Clinical Neuroscience

[NEW METHODS IN THE INVESTIGATION OF BRAIN HYPOXIA]

SZILÁGYI Géza, NAGY Zoltán

NOVEMBER 30, 2006

Clinical Neuroscience - 2006;59(11-12)

[The main challenge is the investigation of mechanism for apoptosis research and the drug development. Mitochondria have a key position in the production of reactive oxygen species and in the evolution of apoptosis. More possible pathway will be known with the apoptosis investigation. For development of neuroprotective molecules could give strategies the investigation of apoptosis. Exact knowledge of apoptosis provides possibility to screen new neuroprotective molecules. We elaborate a research assay, which could provide quantitative and qualitative data about the free radical production and the mitochondrial transmembrane potential using confocal microscope. So thus we could screen drug candidate, neuroprotective molecules.]

COMMENTS

0 comments

Further articles in this publication

Clinical Neuroscience

[THORACIC MENINGOCELE]

FEKETE Tamás Fülöp, VERES Róbert, NYÁRY István

[Herniation of the meninges through a defect of the spinal canal is a spinal meningocele, and is usually located dorsally in the lumbosacral region. Meningoceles are usually part of a complex developmental disorder, or of a systemic disease, or it can be iatrogenic, as well. We report a very rare case of a true anterior thoracic meningocele.]

Clinical Neuroscience

[CONGRESS CALENDAR]

Clinical Neuroscience

[Introduction]

VÉCSEI László

Clinical Neuroscience

[AMYOTROPHIC LATERALSCLEROSIS IN COUNTY BARANYA, HUNGARY]

MERKLI Hajnalka, NAGY Ferenc, PÁL Endre, GÁTI István, KOVÁCS Norbert, KOMOLY Sámuel, ILLÉS Zsolt

[Amyotrophic lateralsclerosis is a progressive neurodegenerative disease resulting in loss of upper and lower motoneurons. Here we analyzed the clinical and epidemiological data of 202 ALS patients admitted to our department between 1950 and 2004. Risk and protective factors influencing onset and progression of the disease were examined. We also analyzed the relationship between first clinical symptoms/signs and prognosis of the disease. Our data suggest the importance of toxic factors in the initiation of the disease and the effect of clinical phenotype on the progression of ALS.]

Clinical Neuroscience

[ANIMAL MODELS OF HUNTINGTON’S DISEASE]

GÁRDIÁN Gabriella

[Huntington’s disease is an autosomal dominantly inherited progressive neurodegenerative disorder. The main symptoms are choreiform, involuntary movements, personality changes and dementia. Huntington’s disease is a member of a group of diseases caused by CAG repeat expansions. One research aim is to determine the earliest molecular changes associated with Huntington’s disease. There is no possibility for this in humans, but various early changes have been identified in an animal model of Huntington’s disease. They are constructed by excitotoxin causing striatal lesion, or mitochondrial toxins inducing energy impairment, or by generating transgenic mice.]

All articles in the issue

Related contents

Lege Artis Medicinae

[Current topics in modern health informatics]

LAKNER Géza

[Development in technology - significant improvement in calculatory and storage capacities of computers - enable such calculation- and data-intensive applications, which were merely theoretical possibilities, even just a decade ago. Selected fields and methods of medical informatics are discussed in the article. Informatics methods became by now essential to biomedical research, drug discovery and development, and healthcare. Furthermore, the article presents a modern mobile information source application, developed in Hungary, which is aimed at supporting the activities and know-how of professionals in drug development and clinical research.]

Hungarian Immunology

[Therapeutic treatment of rheumatoid arthritis by gene therapy-induced apoptosis]

JAMES M. Woods, VOLIN V. Michael

[Gene therapy was initially conceptualized as a treatment for individuals with genetic disorders, where defective genes would be replaced with functional ones. This concept was eventually broadened to include the use of gene therapy as a delivery mechanism for gene products effective in the treatment of diseases. The latter use of gene therapy, essentially as a drug delivery mechanism, was recognized to be particularly useful in the treatment of rheumatoid arthritis because it may have many advantages over traditional therapies. Two groups of target genes that are potentially useful for gene transfer include soluble inflammatory mediators that in theory could suppress the inflammatory process, and apoptotic mediators that may induce cell death, thereby suppressing the accumulation of inflammatory cells in the joint. To date the former group of target genes has received most of the attention, but it is the latter group of apoptosis-inducing targets that will be discussed in this review. We will focus our discussion on target genes that have shown success at inducing apoptosis in animal models of arthritis and will also include discussion of the apoptotic pathways that are altered in the attempts to reduce inflamed synovial tissue.]

