Biomedical subjects

H Budka

Publications and source records attributed to H Budka.

At least 181 records · Page 10Linked to original sources

PubMed1987

Neurofibrillary tangles in Alzheimer's disease and progressive supranuclear palsy: antigenic similarities and differences. Microtubule-associated protein tau antigenicity is prominent in all types of tangles.

The antigenic profile of neurofibrillary tangles (NFT) in Alzheimer's disease (AD), senile dementia of Alzheimer type (SDAT), progressive supranuclear palsy (PSP) and in non-demented aged humans was investigated by light and electron microscopic immunocytochemistry using antisera and monoclonal antibodies to tubulin, microtubule-associated proteins (MAP1, MAP2 and tau), neurofilament proteins and determinants unique to Alzheimer paired helical filaments (PHF). Antibodies to tau proteins labeled NFT in all cases investigated (AD, SDAT, PSP and non-demented aged humans). However, one monoclonal antibody to PHF recognized numerous tangles in AD/SDAT, but only a small minority of the PSP tangles. Antibodies to tubulin, MAP1, MAP2 and neurofilament proteins did not selectively stain NFT. Whereas pretreatment of sections with phosphatase was required for the detection of tangles with Tau-1 monoclonal antibody, digestion of sections with either phosphatase or pronase had no significant effect on the staining pattern obtained with the other antibodies. Our studies show that, as previously described for AD/SDAT, phosphorylated tau polypeptides are also a major antigenic determinant of tangles in PSP, indicating that tangle formation may follow a common pathogenetic pathway in neurofibrillary degenerations. There is, however, at least one epitope in AD/SDAT tangles which seems to be absent on, or at least inaccessible in, the 15-nm straight fibrils of PSP.

Adult↗

PubMed1987

Contribution of histiocytic cells to sarcomatous development of the gliosarcoma. An immunohistochemical study.

The expression of glial fibrillary acidic protein, fibronectin (FN), factor VIII-related antigen (FVIII/RAG), and of three monohistiocytic markers, lysozyme, alpha-1-antitrypsin and alpha-1-antichymotrypsin was examined in five gliosarcomas (GS) by peroxidase-antiperoxidase immunostaining of formalin-fixed and paraffin-embedded specimens, and compared with vascular changes in 16 glioblastomas (GB). In contrast to GB, endothelial proliferations of GS were sheathed by sarcomatous tissue (perivascular sarcoma), which was contiguous with fibrosarcomatous areas. Cells with conspicuous intracytoplasmic FN content (FN+ cells) were seen in the vascular stroma of GB and dominated in the sarcomatous parts of GS. Most FN+ cells of GS were of varying size and shape and clearly neoplastic. Monohistiocytic markers were demonstrable in small infiltrating mononuclear cells as well as in many sarcomatous cells including FN+ cells. FVIII/RAG was restricted to lumen-lining endothelium and was not found in sarcomatous cells. These results suggest that a major part of sarcoma in GS is less likely to develop from proliferated endothelial cells than from histiocytic cells in the perivascular spaces of GB. By FN mediation, histiocytic cells might also guide and promote sarcomatous proliferations of other mesenchymal cells, leading to fibrosarcomatous development. Prominent monstrous giant cells of one GS seemed to be degenerating glioma cells.

Adult↗

PubMed1987

Glioblastoma developing at the site of a cerebellar medulloblastoma treated 6 years earlier. Case report.

The authors report the highly unusual development of a glioblastoma multiforme at the site of excision of a medulloblastoma 6 years earlier. The patient was operated on for a cerebellar medulloblastoma at the age of 13 years. Postoperative treatment included irradiation and chemotherapy. Six years later, a glioblastoma multiforme was found at the original site of the medulloblastoma. Intensive multimodality treatment is considered the likely cause for the later tumor development.

Adolescent↗

PubMed1986

Non-glial specificities of immunocytochemistry for the glial fibrillary acidic protein (GFAP). Triple expression of GFAP, vimentin and cytokeratins in papillary meningioma and metastasizing renal carcinoma.

