Biomedical subjects
Publications and source records attributed to G Vogel.
The present state of streptokinase treatment at a "moderately high dose" was presented. Based on the experience accumulated, recommendations were given for improvement of the thrombolytic therapy.
Five patients with acute massive pulmonary embolism were treated with streptokinase administered via the pulmonary artery as close as possible to the embolus. Streptokinase (Awelysin) was infused at a loading dose of 250,000 IU followed by a maintenance dose of 100,000 IU/hour under haemodynamic and angiographic control. In four of five patients (two patients with cardiogenic shock) the clinical signs, pulmonary artery pressure and the angiographic findings improved or they normalised within 5-12 hours. In one patient with recurrent embolisation over three weeks the clinical condition improved gradually, although the angiographic findings improved only slightly. The results demonstrate that local thrombolysis of acute massive pulmonary embolism is a highly effective form of treatment.
The dose effects of temazepam tablets (15 and 30 mg) were studied at two sleep centres in 48 volunteers who had objective polysomnographic evidence of sleep onset insomnia. Volunteers slept in the laboratory, retiring at their usual bedtime after taking placebo or temazepam 30 min earlier, and were monitored for 8 h using standard polysomnographic techniques. Acute (nights 5-7) and short term (nights 11-13) temazepam, both 15 and 30 mg, improved the sleep of these volunteers by reducing sleep latency and increasing sleep time compared to the placebo baseline (nights 2-4). Dose differences were found primarily on the measurement of sleep staging, with 30 mg having a greater or more consistent effect than 15 mg. No residual effects were observed on the basis of questionnaires and objective tests of performance and no consistent evidence of disturbed sleep after discontinuing treatment was seen.
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Longterm treatment for 5 years of young patients with familial hypercholesterolemia was accompanied by monitoring of plasma levels of calcium, iron, sodium, parathyroid hormone and water- and fat soluble vitamins, since interference of the ion exchange resin with absorption of numerous substances as well as abnormal plasma levels of some of the above had been described in several studies. Treatment was effective in the group with good compliance (lowering of plasma cholesterol at the end of 5 years by 19% and, compared to the control group, by 23%). Adverse drug effects with respect to the above parameters were not found. Plasma levels of carotinoides and vitamin E were elevated in the patients according to elevated concentrations of lipoproteins which are carriers of these vitamins.
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The predatory slime mold, D. caveatum, feeds upon other amoebae by phagocytosis. The D. caveatum amoebae begin feeding upon cells the same size or larger by nibbling pieces of cells. While feeding upon other amoebae as opposed to bacteria, they increase in size. This behavior resembles that of phagocytes in higher organisms. A novel method was used to follow the time course of phagocytosis. A lytic toxin, phallolysin, and mutants resistant to the toxin were utilized in an assay to separate the phagocytes from the prey cells. Since a broad spectrum of cells are sensitive to the toxin, the method has general applicability.
Forty-eight patients complaining of insomnia were studied at two sleep laboratories using an identical protocol to evaluate hypnotic efficacy. All met the screening requirement of a mean sleep latency of 30 min or greater on 3 laboratory nights following an adaptation night. Of these patients 34 still complaining of insomnia were screened a second time 2 to 6 months later. Sixteen of the 34 failed the second screen. Sleep parameters for the 34 on screen 1 compared with screen 2 were the same except for sleep latency (the eligibility criteria), which was significantly shorter. There was no evidence of a systematic difference between laboratories, a change in procedure from screen 1 to 2, or a systematic loss of patients from screen 1 to 2. The data show that the statistical phenomenon of regression toward the mean must be considered in designing hypnotic efficacy studies.
The specific detection of fibrin monomer and fibrin degradation products is of high importance in the laboratory diagnosis of intravascular clotting (disseminated intravascular coagulation, deep vein thrombosis). The methods proposed until now are partly time-consuming, needing special laboratories or insensitive and poorly specific. Applying ristomycin instead of ristocetin (another member of the vancomycin antibiotics) a new simple, specific and sensitive method has been elaborated and recommended for the laboratory diagnosis of intravascular coagulation and its differentiation from primary fibrinogenolysis. The results obtained from in vitro and animal experiments and from human studies are presented.
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The pharmacokinetics and the effects on the haemostatic system of hirudin were assessed in six healthy subjects after single intravenous or subcutaneous dose (1000 AT-U/kg). When hirudin was given intravenously first-order elimination kinetics followed the initial distribution phase. The decline in plasma hirudin concentration was most adequately expressed by a biexponential equation describing a two compartment model. A mean elimination half-life of 0.84 hr and a mean volume of distribution of 12.9 l were calculated. After subcutaneous injection a low hirudin level (approximately 0.5 AT-U/ml) was maintained for a prolonged period of time. In the 24 hour-urine up to 50 per cent of the administered amount of hirudin was excreted in active form. Thrombin time, partial thromboplastin time and prothrombin time measured in plasma samples ex vivo were prolonged dependent on the hirudin plasma level. Platelet counts, fibrinogen level and the fibrinolytic system were unchanged. Bleeding time was prolonged twice at maximum. Subcutaneous or intravenous administration of pure hirudin was tolerated without side-effects.
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A single oral dose of the lyophilized deathcap fungus Amanita phalloides (85 mg/kg body wt) caused gastrointestinal signs of diarrhea, retching, and vomiting in beagles after a latent period of 16 hr. The pathologic lesions; the increases in serum transaminase (GOT, GPT), alkaline phosphatase, and bilirubin, as well as the fall in prothrombin time all indicated that liver damage was maximal at about 48 hr after poisoning. Four of twelve dogs given A. phalloides died with signs of hepatic coma within 35 to 54 hr with the biochemical values in the survivors reverting to normal by the ninth day. Silibinin administration (50 mg/kg) 5 and 24 hr after intoxication suppressed the serum changes and the fall in prothrombin time. The degree of hemorrhagic necrosis in the liver was markedly reduced, and none of the silibinin-treated dogs died.
Two recessive mutations of the cellular slime mould Dictyostelium discoideum, phgA1356 and phgB1351, which express altered phagocytic properties, were characterized using parasexual genetic analysis. The phgA locus was assigned to linkage group VII, and the phgB locus to linkage group IV. Complementation analysis of a further twelve independently derived phagocytosis mutants showed that each fell into one of these two complementation groups.