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Biomedical subjects

R C Janzer

Publications and source records attributed to R C Janzer.

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

[Peripheral nerve and spinal cord complication in intravenous heroin addiction].

The neurological complications observed in 6 HIV negative intravenous drug users are reported. Four developed acute neuromuscular involvement in a lumbosacral or brachial distribution with rhabdomyolysis, myoglobinuria, hypovolemia, renal and hepatic failure in the 3 most severely affected patients. Despite evidence of immunologic abnormalities and especially presence of anti-heroin antibodies, we feel that causative mechanisms include mixed compression and ischemia with an underlying toxic myopathy, resulting in segmental myopathy with secondary compression of peripheral nerves. Two patients developed myelopathy with acute or chronic onset. The mechanisms were vascular with spinal cord infarction in the acute form and probably infectious with secondary compressive arachnoiditis in the chronic form. In these 2 patients with myelopathy, outcome was poor.

Acute Disease↗
PubMed1995

Direct and astrocyte-mediated effects of ethanol on brain-derived endothelial cells.

The effects of ethanol have been studied in the central nervous system, however there exists only scarce information about the effects of ethanol on endothelial cells forming the blood-brain barrier. As some properties of brain endothelial cells are modulated by underlying astrocytes, the effect of ethanol on cerebral microvasculature might be indirect and mediated by astrocytes. To analyse this question, we added to rat brain-derived endothelial cells (rbEC) in culture either only ethanol (0, 15 and 150 mM) or ethanol conjointly with soluble factors secreted by astrocytes. Alternatively, astrocytes were exposed to ethanol and the medium was added to rbEC. The effects of treatments were evaluated on cell growth and expression of specific proteolytic markers of rbEC. The experiments showed that while the addition of ethanol alone to rbEC increased the expression of gamma-glutamyltranspeptidase and cell growth following an initial toxic effect, the most significant effects were seen when ethanol was added to rbEC together with astrocytic factors or when medium conditioned by astrocytes exposed to ethanol was added to rbEC. In particular, the expression of angiotensin converting enzyme in endothelial cells was dose-dependently increased. These results indicate that the hypertensive and toxic effects of ethanol are mediated by ethanol and soluble factor(s) secreted by astrocytes and dependent on the expression of angiotensin converting enzyme in the brain endothelium. Thus, when evaluating in vitro the effects of toxic substances such as ethanol on the cerebral endothelium, the modulating effect of cells surrounding cerebral vessels must be accounted for.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Idiopathic orbital inflammation (orbital inflammatory pseudotumour): an unusual cause of transient ischaemic attack.

A patient with idiopathic inflammation of the right orbit, established by biopsy, developed episodes of transient left sensorimotor hemiparesis. Neuroimaging showed intracranial extension of the disease with pronounced narrowing of the right internal carotid artery in its intracavernous portion. Oral cyclophosphamide induced gradual improvement. Transient ischaemic attack is rarely found in association with orbital disease and indicates possible intracranial extension.

Administration, Oral↗
PubMed1994

Tumor cells suppress cytokine-induced nitric-oxide (NO) production in cerebral endothelial cells.

Nitric oxide (NO) produced by endothelial cells (EC) has been shown to exert cytotoxic activity on tumor cells. In order to analyze events involved in brain metastasis, the modulation of NO production in rat-brain-derived EC was investigated. NO release was increased by tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-1 beta, lipopolysaccharide or forskolin in EC219 cells, a rat-brain-microvessel-derived EC line. Dexamethasone decreased NO release by cytokine-activated EC219 cells. Tumor cells (DHD/K12/PROb, a rat colon-carcinoma cell line) were highly adherent to EC219 cells, and adhesion was not modified by TNF-alpha plus IFN-gamma, or by dexamethasone. Addition of tumor cells or tumor-cell-conditioned medium significantly inhibited NO release induced by any of the stimuli examined, but only if added during the initial phase of endothelial-cell activation. Tumor-derived suppression of NO release was also observed in primary cultures of cerebral EC. NO synthase (NOS) activity in cytosol extracts of the cerebral EC line was Ca(2+)-independent and required both NADPH and tetrahydrobiopterin. NOS activity was increased by TNF-alpha and IFN-gamma, and significantly reduced by tumor-cell-conditioned medium. These results suggest that rat colon-carcinoma cells may have developed a protective mechanism involving the release of (a) soluble factor(s) which inhibit(s) NO production by cerebral EC.