In an extensive immunocytochemistry study for glial fibrillary acidic protein (GFAP) of human neuropathological biopsy or autopsy tissue specimens examined for diagnostic or research purposes, rare non-glial specificities of the GFAP immunostain were observed: Schwann cells of some small nerves in salivary gland, renal capsule, and in epidural fat adjacent to a metastatic carcinoma, Schwann and satellite cells in a spinal ganglion invaded by tumor, chondrocytes of epiglottic cartilage, few cells of a malignant pleomorphic adenoma of salivary gland, most cells of a recurrent papillary meningioma with areas similar to the hemangiopericytic variant, and many cells of a renal carcinoma metastatic to brain; the primary renal tumor had been operated 4 years earlier and focally contained some GFAP-positive cells. To ascertain the specificity of such unexpected immunoreactivities for GFAP and to exclude possible crossreactivities with other intermediate filament (IF) proteins, a panel of different antibodies was used for immunocytochemistry with the peroxidase-antiperoxidase (polyclonal antisera) or labeled biotin-avidin (monoclonal antibodies) techniques: two monoclonal and four polyclonal anti-GFAP, three monoclonal and one polyclonal anti-cytokeratins (CK), and two monoclonal anti-vimentin (VIM) antibodies. Triple expression of GFAP, VIM and CK was found in the papillary meningioma (in patterns suggesting frequent co-localization), in the metastatic carcinoma (in patterns suggesting little co-localization), and in the pleomorphic adenoma (only few GFAP-positive cells). Co-expression of GFAP and VIM was seen in epiglottic chondrocytes and reactive astroglia; another metastatic carcinoma was labeled only for CKs. In the light of previous reports on non-glial specificities of the GFAP immunostain, and of the consistency of our immunostaining results obtained by all monospecific anti-GFAP antibodies as well as the lack of immunocytochemically evident crossreactivity with other IF proteins, authentic GFAP production by some rare non-glial tissues and tumors is suggested.

Aged↗

PubMed1986

Development of stroma in malignant lymphomas of the brain compared with epidural lymphomas. An immunohistochemical study.

The relation of lymphoma cells to gliomesenchymal stroma within nervous tissue was studied by peroxidase-antiperoxidase immunostaining of formalin-fixed and paraffin-embedded surgical specimens for fibronectin (FN), factor VIII-related antigen and glial fibrillary acidic protein in 17 malignant non-Hodgkin lymphomas of the brain. For comparison, 9 non-Hodgkin lymphomas, 6 Hodgkin lymphomas, and 19 plasmacytomas of the spinal or cranial epidural spaces were studied with the same methods. Lymphoma cells were consistently negative for all markers. All lymphomas of the brain showed conspicuous concentric perivascular circles of immunoreactivity for FN in parts infiltrating brain tissue. Such structures are considered to derive from splitting of basal laminae of preexisting brain vessels; they were not seen in tumors of the epidural space. Cells with conspicuous FN content were found in brain as well as in epidural lymphomas. A monohistiocytic origin of those cells was confirmed by presence of monohistiocytic markers lysozyme and alpha-1-anti-chymotrypsin. Thus, additional immunostaining for FN seems to be useful for detecting monohistiocytes/macrophages in brain tumors.

Antigens↗

PubMed1986

Multinucleated giant cells in brain: a hallmark of the acquired immune deficiency syndrome (AIDS).

