Biomedical subjects

H Budka

Publications and source records attributed to H Budka.

225 records · Page 13Linked to original sources

PubMedDate not supplied

An immunocytochemical comparison of the glia-associated proteins glial fibrillary acidic protein (GFAP) and S-100 protein (S100P) in human brain tumors.

Immunostaining patterns of two glia-associated proteins, glial fibrillary acidic protein (GFAP) and S-100 protein (S100P), were compared using the peroxidase-antiperoxidase (PAP) method on adjacent paraffin sections in 100 brain tumors including 52 astroglial tumors, 13 oligodendrogliomas, 14 ependymomas, 13 choroid plexus papillomas and 8 medulloblastomas. Most astroglial tumors showed similar immunoreactivity for both proteins. Fibrillary processes, however, showed a stronger and more crisp staining with anti-GFAP than with anti-S100P, whereas cell nuclei were labeled only for S100P. Focal dissociation of immunoreactivities for the two proteins was prominent in several malignant astroglial tumors including giant cell glioblastoma, and in subependymal giant cell astrocytoma. In oligodendrogliomas, GFAP-positive neoplastic oligodendrocytes also showed immunoreactivity for S100P; a smaller number of tumor cells were immunoreactive only for S100P, comparable to normal mature oligodendroglia. Most ependymomas were characterized by a similar distribution of cells immunoreactive for both proteins. In choroid plexus papilloma, absent or only focal immunoreactivity for GFAP contrasted with diffuse labeling for S100P in all cases; this seems of value for a differential diagnosis of papillary CNS tumors. In medulloblastoma, some tumor cells of a classical type were immunoreactive only for S100P; on the contrary, GFAP positive tumor cells with sparse or absent immunoreactivity for S100P were found in desmoplastic medulloblastomas. Similar immunoreactivities for both proteins in most tumors suggest a generally parallel production of both proteins by glial tumor cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Astrocytoma↗

PubMedDate not supplied

Primitive neuroectodermal tumors including the medulloblastoma: glial differentiation signaled by immunoreactivity for GFAP is restricted to the pure desmoplastic medulloblastoma ("arachnoidal sarcoma of the cerebellum").

Immunoreactivity of tumor cells for glial fibrillary acidic protein (GFAP) is usually regarded as sign of astrocytic histogenesis and/or differentiation. The present study aimed at a systematic evaluation of the significance of GFAP-containing cells in primitive neuroectodermal tumors (PNETs) with special reference to the controversial entity of desmoplastic medulloblastoma (so-called "circumscribed arachnoidal sarcoma of the cerebellum"). Fifty-three PNETs, including 17 pure desmoplastic medulloblastomas were investigated, using GFAP antisera and the peroxidase-antiperoxidase (PAP) technique. Seventy percent of the pure desmoplastic medulloblastomas showed GFAP immunoreactive cells, in 47% indistinguishable from adjacent nonreacting tumor cells. Most immunoreacting cells were found in the reticulin free islands, showing in 6 cases a gradual transition of immunoreacting cells from tumor cells to larger cells shaped like astrocytes. The classical medulloblastomas showed only larger immunoreacting cells which were interpreted as reactive astrocytes. Therefore, the so-called circumscribed arachnoidal cerebellar sarcoma or pure desmoplastic medulloblastoma merits a separate place in the group of PNETs as a tumor with frequent signs of astroglial differentiation; this interpretation appears to be clinically correlated by a difference in age incidence and prognosis of that special tumor-type in comparison with classical medulloblastoma.

Adult↗

PubMedDate not supplied

Diffuse type of Lewy body disease: progressive dementia with abundant cortical Lewy bodies and senile changes of varying degree--a new disease?

The term Lewy body disease (LBD) was proposed earlier to describe a disease classified into three types (A, B, and C) according to the distributional pattern of Lewy bodies in the CNS. Group A (diffuse type of LBD) shows clinical symptoms of "dementia-parkinsonism syndrome". The most remarkable pathologic feature is the widespread appearance of numerous Lewy bodies not only in the brain stem and diencephalon (as in group C), but also in the cerebral cortex and basal ganglia, which is complicated by senile changes of various degrees. Group B is the transitional type between groups A and C. Group C (brain stem type of LBD) is identical with idiopathic Parkinson's disease. In this paper, 12 of our cases with diffuse type LBD were studied clinicopathologically and compared with eight similar cases in the literature. The neuropathologic substrate of progressive dementia in this disease is also discussed. LBD is a clinicopathologic entity; the diffuse type of LBD, a special form of this disease, presents mainly a presenile dementia.

Aged↗

PubMedDate not supplied

[A case of progressive multifocal leucoencephalopathy during chronic lymphocytic leukaemia].

We report here a case of PML in the course of untreated chronic lymphocytic leukaemia. The diagnosis of PML was based on the presence of typical histologic findings in the white matter: focal demyelination, abnormal oligodendroglia with basophilic intranuclear inclusions and enlarged bizarre astrocytes. It was confirmed by immunohistochemistry which revealed JC papova-virus antigens in brain tissue and by in-situ hybridization which showed JC virus genomic DNA in oligodendroglial nuclei. Virus particles in the nuclei of abnormal oligodendrocytes and astrocytes were demonstrated by thin-section electron-microscopy.

Aged↗

PubMedDate not supplied

Neocortical changes in Parkinson's disease, revisited.

