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)

Agonist challenged aortic prostacyclin production was examined in copper-adequate, -marginal and -deficient rats fed AIN-based diets providing 6.7, 1.7 and 0.8 micrograms Cu/g, respectively. Aortic rings were incubated in Krebs-Henseleit salts, 10 mmol/L HEPES buffer, pH 7.4, 95%:5% O2:CO2, 37 degrees C, and equilibrated for 1 h. Equilibrated rings were challenged with buffer (basal), 273.0 nmol/L thrombin and angiotensin II at 84.6 pmol/L and 846.0 pmol/L. Prostacyclin production, determined at 10 minutes by RIA as 6-keto prostaglandin F1 alpha, in basal and 84.6 pmol/L angiotensin II ring incubations was significantly reduced by 28 to 48% in copper-deficient rats. With thrombin or 846.0 pmol/L angiotensin II prostacyclin production was significantly reduced by 18 to 55% in copper-marginal and copper-deficient rats. Copper-dependent superoxide dismutase activity was significantly depressed by 30 and 57% in aortae of copper-marginal and copper-deficient rats. Lipid peroxidation, estimated by the thiobarbituric acid test, was significantly increased by 85% in copper-deficient rats, with a nonsignificant 40% increase in aortae from copper-marginal rats. The results suggest that the decreases in aortic prostacyclin production in aortae from both copper-deficient and copper-marginal rats are associated, in a dose-dependent manner, with copper-dependent superoxide dismutase depression and increases in aortic lipid peroxidation.
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PMID:Copper-marginal and copper-deficient diets decrease aortic prostacyclin production and copper-dependent superoxide dismutase activity, and increase aortic lipid peroxidation in rats. 143 51

During the acute phase of myocardial infarction, the generation of thrombin is reflected in the sudden rise of fibrinopeptide A (FPA) and the thrombin-antithrombin III (TAT) complex in blood. We have systematically determined the FPA and TAT plasma concentrations over a period of 14 days after acute myocardial infarction in 100 patients. Mean levels of both thrombin markers were the highest on admission, remained elevated over the following few days, and then gradually declined after day 5. Still, by the end of the first week two thirds of the patients had distinctly elevated TAT and FPA levels, and by the end of the second week such an abnormality was present in half of them. Continuous intravenous heparin infusion at a dose of 20,000 units/day, administered for 1 week to patients who had either received (n = 21) or not received (n = 17) streptokinase, led to a significant depression (p less than 0.05) of thrombin markers over the first 48 hours, an effect that did not persist over the subsequent days of treatment. In patients not assigned to heparin treatment, those in heart failure had significantly (p less than 0.05) higher mean TAT and FPA values on days 3, 5, and 7 compared with patients in whom heart failure was absent. Infarct extension, pulmonary embolism, and death were also associated with a rise in one or both thrombin markers, often preceding the onset of clinical symptoms. Thrombinogenesis was not accompanied by changes in mean plasma concentrations of prothrombin, antithrombin III, or alpha 2-macroglobulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistent generation of thrombin after acute myocardial infarction. 157 16

The recently developed ELISA for the thrombin-antithrombin III complex (TAT) is a sensitive, specific, and simplified means of detecting intravascular coagulation. For further evaluation of the thrombogenicity of a polyamide (P) and a Hemophan (H) hollow-fibre dialyzer a cross-over study was done in ten stable patients on maintenance hemodialysis. At the same doses of heparin (mean bolus of 30 U/kg bw and maintenance doses of 86 U/kg bw), thrombin time and partial thromboplastin time were significantly lower using H. At the end of dialysis TAT was significantly higher in H (mean +/- SEM before HD 3.57 +/- .56, at 240 min 14.9 +/- 6.5 ng/ml, p less than 0.05, Wilcoxon-test) than in P (before HD 4.36 +/- .98, at 240 min 8.95 +/- 3.0 ng/ml, p less than 0.05 H 240 vs. P 240, Wilcoxon-test). Visible clotting was more pronounced in the H filter. Among other favourable features of blood compatibility the polyamide/polyvinylpyrrolidone copolymer with a hydrophilic/hydrophobic microdomain structure has less thrombogenicity. The modified cellulosic membrane H has advantages in complement activation and leukocyte depression, but thrombogenicity seems less favourable since the incorporated diethyl-amino-ethyl groups with their positive charge bind and inactivate negatively charged heparin.
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PMID:Formation of thrombin-antithrombin III complex using polyamide and hemophan dialyzers. 163 30

