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Biomedical subjects

M Schlenker

Publications and source records attributed to M Schlenker.

12 recordsLinked to original sources
PubMed2000

Tamoxifen-induced hyperplasia of the endometrium.

Greatly thickened endometria are often observed in vaginal sonography in patients taking tamoxifen. The incidence of type I carcinoma of the endometrium is also raised under tamoxifen. Both effects are ascribed to the known partial estrogenic effect of tamoxifen. However, if sonographically hyperplastic endometria are abraded, mostly only atrophic material is obtained. To clarify this contradiction, 89 patients treated with tamoxifen were investigated by means of vaginal sonography at intervals of 6 months. In 33 of them (37%), an endometrial thickness > 8 mm was found. In order to investigate the endometrial thickness throughout, a hysteroscopic loop resection (polyps n = 18, diffuse hyperplasia n = 15) and afterwards histological work-up of the endometrium in serial sections were carried out in all these patients. Hyperplasia of the endometrial stroma without cellular atypia was found in all cases. However, the glandular epithelium was always atrophic. This explains the contradiction between sonographically thick endometrium (stromal hyperplasia) and the scanty abrasion material (atrophy of the glandular epithelium). The 'hyperplasia' found sonographically is not necessarily estrogen-dependent hyperplasia of the glandular epithelium leading to a carcinoma. This raised the question as to the etiological reasons for the increased incidence of carcinomas. We discuss the hypothesis that tamoxifen may also promote the conversion of pre-existent subclinical lesions into manifest carcinomas.

Antineoplastic Agents, Hormonal↗
PubMed1992

Changing patterns of glucose metabolism during the course of subacute sclerosing panencephalitis as measured with 18FDG-positron-emission tomography.

18FDG-positron emission tomography performed at different stages in the course of subacute sclerosing panencephalitis revealed a changing pattern of metabolic disturbance. In clinical stage II patients the inflammation in the basal ganglia appeared to lead to neuronal excitation accompanied by hypermetabolism. Widespread cortical functional inhibition of metabolism followed. The striatal inflammation ended with necrosis and hypometabolism, with resulting functional cortical disinhibition; later, deep midbrain structures and brain stem became hypermetabolic. A patient clinically in remission showed no such changes in cerebral glucose metabolism.

Adolescent↗
PubMed1992

Activity of ornithine decarboxylase and S-adenosylmethionine decarboxylase in transient cerebral ischemia: relationship to the duration of vascular occlusion.

Mongolian gerbils were anesthetized with halothane and forebrain ischemia was induced by occluding both common carotid arteries. After 2, 4, 6, 8, or 10 min of vascular occlusion clips were removed and animals allowed to recover for 8 or 24 h. At the end of the experiments animals were reanesthetized and their brains frozen in situ. Tissue samples were taken from the cerebral cortex, striatum, hippocampus, and thalamus for determination of ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC) activity by measurement of the release of 14CO2 from [14C]ornithine and S-[14C]adenosylmethionine, respectively. A transient increase in ODC activity was found after 8 h of recirculation following cerebral ischemia in all brain structures studied. ODC activity was significantly increased after 8 h of recirculation in the hippocampus of animals subjected to 4 min of ischemia, in the cortex and striatum after 6 min of ischemia, and in the thalamus after 8 min of vascular occlusion. ODC activity had already reached a plateau in the hippocampus after 4 min of vascular occlusion and in the cortex, striatum, and thalamus after 8 min, since there is no further increase in activity even after 10 min of ischemia. After cerebral ischemia and 24 h of recirculation ODC activity returned to control levels throughout the forebrain regardless of the duration of ischemia. SAMDC activity was significantly reduced after 8 h of recirculation following 4 to 10 min of ischemia in the cortex and 8 min of ischemia in the striatum.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosylmethionine Decarboxylase↗
PubMed1992

Neuronal damage after repeated 5 minutes of ischemia in the gerbil is preceded by prolonged impairment of protein metabolism.

The effect of single or repeated episodes of cerebral ischemia on protein biosynthesis and neuronal injury was studied in halothane-anesthetized gerbils by autoradiography of [14C]leucine incorporation into brain proteins and light microscopy. For quantification of the protein synthesis rate, the steady-state precursor pool distribution space for labeled and unlabeled free leucine was determined by clamping the specific activity of [14C]leucine in plasma, and by measuring free tissue leucine in samples taken from various parts of the brain. Control values of protein synthesis were 14.6 +/- 2.2, 5.8 +/- 2.3, 14.2 +/- 3.1, and 10.0 +/- 3.8 nmol g-1 min-1 (means +/- SD) in the frontal cortex, striatum, CA1 sector, and thalamus, respectively. Following a single episode of 5 or 15 min of ischemia, protein synthesis recovered to normal in all brain regions except the CA1 sector, where it returned to only 50% of control after 6 h and to less than 20% after 3 days of recirculation. After three episodes of 5 min of ischemia spaced at 1 h intervals, protein synthesis remained severely suppressed in all brain regions after both 6 h and 3 days of recirculation. Inhibition of protein synthesis after 6 h predicted histological injury after 3 days of recirculation. In animals submitted to a single episode of 5 or 15 min of ischemia, histological damage was restricted to the CA1 sector but injury occurred throughout the brain after three episodes of 5 min of ischemia. These observations demonstrate that persisting inhibition of protein synthesis following cerebral ischemia is an early manifestation of neuronal injury. Prevention of neuronal injury requires restoration of a normal protein synthesis rate.

Animals↗
PubMed1988

Effects of enzymatic blood defibrination in subcortical arteriosclerotic encephalopathy.

Plasma hyperviscosity is a striking abnormality in patients suffering from subcortical arteriosclerotic encephalopathy (SAE) and is thought to perpetuate the chronic ischaemic demyelinating process of the periventricular white matter. Ancrod, a defibrinating enzyme, was given to 10 patients with SAE in an attempt to reduce plasma fibrinogen, which would thus normalise hyperviscosity. This was paralleled by a significant improvement of the initially abnormal retinal arteriovenous passage time, as well as a significant augmentation of the CO2-induced cerebral vasomotor response. This did not lead, however, to any clinical improvement with respect to performance of neuropsychological tests, recurrences of strokes during a 6 month observation period or improvement of various audiological parameters. The findings indicate that hyperviscosity in patients with SAE is merely an epiphenomenon. A potentially reversible, chronic penumbral state of the brain tissue apparently does not exist in SAE.

Aged↗
PubMed1979

[The relative ejection time under different conditions of cardiac stress and in aortic valve disease (author's transl)].

In 51 healthy young people the carotid arterial pulse wave was registered externally during bicycle-exercise in a lying position. The ejection time in relation to the duration of diastole (not pulse period or heart rate!) increased significantly. These results are compared with measurements made by Schulz (15) who found normal ejection times in tachycardia provoked by pacer-stimulation and shortened values during isoproterenol-induced tachycardia. Women have longer ejection times than men especially under physical stress. In 18 patients suffering from aortic insufficiency, ejection times were slightly prolonged and in 28 patients who had a systolic pressure gradient of more than 20 mm Hg between the left ventricle and the aorta ejection times were markedly prolonged. There is also a significant positive correlation between ejection time and pressure gradient. The authors consider that the autonomic innervation plays an important role in the duration of ejection time in normal subjects while in patients with aortic heart disease the ejection time is predominantly influenced by mechanical factors. For the diagnosis of the severity of aortic stenosis measurements of ejection time are only useful in connection with other clinical parameters (pulse pressure, creast time of the arterial pulse wave).

Adult↗