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Muscle Cell Function (muscle + cell_function)

Distribution by Scientific Domains
Medical Sciences50%

Kinds of Muscle Cell Function

  • smooth muscle cell function
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    Selected Abstracts

    EFNS guideline on diagnosis and management of limb girdle muscular dystrophies

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 12 2007
    F. Norwood
    The limb girdle muscular dystrophies (LGMD) are termed as such as they share the characteristic feature of muscle weakness predominantly affecting the shoulder and pelvic girdles; their classification has been completely revised in recent years because of elucidation of many of the underlying genetic and protein alterations in the various subtypes. An array of diagnostic measures is possible but with varying ease of use and availability. Several aspects of muscle cell function appear to be involved in the causation of muscle pathology. These cellular variations may confer some specific clinical features thus permitting recognition of the LGMD subtype and hence directing appropriate levels of monitoring and intervention. Despite an extensive literature on the individual limb girdle dystrophies, these publications may be impenetrable for the general neurologist in this increasingly complex field. The proposed guidelines suggest an approach to the diagnosis and monitoring of the limb girdle dystrophies in a manner accessible to general neurologists. [source]

    Acute effect of antidiabetic 1,4-dihydropyridine compound cerebrocrast on cardiac function and glucose metabolism in the isolated, perfused normal rat heart

    CELL BIOCHEMISTRY AND FUNCTION, Issue 2 2008
    Janina Briede
    Abstract Diabetes mellitus (DM) is an important cardiovascular risk factor and is associated with abnormalities in endothelial and vascular smooth muscle cell function, evoked by chronic hyperglycemia and hyperlipidemia. Chronic insulin deficiency or resistance is marked by decreases in the intensity of glucose transport, glucose phosphorylation, and glucose oxidation, plus decreases in ATP levels in cardiac myocytes. It is important to search for new agents that promote glucose consumption in the heart and partially inhibit extensive fatty acid beta-oxidation observed in diabetic, ischemia. When the oxygen supply for myocardium is decreased, the heart accumulates potentially toxic intermediates of fatty acid beta-oxidation, that is, long-chain acylcarnitine and long-chain acyl-CoA metabolites. Exogenous glucose and heart glycogen become an important compensatory source of energy. Therefore we studied the effect of the antidiabetic 1,4-dihydropyridine compound cerebrocrast at concentrations from 10,10,M to 10,7,M on isolated rat hearts using the method of Langendorff, on physiological parameters and energy metabolism. Cerebrocrast at concentrations from 10,10,M to 10,7,M has a negative inotropic effect on the rat heart. It inhibits L -type Ca2+channels thereby diminishing the cellular Ca2+ supply, reducing contractile activity, and oxygen consumption, that normally favors enhanced glucose uptake, metabolism, and production of high-energy phosphates (ATP content) in myocardium. Cerebrocrast decreases heart rate and left ventricular (LV) systolic pressure; at concentrations of 10,10,M and 10,9,M it evokes short-term vasodilatation of coronary arteries. Increase of ATP content in the myocytes induced by cerebrocrast has a ubiquitous role. It can preserve the integrity of the cell plasma membranes, maintain normal cellular function, and inhibit release of lactate dehydrogenase (LDH) from cells that is associated with diabetes and heart ischemia. Administration of cerebrocrast together with insulin shows that both compounds only slightly enhance glucose uptake in myocardium, but significantly normalize the rate of contraction and relaxation (,±,dp/dt). The effect of insulin on coronary flow is more pronounced by administration of insulin together with cerebrocrast at a concentration of 10,7,M. Cerebrocrast may promote a shift of glucose consumption from aerobic to anerobic conditions (through the negative inotropic properties), and may be very significant in prevention of cardiac ischemic episodes. Copyright © 2007 John Wiley & Sons, Ltd. [source]

    Mast cell-mediated airway remodelling

    CLINICAL & EXPERIMENTAL ALLERGY REVIEWS, Issue 4 2006
    Y. Okayama
    Summary Airway structural changes (remodelling) in asthma include increased smooth muscle mass, mucus gland hypertrophy, deposition of extracellular matrix components, thickening of reticular basement membrane, and angiogenesis. The extent of remodelling correlates with severity of asthma, and since patients with extensive remodelling may be resistant to steroids therapy, prevention of airway remodelling is a promising therapeutic strategy for curing patients with severe asthma. Mast cells play a pivotal role in allergic inflammatory diseases including asthma and rhinitis. Both early-phase mediators such as tryptase and chymase and late-phase mediators such as cytokines released by mast cells are capable of modulating airway smooth muscle cell function and inducing goblet cell hyperplasia. Nasal remodelling in patients with rhinitis seems far less extensive than that which occurs in bronchi of asthmatic patients. Because cytokine production by smooth muscle cells may partly explain the differences in remodelling at these two sites, further investigation of the interaction between human mast cells and airway smooth muscle cells is required to identify new therapeutic strategies for reducing airway remodelling in asthma. [source]

    GENETIC INFLUENCES ON THE ARTERIAL WALL

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2007
    Bronwyn Kingwell
    SUMMARY 1Arterial stiffness, which has independent predictive value for cardiovascular events, seems to have a genetic component, largely independent of the influence of blood pressure and other cardiovascular risk factors. 2In animal models of essential hypertension (stroke-prone spontaneously hypertensive rats and spontaneously hypertensive rats), structural modifications of the arterial wall include an increase in the number of elastin,smooth muscle cell connections and smaller fenestrations of the internal elastic lamina, possibility leading to redistribution of the mechanical load towards elastic materials. These modifications may give rise to mechanisms explaining why changes in arterial wall material accompanying wall hypertrophy in these animals are not associated with an increase in arterial stiffness. 3In monogenic connective tissue diseases (Marfan, Williams and Ehlers,Danlos syndromes) and the corresponding animal models, precise characterization of the arterial phenotype makes it possible to determine the influence of abnormal, genetically determined, wall components on arterial stiffness. 4Such studies have highlighted the role of extracellular matrix signalling in the vascular wall and have shown that elastin and collagen not only display elasticity or rigidity, but are also involved in the control of smooth muscle cell function. 5These data provide strong evidence that arterial stiffness is affected by the amount and density of stiff wall material and the spatial organization of that material. [source]

    Protein chip-based microarray profiling of oxidized low density lipoprotein-treated cells

    PROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 5 2005
    Sergiy Sukhanov
    Abstract Commercially available high-content Ab380 and extensively validated DLM26 homemade protein microarrays were used to profile the effects of the pro-atherogenic molecule, oxidized low density lipoprotein (OxLDL), on human aortic smooth muscle cells. Protein microarrays detected 298 proteins in cell lysates and 54 of these were differentially regulated. Microarray data were validated by immunoblotting for a selected set of up- and down-regulated proteins. The protein microarray data sets were compared with our recent cDNA microarray-based gene expression results in order to characterize the global effect of OxLDL on smooth muscle cell functions. A group of cell-cell interaction molecules was classified as up-regulated by OxLDL, whereas nucleic acid/protein biosynthesis, structural and humoral response proteins/genes were under-expressed in cells treated by OxLDL. These findings reveal the major pattern of OxLDL-induced effects on the human aortic smooth muscle cells functions and also demonstrate that protein chip-based microarrays could be a useful proteomic tool to profile disease-related states of muscle cells. [source]