In a series of 37 Parkinson's disease (PD) brains, cortical changes were reexamined by means of Bielschowsky silver impregnation and anti-ubiquitin immunocytochemistry. Compared to routine HE staining, anti-ubiquitin immunostaining revealed neocortical Lewy bodies (LBs) in a significantly higher percentage (76% vs. 32%). Neocortical senile plaques (SPs) occurred more frequently in brains with neocortical LBs than in cases without LBs (50% vs. 11%; p < 0.05). Semiquantitative assessment of neocortical LB density correlated with the frequency of occurrence and density of neocortical SPs. Dementia was confined to patients with abundant neocortical LBs, thus fulfilling histological criteria of diffuse Lewy body disease. We conclude that neocortical LBs are a very frequent feature of PD, although abundance of cortical LBs is confined only to a small subgroup with prominent dementia: diffuse Lewy body disease.

Aged↗

PubMedDate not supplied

Neuroaxonal dystrophy combined with diffuse Lewy body disease in a young adult.

A 30-year-old woman suffered from a progressive extrapyramidal syndrome, myoclonic jerks, spasticity, and organic brain syndrome; she was clinically suspected to suffer from Creutzfeldt-Jakob disease and died after 4 years of illness. At autopsy, widespread dystrophic axons and Lewy bodies (LBs) were found in her brain. Neuronal loss and diffuse reactive astrogliosis involved the gray matter including the cerebral cortex. Dystrophic axons occurred throughout the nervous system except for the cerebellar cortex and peripheral nerves. LBs involved the cerebral cortex as well as subcortical regions including amygdala and claustrum, brainstem including substantia nigra and locus coeruleus, and spinal cord. LBs were distributed extensively enough to be compatible with diffuse Lewy body disease (DLBD). Ubiquitin immunostaining labeled both dystrophic axons and LBs. The combination of neuroaxonal dystrophy and DLBD may result from cytoskeletal pathology which affects both neuronal cell bodies and axons with subsequent deficient proteolysis and ubiquitination.

Adult↗

PubMedDate not supplied

Langerhans cell histiocytosis of the hypothalamus: diagnostic value of immunohistochemistry.

The immunophenotype of 6 cases of Langerhans cell histiocytosis (LCH) of the hypothalamus and 3 cases of cranial bone manifestation of LCH was investigated by means of immunohistochemistry on paraffin sections. Antibodies against S 100 protein, lysozyme, CD68 (PG-M1), CD68 (KP1), HLA-DR, beta 2 microglobulin, placental alkaline phosphatase (PLAP), the monoclonal antibody MAC 387, and a monoclonal antibody against CD1a were used. All examined cases showed positive staining of lesional cells for S 100 protein, HLA-DR, beta 2 microglobulin, macrophage associated markers and CD1a. According to the "confidence levels" of the Writing Group of the Histiocyte Society [Chu et al. 1987], a "definite diagnosis" of LCH requires the demonstration either of Birbeck granules in lesional cells by electron microscopy, or of CD1a antigenic determinants on the surface of lesional cells. Since electron microscopy of these rare CNS lesions is not possible in many cases, we are now able to give a definite diagnosis of LCH of the hypothalamus by means of immunohistochemistry for CD1 a on routinely fixed and processed tissue.

Adolescent↗

PubMedDate not supplied

Vascular changes in the cerebral cortex in HIV-1 infection: I. A morphometric investigation by light and electron microscopy.

The microvasculature of the cerebral cortex in AIDS brains was investigated by means of stereology at the light and electron microscopic levels. Stereologic parameters for microvessels were determined in formalin-fixed autopsy tissue of 24 AIDS patients and of 35 age- and sex-matched controls. At the light microscopic level these encompassed the measurement of the diameter, volume fraction, surface area density, and length density; at the electron microscopic level profile area, perimeter, diameter of capillaries, endothelial cells, pericytes, and basal lamina as well as the mean thickness of the basal lamina were measured. In AIDS brains a significant increase in the diameter of cortical vessels was noted. The surface area density (Sv) and volume fraction (Vv) of microvessels were likewise significantly increased in AIDS brains. No changes were noted for the length density (Lv) which also indicates that no changes in the number of vessels occur in HIV-1 infection. Ultrastructural thinning of the basal lamina was a consistent finding. Vacuoles occurred in the basal lamina of capillaries and increased in number and size in AIDS brains. Using morphometric methods, significant changes of cortical vessels are detectable at the light and electron microscopic level. These changes most probably represent the morphological substrate of an altered blood-brain-barrier in AIDS brains and may account for the reported hypoperfusion demonstrated in SPECT analyses.

Acquired Immunodeficiency Syndrome↗

PubMedDate not supplied

Cerebral manifestations of Whipple's disease.

A case of Whipple's disease with central nervous system (CNS) involvement has been retrospectively diagnosed. At the age of 50 and after six years of recurrent bouts of pyrexia, anorexia and loss of weight, a man developed a subacute encephalitis. Two episodes of acute loss of vision were followed by changes in mental status, supranuclear ophthalmoplegia and oculo-facio-cervical myorhythmias which remained present until death, one year later. Combined light- and electron microscopic studies have demonstrated: No. 1 the presence in the CNS of nodules containing large amounts of Sieracki cells; No. 2 the existence of bacteria in various stages of degeneration in macrophages or in the neuropile. A review of CNS complications in Whipple's disease is made.

Adult↗