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Biomedical subjects

E Weber

Publications and source records attributed to E Weber.

At least 415 records · Page 23Linked to original sources
PubMed1981

Novel peptide neuronal system in rat brain and pituitary.

Immunohistofluorescence studies of the rat central nervous system with antibodies to Phe-Met-Arg-Phe-NH2 (molluskan cardioexcitatory peptide) revealed a widespread neuronal system in the brain, spinal cord, and posterior pituitary. Immunoreactive axons and cell bodies were mainly located in cortical, limbic, and hypothalamic areas. Immunostaining of serial sections of the brain and pituitary showed that the Phe-Met-Arg-Phe-NH2 immunoreactive neurons were different from neurons labeled by antibodies to either Met-enkephalin or the putative Met-enkephalin precursor Tyr-Gly-Gly-Phe-Met-Arg-Phe, which is structurally related to Phe-Met-Arg-Phe-NH2. Control staining by antiserum absorption and radioimmunoassay indicated that the antibodies that caused the specific immunofluorescence recognized peptides with an amidated Arg-Phe sequence at the carboxyl terminus.

Animals↗
PubMed1981

The clinical pharmacokinetics of buflomedil in normal subjects after intravenous and oral administration.

A dose-ranging pharmacokinetic study of buflomedil was carried out in eight subjects to determine the pharmacokinetic parameters of the drug after oral and intravenous administration. Based on AUC infinity analyses, the pharmacokinetics of buflomedil were found to be linear within the dose ranges studied (50 to 200 mg for i. v. injection and 150 to 450 mg for oral administration). In the oral study, the mean biological half-life of the drug was 2.97 h, while after intravenous dose it was 3.25 h. The apparent volume of distribution after the pseudodistribution equilibrium (Fd beta) and volume of distribution at the steady state (Vdss) were 1.43 +/- 0.24 l/kg and 1.32 +/- 0.26 l/kg, respectively. The mean urinary recovery of intact drug and the metabolite, paradesmethyl buflomedil, after intravenous dosing, were 23.6% and 18.7%, respectively, while after oral dosing, they were 18% and 14.8%, respectively. On the average, 72% of the dose was observed into the systemic circulation after oral administration. This level of bioavailability was attributed to the hepatic first-pass effect.

Administration, Oral↗
PubMed1981

Induction of drug metabolizing enzymes by sulfinpyrazone.

A previous interaction study of sulfinpyrazone (Anturano) suggested that it induced microsomal drug metabolizing enzymes in the liver. To verify this finding the effect of sulfinpyrazone 800 mg per day for four weeks was investigated in ten healthy volunteers. Both the therapeutic actions of sulfinpyrazone, the uricosuric and the antiaggregating effects, were demonstrated (p less than 0.05). The influence on the microsomal drug metabolizing system in the liver was demonstrated by an increase in serum-gamma-glutamyl transpeptidase from 15.1 to 23.3 U/l (p greater than 0.05), a significant increase in the urinary excretion of d-glucaric acid (29.6 to 77.9 microMol/24 h, p less than 0.05) and an increase in antipyrine clearance from 50.3 ml/min to 83.9 ml/min (p less than 0.05). The possibility of enhancement of drug metabolism during treatment with sulfinpyrazone in combination with other drugs should be kept in mind.

Adult↗
PubMed1981

[Interposition of periosteum in joint fractures in adolescents; comparison of operative and conservative treatment (author's transl)].

Interposition of periosteum in joint fractures in adolescents may lead to delayed consolidation of the fracture or even malposition (varus-valgus deformities etc.) by early partial closure of the epiphyseal line. In severe cases, early arthrosis may be sequelar of inappropriate treatment of these patients. 14 cases of joint fractures with interposition of periosteum in adolescents are presented. The results of 5 operated cases are compared with 9 conservatively treated patients. The need for operative treatment is stressed.

Adolescent↗
PubMed1981

[Degradation of Azlocillin and Mezlocillin / I. Behaviour in biological material and buffer (author's transl)].

The degradation of 6-[(R)-2-(2-oxo-imidazolidine-1-carboxamido)-2-phenyl-acetamido] penicillanic acid Na-salt (azlocillin, Securopen) and 6-[(R)-2-[3-methylsulfonyl-2-oxoimidazolidine-1-carboxamido]-2-phenyl-acetamido ] penicillanic acid Na-salt (mezlocillin, Baypen), two chemically related acylureido penicillins, was tested in biological material (plasma and urine) and borate buffer at 37 degrees C over the time period of at least 6 h. In fresh human urine (pH 5.0) no degradation could be observed. In freshly prepared human plasma (pH 7.6) degradation was independent of the initial concentration and amounted to no more than 5%. No difference could be noted between the degradation in plasma or buffer, respectively, indicating that direct aminolysis did not play an important role in the degradation process. The extent of degradation could be demonstrated to be pH-dependent. After 8 h incubation at pH 9.0 azlocillin concentration was decreased to 70% and mezlocillin concentration to 50%, respectively, of the initial concentration. Since urinary pH values up to 8.5 are reported the urinary recovery of the substance could be influenced by alkaline pH.

Azlocillin↗
PubMed1981

Frequency of cancerous and precancerous epithelial lesions in the stomach in different models for enterogastric reflux.

A gastroenterostomy without entero-anastomosis in rats favours the development of adenomatous epithelial lesions at the gastroenteral borderline in dependence of exposition to MNNG. The extent of such changes in the mucosa could be modified by vagotomy, pyloroplasty, or the prevention of duodenogastric reflux (Roux-en-Y method), whereby vagotomy has an enhancing effect on proliferation. A comparison of the mucosal changes at the gastroenteral anastomosis indicates that a multitude of factors causes environmental changes at the gastroenteral borderline, stimulating epithelial proliferation to the point of cancer formation. Thus, it is not possible to accuse any single factor such as intestinal reflux, carcinogens or different surgical techniques as the sole culprit in carcinogenesis.

Animals↗