Acta histochemica. Supplementband最新文献

The right medial cerebral artery of 25 primates (Macaca radiata) was occluded transorbitally with an atraumatic clip. The time courses of infarct volume and capillary morphometric changes in the ischemic lenticular nucleus, caudate nucleus and insular cortex were then determined. Volume changes of ischemic foci were studied morphometrically using an enzyme histotopochemical acid phosphatase stain. During the first 4 hours extension (or spread) of the ischemic area was small and constant. Over the next hours, the ischemic focus increased in volume, becoming maximal in the lenticular nucleus in 24 hours and in the caudate nucleus in 48 hours. In the lenticular nucleus, edema developed 4 hours after onset of ischemia and was characterized by a decrease in capillary diameter and an increase in mean intercapillary distance. In the caudate nucleus and insular cortex, in the first hours after clipping the medial cerebral artery, capillary diameter and volume increased and intercapillary distance decreased. The data demonstrate that the therapeutic window of brain infarct treatment is during the first 4-6 hours after occlusion of the medial cerebral artery.

The effect of nucleotide administration on the regeneration of myelinated nerve fibres following crush injury to the sciatic nerve of the rat was studied using morphometric techniques. In addition morphometrical investigations of peroneal and soleal muscles were performed at different times. After a localized crush lesion of the right sciatic nerve, rats were given nucleotides daily at a dosage of 3.0 mg/kg body wt uridine monophosphate (UM), 2.5 mg/kg body wt cytidine monophosphate (CMP) or 3.0 plus 2.5 mg/kg body wt UMP plus CMP, respectively. Observations were made after 20, 40 and 60 days of common peroneal nerve regeneration for comparison with age-matched crushed or nonoperated controls. Forty days after daily UMP/CMP administration the single fibre conduction velocity of all type II afferents was significantly accelerated. There was a trend towards increased mean fibre area related to increased myelin area. Mean diameter of type II muscle fibres was increased. After 60 days, there was a trend to increase of single afferent fibre conduction velocity in the UMP/CMP group. In the same group automated morphometry revealed a significant increase of nerve fibre area, myelin area and axon area. At this time an increase was found of type I and/or type II muscle fibres in all animal groups. The present results suggest that both axons (neurons) and myelin sheaths (Schwann cells) of regenerating nerve fibres and regenerating muscle fibres are influenced by nucleotide administration.

The development of fluctuations in disability are a main problem of the levodopa long-term treatment in Parkinson's disease. The early combination of low doses of levodopa with a dopamine agonist as lisuride improves the symptoms of Parkinson's disease as much as a monotherapy but prevents the development of fluctuations in disability and dyskinesias at the same time.

The nervous system is frequently affected in patients with the acquired immune deficiency syndrome (AIDS). In addition to opportunistic CNS infections and cerebral lymphomas, approx. 20% of the patients develop HIV-associated encephalopathies. Two major histopathological manifestations are observed. HIV leukoencephalopathy (progressive diffuse leukoencephalopathy) is characterized by a diffuse loss of myelin in the deep white matter of the cerebral and cerebellar hemispheres, with scattered multinucleated giant cells and microglia but scarce or absent inflammatory reaction. HIV encephalitis (multinucleated giant cell encephalitis) is associated with accumulations of multinucleated giant cells, inflammatory reaction and often focal necroses. In some patients, both patterns may overlap. In order to identify the HIV genome in the CNS, brain tissue from 27 patients was analyzed for the presence of HIV gag sequences using the polymerase chain reaction (PCR) and primers encoding a 109 base pair segment of the gag gene. Amplification of HIV gag succeeded in all 5 patients with clinical and histopathological evidence for HIV encephalopathy but was negative in the 20 AIDS patients with opportunistic bacterial, parasitic and/or viral infections or with cerebral lymphomas. These results strongly suggest that the evolution of histopathologically recognizable HIV-encephalopathies closely correlates with the presence and/or tissue concentration of HIV. Since there were no cases with amplified HIV DNA in the absence of HIV-associated tissue lesions, we conclude that harboring and replication of HIV in the CNS rapidly causes corresponding clinical and morphological changes of HIV-associated encephalopathies. In two children with severe HIV encephalomyelitis, large amounts of HIV gag and env transcripts were detected in affected areas of the brain and spinal cord by in situ hybridization.(ABSTRACT TRUNCATED AT 250 WORDS)

The content of the polyamines putrescine, spermidine and spermine, and the activity of their metabolic key enzyme ornithine decarboxylase (ODC) were measured in tissue samples obtained during operation of 45 patients with primary or recurrent gliomas, meningiomas and pituitary adenomas. Biochemical analysis and histopathological classification were carried out in the same tumor samples. In benign tumors ODC activity was less than 10 nmol/g/h, whereas in malignant gliomas values up to 34 nmol/g/h were observed. In rapidly growing tumors pronounced heterogeneity was observed with high values in solid tumor parts and low values in necrotic areas. Thus, high ODC activity represents a reliable biochemical marker of malignancy in brain tumors, but low values do not prove benignity.

Dementia due to vascular and degenerative abnormalities has become more frequent with increasing life expectancy. Although the origin of both dementia types is still unknown, pathobiochemical perturbations comprising energy loss, lactic acidosis, calcium homeostasis and free radical formation have been found in both dementia types in incipient stages at the neuronal level. A therapeutic rational against these abnormalities is discussed.

A retrospective study was conducted into 37 brains of patients, who had died of Grade 2-4 glioma. For assessment of morphological signs of hemorheological failure, microcirculation was checked by H & E, Klüver-Barrera, and Goldner staining as well as by staining for fibrin, using a modified technique according to Zerbino and Lukasewitsh. Microthrombosis was recorded from 30 in the above 37 brains, all of them related to patients with Grade 3 glioma and glioblastoma. Fibrin thrombi represented the predominant variant of microthrombosis. They exhibited differentiated characteristics depending on their localisation in the central and the peripheral regions of the tumour or in surrounding brain tissue. Also included in the study were rates of vascular proliferation and types of necrosis as well as relations between these and microthrombi. The role played by microthrombi in such cases of glial tumours is discussed in some detail.

Specimens from the area 10 of the frontal cortex collected out of 7 patients with severe mental retardation, aged 3 to 24 years and also 8 non-neuropsychiatric age-matched controls were processed according to the Golgi-Kopsch method. The total length of the apical side-dendrites and of the basal dendrites was measured on layer V pyramidal neurons. Compared with controls the total dendritic length of the apical side-dendrites as well as of the basal dendrites was significant reduced in the affected patients (p less than 0.001). The reduced dendritic length represents perhaps a morphological correlate to the mental dysfunction.

After a brief explanation of the mitochondrial function, especially in the relation to the inner-cell coordination, the study analyzed the mitochondrial hypertroph-dilatative cardiomyopathy, myopathy and scrapie which were recently tied to the "D-loop fragment" of the mtDNA. Any primary connection between viral unconventional slow infections and the mitochondrial genome seems unlikely. It is argued in the study that this category of diseases can be much better explained through the transfer of the so-called mobile retroelements.