Biomedical subjects

B Volk

Publications and source records attributed to B Volk.

At least 109 records · Page 6Linked to original sources

PubMed1988

Long-term alcohol consumption reduces the number of neuronal nuclear pores. A morphometric study undertaken in CA3 hippocampal pyramids of rats.

A close relationship between the number of nuclear pores and the cellular protein synthesis activity is known to exist. Previous biochemical investigations lead to admit that the widespread neuronal alcohol-induced degenerative changes could depend on a decrease in the neuronal protein synthesis. The morphometric analysis made on the nuclear pore complexes of CA3 hippocampal pyramids of long-term alcohol-fed rats fully supports this attractive hypothesis, since it has been found a marked reduction in the number of pores per unit surface area of nuclear membrane, together with a reduction in their total number per nucleus.

Alcoholism↗

PubMed1988

Multiple sclerosis presenting as chronic atypical psychosis.

Two patients with multiple sclerosis are reported in whom psychopathological symptoms were present for many years. An exact psychiatric classification of the clinical syndrome was not possible. At no time during the illness were abnormal neurological findings observed. Multiple sclerosis was proven following necropsy in one patient. In the second patient a possible diagnosis of multiple sclerosis was made. This patient was found to have multiple lesions in the white matter which were evident on MRI and in the isoelectric focusing (IEF) of cerebrospinal fluid oligoclonal bands were found.

Adult↗

PubMed1987

The monoclonal antibody Ki-67 as a marker for proliferating cells in stereotactic biopsies of brain tumours.

The monoclonal antibody Ki-67 has been tested as a marker of proliferating cells in 52 stereotactic brain tumour biopsies. The antibody reacts with a nuclear protein expressed in G1,S, G2n and M-phases of the cell cycle. Using the immunoperoxidase technique on squash preparations the percentage of Ki-67 positive cells was determined as a fraction of the total number of tumour cells present. This Ki-67 index was in close correlation with the histological grade. Highest values were found in a pineal germinoma (46.3%) and in 3 primary cerebral non-Hodgkin lymphomas (mean 39.5%). Among the gliomas, the highest fraction of proliferating cells was seen in 2 anaplastic paediatric brain stem gliomas (mean 17.4%) and in an anaplastic ependymoma (12.5%). Anaplastic astrocytomas and glioblastomas varied considerably with mean values of 9.5% and 8%, respectively. To some extent this variability may reflect tumour heterogeneity which is more likely to manifest in small stereotactic samples than in large tissue specimens obtained during open surgery. Pilocytic astrocytomas, mixed gliomas and fibrillary astrocytomas had moderate to low percentages. Ki-67 staining of squash preparations can easily be performed on a routine basis and is, in our experience, superior to frozen sections. This method allows the determination of the growth fraction of an individual tumour and could become an important additional criterion for the decision among alternative and potentially harmful therapeutic regimens.

Antibodies, Monoclonal↗

PubMed1987

[Astrocytoma in a premature twin].

In a premature twin boy (gestational age 34 weeks) two-dimensional echoencephalography, computed tomography, and NMR tomography revealed a brain tumor. The exact diagnosis was confirmed by stereotactic biopsy from the brain. Up to now the clinical course of the child has been surprisingly benign.

Astrocytoma↗

PubMed1986

Resistance to hypoglycemia of cerebellar transplants in the rat forebrain.

Prolonged insulin-induced hypoglycemia causes widespread loss of neurons and permanent brain damage with irreversible coma. Although the deprivation of carbohydrate stores affects all brain regions, the breakdown of energy metabolism and cessation of protein synthesis occur predominantly in the cerebral cortex, caudoputamen and hippocampus. The cerebellum, brain stem and hypothalamus are largely resistant. Following transplantation of the cerebellar anlage of rat fetuses (day 15 of gestation) into the caudoputamen of adult rats, the grafts were allowed to differentiate for a period of 8 weeks. The host animals were then subjected to 30 min of severe hypoglycemia with isoelectric EEG ('coma'). In contrast to the surrounding vulnerable brain structures, protein synthesis was fully preserved within the cerebellar transplant. Grafting of fetal forebrain cortex to the same location did not result in escape from hypoglycemic cell injury. This indicates that resistance to hypoglycemia is part of the programmed differentiation of the cerebellum and develops irrespective of its location and functional integration within the nervous system.

