Примеры использования Myocytes на Английском языке и их переводы на Русский язык
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Cardiac myocytes also possess V1R.
Such cells, including, for example,brain neurons and muscle myocytes, have little or no cell turnover.
It was proved by photon correlation spectroscopy method that the C-99 andC-107 caused an increase of characteristic size of myocytes.
A part of water fraction under this load is likely to change into cardiac myocytes, endotheliocytes and neurite-glial complexes.
Increasing myocytes resistance to ischemia, magnesium orotate has positive effect on the clinical course of myocardial infarction and heart failure.
In this study we have established diverse response of peptides in the right atrial myocytes of rats to salt.
The study of immunolabeled granules of BNP myocytes in rat right atrium enabled to discover a new mechanism of a cardioprotective effect of Mexidol in a long-term post-reperfusion period.
In elevated AP there was reduced synthesis andincreased release of natriuretic peptides in rat atrial myocytes in the periods under study.
ANP and BNP content in atrial myocytes and AP recovered against the background of cardiac myocyte hypertrophy, mitochondrial de-energization and destructive changes in microcirculatory bloodstream.
Reproportion of A- and B-type granules containing atrial andbrain natriuretic peptides in rat atrial myocytes under renovascular hypertension.
Three random observations at the site of arterial wall thickening showed that individual myocytes of tunica media had vacuolated, optically empty cytoplasm, which confirmed their transformation into xanthoma cells Figure 3.
Changes in the proportion of A- and B-types of granules containing atrial andbrain natriuretic peptides in atrial myocytes in vasorenal hypertension in rats.
All myocytes had altered mitochondrial structure: the number of mitochondria in the condition of physiological norm decreased by nearly half; while the number of orthodox mitochondria and vacuolated mitochondria increased Figure 6.
Painful irritation when administered hypotonic solution hydrolysis occurs due to a minor amount of myocytes and their decay products excitation of nociceptors.
Conside ring established kinetic pattern ofcalix[4]arene C-90 inhibitory action on the plasma membrane Ca 2+, Mg 2+-ATPase activity, stationary kinetical model of basal calcium concentration control in unexcited uterus myocytes was develo ped.
Mexidol administered at a dose of 25 mg/kg in a perfusion solution enhances ANP accumulation andrelease processes in atrial myocytes of a rat Langendorf isolated heart, and results in an additional cardioprotective effect.
Mexidol administered at a dose of 25 mg/kg body mass within the first hour reperfusion after 10 min of total ischemia has a positive prolonged effect on BNP: after 60 days of a postperfusion period the processes of peptide accumulation andrelease in atrial myocytes of rats enhance resulting in an additional cardioprotective effect.
Thus, an experimental study of BNPin an early and long-term PRP in a whole body using a quantitative assay of immunolabeled granules of atrial myocytes enabled to reveal a prolonged positive effect of Mexidol at the dose of 25 mg/kg body mass on BNP synthesis and release, and confirm cardioprotective properties of Mexidol.
On the 60 th minute of cardiac functioning on intracardial level, there was found high intensity of synthesis processes, accumulation andsecretion of ANP in atrial myocytes due to stimulating effect of hypoxic and ischemic factors in this period.
Myostatin(also known as growth differentiation factor 8, abbreviated GDF-8) is a myokine,a protein produced and released by myocytes that acts on muscle cells' autocrine function to inhibit myogenesis: muscle cell growth and differentiation.
The steps of myocyte contraction and mechanisms of action of antispasmodics are described in detail.
In the female heart, myocyte turnover occurs at a rate of 10%, 14%, and 40% per year at 20, 60, and 100 years of age, respectively 7.
The intensity of ANP accumulation andrelease were assessed by the quantitative analysis of immunolabeled atrial myocyte granules under a transmission electron microscope.
The intensity of ANP accumulation andrelease processes was assessed by quantitative analysis of immunolabeled atrial myocyte granules in transmission electron microscope.
During this period, in group 3 the change of secretory myocyte ultrastructure was evident as slight clarification of mitochondrial matrix and dilated cisterns of sarcoplasmic reticulum.
It also interacts with myocyte enhancer factor-2(MEF2) proteins, resulting in repression of MEF2-dependent genes.
ACE-031 is an investigational protein which increases myocyte activity by inhibiting molecules that bind to and signal through a cell surface receptor called Activin Receptor Type IIB(ActRIIB).
This creates a freely circulating, decoy version of ActRIIB which removes proteins, such as GDF-8(myostatin) andother related molecules that limit the myocyte activity.
About 75% of mortality in diabetic patients is attributed to CVDs, leading to myocardial infarction(MI) andheart failure while acute MI results in massive necrosis of the myocardium and myocyte cell loss 2.
As a result of the study, it was revealed that patients with compensated hypothyroidism receiving statin therapy have increased frequency of muscle pain with typical for SIM localization,pathogenetically associated with myocyte damage.