Multinucleated giant cells (MGCs) were found in the brains of two patients with the acquired immune deficiency syndrome (AIDS), but were absent in five other AIDS brains. In one case there was a distinctive distribution of MGCs in disseminated clusters; damage of brain parenchyma was minor or absent. In another case, MGCs were restricted largely to the perivascular spaces and were accompanied by lesions of toxoplasmosis and cytomegalovirus infection. In paraffin sections, morphological and histochemical-staining characteristics of MGCs were similar to those of macrophages. Occasional immuno-labeling of MGCs with monoclonal antibody to leukocyte common antigen suggested a hematogenous origin. MGCs were not stained by immunocytochemistry for neural markers glial fibrillary acidic protein, S 100 protein, neurofilament proteins, neuron specific enolase, and myelin basic protein and, therefore, appear unlikely to originate from the neuroepithelium. In the absence of evidence of other infections in case 1, the peculiar tissue reaction found could be a direct result of infection by the AIDS retrovirus. The formation of MGCs is likely to represent a cytopathic effect of the virus on lymphoid or monohistiocytic cells infiltrating the brain (infection of these cells could occur before or after they entered the brain). These assumptions are supported by the finding of similar MGCs in permissive lymphoid cell cultures after infection with the AIDS retrovirus.

Acquired Immunodeficiency Syndrome↗

PubMed1986

Glial fibrillary acidic protein and S-100 protein in human hepatic encephalopathy: immunocytochemical demonstration of dissociation of two glia-associated proteins.

Immunocytochemical staining patterns for glial fibrillary acidic protein (GFAP) and S-100 protein (S100P) were compared in cerebral cortex, basal ganglia and white matter of eight cases with hepatic encephalopathy (HE), including four cases of Wilson's disease and four of liver cirrhosis, and of eight age-matched controls, using the peroxidase-antiperoxidase method on adjacent paraffin sections. The majority of Alzheimer type II glia (Alzg II) showed prominent immunoreactivity for S100P but not for GFAP, resembling normal astrocytes of protoplasmic type; Alzg II might be interpreted as being peculiar types of reactive astrocytes retaining characteristics of protoplasmic astrocytes. A small number of Alzg II cells showed slight perinuclear immunoreactivity for GFAP; some lacked both markers. This suggests a spectrum of metabolic changes in these two proteins in Alzg II. GFAP-positive Alzg II cells were restricted to basal ganglia and white matter adjacent to grey matter, indicating that expression of GFAP in Alzg II might be modulated by local factors. Alzheimer type I cells and Opalski cells in Wilson's disease were immunoreactive for both proteins, confirming their astroglial origin and different character from that of Alzg II. In morphometric comparison, the proportion of GFAP-positive glial cells decreased in the cortex (P less than 0.001) but not significantly in the white matter (0.05 less than P less than 0.1), confirming earlier data that the prominent reduction of GFAP in HE brains is restricted to the grey matter.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

Restricted expression of measles virus proteins in brains from cases of subacute sclerosing panencephalitis.

The presence of five structural proteins of measles virus in brain material obtained at autopsy from four patients with subacute sclerosing panencephalitis (SSPE) was examined by immunofluorescence employing monoclonal antibodies. In addition, the humoral immune response against measles virus antigens in serum and cerebrospinal fluid was analysed by immunoprecipitation in combination with gel electrophoresis, revealing a reduced response mainly to the matrix (M) protein. In none of the brain material were all five structural proteins simultaneously detected. Nucleocapsid protein and phosphoprotein were found in every diseased brain area, whereas haemagglutinin (H) protein was detected in two, fusion (F) protein in three and M protein only in one SSPE case. In two cases, variations in the occurrence of H and F proteins could be observed between regions displaying different degrees of neuropathological changes. No correlation was observed between the humoral immune response and the immunohistological findings. These data support the hypothesis of a restricted synthesis of measles virus proteins, in particular the envelope and M proteins, in SSPE.

Adolescent↗

PubMed1986

Expression of defective measles virus genes in brain tissues of patients with subacute sclerosing panencephalitis.

