Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During pregnancy the activity of coagulation factor VII in plasma increases up to 248% (SEM 16) (n = 18) at 40 weeks even when all precautions to avoid cold activation are taken. This increase is at all times during pregnancy, delivery and puerperium entirely due to the presence in vivo of what is most likely a phospholipid-factor VII complex. This complex is sensitive to phospholipase C, so that treatment with the enzyme reduces the activity of pregnant plasma down to that of non-pregnant controls. When present in the complex factor VII has a higher specific activity and an altered conformation with a more accessible active site as demonstrated by increased susceptibility to inactivation by diisopropylfluorophosphate. Factors II and X are increased to 136% (SEM 4) and 171% (SEM 6) (n = 18) without being sensitive to phospholipase C. The increase during pregnancy and the decrease after delivery of the phospholipase-sensitive factor VII activity have been followed.
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PMID:Clotting factor VII during pregnancy, delivery and puerperium. 394 1

Factor 7 in plasma from 15% of healthy subjects undergoes activation when samples are kept in plastic tubes at 4 degrees Celsius. In women taking oral contraceptives (OCs), this phenomenon is observed more frequently. If this phenomenon occurred under blood bank conditions as well, the transfusion of such plasma from donors taking OCs to patients afflicted by trauma could enhance thromboembolism. Plasma pavks of 72 female donors taking OCs were separated and stored at 4 degrees Celsius for 24 hours in the blood bank. No significant change in factor VII:C level was observed; the initial level was 110.2 +or- 6.2 U/dl (mean +or- SEM), and the 24 hour level was 97 +or- 3.3 U/dl. Among the 72 donors, 10 were identified as cold activators; their factor VII:C level increased from 85.6 +or- 2.5 U/dl (mean +or- SEM) to 222.0 +or- 7.5 U/dl when their plasma samples were kept in plastic tubes for 24 hours at 4 degrees Celsius. In contrast, the factor VII:C level in the plasma packs kept simultaneously in the blood bank at 4 degrees Celsius was only 101.1 +or- 9.0 U/dl at 24 hours. Thus, it appears that plasma from donors taking OCs can be used safely even when not frozen immediately.
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PMID:Factor VII in plasma of women taking oral contraceptives. Lack of cold activation under blood bank conditions. 660 9

To investigate pituitary effects on the vitamin K-dependent coagulation factors, female rats were hypophysectomized (hypox) and treated with growth hormone (GH), cortisone, thyroxine, vitamin K, or saline. After 11 days of treatment, the prothrombin time, platelet count, and factors II, VII, IX, and X were determined. The prothrombin time was 52.9 +/- 1.2% for control rats and 39.1 +/- 0.8% for hypox rats (mean +/- SEM; p < 0.001). All factors decreased after hypophysectomy, reaching significance for factor VII (from 264 +/- 23% to 131 +/- 9%; p < 0.001) and factor IX (from 28.4 +/- 2.2% to 17.1 +/- 2.5%; p < 0.01) while the platelet count was unaffected. When hypox rats were treated with GH, the prothrombin time increased to 50.9 +/- 1.0% (p < 0.001) and factor VII to 299 +/- 10% (p < 0.001). Factor II, IX, and X were slightly increased after GH substitution but not after cortisone, thyroxine, or vitamin K treatment. To summarize, GH is of importance for normal hemostasis in the female rat.
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PMID:Growth hormone deficiency impairs blood clotting and reduces factor VII coagulant activity in rat. 749 70

