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Biomedical subjects

E Matyja

Publications and source records attributed to E Matyja.

At least 37 records · Page 2Linked to original sources
PubMed1996

Cerebral gangliogliomas. Morphological and immunohistochemical study.

Report concerns 6 uncommon cases of cerebral ganglioglioma in adult patients, the majority of whom (4) demonstrated typical classic features, others were anaplastic. Both types presented neuronal and glial components characterized either by NF, NSE and Syn or GFAP immunoreactivity. Only the tumor of the youngest patient presented moderate desmoplasia. Observations indicate at an easy classification of glial component contrary to neuronal component in relation to the origin of neuronal changes.

Adolescent↗
PubMed1996

Mitochondrial damage following exposure of organotypic cultures of human malignant gliomas to 2-chloro- and 2-bromo-2'-deoxyadenosine.

The effects of 2-chloro-2'-deoxyadenosine (cladribine, 2-CdA) and a closely related compound 2-bromo-2'-deoxyadenosine (2-BdA) on organotypic cultures of human malignant gliomas were studied with the use of electron microscopy. The cultures grown from surgical biopsies included six glioblastomas, three anaplastic astrocytomas and low-grade fibrillary astrocytoma. After 6 to 10 days of the in vitro growth the cultures were exposed to 0.3-10 microM 2-CdA or 2-BdA for 1 to 10 days. Mitochondrial swelling and disappearance of cristae following exposure to the tested substances were observed, but only in highly anaplastic (low-differentiated) tumor cells. The mitochondrial toxicity was dose- and time-dependent, and no difference was found between the effect of 2-CdA and 2-BdA.

Antineoplastic Agents↗
PubMed1996

2-chloro- and 2-bromo-2'-deoxyadenosine have no effect on the morphology of rat neural and glial cells in organotypic culture.

Organotypic cultures of hippocampus and cerebellum, established from brains of 1-3 days old rats, were exposed at different stages of development (3, 14 and 21 DIV) to 2-chloro-2'-deoxyadenosine (cladribine, 2-CdA) and 2-bromo-2'-deoxyadenosine (2-BdA) at concentrations up to 10 microM, for up to 10 days. Normal pattern and dynamics of differentiation and maturation of both neurons and glial cells was found with the use of light and electron microscopy. No ultrastructural abnormalities were induced by the substances tested. We conclude that 2-CdA and its sister compound 2-BdA do not exert cytotoxic effects toward normal rat central nervous system tissues in organotypic culture.

Animals↗
PubMed1995

Meningiomas and gliomas in juxtaposition: casual or causal coexistence? Report of two cases.

Two cases of meningioma and glioma established in biopsy material from one or more than one operation are reported. In these cases, an originally benign meningioma was followed by the development of anaplastic astrocytoma in close juxtaposition to the site of first operation. The close juxtaposition of two histologically different tumors suggested that one of them might lead to local proliferation and independent growth of the other.

Brain Neoplasms↗
PubMed1995

Neurofibromatosis type 2. Case report.

A case of a 24-year-old woman with peripheral paresis of the facial nerve, balance disturbance, hearing loss and epileptic seizures for many years is presented. At time of admission to hospital cerebral magnetic resonance imaging (MRI) showed several large tumors situated supra- and infratentorially. Histological examination of the operated tumors revealed bilateral acoustic schwannomas in the cerebellopontine angles and mixed meningioma in the others. The patient was diagnosed as neurofibromatosis type 2 (NF2) according to clinical criteria for neurofibromatoses. Several months after the last operation, she exhibited weakness of all extremities. On spinal MRI an intramedullary tumor in the cervical region and additional focal lesions along central canal were found. Surgical therapy was not performed because of clinical improvement after dexamethasone treatment and location of lesion in cervical medulla. Our case confirms frequently occurring lack of neurocutaneous changes and late appearance of significant neurological symptoms in NF2.

Adult↗
PubMed1995

Occurrence of lamellar bodies in the rat brain organotypic cultures in normal and pathological conditions.