Hungarian Immunology

[On the role of aging in etiology of autoimmunity]

SEMSEI Imre, ZEHER Margit, BAKÓ Gyula

[Several types of diseases, among others autoimmune illnesses, could be coupled with the general processes of aging. The two-edged sword of the immune defense is directed once against environmental attacks and on the other side against the self. However, one has to make a difference between normal (physiological) clearance and autoimmune diseases, although both sides of autoimmunity are influenced by the general processes of senescence. Aging of the thymus seems to be one of the key elements of the etiology of autoimmunity, although other cell types and their aging also play a substantial role in this process. The spontaneous genetic instability, the acquired genetic mutations due to aging and the age-related alterations of the information level of the body together may be important elements of the patomechanism of both the physiological autoimmunity and the autoimmune diseases. Nevertheless, physiological autoimmunity seems to be directed mostly by natural factors (such as aging and apoptosis) but primary autoimmune diseases may be caused by genetic instability that is enhanced by aging as well.]

Clinical Oncology

[Metals and cancer]

VETLÉNYI Enikő, RÁCZ Gergely

[We often tend to forget about our environment when looking for the origin of a disease. Inhaled air, drinking water and food, substances in contact with the skin all have an effect on the human body. Metals are indispensable parts of our everyday lives, their mining, processing and use cause a continuous exposure to them. Metal exert their effects on the body in various ways. Many of them are essential for maintaining homeostasis, but excessive or harmful metal intake can lead to health damage, including tumour formation through multiple attack points. Metals substitute each other during different transport processes and in the structure of proteins, they cause oxidative stress and bind to DNA, thereby damaging it. Applying them appropriately, the proapoptotic effect of the metal compounds is brought to the fore, thus becoming a therapeutic tool for tumours. Nowadays, platinum(II) compounds are widely used as chemotherapeutic agents and there are many ongoing studies to fi nd metal compounds with an ideal therapeutic and side-effect profi le. The aims of this article were to draw the attention to the dangers of metals in relation to cancer and to highlight their diverse application possibilities in current and future cancer therapy and diagnostics.]

Clinical Neuroscience

[EXPERIMENTAL DEMYELINATION CAUSED BY PRIMARY OLIGODENDROCYTE DYSTROPHY Regional distribution of the lesions in the nervous system of mice brain]

KOMOLY Sámuel

[Background and purpose - Heterogeneity of multiple sclerosis lesions has been recently indicated: In addition to T-cell-mediated or T-cell plus antibody-mediated autoimmune mechanisms (patterns I-II) two other patterns (III-IV) were described. Patterns III-IV are characterized by primary oligodendrocyte dystrophy, reminiscent of virus- or toxin-induced demyelination rather than autoimmunity. It was described more than 30 years ago that dietary application of a copper-chelating agent called cuprizone results in primary oligodendrocyte degeneration which is followed by demyelination. The aim of the present study was to examine the regional distribution of cuprizone induced oligodendrocyte dystrophy and demyelination in the nervous system of mice. Material a methods - Demyelination was induced in male weanling Swis-Webster mice by feeding them on a diet containing 0.6% (W/W) cuprizone bis(cyclohexanone)-oxalyldihydrazone (G. F. Smith Chemical, Columbus OH) for 8 weeks. Animals were sacrificed after 3, 7, 14, 27, 35, 56 days of cuprizone administration. Samples were taken from corpus callosum, anterior commissure, optic nerve, cervical spinal cord and sciatic nerve. Samples were examined by immunohistochemistry, in situ hybridization for myelin proteins and myelin protein mRNA-s, respectively. Conventional neuropathological stainings and electron microscopy was also performed. Results - Oligodendrocyte degeneration and demyelination followed a particular standard pattern in the central nervous system. Profound myelin loss developed in the superior cerebellar peduncle, anterior comissure and corpus callosum, whereas the optic nerves, velum medullare anterior and spinal cord showed little or no demyelination. Sciatic nerves were unaffected. No infiltration by lymphocytes or blood-brain barrier damage was observed during cuprizone treatment. Conclusion - Cuprizone induced oligodendrocyte damage and demyelination follows a particular standard pattern in the central nervous system of mice. Cuprizone induced demyelination might be considered as a model for human demyelinating disorders with primary oligodendrocyte dystrophy and apoptosis.]