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Over-activation of the fibrinolytic system may result in proteolytic destruction of fibrinogen. However, the effect of the degradation products formed during fibrinogenolysis on fibrinolytic process and plasminogen/plasmin properties remains unclear. To investigate this effect and its mechanism, the ability of fibrinogen fragments E and D to act on plasminogen and tPA binding, proenzyme activation, fibrin clot lysis and plasmin inhibition by plasma α2-antiplasmin, were studied. It was found that early product fragment EE binds to plasminogen and tissue-type plasminogen activator and enhances plasminogen conversion into plasmin. C-terminal lysine residues of all 3 chains pair and 16 or 23 amino acid residues of Aα- chain are essential for this process. C-terminal lysines of fragment E Aα- and γ-chains and lysine-binding site of tPA kringle 2 are responsible for the interaction between these proteins. Binding of fragment E to plasminogen is provided by N-terminal Aα1–19 and C-terminal Bβ120–122 regions. Late plasmic fibrinogen degradation product fragment EL loses the ability to potentiate plasmin generation but can bind proenzyme and its activator. Fragment D has no binding properties towards plasminogen and tPA. None of fibrinogen fragments protects plasmin from α2-antiplasmin inhibition. It is concluded that at over-activation of the fibrinolytic system and subsequent fibrinogenolysis, the products of fibrinogen degradation, can bind plasminogen and tPA and potentiate generation of plasmin, which will be neutralized under the normal level of the plasmin inhibitor.
The subjects were 8 clinically healthy Polish Primitive Horses at 2-9 years of age. The horses were given E.coli LPS four times, in a dose of 0.1 μg/kg.b.w.; 3 times at 24 hour intervals (LPS-1 , LPS-2, LPS-3 ), and one week after the last infusion (LPS-4). The result analysis indicated that the applied endotoxin dose caused development of tolerance mechanisms related to the platelet count. This phenomenon did not concern changes in fibrinogen concentration. The relatively high sensitivity of horses to LPS may be connected with short duration of endotoxin tolerance in this species.
Congenitally abnormal fibrinogens with impaired fibrin monomer polymerization have been described to contain single amino-acid substitutions localized in certain positions of the γ275-330peptide region. To evaluate the role of the amino-acid sequence in the vicinity of Arg 275 in fibrin monomer polymerization, the peptide fragment corresponding to γ268-282was synthesized and used to obtain peptide-specific antibodies. These antibodies, when purified immunochemically on the immobilized peptide, bound to the intact fibrinogen and fibrin monomers with the same binding affinity. However, they did not recognize the Y268-282epitopes on the denatured and reduced fibrinogen molecules. The lack of influence of antipeptide antibodies on fibrin monomer polymerization indicates that the γ268-282peptide is not directly involved in the structure of the polymerization site in the D domain of fibrinogen. It is suggested that substitution of Arg275either by His or Cys in abnormal fibrinogens results probably in conformational changes which disturb a proper orientation of the polymerization site and reduce its expression.
Angiotensin (Ang) (1-9) is the renin-angiotensin-system peptide found in the plasma of healthy volunteers and after angiotensin-converting-enzyme inhibitors therapy. In vitro experiments proved that Ang-(1-9) may be produced from Ang I. In our study, we tried to expand the poor data about the in vivo properties of Ang-(1-9). We revealed that Ang-(1-9) enhanced electrically stimulated arterial thrombosis in the carotid artery of Wistar rats. Losartan, a selective blocker of AT1 receptor for Ang II, abolished the prothrombotic activity of Ang-(1-9). This peptide increased plasma level of fibrinogen, augments fibrin generation, and similarly to Ang II, potentiated collagen induced platelet aggregation. Using HPLC, we found that after incubation of Ang-(1-9) with platelet homogenates or after intravenous administration this peptide is converted to Ang II. We concluded that Ang-(1-9) exerts an Ang II-like prothrombotic effect due to the conversion to Ang II in the circulatory system of rats and that platelets are involved in this process.
