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)

Circulating mediators have been implicated in the pathophysiology of postburn immunologic depression, suggesting the restorative potential of exchange therapy. Previous reports have stressed the immunosuppressive effects of massive transfusions and major surgical procedures. The effect of plasma exchange (PLA/EX) and surgical excision and grafting (E/G) procedures on postburn lymphocyte function was evaluated retrospectively in one-way mixed lymphocyte reaction assays. Twenty one adult patients with a mean total body surface area (TBSA) burn of 52.6% underwent a total of 54 PLA/EX procedures without complications. The mean volume of plasma exchanged was 5079 ml. PLA/EX was performed at a mean time of 10.4 days after burn injury. Thirty adult patients with a mean TBSA burn of 42.8% underwent a total of 78 E/G procedures. The mean graft size was 2373 cm2 per E/G procedure or 7.25% TBSA. The mean transfusion requirement per E/G was 3355 ml. The initial E/G occurred at a mean of 7.5 days after burn injury. PLA/EX decreased suppression of normal lymphocyte blastogenesis by burn serum from 62.7% to 28.3% (p less than 0.001). The mean duration of improvement in lymphocyte function was 4.8 days. Similarly, the mean suppression by burn serum drawn pre-E/G was 42.2%, while serum suppressive activity post-E/G was 29.1% (p less than 0.05). The mean duration of mixed lymphocyte reaction improvement was 5.0 days. Both PLA/EX and E/G procedures have a significant beneficial effect in restoring lymphocyte function in burn patients.
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PMID:The effect of exchange therapy on postburn lymphocyte suppression. 623 13

Ventricular premature complexes (VPCs) after acute myocardial infarction (AMI) remain important determinants of survival in the post-thrombolytic era. The role of thrombolysis, left ventricular function, and Holter ST-segment depression in modulating VPC frequency is unclear. In a placebo-controlled, randomized study of tissue-type plasminogen activator (t-PA) in 103 patients with AMI (Tissue Plasminogen Activator: Toronto study), VPC frequency and ST depression on Holter monitoring (day 7), ejection fraction by radionuclide scan (day 9), and infarct artery patency and cross-sectional area on day 1 (n = 42) were assessed. After administering t-PA, VPC frequency was 10 +/- 58/hour (mean +/- SD), similar to that after placebo (23.5 +/- 91.7, p = NS). However, patients with ST depression had greater VPC frequency (56 +/- 140/hour) than those without it (1.3 +/- 2.6/hour, p = 0.05). Ejection fraction was negatively correlated with VPC frequency (r = -0.33, p < 0.001). By multivariate analysis, ejection fraction (F = 7.0, p < 0.01) and ST depression (F = 5.8, p < 0.02) were the only independent predictors of VPC frequency. In this placebo-controlled study, VPC frequency after AMI was not related to thrombolytic administration but was associated with ST depression and ejection fraction. This suggests that the underlying extent of both infarcted and ischemic myocardium is important in modulating ventricular arrhythmias after AMI.
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PMID:Importance of ST-segment depression as a determinant of ventricular premature complex frequency after thrombolysis for acute myocardial infarction. Tissue Plasminogen Activator: Toronto (TPAT) Study Group. 752 Feb 9

Random regression models (RRMs) were used to investigate the role of initial severity in the outcome of 4 treatments (cognitive-behavior therapy [CBT], interpersonal psychotherapy [IPT], imipramine plus clinical management [IMI-CM], and placebo plus clinical management [PLA-CM]) for outpatients with major depressive disorder seen in the National Institute of Mental Health Treatment of Depression Collaborative Research Program. Initial severity of depression and impairment of functioning significantly predicted differential treatment effects. A larger number of differences than previously reported were found among the active treatments for the more severely ill patients; this was due, in large part, to the greater power of the present statistical analyses.
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PMID:Initial severity and differential treatment outcome in the National Institute of Mental Health Treatment of Depression Collaborative Research Program. 759 78