The persistence of measles virus in selected areas of the brains of four patients with subacute sclerosing panencephalitis (SSPE) was characterized by immunohistological and biochemical techniques. The five measles virus structural proteins were never simultaneously detectable in any of the brain sections. Nucleocapsid proteins and phosphoproteins were found in every diseased brain area, whereas hemagglutinin protein was detected in two cases, fusion protein was detected in three cases, and matrix protein was detected in only one case. Also, it could be shown that the amounts of measles virus RNA in the brains differed from patient to patient and in the different regions investigated. In all patients, plus-strand RNAs specific for these five viral genes could be detected. However, the amounts of fusion and hemagglutinin mRNAs were low compared with the amounts in lytically infected cells. The presence of particular measles virus RNAs in SSPE-infected brains did not always correlate with mRNA activity. In in vitro translations, the matrix protein was produced in only one case, and the hemagglutinin protein was produced in none. These results indicate that measles virus persistence in SSPE is correlated with different defects of several genes which probably prevent assembly of viral particles in SSPE-infected brain tissue.

Adolescent↗

PubMed1986

Unilateral Creutzfeldt-Jakob disease.

A 73-year-old woman had progressive right hemiparesis, aphasia, and focal motor seizures. EEG showed periodic discharges on the left. She died 8 weeks after onset. At autopsy, there was marked spongiform change, neuronal loss, and severe proliferation of astrocytes predominantly on the left and most prominently in the insular and centroparietal cortex. The changes were consistent with Creutzfeldt-Jakob disease (CJD), but pathology was slight or absent on the right side. This case appears as the first report of what might be called unilateral CJD. Such a condition should be included within the differential diagnosis of progressive unilateral cerebral disorders.

Aged↗

PubMed1985

Shared antigenic determinants between human hemopoietic cells and nervous tissues and tumors.

A panel of nine monoclonal antibodies raised against human hemopoietic cells was used for immunohistological labeling of frozen sections of human nervous tissues and tumors. Three antibodies showed a remarkably consistent labeling pattern when tested on 18 samples of normal or reactive tissue, on 31 neurogenic and 17 non-neurogenic tumors in an indirect immunofluorescence technique. VIM C6, an antibody recognizing cells of the granulocyte series, showed surface labeling of normal and reactive glial cells and of all types of glioma regardless of the grade of malignancy. VIT 13, an antibody recognizing activated T-cells, labeled the processes of normal, reactive, and neoplastic glia in a manner very similar to but not identical with glial fibrillary acidic protein (GFAP). VIB C5, an antibody recognizing B cells and granulocytes, showed surface labeling restricted to malignant cells (malignant gliomas and primitive neuroectodermal tumors) and fetal brain, thus recognizing, within the nervous system, an oncofetal antigen. Due to this operational specificity within the nervous system, some of the antibodies described here might have a role as diagnostic markers for CNS tumors. This study confirms and expands previous data that sharing of antigenic determinants by hemopoietic cells and nervous tissue or neurogenic tumors is common. However, the significance of such cross-recognition is still obscure. It is tempting to speculate that cross-reacting auto-antibodies might contribute to tissue damage in some immune-mediated neurologic diseases (myasthenia gravis, multiple sclerosis, CNS involvement in systemic lupus erythematosus) or to impairment of immunoregulation in multiple sclerosis or glioma patients. Furthermore, sharing of surface determinants might be responsible for the dual tissue tropism of some viruses, including the lymphotrophic virus (HTLV) in the encephalopathy of the acquired immune deficiency syndrome (AIDS).

Antibodies, Monoclonal↗

PubMed1985

Progressive diffuse leukoencephalopathy in patients with acquired immune deficiency syndrome (AIDS).

Two adult patients with acquired immune deficiency syndrome (AIDS) presented with psycho-organic symptoms produced by an extensive cerebral and cerebellar leukoencephalopathy. Diffuse loss of myelin and axons with reactive astrocytosis and distinctive multinucleated giant cells were prominent in the deep white matter, but less so in the subcortical white matter and in compact myelinated pathways. Bilateral involvement of the centrum semiovale produced distal Wallerian degeneration of the descending pyramidal tracts, which in one patient correlated with progressive paraparesis and bladder dysfunction. Although there were morphological indications of cytomegalovirus infection and immunohistochemical evidence of papovavirus antigens, the neuropathology did not resemble that usually associated with infection by these opportunistic agents. The possibility is entertained that the progressive diffuse leukoencephalopathy (PDL) in these patients was directly related to infection with human T-cell lymphotropic virus (HTLV-III/LAV), the etiologic agent of AIDS.

