloaded from the Gene ... Cardiac hypertrophy is an adaptive response to pathological stimuli but prolonged hypertrophy results in cardiac dysfunction ... Ott C, Jung T, Brix S, John C, Betz IR, Foryst-Ludwig A, Deubel S, Kuebler WM, Grune T, Kintscher U and Grune J: Hypertrophy- ... Wang XQ, Xu ZT, Zhang GP, Hou N, Mo QX, Wei J, Jiang X, Liu Y and Luo JD: Endophilin A2 attenuates cardiac hypertrophy induced ...
A77 1726 (leflunomide) blocks and reverses cardiac hypertrophy and fibrosis in mice Zhen-Guo Ma; Zhen-Guo Ma * ... Herein, we found that A77 1726 treatment attenuated pressure overload or angiotensin II (Ang II)-induced cardiac hypertrophy in ... More importantly, A77 1726 was capable of blocking pre-established cardiac hypertrophy in mice. In conclusion, A77 1726 ... However, the effect of A77 1726 on cardiac hypertrophy remains completely unknown. ...
Study: Relationship Between Adenoids Hypertrophy and Food Intolerance. Home » Blog » Food Allergies » Study: Relationship ... Food intolerance is the possible cause of adenoidal hypertrophy. The detection of specific IgG antibodies of food have positive ... To explore the relationship between food intolerance and adenoidal hypertrophy and accordingly to provide evidence for ...
Benign prostatic hypertrophy*Enlargement of prostate*Smooth enlarged prostate*Soft enlarged prostate ...
The Business Research Company offers drugs for benign prostatic hypertrophy market research report 2022 with industry size, ... UK Drugs For Benign Prostatic hypertrophy Market 16.1. UK Drugs For Benign Prostatic hypertrophy Market, Segmentation By Type, ... 5. Drugs For Benign Prostatic hypertrophy Market Size And Growth 5.1. Global Drugs For Benign Prostatic hypertrophy Historic ... 8. Asia-Pacific Drugs For Benign Prostatic hypertrophy Market 8.1. Asia-Pacific Drugs For Benign Prostatic hypertrophy Market ...
Skin hypertrophy is found among people with Nuclear magnetic resonance imaging abdominal abnormal, especially for people who ... What is Skin hypertrophy?. Skin hypertrophy (skin cells enlarges) is found to be associated with 1,039 drugs and 508 conditions ... Do you take medications and have Skin hypertrophy?. Check whether Skin hypertrophy is associated with a drug or a condition How ... Nuclear magnetic resonance imaging abdominal abnormal and Skin hypertrophy. Summary:. Skin hypertrophy is found among people ...
  • T-cell infiltration and the subsequent increased intracardial chronic inflammation play crucial roles in the development of cardiac hypertrophy and heart failure (HF). (
  • Herein, we demonstrate that the in vivo cardiomyocyte specific overexpression of RGS2 eb prevents the development of cardiac hypertrophy in a transverse aortic constriction (TAC) model of experimental pressure overload, as well as functional loss and the expression of "fetal" genes associated with hypertrophy and heart failure. (
  • Doctors who do Adenoid Hypertrophy Treatment in Tennessee. (
  • Current models suggest that growth factors or vasoactive agents produced by cardiac nonmuscle cells or by myocytes themselves in response to hemodynamic stress stimulate the expression of various genes, leading to myocyte hypertrophy. (
  • Furthermore, 1,25(OH) 2 D 3 increased myocyte protein levels and increased cell size, suggesting that it induces cardiac myocyte hypertrophy. (
  • Our findings indicate that 1,25(OH) 2 D 3 and phorbol esters directly regulate myocyte proliferation and induce myocyte hypertrophy. (
  • Tarone G, Lembo G. Molecular interplay between mechanical and humoral signalling in cardiac hypertrophy. (
  • Lipomatous hypertrophy is an uncommon benign lesion of the atrium, generally asymptomatic, characterized by unencapsulated accumulation of adipose tissue entrapping cardiomyocytes. (
  • Lipomatous hypertrophy is a benign cardiac mass characterized by an unencapsulated accumulation of mature adipose tissue within the interatrial septum, rarely in the atrium wall [ 1 ]. (
  • Lipomatous hypertrophy represents a benign though rare condition that should always be considered in the differential diagnosis in case of an atrial mass detected during imaging, surgery, or necroscopy and definitively diagnosed by histological examination. (