The epithelial lining of the airways is subject to injury through several processes, including infections, bronchiolitis, and fume exposures. Because airway fibrin deposition influences the course of local injury, we examined how two inflammatory cytokines influenced fibrin formation and clearance in human tracheal epithelial cells (TEC). TEC were treated with transforming growth factor-beta (TGF-beta) and tumor necrosis factor-alpha (TNF-alpha). TNF-alpha increased release of tissue factor (TF)-related procoagulant activity that, through generation of factor Xa, promotes assembly of the prothrombinase complex at the cell surface. Fibrinolytic activity was plasminogen dependent and due to both urokinase (uPA) and tissue plasminogen activator (tPA). The cells expressed plasminogen activator inhibitor 1 (PAI-1), but relatively little PAI-2. Depression of fibrinolysis by TGF-beta correlated with increased PAI-1. Conversely, TNF-alpha increased plasminogen activator (PA) activity due to increased uPA. Fibrinolytic activity was inhibited by actinomycin D and cyclohexamide, but changes in mRNAs for uPA, tPA, PAI-1, and TF by either cytokine were not appreciable. PAI-2 mRNA was not found. The data indicate that TGF-beta decreases the fibrinolytic capacity of TEC, suggesting that this cytokine promotes fibrin retention. TNF-alpha increases expression of both procoagulant and fibrinolytic activities; this differential regulation could favor both pericellular fibrin formation and dissolution.
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PMID:Effects of TGF-beta and TNF-alpha on procoagulant and fibrinolytic pathways of human tracheal epithelial cells. 781 Jun 74

Patients who have chest pain occurring at rest are at a significant risk of myocardial infarction and or sudden death. Most trials enter patients with anginal rest pain after an initial screening period. Thus, the clinical efficacy of early thrombolytic treatment for patients with rest pain remains unproven. Eighty patients with chest pain at rest and with ECG changes of ST depression of at least 1 mm in any ECG lead, were randomized to alteplase 100 mg infused over 3 h, or placebo. Concomitantly, all patients received intravenous heparin and 300 mg of aspirin daily (unless contra-indicated). Seventy-four patients had coronary angiography (the majority within 72 h of admission) of which 73 were assessable. The patency of the ischaemia-related vessel was not significantly greater in the alteplase treated group (81% vs 78%, P = 0.82). The culprit lesion morphology tended to be more concentric in the alteplase treated group (84% vs 56%, P = 0.06) although alteplase treatment was not associated with a significant reduction in the severity of the culprit lesion stenosis. Intra-coronary thrombi were detected in 7% of patients (3% placebo, 11% alteplase, P = 0.35). The mean left ventricular ejection fraction or the alteplase-treated group was 49 +/- 3% and for the placebo-treated patients 56 +/- 3% (P = 0.05). There was no difference in the total in-hospital cardiac event rate i.e. cardiac death, myocardial infarction and coronary revascularization between patients receiving alteplase (10%, 63%, and 38%) and those receiving placebo (8%, 65%, and 30%) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Double-blind randomized trial of alteplase versus placebo in patients with chest pain at rest. 829 37

Functional interrelations between immune and fibrinolytic systems were studied in 107 patients with disseminated tuberculosis patients. The findings showed a depression in plasminogen activator activity associated with high yield of fibrin degradation products. Lymphocyte blast transformation with PHA decreased, whereas that with PPD increased. Concentrations of IgA and IgG rose in a small drop of IgM in peripheral blood. The above changes were more pronounced in marked clinical symptoms. The results may give rise to further developments in pathogenetic mechanisms of pulmonary tuberculosis and new approaches to its treatment.
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PMID:[Immune reactivity and fibrinolysis in patients with disseminated pulmonary tuberculosis]. 832 38

Plasminogen activator inhibitor (PAI-1), tissue type plasminogen activator (tPA) and von Willebrand factor (vWF) concentrations were measured by ELISA in the supernatant of the following cultures: endothelial cells from human umbilical vein (HUVEC); human colon cancer cells (HRT-18); and co-culture cells of HUVEC + HRT-18. No measurable amount of the three substances was found in the supernatant of HRT-18 cell culture. Compared to the value in the HUVEC supernatant, in the UVEC/HRT-18 co-cultures, tPA concentration was significantly lower (P = 0.0047), PAI-1 significantly higher (P = 0.026) and vWF also significantly higher (P = 0.0048). These data indicate that HRT-18 tumor cells do not produce tPA, PAI-1 and vWF; however, these tumor cells induce endothelial cells to change the production of these substances. As a consequence, the interaction between tumor and endothelial cells in vivo may lead to depression of fibrinolysis and enhancement of platelet adhesion.
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PMID:Expression of tissue-type plasminogen activator, plasminogen activator inhibitor and von Willebrand factor in the supernatant of endothelial cell cultures in response to the seeding of adenocarcinoma cell line HRT-18. 895 58