Amino Acid Oxidoreductases↗
PubMed1994

Further ultrastructural evidence that spirochaetes may play a role in the aetiology of Alzheimer's disease.

Recently it was reported that, at autopsy, in neuropathologically confirmed cases of Alzheimer's disease spirochaetes were found in blood and cerebrospinal fluid using dark-field microscopy. Moreover, the spirochaetes were isolated and cultured from brain tissue. We now show, using scanning electron microscopy and atomic force microscopy that the helically shaped microorganisms isolated and cultured from the Alzheimer brains possess axial filaments. This indicates that these microorganisms taxonomically indeed belong to the order Spirochaetales. A morphometric analysis reinforces this notion.

Alzheimer Disease↗
PubMed1994

[Critical analysis of the results of muscle biopsies and of the methods used in 889 cases of neuromuscular disorders].

The contribution of muscle biopsies to the diagnosis of neuromuscular disorders and the indications of various methods of examination are investigated by analysis of 889 biopsies from patients suffering from myopathic and/or neurogenic disorders. Histo-enzymatic studies performed on frozen material as well as immunohistochemistry and electron microscopy allowed to provide specific diagnoses in all the neurogenic disorders (polyneuropathies and motor neuron diseases), whereas one third of myopathies remained uncertain. Confrontation of neuropathological data with the clinical indications for histological investigations shows that muscle biopsies reveal the diagnosis in 25% of the cases (mainly in congenital and metabolic myopathies) and confirm and/or complete the clinical diagnosis in 50%. In the remaining cases with non specific abnormalities neuropathological investigations may help the clinician by excluding well defined neuromuscular disorders. Analysis of performed studies and results of investigations show the contribution and specificity of each method for the diagnosis. Statistical evaluation of this series indicates that cryostat sectioning for histo- and immunochemical and electron microscopy increases the rate of diagnoses of neuromuscular diseases: full investigation was necessary for the diagnosis in 30% of the cases. The interpretation of the wide range of pathological reactions in muscles requires a close cooperation with the clinician.

Adolescent↗
PubMed1993

Astrocytes secrete a factor inducing the expression of HT7-protein and neurothelin in endothelial cells of chorioallantoic vessels.

Among the most specific markers of the blood-brain barrier phenotype of endothelial cells are the well-characterized immunoglobulin-like surface glycoprotein HT7 and the probably related or identical glycoprotein neurothelin. Both can be induced in chorioallantoic vessels by transplants of embryonic mouse brain. Other blood-brain barrier markers have been shown to be inducible by type-1 astrocytes in endothelial cells of non-neural origin. In the present work we tested the hypothesis that this cellular interaction between astrocytes and endothelial cells is mediated by a soluble factor(s). Chorioallantoic vessels of embryonic day 9 chick embryos were exposed for 4 or 10 days to a constant and localized delivery of astrocyte-conditioned medium by using a piece of gelfoam posed onto the chorioallantoic membrane, as a localized reservoir, which was connected to a miniosmotic pump system delivering astrocyte-conditioned medium at a steady rate. We found that in a significant number of chorioallantoic vessels located near the gelfoam, endothelial cells exposed to astrocyte-conditioned medium for a period of 4 or 10 days, but not to glioma-, fibroblast- or endothelial cell-derived conditioned medium, expressed the HT7 antigen and neurothelin. These results provide evidence that type-1-astrocytes are capable of inducing blood-brain barrier related properties in endothelial cells of non-neural origin through a soluble factor(s).