  • The drug benign prostatic hypertrophy market consists of sales of benign prostatic hypertrophy drugs to treat enlarged prostate glands. (
  • Benign Prostatic Hypertrophy is commonly seen in men older than age 50. (
  • The main types of drugs for benign prostatic hypertrophy are alpha-blockers, 5-alpha reductase inhibitors, phosphodiesterase-5 inhibitors, and others. (
  • This drug for benign prostatic hypertrophy market research report delivers a complete perspective of everything you need, with an in-depth analysis of the current and future scenario of the industry. (
  • The rising male geriatric population globally is driving the market for Benign Prostatic Hypertrophy drugs as the condition is commonly seen in men aged over 50 years. (
  • Combination drugs are increasingly being used in the treatment of Benign Prostatic Hypertrophy as they are more effective and help prevent disease progression. (
  • For instance, Duodart, a combination of dutasteride and tamsulosin hydrochloride is increasingly being prescribed for the treatment of Benign Prostatic Hypertrophy. (
  • Benign prostatic hypertrophy drug manufacturers globally are regulated by various regulatory bodies. (
  • Major players in the drugs for benign prostatic hypertrophy market are Allergan PLC, Astellas Pharma Inc., Boehringer Ingelheim, Eli Lilly and Company, GlaxoSmithKline PLC, Teva Pharmaceutical Industries Limited, Sanofi, Nymox Pharmaceutical Corporation and AEternaZentaris Inc. (
  • Ritter O, Neyses L. The molecular basis of myocardial hypertrophy and heart failure. (
  • Myocardial hypertrophy is an independent risk factor for cardiovascular disease and a key cause of heart failure ( 1 ). (
  • Cardiomyocyte hypertrophy is an indicator of myocardial remodeling and induces decreased myocardial contractility, which progresses to heart failure ( 2 ). (
  • BACKGROUND: Because initially compensatory myocardial hypertrophy in response to pressure overloading may eventually decompensate to myocardial failure, mechanisms responsible for this transition have long been sought. (
  • We evaluated the myocardial protective effect of verapamil cardioplegia on the hypertrophied left ventricle during CPB. (
  • 26.Murach KA, Bagley JR. Skeletal Muscle Hypertrophy with Concurrent Exercise Training: Contrary Evidence for an Interference Effect. (
  • The presence of right ventricular hypertrophy (RVH) accounts for approximately 5-10% in young adults. (
  • He had right ventricular hypertrophy, thickened pulmonary valve leaflets, severe asymmetric left ventricular hypertrophy with outflow tract obstruction, and a thickened and dysplastic aortic valve. (
  • Using a minimally invasive transverse aortic banding (MTAB) mouse model of cardiac hypertrophy, we have assessed fibrosis and cardiac fibroblast proliferation. (
  • The MTAB model used here produces extensive hypertrophy and fibrosis. (
  • To explore the relationship between food intolerance and adenoidal hypertrophy and accordingly to provide evidence for intolerance and adenoidal hypertrophy. (
  • Food intolerance is the possible cause of adenoidal hypertrophy. (
  • The detection of specific IgG antibodies of food have positive significance in the prevention of adenoidal hypertrophy. (
  • Approximately half the animals receiving androstanediol alone and all of those receiving androstanediol plus estradiol fulfill the weight and histologic criteria for prostatic hypertrophy in the dog. (
  • Since both of these steroid hormones are presumed to be normal secretory products of the testis, it is possible that they are involved in the pathogenesis of prostatic hypertrophy in the dog. (
  • Walsh, PC & Wilson, JD 1976, ' The induction of prostatic hypertrophy in the dog with androstanediol ', Journal of Clinical Investigation , vol. 57, no. 4, pp. 1093-1097. (
  • According to generic Viagra review , prostatic hypertrophy is a disease characteristic for elderly men. (
  • One of the largest ever studies in the reversal of left ventricular hypertrophy (LVH) has provided new evidence for the reversal of target organ damage with fixed-dose combination therapy. (