Acquired Immunodeficiency Syndrome↗

PubMed1985

Cross-reactivity between human hemopoietic cells and brain tumors as defined by monoclonal antibodies.

A battery of 24 monoclonal antibodies raised against human hemopoietic cells was tested in an indirect immunofluorescence technique on frozen sections of a variety of human neurogenic and non-neurogenic tumors. Twelve antibodies demonstrated some type of labeling of neurogenic tumors, frequently in patterns characteristic for benign and/or malignant gliomas and/or primitive neuroectodermal tumors (PNETs). Although also some cross-reactivity occurred in non-neurogenic tumors, the apparent operational specificity of some of our antibodies within the nervous system promises some aid in neuropathological tumor diagnosis; this was also demonstrated by combined use of some antibodies on smear preparations in which diagnosis by conventional stains was uncertain. This study confirms and expands previous data that sharing of antigenic determinants by hemopoietic cells and nervous system tumors is common. The significance of these cross-reactivities is at present a matter of speculation; cross-reacting autoantibodies might interfere with immune regulation in tumor patients, and an immune response might be initiated when glioma cells bearing Ia antigens present tumor-associated antigens to T cells.

Adolescent↗

PubMed1985

Occurrence of IgA subclasses (IgA1 and IgA2) in the human nervous system. Correlation with disease.

The occurrence of IgA subclasses in pathological conditions of the nervous system was studied by means of monoclonal antibodies and an indirect immunofluorescence technique. IgA1- and/or IgA2-positive lymphoid (plasma) cells were found in demyelinating diseases comprising multiple sclerosis, Guillain-Barré syndrome, and adrenoleukodystrophy, in various inflammatory diseases, and in tumors, some of which exhibited labeling of tumor cells. Demyelinating and inflammatory diseases with chronic course displayed some prevalence of IgA2-, and tumors some prevalence of IgA1-positive cells. This is the first demonstration of IgA1 and IgA2 in the nervous system.

Alzheimer Disease↗

PubMed1985

Pathology of midline brain tumors. Immunocytochemical tumor markers and classificatory aspects.

Our understanding of the pathology of human brain tumors has considerably increased in recent years thanks to investigation of nervous tissue markers which can be demonstrated by immunocytochemical techniques in sections of neurosurgical tissue specimens. This development is presented here in a review of the most important entities among midline brain tumors. Detection of neural differentiation markers such as glial fibrillary acidic protein (GFAP), S 100 protein (S 100 p), neurofibrillary proteins and neuron-specific enolase (NSE) greatly contributed to clarifying the histogenesis and differentiation potential of undifferentiated small-cell tumors grouped as primitive neuroectodermal tumors (PNETs) which include cerebellar medulloblastomas and pinealoblastomas as well as neuroblastomas and ependymoblastomas. Among medulloblastomas, the desmoplastic variety (formerly called by some "arachnoidal sarcoma of the cerebellum") shows frequent glioneuronal differentiation. Monoclonal antibodies recognizing antigenic determinants specific for tumor types and grades of malignancy/differentiation will gain significance in brain tumor diagnosis, as demonstrated in some examples. Despite the development of more objective ("scientific") criteria for typing human brain tumors, the "art" of classical histopathologic evaluation is not replaced but supplemented by the wealth of data supplied by such modern accomplishments.

Astrocytoma↗

PubMed1984

Glial bundles in spinal nerve roots. An immunocytochemical study stressing their nonspecificity in various spinal cord and peripheral nerve diseases.

