Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 56-yr-old woman with long-standing rheumatoid arthritis exhibited jaundice, pruritus and abdominal discomfort after 8 yr of periodic gold sodium thiomalate injections amounting to a cumulative dose in excess of 2.5 gm. Histopathological examination of the liver biopsy specimen showed submassive loss of parenchyma, collapse of reticulin and mixed cellular inflammatory infiltrates. Macrophages contained dark granules, which displayed the characteristics of aurosomes when examined by transmission electron microscopy and electron microprobe analysis. It is likely that hepatocellular injury occurred when the lysosomal storage capacity for gold was exceeded.
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PMID:Light- and electron-microscopical study of a case of gold salt-induced hepatotoxicity. 190 34

A seriously ill patient with circulatory collapse, fever, acute renal failure, and progressive respiratory failure had dramatic improvement after treatment with imipenem/cilastatin sodium. During the treatment period, a diagnosis of tularemia was established serologically. This case suggests the efficacy of imipenem/cilastatin in the treatment of tularemia.
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PMID:Treatment of tularemia with imipenem/cilastatin sodium. 192 35

The synaptosomal metabolism of glutamine was studied under in vitro conditions that simulate depolarization in vivo. With [2-15N]glutamine as precursor, the [glutamine]i was diminished in the presence of veratridine or 50 mM KCl, but the total amounts of [15N]glutamate and [15N]aspartate formed were either equal to those of control incubations (veratridine) or higher (50 mM [KCl]). This suggests that depolarization decreases glutamine uptake and independently augments glutaminase activity. Omission of sodium from the medium was associated with low internal levels of glutamine which indicates that influx occurs as a charged Na(+)-amino acid complex. It is postulated that a reduction in membrane potential and a collapse of the Na+ gradient decrease the driving forces for glutamine accumulation and thus inhibit its uptake and enhance its release under depolarizing conditions. Inorganic phosphate stimulated glutaminase activity, particularly in the presence of calcium. At 2 mM or lower [phosphate] in the medium, calcium inhibited glutamine utilization and the production of glutamate, aspartate, and ammonia from glutamine. At a high (10 mM) medium [phosphate], calcium stimulated glutamine catabolism. It is suggested that a veratridine-induced increase in intrasynaptosomal inorganic phosphate is responsible for the enhancement of flux through glutaminase; calcium affects glutaminase indirectly by modulating the level of free intramitochondrial [phosphate]. Because phosphate also lowers the Km of glutaminase for glutamine, augmentation of the amino acid breakdown may occur even when depolarization lowers [glutamine]i. Reducing the intrasynaptosomal glutamate to 26 nmol/mg of protein had little effect on glutamine catabolism, but raising the pH to 7.9 markedly increased formation of glutamate and aspartate. It is concluded that phosphate and H+ are the major physiologic regulators of glutaminase activity.
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PMID:Neuronal glutamine utilization: glutamine/glutamate homeostasis in synaptosomes. 197 Oct 10

AHR-13268D (4-[3-[4-[Bis(4-fluorophenyl)hydroxymethyl]-1- piperidinyl]propoxy]benzoic acid, sodium salt) is a potent, long-acting water soluble, antiallergic and antihistaminic agent. AHR-13268D protects sensitive guinea pigs from collapse induced by aerosolized antigen; 1, 5, and 24 h ED50s in the test were 0.27, 0.25, 0.93 mg/kg, PO, respectively. AHR-13268D was also active when given as an aerosol, the 1 h ED50 = 0.29%. In the rat passivefoot anaphylaxis test. AHR-13268D was slightly more active (1.55 times) than AHR-5333B when given orally 1 h prior to challenge and equipotent to cromolyn when given intravenously immediately prior to challenge. AHR-13268D displayed potent, long-acting antihistaminic activity in naive guinea pigs; the 1, 5, and 24 h oral ED50s being in the range of 0.3 mg/kg. AHR-13268D (10 to 20 mg/kg, PO) attenuated the skin responses to ascaris antigen in sensitive dogs and did not alter the EEG pattern or sleep/wake patterns of cats at doses in vast excess of its antihistaminic activity. In vitro, AHR-13268D was a potent inhibitor of histamine release from rat peritoneal mast cells (IC50 = 0.51 nM) and was as potent as the reference 5-LO inhibitor phenidone in inhibiting antigen-induced contractions of guinea pig ileum in the presence of pyrilamine, atropine, and imidazole (IC50 approximately 300 microM). AHR-13268B was bioavailable (approximately 88%) from capsules or from oral solutions.
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PMID:The in vivo and in vitro activity of AHR-13268D, a new antiallergic/antihistaminic agent. 198 1