Lamellar bodies (LB) represent an intracytoplasmic organelles of the cells of different origin and various organs. Their exact function is not known. It has been recently suggested that these organelles may play a role in the protein synthesis and regulation of gene expression. Increased number of LB has been demonstrated in differentiating and growing cells. It suggests their functional relation to enhanced metabolism of the cells. Such conditions for cells establish a tissue culture. We have examined organotypic rat brain cultures maintained under standard conditions, and subsequently exposed to anoxia and neurotoxins: kainic and quinolinic acid. In normal conditions LB were occasionally found in neurons. Their number significantly increased in damaged neurons in the experimental conditions. They have also appeared in some damaged astrocytes. We postulate that LB in the brain are connected with cell degeneration. Their origin from rough endoplasmic reticulum is demonstrated.

Animals↗
PubMed1994

Reaction of microglial cells in human astrocytomas (preliminary report).

Forty human primary brain tumors: twelve protoplasmic, six gemistocytic, four fibrillary and ten anaplastic astrocytomas, eight glioblastomas were submitted for immunohistochemical and histochemical characterization of microglia in tumor tissue and in its surroundings. The following antibodies were used: GFAP, ferritin, CD45RO and lectin RCA-1. It was found that the greatest number of ramified microglia occurred in gemistocytic astrocytomas. In the protoplasmic and fibrillary astrocytomas both the ramified and amoeboid microglia were observed. In glioblastomas and anaplastic astrocytomas the greatest number of amoeboid microglia and very rarely ramified microglial cells were found. It is suggested that differences between the various kinds of astrocytomas determine the difference in the type of microglia reaction. It is assumed that this might be caused by the differences in secreting some factors by these tumors astrocytes.

Antibodies↗
PubMed1994

Intracranial meningiomas following irradiation therapy for brain tumors.

Two cases of radiation-induced meningiomas following therapeutic irradiation given for primary diagnosed malignant brain tumor are presented. The meningiomas, histologically different from the initial brain tumor, appeared 15 and 21 years after high-dose brain irradiation. The possible risk of carcinogenesis within the CNS resulted from therapeutic cranial irradiation is stressed.

Brain↗
PubMed1994

Microcystic meningioma--a rarely occurring morphological variant of meningioma.

Two cases of microcystic meningioma are reported. They were found by retrospective study of 124 human intracranial meningiomas. Both of the examined tumors were characterized histologically by a great number of cysts of various size intermixed with nests of neoplastic tissue of meningothelial meningioma type. Nevertheless, there were two kinds of cystic changes in these tumors. In the first case, numerous microcysts within the tumor were surrounded by stellate-shaped processes of meningioma's cells. The microcystic space were empty or rarely contained eosinophilic material. The latter tumor demonstrated small agglomerations of microcysts and many macrocystic changes, some of them filled with eosinophilic, PAS and mucicarmine negative material. Additionally, in focal areas of the tumor, single mitotic figures and giant cells with hyperchromasia were present. The authors discuss morphologic variability of the examined tumors and its possible clinical consequences. The pathogenesis of microcystic changes in meningioma is discussed with a brief review of the literature.

Adult↗
PubMed1994

Delayed effect of QUIN-neurotoxicity. Ultrastructural study.

The ultrastructural studies of QUIN-injected rat hippocampus were performed in long-term experiment in order to determine delayed neurotoxic effect of this compound. QUIN, in a single dose, was administered stereotaxically into the dorsal hippocampus. The morphological changes were characterized by marked atrophy of neuropil accompanied by remarkable glial pathology. The neuronal changes consisted in loss of many nerve cells, abnormalities of nuclear chromatin in the persisting pyramidal neurons and degeneration of postsynaptic dendrites. The glial changes were represented by electron-lucency of astrocytic cytoplasm and their processes. The mechanism of this reaction is unclear and the suggestion, that electron-lucent astrocytes represent a form of transformed glia especially sensitive to amino acids, releasing from degenerating neurons is discussed.

Animals↗
PubMed1993

Ultrastructural evidence that mercuric chloride lowers the threshold for glutamate neurotoxicity in an organotypic culture of rat cerebellum.

Separate exposure of organotypic cultures, derived from newborn rat cerebellum, to non-toxic concentration of either 100 microM glutamate (GLU) or 1 microM mercuric chloride (MC), for as long as 3 days, produced no distinct ultrastructural changes in neurons and glial cells. By contrast, simultaneous exposure to both agents resulted, as early as after 30 min, in microvacuolar degeneration of neurons and later on in postsynaptic abnormalities, typically accompanying excitotoxic lesions but not heavy metal-induced lesions. The results indicate that MC at low micromolar concentrations lowers the threshold for GLU neurotoxicity.