The pathogenesis of disseminated intravascular coagulation (DIC) in the early stage after burn injury remains still unclear. We investigated 12 burn injured patients by serial determination of anti-thrombin III (AT-III) activities and thrombin-antithrombin III complex (TAT) levels. Of these patients 4 developed DIC (DIC group) and the others had no hematological complications (non-DIC group). The mean levels of TAT increased markedly and peaked at 6 hr; the increment being more pronounced in DIC group (p less than 0.001). A significant correlation was recognized between TAT and Burn Index (r = 0.871, p less than 0.001). We also observed low AT-III activities those inversely related to Burn Index (r = 0.875, p less than 0.001), whereas closely correlated with serum albumin levels (r = 0.864, p less than 0.001), suggesting that this depression might be caused by both massive infusion and shifts of plasma into the extravascular space rather than consumption. These findings suggest that massive thrombin generation and decrease of anticoagulant activity, correlated to the severity of burns, might concurrently develop. Non-DIC group may remain to latent activation of coagulation cascade where anticoagulants could inactivate thrombin generated. This compensatory mechanism may fail in severe burn patients who have Burn Index of more than 90, developing DIC with high levels of TAT (316.3 +/- 104.5 ng/ml) and low AT-III activities (19.5 +/- 8.7%).
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PMID:[Disseminated intravascular coagulation in the early stage after severe burn: the role of excessive thrombin generation]. 194 44

A study was made of the blood and tissue oxygen regime in patients with vibratory disease (VD) induced by local vibration and of the importance of lipid peroxidation (LPO) in oxygenation disorders. Venous hyperoxia, a decrease of the arteriovenous difference according to oxygen, the percentage of oxygen utilization by tissues, shift of the acid-base balance towards metabolic acidosis were established, attesting to tissue hypoxia that increased with the gravity of VD. The importance of a steady activation of LPO and depression of the antioxidant system in the pathogenesis of hypoxia associated with VD was supported by the correlation analysis data on oxygen balance and LPO, the functional and metabolic characteristics of red blood cells (according to the viscosity of red blood cell suspension and the content in the cells of SH-groups, lipoproteins and histidine) and platelets (according to aggregation in response to ADP and thrombin) as well as by the level of blood serum fluorescence. The authors provide evidence for the use of antioxidants (a complex of alpha-tocopherol with ascorbic acid and methionine and calcium antagonists of the nifedipine group), giving a membranostabilizing effect, in multimodality treatment of patients afflicted with VD.
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PMID:[Cell-membrane aspects of the pathogenesis of hypoxia in vibration disease induced by local vibration]. 204 32

A rat platelet factor has a high antiheparin activity. It also decreases nonenzymatic fibrinolytic activity of normal rat plasma and antithrombin III-heparin complex. The platelet factor 4 formed inactive complexes with heparin in molar ratios of 1:1 and 2:1. Intravenous injection of the platelet factor 4 before injection of albino rats with tissue thromboplastin prevented the reaction of anticoagulation system inactivated the synthesis of endogenous thrombin. This effect is accompanied by high hypercoagulation and depression of nonenzymatic fibrinolysis in blood.
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PMID:[The antiheparin thrombocyte factor 4 and its interaction with heparin]. 207 38

Expression of tumor necrosis factor (TNF alpha), tissue factor (TF), and interleukin 1-beta (IL-1 beta) mRNA was evaluated in monocytes isolated from patients infected with human immunodeficiency virus (HIV). There was a significant depression (66%) of the induced level of TF mRNA expression in response to lipopolysaccharide. Conversely, the response of TNF alpha and IL-1 beta, following LPS induction, was "normal." TF mRNA reduction was also observed to a lesser degree in AIDS-related complex patients (20%) but not in asymptomatic seropositives. TF is necessary for initiation of the coagulation protease cascade, leading to thrombin production and fibrin deposition, which play a role in inflammatory responses. Its selective reduction may be a factor in the diminished resistance to secondary infections observed in AIDS. Further, since the TF defect increases as patients progress toward AIDS, it may serve as a marker for disease progression.
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PMID:A selective defect in tissue factor mRNA expression in monocytes from AIDS patients. 229 2