  • ECG left ventricular hypertrophy with strain is associated with an adverse prognosis in aortic stenosis. (
  • Background: Left ventricular hypertrophy (LVH) is a common cardiovascular complication and an independent risk factor for cardiovascular death in hemodialysis (HD) patients. (
  • Middleton, R.J., Parfrey, P.S. and Foley, R.N. (2001) Left Ventricular Hypertrophy in the Renal Patient. (
  • Silberberg, J.S., Barre, P.E., Prichard, S.S. and Sniderman, A.D. (1989) Impact of Left Ventricular Hypertrophy on Survival in End-Stage Renal Disease. (
  • Left ventricular hypertrophy is a thickening of the wall of the heart's main pumping chamber. (
  • Left ventricular hypertrophy is thickening of the walls of the lower left heart chamber. (
  • During left ventricular hypertrophy, the thickened heart wall can become stiff. (
  • Uncontrolled high blood pressure is the most common cause of left ventricular hypertrophy. (
  • Treatment of left ventricular hypertrophy depends on the cause. (
  • Left ventricular hypertrophy usually develops gradually. (
  • Left ventricular hypertrophy itself doesn't cause symptoms. (
  • If you have high blood pressure or another condition that increases the risk of left ventricular hypertrophy, your provider is likely to recommend regular health checkups to check your heart. (
  • Anything that puts stress on the heart's lower left chamber can lead to left ventricular hypertrophy. (
  • Left ventricular hypertrophy also may be caused by gene changes that affect the heart muscle's structure. (
  • Also called hypertension, this is the most common cause of left ventricular hypertrophy. (
  • Treating high blood pressure can help reduce left ventricular hypertrophy symptoms and may even reverse it. (
  • If left untreated, facet hypertrophy can cause several other conditions including stenosis and radiculopathy. (
  • Pathological left ventricular hypertrophy is a maladaptive cardiomyocyte growth response to various cardiovascular conditions such as hypertension, and is a major risk factor for heart failure and stroke. (
  • Effects of Verapamil Cardioplegia on the Hypertrophied Left Ventricle Undergoing Cardiopulmonary Bypass. (
  • There is a close correlation between the level of hypertension, left ventricular hypertrophy, deterioration of GFR, and the progressive enlargement of the cystic kidneys in adult ADPKD. (
  • Randomized clinical investigation indicates that ACEI and a BP goal of 120/80 mmHg are associated in a 7-yr study to reverse left ventricular hypertrophy. (
  • Optimal threshold value for left ventricular hypertrophy in blacks. (
  • Exposure to traffic-related air pollution is linked to left ventricular hypertrophy, heart failure, and death. (
  • Excess dietary intake of sodium increases blood pressure (1) and can increase the risk of cardiovascular disease, renal disease, gastric cancer, osteoporosis, and left ventricular hypertrophy (2,3). (
  • The work will pave the way for a better understanding of the underlying mechanisms of adipocyte hypertrophy as well as the identification of therapeutic strategies targeting adipocytes. (
  • Furthermore, Res ameliorated isoprenaline‑induced cardiac hypertrophy, significantly improving cardiac dysfunction in vivo experiment (echocardiography, the degree of ventricular hypertrophy, etc. (
  • An infant with subvalvar and valvar aortic stenosis, subvalvar and valvar pulmonary stenosis, severe biventricular hypertrophy and pulmonary hemorrhage. (
  • Herein, we found that A77 1726 treatment attenuated pressure overload or angiotensin II (Ang II)-induced cardiac hypertrophy in vivo , as well as agonist-induced hypertrophic response of cardiomyocytes in vitro . (
  • Conclusions - Downregulation of I to , APD prolongation, and cardiac hypertrophy occur early after AS, and in vivo gene transfer of Kv4.3 can restore these electrical parameters and abrogate the hypertrophic response via the calcineurin pathway. (
  • abstract = "Background - Prolongation of the action potential duration (APD) and decreased transient outward K+ current (Ito] have been consistently observed in cardiac 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). (
  • Facet Hypertrophy is the term used to describe a degeneration and enlargement of the facet joints. (