Allantois↗
PubMed1993

The blood-brain barrier: cellular basis.

Perfusion experiments with horseradish peroxidase have established that the morphological substrate of the blood-brain barrier is represented by microvascular endothelial cells. They are characterized by complexly arranged tight junctions and a very low rate of transcytotic vesicular transport. They express transport enzymes, carrier systems and brain endothelial cell-specific molecules of unknown function not expressed by any other endothelial cell population. These blood-brain barrier properties are not intrinsic to these cells but are inducible by the surrounding brain tissue. Type I astrocytes injected into the anterior eye chamber of the rat or onto the chick chorioallantoic membrane are able to induce a host-derived angiogenesis and some blood-brain barrier properties in endothelial cells of non-neural origin. Recently we have shown that this cellular interaction is due to the secretion of a soluble astrocyte derived factor(s). Astrocytes are also implicated in the maintenance, functional regulation and the repair of the blood-brain barrier. Complex interactions between other constituents of the microenvironment surrounding the endothelial cells, such as the basement membrane, pericytes, nerve endings, microglial cells and the extracellular fluid, take place and are required for the proper functioning of the blood-brain barrier, which in addition is regionally different as reflected by endothelial cell heterogeneity.

Animals↗
PubMed1993

Cellular schwannomas of the intracranial and intraspinal compartment: morphological and immunological characteristics compared with classical benign schwannomas.

The concept of cellular schwannoma as an unusual benign tumor is well established for peripheral nerves but has never been tested in neurosurgical series. In order to test the validity of this concept in cranial nerves and spinal roots we performed an analysis of the clinical and morphological characteristics of 12 cellular and 166 classical benign schwannomas. Immunohistochemical detection of antigen expression in Schwann cells including proliferating cell nuclear antigen (PCNA) was also performed. This study shows that cellular schwannomas in neurosurgical series manifest at a lower age than the classical benign variant and occur mainly in the spinal roots. Mitotic activity and sinusoidal vessels appear more frequently in cellular schwannomas and constitute with high cellularity, the most valuable criteria separating both entities. The postoperative course in both types of tumors was free of metastases or sarcomatous changes. Immunoexpression of S-100 protein, vimentin, epithelial membrane antigen and glial fibrillary acidic protein is not statistically different between the two variants. In contrast, PCNA is more highly expressed in cellular schwannomas. These These results confirm the concept that cellular schwannomas are a clinico-pathological variant of benign schwannomas and provide significant support for the introduction of this entity in neurosurgical oncology.

Adult↗
PubMed1993

Motor conduction block and high titres of anti-GM1 ganglioside antibodies: pathological evidence of a motor neuropathy in a patient with lower motor neuron syndrome.

A patient with a progressive lower motor neuron syndrome and neurophysiological evidence of motor axon loss, multifocal proximal motor nerve conduction block, and high titres of anti-ganglioside GM1 antibodies. Neuropathological findings included a predominantly proximal motor radiculoneuropathy with multifocal IgG and IgM deposits on nerve fibres associated with a loss of spinal motor neurons. These findings support an autoimmune origin of this lower motor neuron syndrome with retrograde degeneration of spinal motor neurons and severe neurogenic muscular atrophy.

Aged↗
PubMed1992

Induction of the blood-brain barrier specific HT7 and neurothelin epitopes in endothelial cells of the chick chorioallantoic vessels by a soluble factor derived from astrocytes.

Some blood-brain barrier properties of microvascular endothelial cells have been shown to be inducible by astrocytes. We tested the hypothesis that this cellular interaction is mediated by a soluble factor(s). Chick chorioallantoic vessels in ovo were constantly exposed to astrocyte-conditioned medium. We found that endothelial cells exposed to astrocyte-derived factors, but not to glioma- or endothelial cell-derived factors, expressed the HT7 antigen and neurothelin, two specific markers of the blood-brain barrier phenotype. These results indicate that a soluble factor(s) secreted by astrocytes is capable to induce specific blood-brain barrier properties in endothelial cells of non-neural origin.

