PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Modifiable factors”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMed1997

The impact of disease states as a modifying factor for nutrition toxicity.

Acquired kidney and liver diseases are relatively common diseases that can raise the potential for nutrient intoxication. For example, high-protein diets increase glomerular blood flow and the blood pressure gradient across the glomerular capillary wall in the kidney, which can result in injury to membranes. Likewise, the liver can increase nutrient intoxication because it is involved in the intermediary metabolism of many nutrients, serves as the storage organ for many nutrients, and is important in the biotransformation and excretion of nutrients. In this paper, vitamin A serves as an example to illustrate how kidney disease and liver disease can increase a single nutrient's toxicity.

Anemia, Pernicious↗
PubMed1985

Ethanol diuresis in rats: possible modifying factors.

Ethanol has been shown to produce a biphasic dose-dependent effect on urine output in rats. Experiments were carried out to examine factors which may influence ethanol diuresis. Immobilization stress (30 min) decreased and ethanol (2.5 g kg-1) increased urine output of intragastrically hydrated rats. In stressed rats, ethanol had a more pronounced diuretic effect compared with home cage control rats. This increased sensitivity to ethanol disappeared when rats were immobilized daily for four days, indicating development of tolerance. The diuretic action of ethanol was not influenced by adrenalectomy.

Adrenalectomy↗
PubMed2006

Factors modifying the frequency of spontaneous activity in gastric muscle.

The cellular mechanisms that determine the frequency of spontaneous activity were investigated in gastric smooth muscles isolated from the guinea-pig. Intact antral muscle generated slow waves periodically; the interval between slow waves was decreased exponentially by depolarization of the membrane to reach a steady interval value of about 7 s. Isolated circular muscle bundles produced slow potentials spontaneously or were evoked by depolarizing current stimuli. Evoked slow potentials appeared in an all-or-none fashion, with a refractory period of approximately 2-3 s. Low concentrations of chemicals that modify intracellular signalling revealed that the refractory period was causally related to the activity of protein kinase C (PKC). Activation of PKC increased and inhibition of PKC activity decreased the frequency of slow potentials. Chemicals that inhibit mitochondrial functions reduced the frequency of slow waves. Inhibition of internal Ca(2+)-store activity decreased the amplitude, but not the frequency of slow potentials, suggesting that the amplitude is causally related to Ca(2+) release from the internal store. The results suggest that changes in [Ca(2+)](i) caused by the activity of mitochondria may play a key role in determining the frequency of spontaneous activity in gastric pacemaker cells.

Animals↗
PubMed1975

Animal model for determining the no-effect level of an antimicrobial drug on drug resistance in the lactose-fermenting enteric flora.

Mature beagles were fed a ground-meal diet containing 0, 2, or 10 mug of oxytetracycline per g for 44 days. The 10-mug/g diet resulted in a shift from a predominantly drug-susceptible population of enteric lactose-fermenting organisms to a multiply antibiotic-resistant population which peaked at 78% resistant organisms. Since a shift to drug-resistant organisms did not occur in the group fed 2 mug/g, the level of oxytetracycline that results in increased incidence of antibiotic resistance lies between 2 and 10 mug/g in this dog model. Rats and hamsters fed diets containing oxytetracycline (10 mug/g or greater) or dihydrostreptomycin (10 mug/g), and provided suspensions of drug-susceptible Escherichia coli, did not develop a population of antibiotic-resistant organisms.

Animals↗
PubMed1985

Klebsiella 'modifying factor': binding studies with HLA-B27+ and B27- lymphocytes.

On the basis that extracts of some klebsiella organisms bind selectively to the lymphocytes of HLA-B27+ individuals and induce the appearance of new antigens, attempts were made to detect the binding of klebsiella products to HLA-B27+ and B27- lymphocytes by a number of different techniques. Firstly, blocking of the binding of two different HLA-B27 specific monoclonal antibodies to HLA-B27+ lymphocytes has been examined following exposure of the lymphocytes to a cell-free culture filtrate from K. pneumoniae K21 and K43. There was no reduction in the cytotoxicity of either antibody, suggesting that neither of the epitopes detected by the anti-HLA-B27 monoclonal antibodies is a binding site for klebsiella products. Secondly, we have studied the binding of partially purified, radiolabelled klebsiella products to healthy HLA-B27+ and B27- lymphocytes. There was no significant difference either in terms of numerical counts bound or by comparing, by SDS-PAGE analysis, the molecules bound to each cell type. At the level of sensitivities of these techniques we can detect no difference in binding of klebsiella products to the lymphocytes of healthy HLA-B27+ and B27- individuals.

Antibodies, Monoclonal↗
PubMed1982

Factors modifying contraction-relaxation cycle in vascular smooth muscles.

Contraction-relaxation cycles in vascular smooth muscles are largely dependent on the regulation of free Ca2+ in the myoplasm, as is the case in skeletal and cardiac muscles. In this article we describe the varieties of contraction-relaxation cycles of vascular smooth muscles determined at cellular and subcellular levels. To discuss the excitation-contraction and pharmacomechanical coupling mechanisms in vascular tissues, passive and active membrane properties and ionic movements measured by various procedures are briefly introduced. In vascular smooth muscles the sources of Ca2+ contributing to the activation of contractile proteins are extra- and intracellular. Influxes of Ca2+ across the membrane are enhanced by the calcium spike and electrical and chemical depolarizations or activations of autonomic receptors.l However, the Ca2+ influx during the generation of action potential does not directly increase the free Ca2+ in the cell; rather, this ion is sequestered in the storage site and activates the calcium-induced calcium-release mechanism in the storage sites with a subsequent increase in the levels of free Ca2+. In some vascular tissues depolarizations induced by activations of autonomic receptors are not a prerequisite for generation of the contraction, as these mechanical responses appear with hyperpolarization of the membrane or without a change in the membrane potential. Possible functional links between the myoplasmic membrane where the receptors are distributed and the Ca2+ storage and releasing sites (mainly sarcoplasmic reticulum) in the cell are discussed. In addition, small arteries possess possibly more than three subtypes of alpha-adrenoceptors, including the presynaptic alpha 2-adrenoceptor. The roles of sarcoplasmic reticulum and the calcium receptor of contractile proteins (calmodulin or leiotonin C) from the chemically skinned muscles of vascular tissues were compared with those of intact muscles. The relaxation of vascular tissues as induced by activations of beta-adrenoceptors, nitrites, and other chemicals is also briefly introduced.

Action Potentials↗