Glial bundles (GBs) in spinal nerve roots in 86 autopsy cases with various spinal lesions were examined using the peroxidase-antiperoxidase technique for glial fibrillary acidic protein (GFAP). In 19 of 22 cases of Werding-Hoffmann disease (WHD), GBs were present in the anterior roots (ARs) but absent in the youngest age group (age less than 1.5 months at death). GBs were numerous in classical cases (age 3-24 months), accompanying severe damage of the anterior horns and roots, but were less prominent in most cases of protracted course (age 2-8.5 years). Thus, development of GBs in the ARs of motor neuron disease at a young age seems to depend on the clinical type (age at onset and disease duration) and degree of damage to motor neurons and ARs. Varying numbers of GBs were found also in the posterior roots (PRs) of 12 cases of WHD. In 13 patients with amyotrophic lateral sclerosis (ALS), few GBs were observed in the ARs of two and PRs of five cases without apparent relation to other clinicopathologic data. GBs in the PRs of both WHD and ALS might indicate spreading of the degenerative process to sensory neurons despite the absence of pathology detectable by routine histological stains. Numerous GBs were found also in adults affected with polymyelitis in childhood. Varying numbers of GBs were present, however, in many different diseases, such as Friedreich ataxia, Guillain-Barré syndrome, various polyneuropathies, cervical spondylosis, ataxia telangiectasia, metachromatic leukodystrophy, and Leigh syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1984

Glial fibrillary acidic protein (GFAP) in oligodendroglial tumors: gliofibrillary oligodendroglioma and transitional oligoastrocytoma as subtypes of oligodendroglioma.

Immuno-reactivity to glial fibrillary acidic protein (GFAP) is mainly regarded as a sign of astroglial histogenesis and/or differentiation. The presence of astrocytes in oligodendrogliomas is a well known phenomenon; in addition, GFAP-positive neoplastic oligodendrocytes have also been described but have not yet been studied systematically. Using an anti-GFAP serum in the peroxidase-antiperoxidase antiperoxidase (PAP) technique, 50 oligodendrogliomas and 16 mixed oligodendrocytomas were investigated; they had been diagnosed by routine histological stains. In half of all oligodendrogliomas, and only in a few (12%) of the mixed oligoastrocytomas, GFAP-positive oligodendrocytes were found in some areas of the classical honey-comb texture with a prominent vascular stroma. The term 'gliofibrillary oligodendrocyte' (gfoc) is proposed for these immuno-reactive cells. The existence of a tumour cell combining morphological characteristics of oligodendroglia with GFAP production in its cytoplasm may be considered analogous to transient GFAP expression by myelin-forming glia during normal development (Choi and Kim 1984), thus suggesting the return to a foetal behaviour by some neoplastic oligodendrocytes. Three tumours of the present series consisted largely of gfocs and, therefore, may be termed gliofibrillary oligodendrogliomas. In about 32% of all oligodendrogliomas, but only once in the mixed tumour group, a gradual morphological transition from gfocs to gemistocytic astrocytes was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Neoplasms↗

PubMed1984

Production of glial fibrillary acidic protein (GFAP) by neoplastic cells: adaptation to the microenvironment.

In 80 specimens of human glioma the production of glial fibrillary acidic protein (GFAP) by tumour cells invading meninges or connective tissue was studied immuno-cytochemically by the PAP technique. In 38 of 55 cases of astrocytoma, glioblastoma, gliosarcoma, and oligoastrocytoma, GFAP immunoreactivity was greater in the invading cells as compared with the main part of the neoplasm. Fifty-eight percent of the astroglial tumours invading the leptomeninges, all astroglial tumours invading connective tissue and all gliosarcomas showed enhanced GFAP immuno-reactivity of tumour cells getting in contact with collagenous tissue, whereas meningeal infiltrates of 25 non-astroglial tumours (oligodendroglioma, ependymoma, medulloblastoma) remained GFAP-negative like the main part of the respective tumours. In the majority of astroglial tumours an increase of GFAP immunoreactivity was found also in perivascular cells of the main part of the tumour. It is concluded that glioma cells are capable of adapting their cytoskeleton to their micro-environment. Contact with dense collagenous tissue appears as an important factor able to induce an increased production of GFAP by adjacent glial cells.

Astrocytoma↗