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Biomedical subjects

N Böhm

Publications and source records attributed to N Böhm.

At least 109 records · Page 6Linked to original sources
PubMed1977

[Vena cava occlusion-syndrom by leiomyosarcoma. Two case reports (author's transl)].

Two cases of occlusion of the inferior vena cava by leiomyosarcoma are reported. This localisation is extremely rare for mesenchymal tumors. The neoplasm originated from the wall of the vena cava, expanded forward into the lumen of the vessel, in one case up to the right atrium. Collateral circulation, anasarca edema and varices develop by this occlusionsyndrome. The fatal outcome of the disease is usually determined by right heart failure and not by metastases directly. In most cases diagnosis is made by autopsy. In cavography the differential diagnosis of thrombosis might include the rare possibility of leiomyosarcoma of the caval vein. Only early diagnosis makes succesful surgical therapy possible.

Aged↗
PubMed1976

[Reversible hyperplasia and hypertrophy of the mouse liver induced by a functional charge with phenobarbital].

INTRODUCTION: Administration of phenobarbital to rats and mice is well known to cause enlargement of the liver, where the drug is metabolized by hydroxylation and oxydation. The increase of the liver weight is thought to be due to and enlargement of the individual hepatocytes (hypertrophy) caused by an augmentation of the smooth endoplasmic reticulum, as well as to cell multiplication (hyperplasia). The present investigation deals with the nuclear DNA content of mouse hepatocytes during and after administration of different doses of phenobarbital. The data are related to liver weight with due consideration of mitotic activity and cell loss by necrobiosis. MATERIAL AND METHODS: 172 five to six weeks old male albino NMRI mice with a body weight of 23 to 33 gms were randomly divided into four groups, one of which served as the controls. The three test groups received 75 mg and 150 mg phenobarbital per 1 kg body weight intraperitoneally once every day for a total of 10 days. Thereafter the administration of the drug was discontinued. Beginning with the third day of the experiment 3 animals of each group were sacrificed by exsanguination every secound day after their body weight had been carefully determined. Then the liver weights were measured. The nuclear DNA content of the hepatocytes was determined from liver smears by means of acriflavine-Feulgen fluorescence cytophotometry. The number of mitotic figures and of necrobiotic liver cells was counted in histologic sections. RESULTS: With animals receiving 150 mg and 100 mg phenobarbital per 1 kg body weight a rapid increase of the relative liver weight (up to 74% above the controls) was observed, which was reduced back to normal levels within 10 days after discontinuation of the drug. Parallel with the increase of the liver weight a striking DNA-polyploidisation of the liver nuclei occurred which proved to be reversible during the reduction phase. Mitotic figures were found only in the initial phase of the experiment (third to fifth day), while the number of necrobiotic hepatocytes was increased after the drug was discontinued. Similar but markedly less pronounced effects were encountered with animals of the 75 group. DISCUSSION: It is concluded that the increase of the liver weight of mice after phenobarbital administration is partly due to cell multiplication (hyperplasia) - as is shown by a high number of mitotic figures in the initial phase of the experiment-, partly due to the enlargement of hepatocytes with concommitant polyploidisation of the muclei (hypertrophy). When the drug administration is discontinued the liver weights return to normal levels within 10 days. Since at the same time the number of high-ploidy nuclei is reduced with no evidence of an increased mitotic activity, the reduction of the liver weight should be partly caused by an elimination of high-ploidy hepatocytes, which are no longer required after the hyperfunctional stimulus has ceased...

Animals↗
PubMed1976

[Cystinosis (author's transl)].

Cystinosis (syn. crystine storage disease) is inherited as an autosomal recessive trait. The severety of clinical symptoms may vary considerably. The most severe form of nephropathic cystinosis causes death of the affected patients at the age of 2 to 4 years (subacute course) or before puberty (primary chronical course). Three autopsy cases are demonstrated. Each of these children died from complications of chronic renal failure, caused by kidney contraction as a sequela of chronic interstitial nephritis. Cristalline cystine deposits were found in the renal interstium as well as in the RES cells of spleen and liver. Because of water solubility of L-cystine aqueous fixation and staining solutions must be avoided. Diagnostic doubly refractive brick- or needle-shaped cystine cristals can be demonstrated in frozen sections or tissue smears from spleen, liver, lymphnode and bone marrow.