The release of sodium and potassium and the uptake of sucrose molecules was studied in pig lenses incubated in isosmotic sucrose solution in either the presence or absence of 1% Triton X-100 (a non-ionic detergent). This Triton X-100 treatment has been shown to cause severe disruptions of cell membrane integrity. If sodium and potassium were free in the lens fibers as in a dilute aqueous solution, they would be expected to diffuse three to four times faster than sucrose. However, measurements of sodium and potassium release and sucrose uptake in the Triton X-100 treated lenses show a 1:1 equilibration. When pig lenses were incubated in the same solution without detergent, the sucrose uptake was significantly less than the potassium and sodium release. It is postulated that a slow, detergent mediated collapse of protein-water-ion interactions within the lens is the rate-limiting step of the observed equilibration of monovalent cations and sucrose molecules.
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PMID:Proportional equilibration of K, Na ions, and sucrose molecules in pig lenses incubated in the presence of the non-ionic detergent Triton X-100. 202 94

Propionic acid induces a calcium mobilization in human neutrophils which is prevented by pretreatment with phorbol ester or pertussis toxin. The effect is reminiscent of that of chemotactic factors and leukotriene B4 and was attributed to cytoplasmic acidification (Naccache, P.H. et al. (1988) J. Cell. Physiol. 136, 118-124). We show there that other weak acids also induced cytoplasmic alkalinization and calcium mobilization. However, addition of trimethylamine together with propionic acid prevented the cytoplasmic acidification without modifying the calcium mobilization. Propionic acid increased the production of inositol phosphates but this effect was largely prevented by the joint addition of trimethylamine. The ionophores nigericin and monensin can both be forced to produce either cytoplasmic acidification or alkalinization by manipulating the extracellular concentrations of Na+, K+ or H+. Both ionophores produced calcium mobilization in all the cases, irrespective of the direction of the cytoplasmic pH shift. The ionophores were documented to collapse existing pH gradients among the cytoplasm and intracellular compartments. We conclude that the calcium-mobilizing effect of propionic acid and other weak acids is not due to the acidification of the cytoplasm. Our results are consistent, however, with calcium mobilization induced by weak acids and ionophores arising from acidification of an alkaline intracellular compartment.
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PMID:The role of intracellular acidification in calcium mobilization in human neutrophils. 204 5

Adult female Wistar rats were injected with 125 mg/kg b.w. of human methemoglobin (M-Hb) in order to induce a first episode of hemodynamically-mediated acute renal failure (HMARF). Eleven days after the injection of M-Hb, other groups of rats received another equal dose of the drug in order to induce a second episode of HMARF. Evaluation of renal function, histopathology studies, and determinations of plasma and kidney erythropoietin (Epo) titers by radioimmunoassay in normoxic and hypoxic conditions were performed 1, 2, 3, 5 and 10 days after M-Hb administration. Treatment induced transient increases in plasma urea concentration, fractional sodium excretion, and urine volume, and significant depression in urine osmolality. In every case, the maximal effect of the first injection of M-Hb on the individual parameters was always greater than that of the second injection, and observed on the 5th post-injection day. Histologic sections showed interstitial cellular infiltration, desquamation of the proximal tubular epithelium and collapse or dilation of the tubular lumen. Treatment with M-Hb depressed Epo titers in both kidney homogenates and plasma in normoxic as well as hypoxic rats. Here again, the effect of the first injection of the drug was higher than that of the second one. These observations indicate that there is a negative correlation between kidney tubule injury and Epo production in normoxic and hypoxic conditions. The findings give support to the concept that Epo production is related to proximal tubular function.
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PMID:Depressed plasma erythropoietin levels in rats with hemodynamically-mediated acute renal failure. 209 64

