Biomedical subjects
Publications and source records attributed to N Böhm.
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Brain tissue embolism in the coronary, leptomeningeal and pulmonary arteries was discovered microscopically following the autopsy of a female newborn. Death occurred 8 h after breech delivery, which had been complicated by both arms being turned up beside the head. The dislodged brain tissue originated from the left cerebellar hemisphere and had entered the venous blood stream through a rupture of the left sinus transversus. Both "paradoxical" systemic and pulmonary artery embolization ensued. The baby died from the combined effects of cerebral haemorrhage, pulmonary embolism, myocardial infarction and shock.
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Two brothers are described who manifested primary adrenal insufficiency, dystrophic myopathy, severe psychomotor retardation, failure to thrive, fatty degeneration of the liver, megalocornea, chronic constipation, and terminal bladder ectasia until their death at 3 8/12 and 1 7/12 years, respectively. The differential diagnosis to similar syndromes is discussed. This combination of problems apparently has not yet been described. The term adrenomyodystrophy is suggested.
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It has been well documented in laboratory animals that beta-sympathicomimetics, such as isoprenalin, can cause myocardial lesions. Other so called "beta2-selective" symphaticomimetic drugs, which nevertheless induce beta1-cardiostimulatory side effects, are now widely used for suppression of premature labor. We examined the hearts of 25 newborns whose mothers had been treated with beta-sympathicomimetics for various lengths of time (24h to 8 weeks). Three types of lesions were detected: (1) focal subendocardial necroses (3 cases), similar to isoprenalin-induced myocardial necroses in animal experiments, (2) diffuse fatty degeneration of myocardial cells (3 cases), and (3) nuclear polyploidization in the subendocardial layer of the right ventricular wall (14 cases). However, the immediate causes of death could not be directly related to the tocolytic treatment in any of the cases.
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Phenobarbital was injected intraperitoneally into male white NMRI mice aged 0.5, 1. 1.5, 3, 6 and 12 months at a dose of 120 mg/kg body weight for 10 consecutive days. The 0.5 month-old mice did not tolerate the phenobarbital dose and died. The experimental animals and one of the controls were sacrificed 1, 3, 5, 10, 15 and 20 days after phenobarbital administration was started. Liver weights were recorded and liver cells were isolated. The number of nuclei per cell was determined and the DNA-content of each single nucleus was measured by Feulgen fluorescence cytophotometry. Liver weights showed an increase of 25--30% during phenobarbital treatment and returned slowly to lower values after cessation of drug application. The hepatic enlargement was accompanied by an excessive and likewise reversible nuclear and whole cell DNA-polyploidization, i.e. polyploidization beyond the physiological age-dependent ploidy level; for example, mean values of 7.7 c per nucleus (versus 4.2 c in the controls) and 14.3 c for whole liver cells (versus 7.5 c in the controls) were found in 3 months-old animals after 5 days of treatment. As with the induction of microsomal enzymes, the augmentation of smooth endoplasmic reticulum, and the increase of RNA- and protein-synthesis, excessive DNA-polyploidization of liver cell nuclei appears to be an expression of hepatocellular hypertrophy due to the functional or metabolic stress imposed upon the liver by large quantities of phenobarbital. After cessation of drug administration the abnormally high ploidy cells are eliminated - probably by necrobiosis - and the liver cells return to their normal age-dependent DNA-ploidy level. The liver cells of the one-month-old animals revealed the physiological polyploidization to be slightly inhibited. This is probably due to some toxic effect of phenobarbital. Phenobarbital did not alter the number of nuclei per liver cell.
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3 cases of unilateral angiomyolipoma of the kidney are presented. Angiography was unsuccessful in diagnosing angiomyolipoma in these cases observed by us. The diagnostic problems of the angiomyolipoma are discussed on the basis of histologic and angiographic findings. No patient showed simultaneously tuberous sclerosis.
Pretreatment with protein-free diet (PFD) or pregnenolone-16 alpha-carbonitrile (PCN) markedly reduces th toxicity of dimethylnitrosamine (DMN) in rats. PFD causes a shift in DMN metabolism form liver to kidney with a consequent increase in the incidence of kidney tumours. The present study was designed to evaluate the effect of PCN on the carcinogenicity and metabolism of DMN. After pretreatment with PFD, PCN or a combination of both, adult female Wistar rats received a single i.p. dose (60 mg/kg) of DMN. Animals pretreated with PFD and PFD + PCN developed a similar incidence of kidney tumours (83-85%) after a mean survival time of 357 and 396 days, respectively, Animals pretreated with PCN alone had a 50% incidence of renal tumours after a mean survival time of 672 days. This correlates with the initial extent of DMN-induced methylation of kidney DNA. Concentrations of 7-methylguanine and O6-methylguanine were highest and very similar in PFD- and PFD + PCN-pretreated rats, whereas in PCN-conditioned animals the extent of base methylation was 38% lower. Extrarenal tumours, in particular large cystic cholangiomas of the liver, were most frequent in PCN-pretreated rats, probably due to their longer survival time. In contrast to animals pretreated with either PCN or PFD, hepatic DNA methylation was markedly reduced (54-60%) in animals pretreated with both PFD and PCN.
After Feulgen staining with acriflavine-Schiff, the DNa content of glial and neuronal nuclei from various sites of the human CNS (pre- and post-central gyrus, cerebellar cortex and spinal cord) were determined by fluorescence cytophotometry. The specimens were obtained from twelve adult human autopsy cases. Glial cell nuclei always revealed a biomodal DNA distribution pattern with a large 2c and a smaller 4c peak. The 4c peak was most prominent in the cerebellum. A few 8c glial nuclei were found. Neuronal cell nuclei disclosed DNA histograms with hyperdiploid means in the range 2.2-2.5c (1.8-2.9c for the individual populations). Tetraploid 4c DNA values were not observed, neither in Purkinje cells, nor in pyramidal cells. In eleven out of a total of forty-four slides the higher DNA means of neuronal nuclei were found to be statistically significant (P greater than 0.05) when compared with a population of 2c hepatocytes on the same slide. The results indicate the existence of some 'extra DNA' in human neuronal cell nuclei, the biological significance of which has still to be elucidated. It is however, suggested that it may play an important role in the functional activity of the CNS.
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