High plasma levels of fibrinogen and plasminogen activator inhibitor (PAI-1) are reported to be correlated with coronary heart disease. Therefore the level of fibrinogen concentration in plasma was examined and verified for the possible correlation with the previously explored PAI-1 antigen and PAI-1 activity in the pathogenesis of premature atherosclerosis (Grzywaczet al., 1998,Blood Coagul Fibrinol. 9, 245-249). Examination included only men, aged 33-46 years, who were in a stable condition for at least six months after the acute event. They were divided into two subgroups: group A (n = 14) with and group B (n = 15) without ischaemic changes in 24 h Holter electrocardiogram. The number of involved vessels visible on the coronarography picture was similar in both groups. In the patients of group A the mean level of fibrinogen (3.92 vs 3.23 g/l, P < 0.05) was higher than in the controls (n = 15). No statistically differences were found between group B and control healthy subjects in any of the parameters measured. There were no correlation between fibrinogen concentration and PAI-1 antigen and activity levels, which were elevated in both groups of patients according to our previous study. Our results indicate that elevated levels of plasma fibrinogen and PAI-1 appeared in the group of patients with more severe disease, as revealed by silent myocardial ischaemia.
Sulfatide (galactosylceramide I3 -sulfate) has been reported to activate blood coagulation factor XII (Hageman factor), which suggests that it exhibits coagulant activity (Fujikama et al., 1980 Biochemistry 19, 1322-1330) However, sulfatide administered into animals as a bolus shot without subsequent thrombus formation, prolonged conventional clotting times and bleeding time (Hara et al., 1996 Glycoconjugate J. 13, 187-194). These findings suggest that it may exhibit anticoagulant rather than coagulant activity. Following this suggestion we found in vitro that binding of sulfatide to fibrinogen resulted in disturbance of fibrin formation. To examine a possible pharmacological effect of sulfatide on blood coagulation in vivo we continuously infused sulfatide into rats through plastic cannulae and found formation of giant thrombi around the tips of the cannulae. These data suggest that sulfatide may exhibit contradictory functions in the blood coagulation system.
The aim of the present study was to identify any possible protective effects of wild greens on certain biochemical cardiovascular disease (CVD) risk factors in elderly women leaving in rural Crete. For the needs of the study a region with high consumption of wild greens (Avdou) and a region with low consumption (Anogia) were identified and a representative population from each area was recruited (n= 37 and n=35 respectively). Serum lipids and fibrinogen levels, total antioxidant capacity (TAC), soluble intercellular adhesion molucule-1 (sVCAM-1), soluble vascular adhesion molucule-1 (s-ICAM-1) and haematological factors were measured in both regions during winter and summer time when wild-green plants consumption is high and low, respectively. Regarding classic lipid risk factors for arteriosclerosis no significant different between the two regions were detected. TAC was found higher in Avdou compared to Anogia during winter screening, but null in both regions during summer. Fibrinogen was found higher in Avdou compared to Anogia while no differences between the two regions were detected for sVCAM-1 and s-ICAM-1 in both screenings. The significantly higher TAC and fibrinogen values detected in Avdou could be attributed to the higher wild green consumption in that region since resent data indicated that their content in vitamin C and E as well as flavonoids is particularly high.
The purpose of the present research is compare the effects of coagulation factors in non-athletes gilrs after exhaustive anaerobic activity sessions in the morning and evening. Present study was semi-emprical that was done on 12 non-athlete female students in range of 18-24 years. Exercise protocol was RAST test, that in which each person passed amain 35 meters of distance for 6 times and rest 10 seconds between each stage. Blood sampling was performed Once in the morning (8 am) and a later week in evening (5 pm) in two stages (before and after). Datas were analyzed with Kolmogorov Smirnov test, Levine's test and two-way ANOVA level (p < 0/05 ). The results showed that there was not significative difference between the effects of an anaerobic activity in the morning and in the evening on hematocrit, platelet, partial time Thromboplastin (PTT), Prothrombin time (PT) and fibrinogen in non-athletic subjects. Findings showed that training for normal persons, non-athletes and patients, especially patients with clotting problems, and cardiovascular disease will be suggeste, each activity to be act with caution at morning and during the day.
The purpose of the present research is compare the effects of coagulation factors in nonathletes gilrs after exhaustive anaerobic activity .Present study was semi-emprical that was done on 12 non-athlete female students in range of 18-24 years. Exercise protocol was RAST test, that in which each person passed amain 35 meters of distance for 6 times and rest 10 seconds between each stage.Blood sampling was performed in two stages (before and after).Datas were analyzed with Kolmogorov Smirnov test, Levine's test and two-way ANOVA level (p < 0/05 ). The results showed that anaerobic exercise had a significant influence on partial time Thromboplastin (PTT), and fibrinogen in non-athletic subjects.But there was not significative difference on Prothrombin time (PT), platelet and hematocrit.Findings suggested that a meeting of anaerobic exercise on blood coagulation factor, effectiveness and changes in some of the invoices for training program Drafradghyrfal is important.
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