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Biomedical subjects

J Musiał

Publications and source records attributed to J Musiał.

At least 55 records · Page 3Linked to original sources
PubMed1994

[Laboratory methods of estimating blood platelet activation].

Important discoveries of the last twenty years indicate that blood platelets play an important role in the etiopathogenesis of many serious diseases. These include atherosclerosis with its acute vascular complications like myocardial infarction and many forms of disseminated intravascular coagulation. Their role is not limited here to platelet participation in thrombus formation. This is why we are constantly searching for a method which will allow to detect platelet activation in vivo before any important damage to vital organs and tissues will take place. Despite the implementation of sophisticated modern laboratory techniques reliable assessment of such activation poses still a clinical and laboratory problem.

Flow Cytometry↗
PubMed1994

Thrombinogenesis and its pharmacological modulation in atherosclerosis.

Appearance of thrombin in circulating blood can be monitored in the clinical setting by measuring specific thrombin markers, such as fibrinopeptide A, thrombin-antithrombin III or prothrombin fragment 1 + 2. In myocardial infarction monitoring of thrombin activity is of growing clinical interest. High levels of thrombin markers indicate an increased risk to a patient with myocardial infarction. Persistent, high thrombin marker levels, despite heparin anticoagulation, point to ongoing thrombin generation that may necessitate more anticoagulation, increased antiplatelet treatment, angioplasty or, in the future, use of new antithrombotic drugs. Recently, new sensitive methods have been developed to study the reaction of thrombin generation in clotting blood. These methods permitted to demonstrate that, aspirin, contrary to several other antiplatelet drugs, delay the process of thrombin formation. Continuous dampening of thrombin formation by aspirin might be one of the mechanisms responsible for its prophylactic and therapeutic efficacy. Hypercholesterolemic subjects might profit less than others from this type of treatment, since aspirin dampening effects are not so evident in hypercholesterolemia.

Animals↗
PubMed1991

[Lipoproteins (A) after a history of myocardial infarction, arteriosclerosis obliterans, hypertension and hyperlipidemia].

Serum lipoprotein(a) concentration in men with hypertension, arteriosclerosis obliterans, hypercholesterolemia and after myocardial infarction was measured using Laurell's immunoelectrophoresis. Lp(a) distribution and mean serum concentrations did not differ significantly from the controls, with the exception of a group of premature myocardial infarction (age below 45), in which high values were more frequent.

Adult↗
PubMed1991

[Treatment of respiratory tract infections with pefloxacin].

Pefloxacin, a 4-quinolone derivative, was administered in the dose of 800-1200 mg for the mean of 12 days to 24 patients with respiratory tract infection complicating chronic bronchial asthma or chronic obstructive lung disease. Patients with positive sputum culture and bacteria sensitive to pefloxacin were included in the study. Total eradication of the offending microorganisms was achieved in 54% of patients, and partial--in the next 20%. A poor efficacy of pefloxacin against Streptococcus species has been confirmed. In a few cases we have observed the development of resistance of isolated bacteria to pefloxacin during the course of treatment.

Adult↗
PubMed1986

Fibrinolytic activity of prostacyclin and iloprost in patients with peripheral arterial disease.

We studied the effects of prostacyclin (PGI2) and its stable analog, iloprost, on blood fibrinolytic activity in 33 patients with peripheral arterial disease. Ten subjects (group A) received three 5-hour infusions of iloprost on three consecutive days. The remaining 23 patients received three different 5-hour infusions (placebo, iloprost 2 ng/kg/min, PGI2 5 ng/kg/min). Tissue plasminogen activator (t-PA), total plasma fibrinolytic activity and euglobulin clot lysis time (ECLT) were determined in patients before and after each infusion, both in freely flowing blood samples and following 10 min venous occlusion. In patients of group A, ECLT at rest was significantly shortened after all three iloprost infusions (on average by about 5-11%). First and third infusions produced also shortening of ECLT after venostasis (by 21 and 32%). Statistically significant rise in t-PA activity (by about 68% on average) accompanied only the first infusion. In patients of the group B iloprost provoked significant fall in ECLT at rest (by about 19% on average) only. PGI2 shortened ECLT both at rest and after venous occlusion (by about 17% and 20% on average, respectively) and led to a rise in t-PA activity after venous occlusion by about 33% on average. Our results indicate that prostacyclin and its stable analog, iloprost, enhance fibrinolytic activity in man by releasing or facilitating the release of tissue plasminogen activator from the vessel wall.

Adult↗
PubMed1978

Thromboxane generation and platelet aggregation in survivals of myocardial infarction.

Arachidonic acid (AA)-induced platelet aggregation was studied in platelet-rich plasma of 30 male patients who survived myocardial infarction and in 30 healthy men of similar age. Mean platelet aggregation thresholds to AA were 746 +/- 62 micrometer, and 869 +/- 57 micrometer, respectively. Only in 2 healthy subjects, but in 12 patients, irreversible platelet aggregation was induced consistently with low concentrations of AA, under 500 micrometer. The rate of conversion of AA to thromboxane A2 (TXA2) by platelets of these patients was augmented. Furthermore, less endogenous TXA2 was required to trigger aggregation of their platelets as compared to the controls. We have also shown that in platelet-poor plasma of these patients with "hyperreactive" platelets there exists a transferable factor which makes platelets of healthy subjects more prone to aggregatory action of AA. It is proposed that the assessment of platelet aggregability with AA provides a tool for identifying a subgroup of patients with coronary heart disease who might substantially benefit from the secondary preventive treatment with aspirin and with other antiplatelet drugs which inhibit the generation of TXA2 in platelets.

Adult↗