  • Facet Hypertrophy is a condition in which there is a swelling, or enlargement, of the facet joint. (
  • Whatever the exact mechanism of cardiac hypertrophy, it eventually reaches a limit beyond which enlargement of muscle mass is no longer able to compensate for the increased burden, and cardiac failure ensues. (
  • Although we further hypothesized that the expression of RGS2 eb in Rgs2 --/- mice (which are highly sensitive to hypertrophy and heart failure following pressure overload) could compensate for the loss of endogenous RGS2, we were limited in our characterizations by poor survival rates in Rgs2 -/- animals following TAC surgery. (
  • CONCLUSIONS: These and additional corroborative data show that increased cardiocyte microtubule network density is an important mechanism for the ventricular contractile dysfunction that develops in large mammals with adult-onset pressure-overload-induced cardiac hypertrophy. (
  • Adipocyte hypertrophy is irrespective of body fat and causes a wide range of pathological conditions including cardiometabolic diseases. (
  • RGS2 is a GTPase activating protein which limits G q - and G s -mediated signalling, which are known to play major roles in the development of pathological cardiac hypertrophy. (
  • These images are a random sampling from a Bing search on the term "Tonsillar Hypertrophy Grading Scale. (
  • Tonsillar hypertrophy, or enlarged tonsils, can be caused by an ongoing (chronic) condition or be a temporary effect of an infection. (
  • Patients with isolated valvular pulmonary stenosis may have a reactive infundibular hypertrophy that could elicit a reactive infundibular obstruction. (
  • The mechanisms of cardiac muscle hypertrophy involve many signal transduction pathways, leading to the induction of a number of genes, which in turn stimulate synthesis of numerous cellular proteins. (
  • A total of 444 targets associated with cardiac hypertrophy and 229 potential disease‑associated targets of Res were identified, from which 8 overlapping genes were demonstrated. (
  • Lipid droplets (LDs) hypertrophy in adipocytes is the main cause of energy metabolic system dysfunction, obesity and its afflictions such as T2D. (
  • Derived from workspace Guyton, Heart Hypertrophy or Deterioration, 2008 at changeset bf2aede8c806 . (
  • RESULTS: The ventricular segments most affected by hypertrophy are those of the septal region. (
  • Thus, we hypothesized that the in vivo expression of RGS2 eb could limit the development of experimentally induced hypertrophy. (
  • The relation between electrical remodeling and cardiac hypertrophy in vivo is unknown. (
  • Adipocyte hypertrophy is a condition associated with larger than normal lipid droplets (LDs), the adipocyte organelles that store energy in the form of triglycerides. (
  • The scope of the EU-funded SPHERES project is to investigate the hypothesis that disturbances in the interaction between LD proteins and LD lipid composition lead to adipocyte hypertrophy. (
  • In conclusion, Res inhibited cardiac hypertrophy via downregulation of the apoptosis signaling pathway and upregulating the autophagy pathway. (
  • Female Sprague-Dawley rats were treated with either simvastatin (a novel competitive inhibitor of HMG CoA reductase) or phenobarbital (positive control) to ascertain the possible relationship between the effects of simvastatin on hepatic metabolism and the thyroid hypertrophy and follicular cell adenomas which it produces in this strain of rat. (
  • However, the mechanisms by which Res ameliorates cardiac hypertrophy have not yet been fully elucidated. (
  • It was concluded that the chronic administration of SMS reduced glomerular hypertrophy without altering renal functions in this experimental model. (
  • 6 ,7 These findings are supported by rat studies that show 1,25(OH)2D3 administration attenuates the development of glomerulosclerosis and the progression of proteinuria through parathyroid hormone-independent antiproliferative actions and decreases in podocyte loss and podocyte hypertrophy. (
  • Variants (also known as mutations) in the MSTN gene cause myostatin-related muscle hypertrophy. (