The effects of melatonin on platelet aggregation and thromboxane-B2 (TxB2) production induced by 1-4 x 10(-6) M adenosine diphosphate (ADP) or 0.6 x 10(-3) M arachidonic acid (AA) were assessed in platelet-rich plasma (PRP). Micromolar concentrations of melatonin inhibited in a dose-dependent way ADP-induced platelet aggregation with individual inhibitions 40% or more at 10(-6)-10(-5) M. A significant depression of AA-induced platelet aggregation was observed only at 10(-5)-10(-4) M melatonin. Morning (0830 h)-evening (1800 h) studies of ADP-induced platelet aggregation in seven normal men showed a higher sensitivity at 1800 h when analyzed as a global inhibitory effect of melatonin (P less than 0.01). Moreover, only during the evening hours did melatonin induce reversible aggregation, an index of inhibition of the platelet secretory process elicited by ADP exposure. No diurnal variability in melatonin inhibition of AA-induced aggregation was detected. TxB2 production elicited by AA in the evening was inhibited significantly in a concentration-related manner by a 2-min preincubation with 10(-9)-10(-5) M melatonin, while during the morning hours the inhibition was significant only at 10(-6) M or higher melatonin concentrations. In the case of ADP, the inhibition of TxB2 release attained significance at 10(-5)-M (0830 h) or 10(-6)-M concentrations (1800 h). In the presence of either stimulatory agent, melatonin depression of TxB2 generation was about 2-fold greater at 1800 h than at 0830 h. The diurnal changes in melatonin effect on TxB2 production were also observed in thrombin-stimulated washed platelets. The present data indicate the existence of circadian variations in platelet responsiveness to melatonin in humans.
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PMID:Inhibition of human platelet aggregation and thromboxane-B2 production by melatonin: evidence for a diurnal variation. 229 33

The effects of marine oil-enriched diets on the fatty acid composition of lipids in guinea pig megakaryocytes (MK) and platelets were studied to obtain a better understanding of the mechanisms for changes in platelet fatty acid composition and platelet function. Animals were fed 2%, 5% and 10% menhaden oil-enriched diets for up to 35 days. Platelets and MK were isolated and MK subpopulations at various stages of development were prepared. The diets did not cause a change in the cholesterol/phospholipid ratio in MK or platelets. The diets induced a dose related incorporation of eicosapentaenoic (20:5) and docosahexaenoic acid (22:6) and an associated decrease in linoleic acid (18:2) in both MK and platelets. However, there was a considerable greater depression of 20:4 in platelets than in MK. These changes were evident with 2% marine oil diets and maximal with 10% diets. Half maximal changes in fatty acid composition occurred after 3 days and maximal changes at 10 days after the initiation of the diets and no further changes occurred up to 35 days. Based on percent of total fatty acids in individual phospholipids, 20:5 had been primarily incorporated into phosphatidylethanolamine (PE) and phosphatidylinositol (PI) and 22:6 into PE and phosphatidylserine (PS) in both MK and platelets. 18:2 was decreased in all phospholipids. 20:4 was decreased only in PI in MK while 20:4 was decreased in PE, PI and PS in platelets. In animals on the 10% marine oil diet, more 20:5 and 22:6 were incorporated into mature than immature MK but the greatest amount of 20:5 and 22:6 had accumulated in platelets. Ingestion of marine oil-enriched diets did not cause thrombocytopenia or affect MK maturation based on the analysis of morphologic stage, ploidy or size. Marine oil-enriched diets caused a decrease in thromboxane synthesis in response to thrombin and calcium ionophore in platelets and MK at all stages of maturation. In platelet-rich plasma, collagen induced platelet aggregation, ATP secretion and thromboxane synthesis were decreased to a greater degree at 35 days than 10 days. Thus, the study indicates that the ingestion of marine oil-enriched diets resulted in the compartmentalization of 20:5 and 22:6 in acidic phospholipids in mature MK and platelets. The observation that marine oil-enriched diet induced maximal changes in lipid composition in MK and platelets within 10 days but caused progressive inhibition of platelet function for up to 35 days indicates that as yet undefined membrane and cellular changes may occur at later time points.
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PMID:Effects of marine oil-enriched diets on guinea pig megakaryocyte and platelet lipids: effects on thromboxane synthesis and platelet function. 230 2

Hemostasis was investigated in 2 groups of patients with systemic scleroderma (SSD) with minimal (12 patients) and moderate (9 patients) activity of the process. It has been shown that in SSD, the triggering factor of intravascular blood coagulation is the release of Willebrand's factor, an activator of platelets, from the impaired endothelium. Hyperaggregation and labilization of platelets characterizes the course of SSD irrespective of the disease activity. The main changes in coagulation hemostasis are related to the dramatically accelerated triggered thrombin formation and deficiency of the antithrombin potential. The status of fibrinolysis confirming the thrombogenic situation is marked by a number of features: depression of contact lysis is maximally pronounced in chronic SSD with minimal activity, accumulation of the soluble complexes of fibrin monomer only correlates with the disease activity, and no significant rise of the level of fibrin/fibrinogen degradation products has been discovered.
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PMID:[The mechanisms of intravascular blood coagulation in patients with systemic scleroderma]. 239 20


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