Animals↗

PubMed1986

Diagnostic value of ultrasound in duodenal stenosis.

Radiology and endoscopy are usually used to diagnose stenosis of the duodenum, but the cause of the stenosis may still escape detection. Three pathologic processes--multiple duodenal polyps, duodenal wall cysts, and annular pancreas--are presented to demonstrate how ultrasound, under specific conditions, can provide decisive diagnostic information. The cause of the stenosis may be made accessible to sonographic study through administration of oral fluids and intravenous hyoscin-n-butylbromid (Buscopan).

Adult↗

PubMed1986

Degeneration of granule cells following chronic phenytoin administration: an electron microscopic investigation of the mouse cerebellum.

Fifteen male mice (C57/Bl6J) were fed the liquid diet "Stardit" supplemented with vitamins together with phenytoin for 8 weeks; experimental animals and controls were pair-fed. After 8 weeks of treatment, the anesthetized animals were perfused with 3.5% glutaraldehyde. Tissue samples of the cerebral cortex (area 3), cerebellum (vermis), thalamus, hypothalamus, and liver were embedded in Araldite. All phenytoin-treated animals displayed a hepatomegaly. Semithin sections and ultrastructural investigations of the cerebellar vermis showed pyknoses of granule cells and an enlargement and swelling of parallel fibers in presynaptic areas in the molecular layer. The swollen axons showed an accumulation of tubular structures which represented proliferated smooth endoplasmic reticulum. Similar tubular structures were observed in hepatocytes of experimental animals. It is proposed that phenytoin caused an induction of the microsomal system of hepatocytes and granule cells which led to a proliferation of the smooth endoplasmic reticulum. The transport of these organelles to the axon terminals of parallel fibers via the axoplasmic flow is assumed to cause a swelling of the presynaptic area. A dying-back process may then lead to pyknosis of granule cells. Chronic phenytoin administration to mice is a new experimental model of neuroaxonal dystrophy.

Animals↗

PubMed1986

[CT stereotactic biopsy in the differential diagnosis of deeply situated intracerebral hematomas].

The diagnosis of intracerebral haematomas, especially of those which are relatively small, occupy little space and are deeply situated, presents considerable problems. The problem is even greater when the expected acute case history and the acute beginning of the symptoms do not occur and unusual localisations are found. The consequences of this are false diagnoses and the treatment of these patients within the framework of blanket diagnosis "intracerebral tumours" or "space occupying processes" without any confirmation of the histological diagnosis. - Using a sample of 26 patients where the histological diagnosis of non-recent intracerebral hemorrhages had been confirmed (out of a series of 818 CT-stereotactically biopsied patients punctured by us from the beginning of 1983 until the end of 1984), the problem of establishing a diagnosis is exposed. - A histological diagnoses should in any case be confirmed before any thorough and deep-reaching therapy is begun, since false diagnoses and misinterpretations can cause serious consequences for the patient.

Biopsy↗

PubMed1986

Chronic alcohol consumption induces plastic changes in granule cell synaptic boutons of the rat cerebellar cortex.

The reduction of cerebellar cortex molecular layer afferents, as a consequence of an alcohol-induced granule cell degeneration, is followed by a remodeling activity which leads to marked structural changes. Using Golgi, ultrastructural and combined Golgi-ultrastructural methods, it was evaluated the role played by granule cell synaptic boutons in this plastic process and, furthermore, determined whether there were differences between the boutons located in the ascending portions of the axons and those belonging to parallel fibers. No significant differences were found in the number of boutons per unit length of axon when the alcohol-fed animals were compared to the controls, despite a significant increase in the volumetric density of nerve terminal profiles after 12 months of alcohol intake. This increase is likely to depend on variations in the size of the nerve terminals rather than on their number.

Alcoholism↗

PubMed1985

Lipofuscin granules in cerebellar interneurons after long-term alcohol consumption in the adult rat.