Animals↗
PubMed1992

A modified Hortega-Globus stain is superior to Bielschowsky and Bodian stains for demonstrating neuritic plaques.

The quantitative assessment of the age-dependent number of neuritic plaques is essential for the diagnosis of Alzheimer type dementia. This study reports the superiority of a modified Hortega-Globus stain compared to Bielschowsky and Bodian stains applied to samples obtained from ten brains of patients with a clinical history of progressive dementia. In two of ten cases only the modified Hortega-Globus stain allowed confirmation of the diagnosis of senile dementia of the Alzheimer type (SDAT). The counts of neuritic plaques in sections stained by other methods were not sufficient to establish the histological diagnosis of SDAT. These results indicate that the choice of the most sensitive staining method is critical for the correct histopathologic diagnosis of the Alzheimer type dementia.

Aged↗
PubMed1991

Acute fatal myeloencephalopathy after combined intrathecal chemotherapy in a child with acute lymphoblastic leukemia.

We report a case of a fatal toxic encephalomyelopathy in a 12-year-old girl due to prophylactic intrathecal injection of methotrexate and cytosine arabinoside, with a characteristic progressive symptomatology leading to death after 28 days. The location and type of neuropathological changes support the hypothesis of a direct toxic effect of methotrexate and/or cytosine arabinoside on structures directly exposed to the cerebrospinal fluid.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1991

Clinical growth rate of acoustic schwannomas: correlation with the growth fraction as defined by the monoclonal antibody ki-67.

The growth rate of acoustic tumors, although slow, varies widely. There may be a continuous spectrum or distinct groups of tumor growth rates. Clinical, audiologic, and conventional histologic tests have failed to shed any light on this problem. Modern immunohistochemical methods may stand a better chance. The Ki-67 monoclonal antibody stains proliferating cells and is used in this study to investigate the growth fraction of 13 skull base schwannomas. The acoustic tumors can be divided into two different growth groups, one with a rate five times the other. The literature is reviewed to see if this differentiation is borne out by the radiologic studies. Distinct growth rates have been reported: one very slow, taking 50 years to reach 1 cm in diameter, a second rate with a diameter increase of 0.2 cm/year, and a third rate five times the second, with a 1.0 cm increase in diameter per year. A fourth group growing at 2.5 cm/year is postulated, but these tumors cannot be followed for long radiologically, since symptoms demand surgical intervention. The clinical implications of these separate growth rates are discussed.

Journal Article↗
PubMed1991

Arteriovenous malformation in meningothelial meningioma: case report.

An unusual association of a meningioma and an arteriovenous malformation is reported. A 68-year-old man developed left homonymous hemianopsia, left hemiparesis, and gaze palsy. Magnetic resonance imaging showed a right occipital mass lesion containing multiple signal-void areas with tubular and honeycomb appearance, suggesting a marked vascular component. An angiogram showed abnormal vasculature in the mass supplied by the posterior cerebral artery and a dural arteriovenous malformation on the tentorium. Neuropathological examination after total removal of the mass revealed a meningothelial meningioma including major portions of an arteriovenous malformation that extended from the dura and leptomeninges, through the meningioma, and into the occipital lobe, where the tumor was located.

Aged↗
PubMed1990

Meningovascular form of neuroborreliosis: similarities between neuropathological findings in a case of Lyme disease and those occurring in tertiary neurosyphilis.

Recent observations have delineated the neurological manifestations of Lyme disease, but, to our knowledge, no detailed neuropathological study from autopsy cases has been reported. In this report we describe the neuropathological findings in a case of Lyme neuroborreliosis. The chronic meningitis, the occlusive meningovascular and secondary parenchymal changes that we found are similar to those occurring in the meningovascular form of neurosyphilis. Thus, we suggest that the case described here represents the meningovascular form of tertiary Lyme neuroborreliosis.

Humans↗