The use of OKT3 as prophylaxis in renal transplantation carries an increased risk of intragraft thrombosis, which is related to the systemic activation of the coagulation system that consistently occurs after the first dose of OKT3. As only a few patients develop thrombosis after OKT3 therapy, we searched for possible additional risk factor by comparing the demographic and clinical parameters of the 13 patients who developed thrombosis in our institution to those of 218 patients who did not. Multivariate analysis showed a relationship between the dose of methylprednisolone (mPDS) given before the first OKT3 injection and the risk of thrombosis: 6 out of 42 patients (14%) who received high (30 mg/kg) mPDS experienced a thrombotic event, as compared to 7 out of the 189 patients (3.7%) who received < or = 8 mg/kg of mPDS (P < 0.01). This led us to study the effects of mPDS on the procoagulant activity induced by OKT3 on peripheral blood mononuclear cells (PBMC) in vitro. The procoagulant activity of unstimulated PBMC (mean +/- SEM: 0.6 +/- 0.1 mU/ml) reached 3.0 +/- 0.7 mU/ml after OKT3 stimulation (P = 0.0062) and further increased to 7.4 +/- 2.0 mU/ml when PBMC were first preincubated overnight with mPDS before OKT3 stimulation (P = 0.018 as compared to OKT3 alone). This process involved the tissue factor/factor VII pathway, as shown by increased membrane expression of tissue factor on monocytes as well as by a marked reduction of the induced procoagulant activity when the clotting assay was performed with factor VII-deficient plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High-dose glucocorticosteroids increase the procoagulant effects of OKT3. 770 16

The hypothesis that myristic acid (C14:0) has a stronger cholesterol-increasing potential than does palmitic acid is based on very few experimental observations. A randomized, strictly controlled dietary study was therefore designed to investigate the effect of a synthetic fat that was high in myristic acid, and palm oil, which is high in palmitic acid, on lipoproteins and hemostatic variables. Twelve men were served two diets (40% of energy as fat) with 41% of fat as myristic (diet M) or palmitic acid (diet P) for 3 wk with 1 mo between the two dietary schedules. Plasma HDL cholesterol was 8% higher with diet M than with diet P: 1.10 +/- 0.06 (mean +/- SEM) vs 1.01 +/- 0.05 mmol/L (P < 0.006). Diet M raised factor VII coagulant (F VIIc) activity to 98% (77-117%) vs 96% (71-109%) (medians and ranges) after diet P (P = 0.02). Total and LDL-cholesterol concentrations did not differ between the diets. In conclusion, the myristic acid test fat was not more cholesterolemic than was palm oil, but it did induce a minor rise in F VIIc activity.
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PMID:Effect on blood lipids, coagulation, and fibrinolysis of a fat high in myristic acid and a fat high in palmitic acid. 776 35

The effect of incubation of plasma with lipoprotein lipase on factor VII coagulant (FVII:C) activity was examined in 40 patients, 22 male and 18 female, aged 28 to 77 years, with history of venographically proven deep venous thrombosis (DVT). While the mean (+/-SEM) FVII:C activity of the 40 patients was 100.9 +/- 4.1%, 19 patients had FVII:C activity less than 100%, 11 had 100 to 120% activity and 10 patients had greater than 120% FVII:C activity. The mean triglyceride level of all the patients was 84.0 +/- 6.5 mg/dl. The FVII:C activity correlated significantly with triglyceride (r = 0.36; n = 40; p = 0.021). There was about 30% average loss of FVII:C activity upon incubation of plasma with lipoprotein lipase. The mean activity loss increased from 23.8% to 31.5% and 42.6% in patients whose FVII:C activity levels were less than 100%, between 100 and 120% and more than 120% respectively, the variation in the means being statistically significant (p < 0.001). While according to current opinion, FVII:C activity represents the total FVII mass (FVII plus FVIIa) and activity state, the present findings demonstrate a lipid dependence of FVII:C activity, and raises the possibility of a therapeutic option of controlling FVII:C by controlling triglyceride levels.
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PMID:Triglyceride dependence of factor VII coagulant activity in deep venous thrombosis. 890 84