Lipofuscin deposition in nerve cells is one of the most reliable and consistent neurocytological features correlated with ageing. Purkinje cells of long-term alcohol-fed rats show large agglomerates of lipofuscin granules after six months of alcohol experiment, whereas in normal biological ageing, this happens only after 25 months of age. Cerebellar interneurons have specific patterns of lipofuscin accumulation during ageing concerning both its morphological type and chronology of deposition. We studied the effects of chronic alcohol treatment on cerebellar interneurons taking particular account of lipofuscin pigment accumulation. Control and alcohol-fed groups for 1, 3, 6, 12 and 18 months were used. A precocious and progressive accumulation of lipofuscin granules occurred in granule, Golgi and basket cells. Stellate cells remained pigment-free. The lipofuscin deposited in the granule and Golgi cells was of the granular type, whereas that of basket and stellate cells was lamellar (fingerprint-like pattern). These results parallel those observed during normal ageing, and reinforce the hypothesis of the existence of a close relationship between chronic alcohol consumption and precocious nerve cell ageing.

Aging↗

PubMed1985

Damage of Purkinje cell axons following chronic phenytoin administration: an animal model of distal axonopathy.

An animal model of central distal axonopathy following chronic administration of phenytoin is described. Male C57/BL6J mice received diphenylhydantoin (DPH) in the daily diet (liquid diet 'Stardit', supplemented with vitamins) over a period of 8 weeks. Control and experimental animals were pair-fed. Twelve mice of both groups were perfused via the left ventricle with glutaraldehyde. Representative samples of the cerebral cortex (area 3), cerebellum (vermis and deep cerebellar nuclei), thalamus, hypothalamus, and liver were embedded in araldite. Semi-thin sections and electron microscopy of the cerebellar vermis revealed marked dystrophic changes in the Purkinje cell axons. The presynaptic segments of Purkinje cell axons in the deep cerebellar nuclei showed massive enlargement and swelling due to accumulation of spherical particles and tubular structures in the axoplasm. These structures represent a proliferation of the smooth endoplasmic reticulum. Identical changes were found in hepatocytes of treated animals. Because phenytoin induces hepatic microsomal enzymes, we suggest that phenytoin-related Purkinje cell damage may be produced by an induction of Purkinje cell microsomes with proliferation of the smooth endoplasmic reticulum which causes a swelling and enlargement of presynaptic segments of Purkinje cell axons in deep cerebellar nuclei. Chronic phenytoin administration to mice is a new model of phenytoin-induced encephalopathy and of distal axonopathy of cerebellar neurons.

Animals↗

PubMed1985

Nuclear inclusions following chronic ethanol administration. An electron-microscopic investigation of the rat parietal cortex.

Wistar rats with an average initial body weight of 180 g received a 15% (v/v) ethanol-water solution over a period of 6 months. Neurons of the parietal cortex (area 3) showed a significant increase of nuclear inclusions which consisted of parallel filaments and tubular systems. Furthermore, we observed an augmentation of lipid droplets, nemetosomes, and straight filaments. The latter could not be identified in control animals. It is discussed whether the occurrence of these structures might be enhanced by an altered cellular metabolic activity during the chronic ethanol administration.

Animals↗

PubMed1985

Nafenopin-induced rat liver peroxisome proliferation reduces DNA methylation by N-nitrosodimethylamine in vivo.

The hypolipidaemic drug nafenopin (NAF) has been shown to enhance the hepatocarcinogenic effect of N-nitrosodimethylamine (NDMA) and N-nitrosodiethylamine in rats. We have investigated whether the NAF-induced peroxisome proliferation in hepatocytes interferes with NDMA's metabolism and interaction with DNA. Adult male Wistar rats received a single i.p. injection of [14C]NDMA (2 mg/kg) and were killed 4 h later. DNA was isolated from liver and kidney, hydrolysed in 0.1 N HCl and analysed by Sephasorb chromatography. In rats pre-treated with NAF (0.2% in the diet over a period of 3 weeks), the concentration of N7-methylguanine in hepatic DNA (mumol/mol guanine) was 46% below control values. This is probably due to the greater amount of target DNA, as NAF caused a marked hepatomegaly with a 50% increase in total liver DNA content. Concentrations of N7-methylguanine in kidney DNA were twice as high in NAF-pre-treated animals when compared to control rats. This is unlikely to result from a shift in the metabolism of NDMA from liver to other rat tissues since the time course and extent of the conversion of [14C]NDMA to 14CO2 and 14C-labelled urinary metabolites were identical in NAF-treated and control animals. There was no indication that NAF inhibits the activity of the hepatic O6-alkylguanine-DNA alkyltransferase.

Animals↗

PubMed1985

Histological diagnosis of liver hemangiomas using ultrasound-guided fine needle biopsy.

