Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method has been developed for isolation of cells from the efferent ductules of the rat epididymis to obtain a population of epithelial cells. The technique depends on a transfer of segments of the ductules into a new isolation medium and gradual purification from fat cells, fibroblasts, collagen fibres and smooth muscle cells. Segments of the ductules so isolated were further separated into single cells or their aggregates. The mode of isolation applied allowed to obtain morphologically unchanged and functionally fully efficient cells. When transferred to culture they rapidly formed a single layer and further developed into a multi-layer culture. The cells divide and preserve their ability of producing secretion. They react to the absence of androgenous hormones by a considerable depression of the number of mitotic divisions and reduction of their secretion.
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PMID:Isolation technique and identification of epithelial cells from efferent ductules of the rat epididymis. 384 20

This study was carried out to evaluate the mechanism of action of a reticuloendothelial (RE)-depressing substance. This RE-depressing substance was obtained from the plasma of dogs subjected to 3 hr of intestinal ischemia. RE-depressing substance was partially purified by dialysis and reverse-phase column chromatography. The assay of RE-depressing activity was based on the depression of the rate of clearance of colloidal carbon from the blood of rats or mice. The effect of RE-depressing substance on three other RE system (RES) test particles (gelatinized lipid emulsion, formalinized sheep erythrocytes, and IgM-coated erythrocytes) was determined. RE-depressing substance did not affect the clearance rate or the organ localization of these three test particles. Therefore, RE-depressing substance affected only the clearance of colloidal carbon. Since platelet aggregation has been shown to contribute to the clearance of colloidal carbon, the effect of RE-depressing substance on platelet aggregation was evaluated. RE-depressing substance depressed in vitro platelet aggregation induced by ADP or collagen. It was concluded that the effect of RE-depressing substance on the clearance of colloidal carbon was due to a depression of platelet aggregation rather than to a depression of hepatic macrophage phagocytic function.
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PMID:Reticuloendothelial-depressing substance: studies on the mechanism of action. 386 28

The inhibitory effects of sulfinpyrazone are more marked ex vivo than in vitro, suggesting biotransformation to potentially active metabolites such as the sulfide and sulfone metabolites. As a platelet inhibitor, the sulfide metabolite is 10 times as potent as the parent and because of its long t1/2, the former may lead to cumulative inhibition of platelet function in vivo during chronic sulfinpyrazone dosing. In our study, healthy subjects received sulfinpyrazone, 200 mg four times a day, for 6 days. Plasma levels of the sulfide metabolite rose slightly from 2.1 +/- 0.8 micrograms/ml 12 hr after the fourth dose to 2.8 +/- 0.8 microgram/ml 12 hr after the twenty-fourth dose. This was associated with increasing inhibition of ex vivo platelet aggregation induced by platelet-activating factor during the dosing period, but inhibition of arachidonic acid-induced aggregation did not increase cumulatively during dosing and collagen-induced aggregation was not inhibited. Inhibition of platelet aggregation was no longer evident 24 hr after the final dose of sulfinpyrazone. The effects of sulfinpyrazone on cyclooxygenase activity were assessed by measurement of thromboxane B2 production by thrombin-stimulated platelets ex vivo and urinary excretion of the major prostacyclin metabolite 2,3-dinor-6-keto-PGF1 alpha. During sulfinpyrazone dosing, thromboxane formation and prostacyclin biosynthesis were correspondingly lowered 50% to 60%. The extent of this depression was of the same order on days 2 and 5 of dosing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclooxygenase inhibition, platelet function, and metabolite formation during chronic sulfinpyrazone dosing. 391 87

Cepharanthine incorporated into rabbit platelets dose dependently, inhibited calcium influx as well as aggregation in response to collagen, and also inhibited arachidonate release in response to collagen and A23187 in the same concentration ranges. The latter action of cepharanthine was shown not to be due to the direct action on phospholipase A2 molecules but to the depression of susceptibility of substrate phospholipids to enzymatic hydrolysis. These depressed functions, as well as the inhibited aggregation, were almost restored by removing the bound drugs from the platelets. Arachidonate-induced aggregation and prostaglandin synthesis from externally added arachidonate were not suppressed by the addition of cepharanthine. These results suggest that cepharanthine physically changes the lipid properties and thereby inhibits the function of the calcium channel or the susceptibility of substrate phospholipids to enzymatic hydrolysis by phospholipase A2.
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PMID:Inhibitory effect of cepharanthine on collagen-induced activation in rabbit platelets. 392 12

Forty-six elderly patients (mean age 60 years) suffering from diabetes mellitus (DM), or essential or arteriosclerotic hypertension (HT) were divided into 4 groups. Group 1 served as a control, group 2 was administered 1500 mg niceritrol, group 3 was administered 162 mg acetylsalicylic acid (ASA), and group 4 was administered both 1500 mg niceritrol and 162 mg ASA/day for 8 weeks. Niceritrol lowered serum levels of beta-lipoprotein and total cholesterol and increased HDL cholesterol, usually in 8 weeks. ASA did not affect the lipid-lowering effects of niceritrol. Platelet aggregation induced by epinephrine (1 microgram/ml), collagen (1 microgram/ml), and ADP (2 microM) was depressed in groups 2, 3 and 4. Degrees of depression were higher in groups administered ASA (groups 3 and 4) than in the group administered niceritrol alone (group 2). Plasma fibrinogen levels were lowered in groups administered niceritrol (groups 2 and 4) in 8 weeks. Apparent whole blood viscosity measured at shear rates of 37.6/s and 376/s was improved only in group 4 in 8 weeks, while hematocrit did not change during the study. Because flushing, the most frequent side effect of niceritrol, can be easily controlled by a low dose of ASA, and because the combination of the 2 drugs has some beneficial effects on blood rheology, this combination is considered worthwhile for treatment and prevention of atherosclerosis.
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PMID:The effects on lipids, blood viscosity and platelet aggregation of combined use of niceritrol (Perycit) and a low dose of acetylsalicylic acid. 400 83