  • Cardiac hypertrophy, however, is associated with reinduction of ANF gene expression . (
  • What are the triggers for hypertrophy and for these changes in gene expression? (
  • At the microscopic level, thyroid hypertrophy was observed in all phenobarbital-treated rats and to a lesser degree in most simvastatin-treated animals. (
  • Reduced glomerular hypertrophy by somatostatin analog, SMS 201-995, in the subtotal nephrectomized rats fed high-protein meals. (
  • AS rats infected with Ad.β-gal developed cardiac hypertrophy compared with sham rats, as assessed by cellular capacitance and heart weight-body weight ratio. (
  • Is mild facet hypertrophy serious? (
  • Hypertrophy in your facet joints is related to spinal arthritis, and like spinal arthritis, it usually occurs as the effects of age, wear and tear, poor posture and/or injuries take root. (
  • Facet Hypertrophy. (
  • Facet Hypertrophy refers to degenerative and arthritic changes (osteoarthritis and osteophytosis or bone spur) impacting the facet joints. (
  • The radicular symptoms often result from lateral recess stenosis from facet and ligamentous hypertrophy, disk herniation, or both. (
  • I'm not talking about "shaved dudes posing in thongs" bodybuilding, but the good old hypertrophy-inducing strength-training from the days of the past. (
  • Therefore, it is necessary to determine factors offering a protective effect against cardiac hypertrophy to decrease the incidence of heart failure and subsequent mortality. (
  • Here it is: Hypertrophy and strength training don't have to be two separate entities. (
  • We have investigated whether calcium/calmodulin-dependent protein kinase IIδ (CaMKIIδ) regulates proliferation in fibroblasts isolated from normal and hypertrophied hearts. (
  • CaMKIIδ protein expression and activity is upregulated in MTAB hearts and, specifically, in cardiac fibroblasts isolated from hypertrophied hearts. (
  • Myostatin-related muscle hypertrophy is a rare condition characterized by reduced body fat and increased muscle size. (
  • Myostatin-related muscle hypertrophy is not known to cause any medical problems, and affected individuals are intellectually normal. (
  • Myostatin-related muscle hypertrophy has a pattern of inheritance known as incomplete autosomal dominance. (
  • Myostatin mutation associated with gross muscle hypertrophy in a child. (
  • That's probably because more is understood about the nervous system than muscle soreness, or maybe it's because most of the writers who are only concerned about hypertrophy training are imbeciles who can't even build muscle on themselves. (
  • I've never designed a program that was based solely on "hypertrophy" training, yet my clients have gained a ton of muscle over the years. (
  • Assuming all is normal with your physiology, even the best hypertrophy program won't build appreciable amounts of muscle if there are insufficient nutrients. (
  • Let's dig into some real hypertrophy methods so you can apply them to your current program in exchange for more functional muscle. (
  • Once you're comfortable breaking every "hypertrophy" rule in the book, you can rapidly build muscle with this program. (
  • For example, during muscle hypertrophy, the α-myosin heavy chain is replaced by the β form of the myosin heavy chain, which leads to decreased myosin adenosine triphosphatase (ATPase) activity and a slower, more energetically economical contraction. (
  • Scientists found that changes in myokine levels correlate to changes in lean mass, indicating that muscle hypertrophy is a key driver of serum myokine levels. (
  • Molkentin JD, Dorn GW: Cytoplasmic signaling pathways that regulate cardiac hypertrophy. (
  • The atrophy-hypertrophy complex (AHC) refers to the controlled restoration of liver parenchyma following hepatocyte loss. (
  • The term "true macroglossia" refers to macroglossia caused by histologic abnormalities within the tongue secondary to an underlying condition, such as muscular hypertrophy and vascular malformation. (
  • Subsequent elevation of end-diastolic pressure and decreased compliance of the RV, consequent to the hypertrophy, lead to elevated right atrial (RA) pressure and dilatation of that chamber. (