Acta histochemica. Supplementband最新文献

Neurofibromatosis (NF) is subdivided into at least two different forms: NF-1, which is characterized by café-au-lait spots, cutaneous neurofibromas, Lisch nodules and osseous dysplasias, and NF-2, the hallmarks of which are bilateral acoustic neuromas. Neuropathological findings in 5 cases of NF-1 and 3 cases of NF-2 are presented.

Parallel primary cultures have been prepared from dispersed cells of adult human pituitary anterior lobes and can be used as a model system for cell-biological studies. The cultured cells were able to secrete all the known hormones of the adenohypophysis. Bromocriptine administration markedly reduced prolactin release into the medium while slightly enhanced growth hormone release. The adequate response of somatotrophs to GRF and SRIF could not be demonstrated.

The autopsy findings in 3 cases of type I ("classical") and 3 of type II ("hydrocephalic") lissencephaly are presented. The characteristic pathomorphology is described and some aspects about pathogenesis are considered.

Aluminium was detected by electron spectroscopic imaging and electron energy loss spectra in the lysosomes of all cell types of the nephron in rats treated with aluminium chloride after 5/6 nephrectomy. The lysosomes of kidney cells of untreated rats did not demonstrate any detectable amounts of aluminium. Electron energy loss spectra showed the regular occurrence of iron (and also other elements) in the lysosomes of both groups of rats.

Histoautoradiographic and immunohistochemical studies of biopsies from 27 brain tumors yielded the following preliminary conclusions: 3H-thymidine labeling indices and Ki-67 growth fraction indicate the proliferative activity more reliable than counting of mitoses, the fraction of DNA synthesizing tumor cells and the Ki-67 growth fraction show an equal behaviour, as expected, the immunohistochemical values are higher than the labeling indices because all tumor cells within the proliferation cycles express the nuclear antigen. By the increase of the number of tumors and the use of the different cell kinetic methods on the same tumor tissue the prerequisite to grading of brain tumors as a basis of therapeutic strategy can be improved.

In some cases of pituitary adenomas, the immunohistochemical proof of a hormone production does not correspond with the clinical findings. False negative results are caused by different functional stages of the adenoma cells when hormone granules are largely released. Then, the intracellular content of hormone granules lies under the immunohistochemical demonstrability although clinical findings show high serum values of the hormone in question. Especially in prolactinomas, sparsely granulated forms are not rare. In these cases, the proof of a hormone production is possible by means of immuno-electronmicroscopy. Preoperative application of a bromocriptine therapy may falsify the results too. False positive results may occur in "plurihormonal" adenomas. True plurihormonal adenomas--especially the combinations GH/PRL and FSH/LH--exist but frequently reported combinations of several hormones should be seen with care. Often, the operatively removed tissue is cut into small pieces not only containing adenomatous tissue but also parts of the neighbouring normal pituitary gland with a production of several or even all hormones investigated. By use of GFAP or S-100 protein for the detection of folliculostellate cells, adenomatous and normal pituitary tissue can be differed. Folliculostellate cells can only be found in normal pituitary but not in adenomas.

During the last several decades, immunohistochemical studies of tumors, along with other approaches, have suggested that the clinical and biological progression results, at least in part, from the sequential appearance within the neoplasm of cellular subpopulations whose new characteristics reflect specific somatic genetic changes. However, CNS may provide a different microenvironment for activation and proliferation than other tissues. The tissue-specific distribution of intermediate filament proteins, in particular the keratins, permits their use as marker in histopathology, but several important exceptions are recognized. In this connection, it is of interest that, according to the other reports, glial tumors may be positive for different anti-keratin antibodies. However, the gliomas did not show an immunoreaction in any of the cases when HEA-125 and Ber-EP4 were applied. The great number of multihormonal pituitary adenomas and possible change of the immunohistochemically detectable hormone status in cases of recurrent tumors have particularly re-emphasized the need for new thinking about patterns of classification. The diagnosis of malignant melanoma has been considerably facilitated recently by the introduction of immunohistological labelling with antibodies selective against melanoma antigen (HMB-45). Our results confirmed the necessity of cautious interpretation of HMB-45 immunoreactivity because a HMB-45 expression can be observed in several non-melanotic tumors.

Type VIII collagen has been localized to specialized extracellular matrices in fetal tissues and has been suggested to be associated with cellular proliferation and angiogenesis (Sage and Iruela-Arispe 1990). In view of this hypothesis we studied its distribution in the normal and diseased human brain. Focal immunoreactivity was seen in histologically abnormal vessels of all 10 angiomas and 40 of 52 brain tumors. Staining was very weak in 3 embryonal and fetal brains, and it was absent in 20 normal adult brains and in 15 adult brains showing various cerebrovascular abnormalities. Our results provide additional evidence for the participation of type VIII collagen in some types of angiogenesis.

Neurohistochemical and electron microscopic investigations of the autonomic nervous system (ANS) of man and animals suggest that its ontogenesis can be divided into the premediatory, mediatory and postmediatory periods of development. The postmediatory period begins heterochronically in various ganglia of the ANS. A normal process of early cardiac desympathization usually occurs at the age of 35 to 60 years. Specific changes of preceding sudden cardiac death are elicited in different parts of the ANS and adrenal glands. This is accompanied by focal myocardial desympathization. Coronary vessels and conducting system which may influence myocardial hypersensitivity zones to catecholamines are involved in the process of destabilization of the cardiac function. Moreover, relationships are demonstrated which exist between the atherosclerotic lesions of the aortic wall and the status of its nerve plexuses.