The influence of calcium ions on the electrophoretic properties of phospholipid stabilized emulsions containing various quantities of the sodium salts of oleic acid (SO), phosphatidic acid (SPA), phosphatidylinositol (SPI), and phosphatidylserine (SPS) was examined. The critical flocculation concentration of calcium corresponded to a critical zeta potential in all but one of the systems. Systems of approximately equal zeta potential in 0 mM Ca++ had different zeta potentials in dilute solutions of Ca++. A comparison of emulsions of similar polydispersity suggests that these differences may be largely related to differences in particle size and surface area of the emulsions. The influence of Ca++ on the monolayer properties of mixed films containing phosphatidylcholine (PC) with either SPA or SO was also examined at the air-water interface. Films containing PC with SPA were more expanded on a subphase containing calcium compared to a subphase with no calcium. In addition, the compression of films containing PC with SO demonstrated two collapse pressures while SPA was relatively more miscible in the film. This suggests that phase separation of interfacial lipids occurs more easily in systems containing PC and SO. These results may help to explain differences in the flocculation and coalescence of emulsions stabilized by lipid films of different composition.
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PMID:The influence of charged lipids on the flocculation and coalescence of oil-in-water emulsions. II: Electrophoretic properties and monolayer film studies. 225 Feb

We investigated the protective effect of the high-viscosity substances sodium hyaluronate (1%) and methylcellulose (2%) on corneal endothelium in the face of severe mechanical insult. An intraocular lens was drawn across the endothelium of porcine corneas with standardized conditions. We used different compression forces. Methylcellulose and sodium hyaluronate were used as lubricating substances in the experimental groups, while balanced salt solution (BSS PLUS) was used in the control group. In this study no significant protective effect of high-viscosity substances against strong direct mechanical damage was generally demonstrable. Only one group in which a moderately strong compression force was applied showed significantly less smaller endothelial cell loss when methylcellulose was used. The most important function of viscous substances is therefore to prevent a collapse of the anterior chamber and to prevent any contact of the intraocular lens or of instruments with the endothelium. Any mechanical contact with the endothelium means an irreversible endothelial cell loss.
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PMID:[Endothelium protective effect of the high viscosity substances hyaluronic acid and methylcellulose in mechanical damage]. 227 77

Monensin, a carboxylic ionophore, collapse Na+ gradient across biological membranes, increases intracellular pH and affects many processes involved in transport, posttranslational modification and secretion of proteins, moreover endocytosis and degradation in lysosomes. Concerning the liver, the action of monensin in vitro or in perfused liver, showed an altered secretion of protein and altered transport of VLDL; in bile-fistula rats, monensin caused a decrease of bile flow, altered protein profile and bile acids secretion. Because the effects of monensin seem to be complicated, in this note it has been studied the action of monensin on the morphology of liver cells to have a picture not only of the parenchymal cells, but also of the sinusoidal cells, which cooperation with the general liver functions become increasingly evident. The results obtained after staining of liver biopsies with Sudan Black, Sudan III and Sudan IV showed that monensin induces a diffuse cholestasis and islands of hepatocytes in steatosis, in agreement with the data in literature. Cells lining the sinusoid with phagocytic activity and that might be identified with fat-storing cells, showed an increase of their lipid droplets that might be attributed to vitamin A.
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PMID:[Morphologic changes in the liver of rats treated with monensin]. 228 46


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