Obstructive sleep apnoea syndrome (OSAS) is a very common disorder. Patients with OSAS are at an increased risk for cardiovascular events. It has also been reported that a 25% rise in factor VII clotting activity (FVIIc) is associated with a 55% increase in ischaemic heart disease death during the first 5 years. We examined the effects of nasal continuous positive airway pressure (NCPAP) treatment on FVIIc in patients with OSAS. FVIIc was investigated prospectively in 15 patients with OSAS before (mean +/- SEM apnoea and hypopnoea index (AHI) 61.5 +/- 4.2 and after (AHI 3.0 +/- 0.9) NCPAP treatment for immediate relief, at 1 month after treatment and at over 6 months. FVIIc levels gradually decreased after NCPAP treatment. After 6 months of NCPAP treatment, FVIIc levels had decreased significantly (before 141.1 +/- 11.7% vs. after 6 months 110.7 +/- 6.2%; p < 0.01). Six of the seven patients whose FVIIc levels were over 140% before the NCPAP treatment had FVIIc levels below 130% after 6 months or 1 year of NCPAP treatment. This decrease in FVIIc after long-term NCPAP treatment could improve mortality in OSAS patients. If patients, especially obese ones, present with high FVIIc of unknown origin, it would be prudent to check for OSAS.
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PMID:Improvement of factor VII clotting activity following long-term NCPAP treatment in obstructive sleep apnoea syndrome. 1002 17

To determine whether the hypercoagulable state of patients with complications of diabetes can be reversed toward normal, a group of insulin-dependent individuals with proteinuria was treated with intensive insulin protocols. A statistically significant (P<.001) improvement in control of diabetes was achieved (mean +/- SEM glycosylated hemoglobin, 9.51% +/- 0.35% at baseline to 8.36% +/- 0. 39% at 12 months; and mean +/- SEM advanced glycosylated end products, 14.8 +/- 2.8 U/mL at baseline to 8.4 +/- 1.5 U/mL at 12 months). There were statistically significant decreases in 2 procoagulant factors: mean +/- SEM baseline elevated plasma factor VII, 128.69% +/- 5.63% at baseline to 106.24% +/- 3.43% at 12 months (P =.002); and mean +/- SEM plasma fibrinogen, 12.3 +/- 0.7 micromol/L (417.3 +/- 24.7 mg/dL) at baseline to 10.2 +/- 0.7 micromol/L (348.8 +/- 22.6 mg/dL) at 12 months (P =.04). Throughout the study, lipid fractions did not change significantly. Because plasma factor VII and fibrinogen concentrations were elevated while cholesterol and triglyceride concentrations were not, more attention should be paid to procoagulants as markers for thromboembolic complications in diabetic patients undergoing intensive insulin therapy.
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PMID:Fibrinogen and factor VII levels improve with glycemic control in patients with type 1 diabetes mellitus who have microvascular complications. 1114 4

The cellular initiation of coagulation by the tissue factor (TF)-activated factor VII complex is transiently inhibited by endogenous tissue factor pathway inhibitor-1 (TFPI-1), whereas exogenously added TFPI-1 is targeted to a degradation pathway. This study investigates the relevance of glycosyl phosphatidylinositol (GPI) anchoring for the anticoagulant properties of TFPI-1. Experiments were performed with the human cell line ECV304 using liposomal gene transfer. For GPI anchoring of TFPI-1 we used a fusion protein of TFPI-1 and the GPI attachment sequence of decay-accelerating factor (GPI-TFPI-1), and compared it with wild-type TFPI-1. We measured TF and TFPI-1 surface expression by flow cytometry and TF proteolytic activity by a chromogenic assay for activated factor X generation. After transfection of GPI-TFPI-1, surface expression of TFPI-1 increased to 134 +/- 9% of mock transfected cells (mean +/- SEM, P = 0.004), and transfection with wild-type TFPI-1 did not significantly alter TFPI-1 surface expression. After transfection with GPI-TFPI-1, TF activity was reduced by 18 +/- 9% compared with mock transfections (P = 0.003), whereas after transfection with TFPI-1 wild type no significant inhibition was observed. This effect was not due to altered TF expression. GPI anchoring is an essential prerequisite for surface expression of TFPI-1 and inhibition of TF activity. Gene transfer of GPI-anchored TFPI, therefore, may be an efficient tool to inhibit local TF-induced coagulation.
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PMID:Overexpression of glycosyl phosphatidylinositol-anchored tissue factor pathway inhibitor-1 inhibits tissue factor activity. 1296 Jun 6