Child↗
PubMed1976

[Congenital mesoblastic nephroma - a semimalignant fibroleiomyomatous kidney tumor of the newborn (author's transl)].

The congenital mesoblastic nephroma is a distinct tumor entity, which should be clearly distinguished from Wilmus-tumor. The pure mesenchymal tumor is usually present at birth and palpated as a mass in the kidney. Macroscopically the tumor reveals a striking resemblance with an uterine fibroid. Histologically the tumor tissue ist characterized by 1. interlacing bundels of spindle cells with uniform cell nuclei and regular mitotic figures, 2. collagen fibres between the tumor cells, 3. an angiomatous marginal zone, no tumor capsule, 4. hematopoetic foci and dysplastic glomeruli and tubuli in areas where normal kidney parenchyma mixes with tumor tissue, 5. small myxomatous areas within in the tumor, 6. no invasion of blood vessels or pelvis. Prognosis of the congenital mesoblastic nephroma is much better than in Wilms-tumor. Metastases have not been described so far. If, however, the tumor tissue is incompletly removed during operation, the neoplasm may recur and prove fatal. Ultrastructural and DNA cytophotometric studies suggests a low grade malignancy rather than a truely benign behaviour of this tumor.

DNA, Neoplasm↗
PubMed1975

[The fructose induced "glycogenosis". I. Ultrastructural and morphometric analysis of rat hepatocytes 7 days after fructose overload (author's transl)].

INTRODUCTION: Infusion of fructose has been shown to stimulate the SER and to reduce the RER in rat liver cells. After feeding fructose of 7 days a glycogenosis of unknown pathogenesis occurs, which was analysed morphometrically. MATERIAL AND METHODS: 60% fructose in water, was given as drinking water to animals deprived of other food. Controls had free access to Altromin-R-standard diet and drinking water. Liver tissue was analysed morphometrically according to the methods described by Weibel. RESULTS AND DISCUSSION: Rat hepatocytes accumulate a material with histochemical properties of glycogen. The enlargement of hepatic nuclei is probably due to a pathological edema. The SER is decreased suggesting a drop of glycogen catabolizing enzymes. The drastic reduction of the RER and the non-membrane bound ribosomes are signs of inpeeded protein synthesis. According to this, the peroxisomes, which arise from the RER, are decreased in volume and number. The hepatocellular chondrioma is transformed morphometrically in a smaller number of larger, pleomorphic and cup-shaped mitochondria. The ATP level drops while, on the other hand, the cristeal membranes increase. This might be caused by a negative feed back mechanism. The hepatocellular cytoarchitecture described is similar to the one found in glycogenosis type I and in the cerebrohepato-renal syndrom.

Animals↗
PubMed1975

[Familial glucocorticoid insufficiency (author's transl)].

Familial glucocortivoid insufficiency--also called hereditary lack of response of the adrenals to ACTH-has not yet been described in Europe. Isolated glucocorticoid insufficiency combined with intact secretion of aldosterone and high plasma level of ACTH are characteristic. The diagnostic difficulties are demonstrated by the deaths before diagnosis of 13 siblings of 21 patients from 9 families. One such family is described. The first of 3 children died at the age of 3-1/2 years after a two day illness interpreted as encephalitis. Another boy, aged 4-1/2 years, had a hypoglycemic attack. 3 months later he died in status epilepticus after a short feverish illness. At autopsy the adrenals were very small. Histologically only the glomerulous zone was developed. An the hypophysis there was hyperplasia of the R cells producing ACTH. The 6 year old sister had been pronouncedly pigmented from the age of a few months onwards. Age in terms of height and bone development corresponded to 8-1/2 and 7-1/2 years. After intravenous insulin and synacthen plasmacorticoids could not be found. With normal and low supply of salt, the following data were found: Renin-activity 2.9 and 5.6 ng/ml p.h. respectively; rate of aldosterone secretion 62.6 and 151.5 mug/24 hrs.; average aldosterone plasma concentration 9.39 and 27.7 ng/100 ml respectively; MCR 666 and 5471 p/24 hrs. Plasma ACTH in this patient (5086--7200 pg/ml) and, post mortem, in her brother (8100 pg/ml), were extremely reaised.

Adrenal Glands↗