Six-week-old mice were exposed by inhalation to an aerosol of 239PuO2 (activity median aerodynamic diameter 2.2 microns) to establish mean alveolar depositions at 2 days after exposure of 4, 40, and 930 Bq of 239Pu. Animals were killed serially after 3, 6, 12, and 18 months at which times the development of the pulmonary fibrotic lesion was assessed by both biochemical and histopathological techniques. Individual measurements of both fresh and dry weights, protein, DNA, and hydroxyproline were made on whole lung and also on each of the five constituent lobes. Early and sustained increases in lung mass, lung protein, and total lung collagen were found, together with a depression of the total cellularity of the lung at 6 and 12 months after exposure. Although at later times compensatory hypertrophy of less affected areas distorted the relationship, systematic trends in the severity of responses between lobes were found. These trends were related to the initial lobar concentrations of 239Pu.
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PMID:The development and interlobar distribution of plutonium-induced pulmonary fibrosis in mice. 407 May 58

In a previous experimental study it was shown that bowel rest with low residue diet led to a reduction of the non-collagenous substances in the intact, unoperated colon, while the collagen content remained unchanged. In the cecum, both the collagen content and the non-collagenous substances were markedly increased. In the present investigation the effect of relative bowel rest on collagen synthesis in the colonic wall was studied. Further, a possible influence on mechanical properties was evaluated. It was found out that bowel rest led to a marked decrease of collagen and protein synthesis in the colon. In the cecum, there was an unchanged collagen synthesis but an increased protein synthesis. It can be deduced that lysis of collagen is decreased in all parts of the colon. The depression of collagen turnover in the colonic wall was not accompanied by measurable changes in mechanical strength. It remains to be studied whether the observed changes in collagen metabolism do affect colonic healing.
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PMID:The effect of relative bowel rest on collagen metabolism and suture holding capacity in the colonic wall. Studies in the rat. 609 10

BM 13.177 (0.1-100 microM) produced a concentration-dependent reduction of the platelet shape change, aggregation and (3H)serotonin release induced by the stable PGH2 analogues U 46619 and U 44069 or exogenous and endogenous arachidonic acid, the latter mobilized by hydrogen peroxide or collagen. BM 13.177 (100 microM) did not inhibit the primary platelet activation by ADP, serotonin, thrombin or collagen in washed platelets or citrated PRP that had been pre-treated with ASA (acetylsalicylic acid). The formation of TXB2 triggered by 100 microM hydrogen peroxide or 10 microM arachidonic acid was not influenced by BM 13.177 (10 microM). In spiral strips of rat and rabbit aorta, BM 13.117 markedly reduced the vasoconstriction triggered by U 46619 and PGF2 alpha. BM 13.177 did not inhibit the K+-or noradrenaline-induced constriction. The concentration/response curves of the U 46619-stimulated platelet shape change and of the vasoconstriction induced by U 46619 and PGF2 alpha were shifted in parallel to the right by BM 13.177, implicating a competitive antagonism. The pAx values were about the same in these models which indicates that BM 13.177 does not differentiate between the thromboxane receptors in human platelets and rabbit aorta. In mice, BM 13.177 prevented in a dose-dependent fashion the sudden death and the symptoms of respiratory depression and shock induced by i.v. injections of U 46619 or arachidonic acid. BM 13.177 did not exert partial agonist activity in the in vitro and in the animal models.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibitory effects of the selective thromboxane receptor antagonist BM 13.177 on platelet aggregation, vasoconstriction and sudden death. 609 35

Manganese, zinc and copper are essential for normal prenatal and neonatal development. Manganese deficiency causes skeletal abnormalities, congenital ataxia due to abnormal inner ear development, and abnormal brain function. Depression of mucopolysaccharide synthesis and manganese superoxide dismutase activity may be fundamental to ultrastructural and other defects. In copper deficiency, neurological and skeletal abnormalities are due to impairment of phospholipid synthesis and collagen crosslinking, and possibly to low activity of copper metalloenzymes. The fundamental defect leading to the extremely teratogenic effects of zinc deficiency is related to depressed synthesis of DNA. In the neonatal period, poor survival and growth and depressed function of the immune system are salient features. Developmental patterns of trace element concentrations in various tissues suggest that important changes in metabolic regulation of trace elements may occur during the neonatal period. This hypothesis is being investigated by studies of molecular localization of trace elements in certain neonatal tissues, in conjunction with similar observations in milk.
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PMID:The roles of trace elements in foetal and neonatal development. 611 92

Blood sampled from the coronary sinus was compared with blood collected simultaneously from the superior caval vein in 50 men with angiographically proven coronary heart disease. Primary, ADP-induced aggregation in coronary sinus blood was reduced by 14 per cent, collagen-induced aggregation by 10 and platelet retention by 16 to 30 per cent as compared with blood from the caval vein. The plasma levels of beta-thromboglobulin, platelet counts and number of circulating platelet aggregates were similar in parallel samples. The reduced platelet function in coronary sinus blood hardly reflects refractoriness after previous platelet stimulation, since no release or irreversible aggregation was induced. A reduced function might be the effect of direct depression induced in the coronary circulation. Most surprisingly, a selective thromboxane synthetase inhibitor (Dazoxiben) and acetylsalicylic acid normalized platelet aggregation but did not affect the low platelet retention response in coronary sinus blood. Thus, the reduced platelet function in coronary sinus blood is not only mediated via prostaglandins.
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PMID:Platelet function in blood from the coronary sinus in patients with arteriosclerotic heart disease. 622 29


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