Forty patients with coronary heart disease (CHD) concurrent with hyperlipidemia were divided into 2 groups according to the baseline fibrinolytic activity. The group with the depressed fibrinolytic system displayed the highest atherogenicity index and levels of cholesterol, low and very low density lipoprotein cholesterol and half levels of high density lipoproteins. After 45-day ingestion of docanol, a new Russian food additive containing docosahexanoic and eicosapentaenoic acids there were positive changes in the lipid spectrum in the both groups. The fibrinolytic changes were heterodirectional: activator and plasma activities increased in the group of fibrinolytic depression while in the group of baseline normal fibrinolysis the activity of plasminogen activator fell.
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PMID:[Effect of docanol on the status of hemostasis and fibrinolysis systems, as well as lipid spectrum in patients with ischemic heart disease depending on the initial level of fibrinolytic activity]. 899 61

Insulin-like growth factors (IGF-I and -II) play an active role in cell proliferation. In biological fluids, they are non-covalently bound to high-affinity binding proteins (IGFBPs), at least 6 species of which have been identified to date, but with poorly defined functions. One of these IGFBPs, IGFBP-2, is secreted by most cell lines and appears to be involved in cell proliferation. A human epidermoid carcinoma cell line, KB 3.1, which produces IGFBP-1 and -3 and small amounts of IGFBP-4, but no IGFBP-2, was stably transfected with an expression vector comprising IGFBP-2 complementary DNA (cDNA), whose expression was placed under the control of the constitutive and ubiquitous cytomegalovirus promoter. After an s.c. injection of these IGFBP-2-expressing KB 3.1 cells into nude mice, tumours developed more quickly than in controls, they were 3 to 4 times larger and grew about 3 times as fast. Concomitant with IGFBP-2 expression in these tumours, were a decrease in IGFBP-1 expression and an increase in IGFBP-3 proteolysis, both of which increase the bioavailability of the IGF-II produced by the cells. The increased IGFBP-3 proteolysis most probably resulted from amplified expression of tissue-type plasminogen activator (t-PA) and depression of its inhibitor (PAI-I) observed in IGFBP-2-expressing xenografts. Our findings suggest that IGFBP-2 plays a role in this model of experimental tumorigenesis via a mechanism that remains unclear, but appears to involve increased protease activity and IGF-II bioavailability.
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PMID:IGFBP-2 expression in a human cell line is associated with increased IGFBP-3 proteolysis, decreased IGFBP-1 expression and increased tumorigenicity. 971 57

A number of behavioural and cellular studies have suggested that activity-dependent synaptic plasticity associated with learning and memory may lead to the expression of various genes whose protein products can play a critical role in memory acquisition and consolidation. Long-term potentiation (LTP) and long-term depression (LTD) represent two forms of synaptic plasticity which have been widely studied by electrophysiological techniques. However, the molecular mechanisms at target gene involved in the generation of long term depression remain to be determined. To elucidate the molecular mechanism underlying activity dependent synaptic remodeling in striatal long term depression, we used the mRNA differential display technology to isolate genes that are induced or modulated by high frequency stimulation of the corticostriatal pathway in a rat brain slice preparation. We have differentially displayed, by means of reverse transcriptase-polymerase chain reaction, mRNA species isolated from striatal slices in which long term depression was induced by tetanic stimuli as well as from slices stimulated at low frequency. We then compared radio-labeled RT-PCR banding patterns to isolate cDNAs that are differentially expressed. Three independent cDNAs were isolated and identified whose mRNA level were enhanced by tetanic stimulation inducing long term depression. We provide evidence that two of these genes encode proteins involved in synaptic vesicle trafficking (dynamin I and amphiphysin II). Moreover, expression of tissue plasminogen activator (t-PA) gene was also increased following striatal long term depression. Our data suggest that a complex pattern of genes acting at presynaptic level and extracellularly may be involved in LTD-associated synaptic remodeling.
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PMID:Modulation of gene expression following long-term synaptic depression in the striatum. 1052 2


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