Hemangiomas of the liver are a common fortuitous finding during ultrasonographic studies of the liver. Although they often present a characteristic ultrasonographic pattern, it is not always possible to exclude malignant disease. Diagnostic difficulties may arise when known malignant disease is present. Computed tomography and angiography do not exclude misinterpretations. In nine patients, six of whom had known malignant disease, liver tumors were detected at ultrasonography. Using a new type of fine needle and ultrasonographic control, biopsy provided the histological diagnosis of hemangioma in all cases. Complications were not observed.

Adult↗

PubMed1984

Morphologic evaluation of stereotactic brain tumour biopsies.

The validity of morphologic diagnosis of stereotactic brain tumour biopsies was evaluated in a series of 600 patients treated since 1977 at the University Hospital, Freiburg. Combined cytological (smear preparations) and histological examination of paraffin-embedded samples revealed the tumour type and approximate grading in 492 (82%) of cases. In 66 patients a clinically suspected neoplasm could be ruled out. In the remaining 42 cases (7%), the presence of a tumour was confirmed but the available samples did not allow an unequivocal classification of the neoplasm. Inaccurate diagnoses were most frequently due to sampling errors in non-homogeneous tumours, i.e. biopsies taken from sites not representative for the entire neoplasm (tumour necroses, infiltration zone). In the future, the use of immunohistochemical methods for the identification of tumour markers and cytoskeleton proteins may partially compensate for the limited size of stereotactic biopsy samples.

Brain↗

PubMed1984

Cerebellar histogenesis and synaptic maturation following pre- and postnatal alcohol administration. An electron-microscopic investigation of the rat cerebellar cortex.

Fetal alcohol syndrome was produced in rats by feeding an ethanol-enriched, vitamine -supplemented liquid diet over a period of 4 weeks before mating and throughout pregnancy. The amount of ethanol was equivalent to 38-40% of the daily calories; control animals were fed an isocaloric amount of sucrose. The offspring of experimental animals displayed a diminished birth weight. In contrast to previous experiments, the ethanol diet was also administered during the lactating period. On postnatal day 7, experimental animals and controls were killed by perfusion and the cerebella prepared for electron microscopy. Morphometric analysis showed a reduced number of Purkinje cells. On day 12, Purkinje cells of experimental animals displayed ultrastructurally fewer organelles. Furthermore, a delayed synaptogenesis in the molecular layer was demonstrated with osmium-zinc iodide and ethanolic phosphotungstic acid showing an immature appearance of the presynaptic grid and weaker stained synaptic cleft material. The following discussion deals with possible mechanisms underlying these alcohol-induced alterations of cerebellar synaptogenesis.

Animals↗

PubMed1984

Histology of congenital nevi during the first year of life. A study by conventional and electron microscopy.

We studied 14 biopsies of congenital melanocytic nevi of children up to 1 year of age. In 11 biopsies we found two different types of melanocytic cells. In the reticular dermis, they were small cells. They had small nuclei, little cytoplasm, and no detectable pigment. They did not come in nests, but were scattered between the collagen bundles. The other type of cells was found within the epidermis or closely under it. These cells were large and round, and had abundant cytoplasms and evenly distributed melanin. Sometimes these cells were arranged in nests and in two moles they were also found in the epithelia of follicles. In all of these biopsies (with three exceptions) the superficial, large pigmented cells were separated from the deep, small, nonpigmented ones by a zone of tissue without any melanocytic cell. Early in life both types of cells are clearly separated, and the superficial ones are few. At later ages the superficial large cells are found in increased numbers, whereas the number of the deep ones does not change with age.

Biopsy↗

PubMed1983

The lectin properties of gluten as the basis of the pathomechanism of gluten-sensitive enteropathy.

The pathogenesis of gluten-sensitive enteropathy is as yet unknown. According to one theory gluten may act as a lectin with toxic properties for the intestinal cells. We can now confirm this theory by laser nephelometric measurements and demonstrate the oligomannosyl specificity of this lectin-like protein gluten. Furthermore, we demonstrate the highly more intensive binding capacity of gluten for the glycoproteins of the immature crypt cells of the intestinal brush border compared to those from the mature villous zone. It is discussed that gluten-sensitive enteropathy is caused by a genetically determined defect-glycosylation of intestinal glycoproteins with the synthesis of more mannosylated glycoproteins.

Celiac Disease↗