Acta histochemica. Supplementband最新文献

The frequent use of methods different from enzyme histochemistry evokes the question, whether it is still useful to apply methods of catalytic enzyme histochemistry to study the nervous system. In this brief overview it is shown, that catalytic enzyme histochemistry can still contribute to a better understanding of nervous system function. This was enabled by methodological progress, i.e., the modification of already existing procedures or the development of new techniques for the visualization and measurement of enzymes in tissue sections using their catalytic properties. The methods for acetylcholinesterase, monoamine oxidase as well as certain exoglycosidases and phosphatases will be given as examples. The application of these procedures as well as of methods for proteases, oxyradical-generating oxidases and enzymes involved in the metabolism of amino acid and other transmitters will illustrate, that qualitative (localization) and quantitative (measurement) catalytic enzyme histochemistry can still contribute to a better understanding of nervous system function.

Imaging of different brain tumor types by computed tomography (CT) or contrast-enhanced CT scans is often very similar. Therefore, the exact preoperative CT diagnosis of intracranial neoplasms is difficult. Among 100 cases (88 primary brain tumors, 12 brain metastases), the preoperative classification by CT was correct in 51 and partially correct in 22 cases. A corresponding presumptive CT diagnosis was made in 22 brain neoplasms. 5 cases were misinterpreted. Examples of CT scans and histological pictures are compared and analysed according to the literature.

The presented methodical contribution demonstrates the suitability of rhodamine-labelled latex microspheres with a defined mean diameter of around 20 nm for retrograde neuronal tracing. After small injections of about 200 nl red fluorescent tracer into visual cortex of mice afferent neurons were labelled in cortical and subcortical structures. Basal forebrain neurons containing the tracer were further characterized by the concurrent visualization of choline acetyltransferase, a marker for cholinergic neurons, and parvalbumin, a putative marker of GABAergic neurons, by immunofluorescence.

Muscle biopsies from control subjects, patients with neuromuscular diseases and premature infants and neonates were investigated for myoadenylate deaminase activity (MAD) by histochemistry. A histochemically picture of MAD-deficiency is more frequently then the clinically defined MAD-deficiency syndrome with an autosomal recessive pattern of inheritance. The high incidence of the carrier state, secondary MAD-deficiency and connections with other diseases are the causes. An individual predisposition for loading crisis of these patients in a high physical stress situation is probable.

Senile plaques in the cerebral neocortex, entorhinal cortex and hippocampus are reactive for Acetylcholinesterase (AChE). The same types of plaques are observed, as with immunostains for beta-protein, including the very simple ones, consisting nearly exclusively of loose deposits of beta-protein. If there are many plaques, the normal network of AChE-positive axons disappears. Explanations for both, the apparent shift of AChE from the axons to the plaques on the one hand and the very early development of AChE positive deposits during the plaque development on the other hand are sought.

An 8-year-old boy with perinatal HIV infection developed a large fusiform aneurysm in the circle of Willis two years prior to death which was confirmed by radiological studies. The postmortem examinations revealed a predominantly intimal, proliferative lesion, and partial destruction of the internal elastic lamina in the involved arteries. Within the intima hyperplasia of fibroblasts and smooth muscle cells was observed. No inflammatory alterations, no granulomas and no multinucleated giant cells could be noted in the vascular walls and in the cerebral parenchyma. A small ischemic infarct was present in the left thalamus. Cerebellum, brainstem and medulla showed multiple areas of progressive multifocal leukoencephalopathy (PML). Immunohistochemistry with anti-gp41, a monoclonal antibody against HIV envelope did not exhibit any positive results. These findings implicate that the vascular lesion might be attributed to primary infection of the brain by HIV which led to a defect of elastic lamina and consecutive intimal hyperplasia. A second hypothesis could be based on the effect of extremely high dose AZT therapy avoiding inflammatory reaction after HIV infection.

In a pediatric case of necrotizing CMV myelitis after perinatal HIV infection characteristic cytomegalic cells, which could not be attached to a particular cell line by cell morphology, were studied after immunostaining with monoclonal and polyclonal antibodies raised against GFAP, S100 protein, NSE, synaptophysin, factor VIII, vimentin, macrophages, leukocytes, CMV, HSV I + II, toxoplasma, and HIV 1 gp41. Astrocytes, oligodendrocytes, neurons, ependymal and endothelial cells, macrophages, and Schwann cells stained positively with CMV antiserum. With regard to their immunological features the majority of cytomegalic cells ("owl eye cells") was identified as astrocytes, and in decreasing frequency, the remainder was characterized as macrophages, mesenchymal, and endothelial cells. It is concluded that CMV giant cells represent one phase of virus induced cell transformation, not only one single, but numerous cell types are exposed to after CMV infection.

This report concerns a 11-year-old girl--at the time of death--who developed normally until the age of 2 years when further psychomotoric maturation stopped and then regressed. The disease was diagnosed as neuroaxonal dystrophy (NAD) by sural nerve biopsy at the age of 7. Further course was characterized by complete loss of all motoric and sensory functions and dementia as well. Finally there was decerebration. The autopsy revealed generalized NAD associated with pallidal deposition of iron pigment to classify as generalized intermediate NAD type II according to Gilman and Barrett (1973). The main histological findings were axonal swellings and spheroids consisting ultrastructurally of membrano-tubular profiles, lamellar structures, vacuoles, glycogen granules and mitochondrial aggregates. Immunohistologically there was partial positive expression of synaptophysin and neurofilament protein in the spheroids. Firstly described electron microscopical findings in the retina include the typical axonal lesions largely in interior layers. Photoreceptors and their synaptic contacts were preserved. The present blindness is of the neuronal type. The current etiopathogenetic opinions, aspects of bioptic diagnosis and problems of classification of primary NADs are discussed.

The cells of primitive neuroectodermal tumours may undergo differentiation and, eventually, may be transformed to neurons, glial cells, and ependymal cells. Early stages of neuroectodermal differentiation may primarily be determined by means of immunohistochemical methods. Immunohistochemical investigations were performed on brains of human foetuses obtained from the 18th to 36th weeks of pregnancy, with a view to elucidating the process of maturation during foetal development and to determining the antigens identifiable in cells in the course of differentiation, following fixation in formalin and embedding in paraffin. Gliafibrillar acid protein (GFAP) and vimentin proved to be of particularly high stability and, consequently, were easily detectable from paraffin material. The same antigens were focally recordable also from eight of 17 primitive neuroectodermal tumours. Clues were rare in these tumours as to neuronal differentiation. This was attributed to instability of neurofilament proteins under conditions of formalin fixation and paraffin embedding.

Malignant angioendotheliomatosis, so called intravascular malignant lymphomatosis or angiotropic lymphoma, was found in cerebral hemispheres, spinal cord and nerve roots of a 50-year-old woman who died 4 months after onset of neurological symptoms. The pathological findings were characterised by neoplastic cells within the lumina and wall of small vessels as well as by multiple infarcts in the CNS. Vascular occlusions were caused by tumor cells and secondary changes of the wall. Positive reactions of Common Leucocyte Antigen and B-cell-markers support the idea of a lymphoid origin for the tumor cells. The differentiation to the angiocentric lymphoma as a T-cell tumor and the obscure pathogenesis of this neoplastic process must be clarified in the future.