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Biomedical subjects

A Bayas

Publications and source records attributed to A Bayas.

8 recordsLinked to original sources
PubMed2005

[Autoimmune neuropathies--current aspects of immunopathologic diagnostics and therapy].

The group of autoimmune neuropathies includes the Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuritis, multifocal motor neuropathy, neuropathies associated with monoclonal gammopathies, and vasculitic neuropathies. This educational review first addresses diagnostic pathways that facilitate more rational diagnostic decisions. Many therapies are effective for treating immune neuropathies. Unfortunately, none of the available therapies are specific. In the acute phase, glucocorticosteroids, plasmapheresis, and intravenous immunoglobulins play key roles. The list of long-term therapies includes azathioprine, cyclosporine, cyclophosphamide, and immunoglobulins. The therapeutic mechanisms involved are not clear for most of these compounds. Modern immunotherapy has to consider medical aspects, available therapeutic evidence, and long-term economic burden.

Autoimmune Diseases of the Nervous System↗
PubMed2003

Modulation of cytokine mRNA expression by brain-derived neurotrophic factor and nerve growth factor in human immune cells.

Brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) exert various effects on immune cells. Here we studied, whether they influence the cytokine expression pattern in peripheral blood mononuclear cells (PBMCs) or antigen specific T-cells. In PBMCs BDNF and NGF had interindividually variable effects on T helper cell type (Th)1- and Th2-cytokines. However, there was a high correlation between the modulating properties of these neurotrophins (r=0.97) concerning the expression of interleukin (IL) 4, transforming growth factor-beta and tumour necrosis factor-alpha mRNA at a concentration of 100 ng/ml. In myelin basic protein-specific T-cell lines BDNF and NGF increased interferon -gamma mRNA to a moderate extent, but not IL4. No major effects were detected at the cytokine protein level. In conclusion, our results suggest a partial effect of neurotrophins on immune cells, which may be modified by other signals.

Brain-Derived Neurotrophic Factor↗
PubMed2003

[Diagnostic principles in myopathies].

Myopathies include a broad range of disorders. Diagnostic steps in muscle disorders should therefore be followed sequentially, in order not to miss important information and to avoid unnecessary and cost intensive diagnostic procedures. Specific care should be applied in taking patient's history to ascertain myopathy related complaints, triggers and concomitant diseases possibly being accompanied by a myopathy. Clinical examination may reveal a distribution pattern already suggestive for a specific disorder. An elevated creatine kinase, often leading to neurological evaluation, should at least be repeated once after resting. Metabolic myopathies might be detected by exercise testing. Electromyography, muscle imaging and, usually as the last diagnostic step, muscle biopsy represent further diagnostic tools in the assessment of myopathies. In some disorders molecular genetic techniques can be applied.

Biomarkers↗
PubMed2002

Human cerebral endothelial cells are a potential source for bioactive BDNF.

Inflammatory stimuli within the central nervous system may not only induce tissue damage but may also convey neuroprotection. It has been shown that brain derived neurotrophic factor (BDNF) is a neuroprotective candidate. Here we show that BDNF is constitutively expressed in cultured human cerebral endothelial cells (HCEC) and can further be upregulated under proinflammatory conditions. TNF-alpha treatment resulted in an increase in BDNF mRNA expression and protein levels were significantly elevated after 72 h (69+/-33%, P<0.01). Using functional assays it was demonstrated that BDNF produced by HCEC is bioactive and supports motoneuron survival. In contrast, BDNF expression was reduced by TNF-alpha in human umbilical vein endothelial cells (HUVEC). We conclude that HCEC likely to contribute to neuronal survival under physiological and inflammatory conditions.

Brain-Derived Neurotrophic Factor↗
PubMed2001

Production of MMPs in human cerebral endothelial cells and their role in shedding adhesion molecules.

Matrix metalloproteinases (MMPs) are Zn2+-endopeptidases that seem to play an important role in chronic inflammatory diseases of the central nervous system by disrupting the blood-brain barrier (BBB) and mediating the destruction of myelin components. We therefore investigated the influence of the pro-inflammatory cytokine TNF-alpha. on the expression and activation of several MMPs in human cerebral endothelial cells (HCEC). HCEC constitutively express MMP-2 and MMP-3 mRNA, but only MMP-3 is upregulated on mRNA and protein level after TNF-alpha stimulation. MMP-9 and MMP-12 mRNA could only be detected under inflammatory conditions. Furthermore, MMPs are involved in shedding of cell surface molecules. We therefore investigated the influence of MMPs on the release of soluble adhesion molecules using marimastat, a specific broad-spectrum MMP inhibitor and other protease inhibitors like aprotinin or leupeptin. Only marimastat inhibited the TNF-alpha mediated release of sVCAM-1 in the supernatants of HCEC. Western blot results of culture supernatants supported the time dependent release of the complete extracellular portion of the VCAM-1 molecule. These data suggest that MMPs produced by HCEC are actively involved in the shedding of soluble adhesion molecules at the BBB.

Alternative Splicing↗
PubMed2000

Managing the adverse effects of interferon-beta therapy in multiple sclerosis.

Interferon-beta is an established therapy in relapsing-remitting multiple sclerosis. Recently, it has also been shown that interferon-beta-1b is effective in secondary progressive multiple sclerosis. However, adverse effects of interferon-beta treatment are common, particularly during the first weeks of treatment, and are a major concern. Flu-like symptoms, injection site reactions and laboratory abnormalities are the most common adverse effects, and may result in reduced compliance or even discontinuation of treatment in a number of patients. Therefore, efforts to minimise these reactions, e.g. appropriate comedication with analgesic/antipyretic drugs, use of correct preparation and injection technique and sometimes modification of the dosage of interferon-beta, are of considerable importance. This article provides an overview of the management of clinically relevant adverse effects related to treatment with interferon-beta, based on a literature review and personal experience. Essential aspects of patient information are also stressed. If these recommendations are followed, adverse effects related to interferon-beta may be substantially reduced in the majority of patients.

Clinical Trials as Topic↗
PubMed1994

Interphase cytogenetics of glioblastoma and gliosarcoma.

Interphase cytogenetics, i.e., in situ hybridization using probes to chromosome-specific DNA, enables histological identification of cells bearing numerical chromosome aberrations and cytogenetic analysis of composite tumors. We studied routinely processed tissues from seven glioblastomas and three gliosarcomas using biotinylated probes to pericentromeric alpha-satellite sequences on chromosomes 10, 17 and X. By applying various pretreatment protocols, an evaluable compromise between morphology and signal intensity was obtained in most cases. Compared to vascular cells with normal chromosomal counts, a significant subpopulation of glioblastoma cells showed monosomy 10 (four of five cases), monosomy 17 (one of seven cases) and loss of one X chromosome (one of seven cases). All monosomy 10 cases comprised additional areas where two copies of chromosome 10 were retained. Among the gliosarcomas, both the glioma and the sarcoma portion showed monosomy 10 in one case and monosomy 17 in another case. In contrast, in the third case of gliosarcoma, monosomy 10 was found only in the glioma portion, whereas a gain of chromosome X was observed in the sarcoma portion. We conclude that: (1) numerical chromosome aberrations can be detected in routinely processed brain tumor biopsy specimens using interphase cytogenetics, making retrospective studies feasible; (2) glioblastomas show intratumoral cytogenetic heterogeneity with formation of monoclonal cell clusters; and (3) sarcoma and glioma elements in gliosarcomas may exhibit the same or different numerical chromosome aberrations, suggesting various histogenetic pathways of the sarcoma-like portion.

Adult↗