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Страница 1 од 201 резултати
Expression of hypoxia-inducible factor 1α mRNA in hearts and lungs of broiler chickens with ascites syndrome induced by excess salt in drinking water.
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Hypoxia-inducible factor 1 (HIF-1) is a ubiquitously expressed heterodimeric transcription factor that mediates adaptive responses to hypoxia in all nucleated cells of metazoan organisms. Hypoxia-inducible factor 1α is involved in the pathogenesis of pulmonary hypertension in humans and animals, but
Ultrastructural demonstration of mitochondrial calcium overload in myocardial cells from broiler chickens with ascites and induced hypoxia.
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Two groups of young broiler chickens, namely, naturally occurring field cases of ascites and those with an induced hypoxia, were used in an ultrastructural study to examine the localisation and distribution of intracellular Ca2+ in cardiomyocytes. Age-matched healthy flockmates were used to control
No significant overreplication occurs in Ehrlich ascites cells during and after reversal of hypoxia.
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Labeling with bromodeoxyuridine and analysis by isopycnic banding for emergence of DNA-helices density-labeled in both strands (HH-DNA) were used to examine whether transient controlled hypoxia induces significant overreplication in the DNA of cultured Ehrlich ascites cells within a single cell
Hypobaric hypoxia in ascites resistant and susceptible broiler genetic lines influences gut morphology.
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Genetic selection based on rapid growth rates, improved feed conversion, and increased body weights has led to a predisposition to ascites in broiler populations. Sire-family selection was applied to a commercial elite line to produce divergent lines of ascites-resistant (RES) and
Studies on the modification of the cellular response to injury: effect of mannitol on Ehrlich ascites tumor cells following injury by anoxia or p-chloromercuribenzenesulfonic acid (PCMBS).
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The possible protective effects of 30 and 180 mM mannitol added to the extracellular medium were studied in Ehrlich ascites tumor cells (EATC) injured by the nonpenetrating mercurial p-chloromercuribenzenesulfonic acid (PCMBS) or by anoxia. Protection was provided with 180 mM mannitol as observed by
Application of hypoxia-induced shut down of replicon initiation to the analysis of replication intermediates in Ehrlich ascites cells.
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Cultured Ehrlich ascites cells were subjected to hypoxic conditions for about 2 h, then reaerated or allowed to remain hypoxic. The newly formed DNA of hypoxic or reaerated cells was labeled with [3H]thymidine using different pulse and pulse/pulse-chase protocols. The chain length distribution of
Effect of perfluorodecalin on viability of Ehrlich ascites tumor cells under conditions of hypoxia.
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Perfluorodecalin increased survival rate of Ehrlich ascites tumor cells under pathological conditions of hypoxia in combination with hyperkalemia. High potassium medium increased the content of lysophospholipids in samples, while in the presence of perfluorodecalin, phosphatidylethanolamine level
Effects of glucose, anoxia, and adriamycin on the chemiluminescence of Ehrlich Ascites cells.
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Glucose and anoxia accelerate the photocount due to luminescence of Ehrlich Ascites cells. Adriamycin also has this effect if glucose is present. Comparison with a chemical standard combined with estimates of cellular and population transmittance yield a photon generation rate of at least 10 . s-1 .
Studies of cellular recovery from injury. I. Recovery from anoxia in Ehrlich ascites tumor cells.
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The reversibility of changes in ultrastructure, K+, and ATP content was studied in experimental injury of Ehrlich ascites tumor cells. Different grades of injury resulted from incubations in N2 atmosphere and omitting substrate after which air and glucose were reinstated. The changes observed in
Reversible shutdown of replicon initiation by transient hypoxia in Ehrlich ascites cells. Dependence of initiation on short-lived protein.
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The O2-dependent regulation of replication in Ehrlich ascites cells, characterized by a reversible shutdown of replicon initiation during hypoxia, was scrutinized with respect to the involvement of gene expression. Synchronous and asynchronous cells were subjected to transient hypoxia and examined
Role of hypoxia in anticancer drug-induced cytotoxicity for Ehrlich ascites cells.
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A review of the literature on the effect of hypoxia on in vitro drug sensitivity had suggested that there was consistently more cytotoxicity under hypoxic conditions for the drugs misonidazole and mitomycin C while there was much conflicting data for the drugs Adriamycin and bleomycin. We have
Effect of dietary flax oil and hypobaric hypoxia on right ventricular hypertrophy and ascites in broiler chickens.
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1. The effect of dietary flax oil on growth rate, blood haemoglobin content, mortality and incidence of pulmonary hypertension and ascites in broilers at ambient pressure and at reduced atmospheric pressure was examined. 2. Birds were housed either in hypobaric chambers simulating 1000, 1500 or 2200
Towards a further understanding of the growth-inhibiting action of oxygen deficiency. Evaluation of the effect of antimycin on proliferating Ehrlich ascites tumour cells.
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The effect of 1 microM antimycin on the proliferative properties, metabolism and basic cell composition of Ehrlich ascites tumour cells cultured in the second in vitro passage was studied. Continuous drug exposure of asynchronous cells caused rapid cessation of cell growth, characterized by the cell
Effect of chronic hypoxia during embryonic development on physiological functioning and on hatching and post-hatching parameters related to ascites syndrome in broiler chickens.
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The present study was designed to investigate the effect of different atmospheric pressure on the endogenous functions of broiler chickens during embryonic, hatching and growing periods related to ascites. Eggs from a commercial broiler line were incubated in two similar commercial incubators at
On the role of dihydroorotate dehydrogenase in growth cessation of Ehrlich ascites tumor cells cultured under oxygen deficiency.
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In pyrimidine biosynthesis the oxidation of dihydroorotate is catalyzed by dihydroorotate dehydrogenase, which is linked to the mitochondrial electron transport chain in vertebrates. In order to elucidate the role of this oxygen-dependent anabolic process in the arrest of cell proliferation under
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