Animals↗
PubMed1993

Ultrastructural evaluation of neuronal damages induced by low doses of quinolinic acid in dissociated hippocampal culture.

The effect of a subtoxic level of quinolinic acid (QUIN) on the morphological picture of the rat hippocampus in dissociated cultures was investigated. Addition of 50 microM of QUIN to the culture medium induced only slight advanced and reversible changes of the postsynaptic elements, whereas the majority of pyramidal neurons were undamaged. The results suggest that subtoxic concentration of QUIN is insufficient to produce stable depolarization of cell membranes and severe neuronal damage.

Animals↗
PubMed1993

Verapamil reduces quinolinic acid-induced neuronal damage in rat hippocampus in vitro.

The effect of the organic calcium channel blocker, verapamil, on quinolinic acid (QUIN) neurotoxicity in rat hippocampal cultures was studied. Verapamil and QUIN, both in 100 microns concentration, were added simultaneously to the culture medium. Ultrastructural analysis showed that verapamil was able to reduce typical QUIN-induced tissue damages. Especially, 3 and 7 days after exposure to the two agents, majority of both neurons and postsynaptic dendrites revealed normally appearing morphological features. The results support the suggestion of the important role of calcium entry in the development of QUIN neurotoxicity.

Animals↗
PubMed1992

Cerebral ganglioglioma with long history and unusual prominence of the mesenchymal elements. Case report.

A case of cerebral ganglioglioma, a relatively rare and controversial tumor of the central nervous system, is reported. The histological pattern of the tumor consisted of differentiated neuronal cells and glial elements displaying a various extent of cytologic abnormalities. Beside these two typical components for ganglioglioma, an abundance of collagen fibrils and numerous blood vessels were encountered. The long clinical course manifested by temporal epilepsy preceding clinical diagnosis of brain tumor and peculiar histological appearance seem to be of considerable interest.

Brain Neoplasms↗
PubMed1992

Hippocampal damage in vitro after different periods of oxygen deprivation.

The dynamics and pattern of postanoxic ultrastructural changes in organotypic culture of rat hippocampus was studied. The experiments were performed on 14-day-old cultures of rat hippocampus exposed to pure nitrogen atmosphere for 10- and 20-minutes and processed for electron microscope 2 and 24 h, 3 and 7 days post anoxia. The earliest changes following 10-min anoxia consisted of marked swelling of mitochondria and Golgi complex of neurons. The presynaptic terminals were preferentially affected. The protoplasmic astrocytes revealed swelling of the cytoplasm whereas the fibrous ones were relatively well preserved. Longer, 20-min anoxia resulted in profound ultrastructural changes even after short survival time. The tissue culture model of anoxia allow to study the direct effect of oxygen deprivation on cell morphology independently of any vascular and/or vasogenic factors.

Animals↗
PubMed1991

Protective effect of nimodipine against quinolinic acid-induced damage of rat hippocampus in vitro.

The study was undertaken to examine the effect of nimodipine, calcium channels blocker, on the morphological alterations induced by quinolinic acid (QUIN). The experiment was performed on 21-day-old organotypic rat hippocampal cultures. Nimodipine was applied to the nutrient medium simultaneously with QUIN (both at 100 microM). Ultrastructural changes were evaluated 24 h, 5 and 7 days after the exposure to tested agent. It was shown that nimodipine induced distinct cytoprotective effect, especially considering the development of late neurotoxic injury produced by QUIN. However, the protection was not complete, indicating the participation of the other factors in the pathomechanism underlying structural damage produced by QUIN.

Animals↗
PubMed1990

Prevention of quinolinic acid neurotoxicity in rat hippocampus in vitro by zinc. Ultrastructural observations.

The effect of zinc on the development and evolution of quinolinic acid-induced alterations in the rat hippocampus in culture was studied ultrastructurally. Zinc, although it possesses intrinsic cytotoxic properties, after application in concentrations comparable with those encountered in vivo, was able to prevent typically observed responses after quinolinic acid exposure, either early or late damage to hippocampal neurons. The results further support the concept of a potential protective effect of zinc against the neurotoxicity of particular excitotoxins.

Animals↗