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BACKGROUND AND AIMS: Biomarkers are biological indicators that permit qualitative study and quantitative evaluation of various conditions, phenomena or biological features. In modern medicine biomarkers are used for precise and relatively easy diagnosis of chronic diseases, and the assessment of likelihood of their occurrence. Nowadays, it is intensively explored research area for new therapies and biochemical, physiological, histological, morphological, or behavioral types of biomarkers are distinguished. The aim was to explain previously poorly explored correlation between biological markers of stress and neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease and systematization of knowledge. METHODS: PubMed search was used to find the available literature data, key words: biomarkers, Parkinson’s disease, Alzheimer’s disease, blood, cerebrospinal fluid. RESULTS: Parkinson’s disease (PD) is a degenerative disorder of the central nervous system that involves degeneration of dopaminergic neurons in the substantia nigra pars compacta resulting in impairing the motor skills, cognitive process and other function. However, it has been shown that noradrenergic (NAergic) cells from the locus coeruleus also degenerate in this disease. On the other hand, Alzheimer’s disease (AD) is manifested by neocortical and hippocampal atrophy, the deposition of Aβ peptides and the formation of neurofibrillar tangles. AD is a progressive degeneration of cholinergic nuclei in the basal forebrain and of NAergic nuclei in the brainstem. It is considered that neuronal loss is greater in NAergic neurons than cholinergic neurons. CONCLUSIONS: Presented is a succinct review of the role and designation of biological markers in neurodegenerative diseases.
BACKGROUND AND AIMS: This interdisciplinary project, linking neurophysiology, neuroendocrinology and psychology, aims to explore biomarkers of stress among rescue personnel under emergency situations (catastrophe) and correlating the results of psychophysical features. We expect that an catastrophe produces significant changes in the concentration of biological indicators of stress that may be related to differences in the style of coping with stress. Our hypothesis is that the differences in the concentrations of biomarkers of stress depend on the temperament and ability to learn, assessed by appropriately selected psychological tests. Furthermore, the released hormones affect behavior and, therefore, performance.  The expected results will explain and systematize knowledge about so far poorly explored correlation between the biological markers of stress and psychological parameters in selected professional group. METHODS: The harmful effect of the stressor interpreted as a threat to the individual can affect a variety of intellectual functions. According to Janis (1982) stress is the cause of disturbances in the evaluation and decision-making because it replaces creative ways of responding with rigid and stereotyped thinking (Zimbardo 1999). Activity of the endocrine system will be measured using high performance liquid chromatography (HPLC), while ability to learn, style of coping with stress and temperament would be measured using carefully selected questionnaires and psychological tests under psychologist supervision. RESULTS: In our preliminary research we found that stress associated with start of the practical driving course caused a rise in salivary cortisol that depended only on the time of sampling. CONCLUSIONS: The results may be important by contributing to the development of biological tests to assist in determining the effectiveness of performance under stress conditions. The approach is discussed in the context of current research in the world.
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Although addiction to amphetamine (AMPH) is a serious social and medical problem, the data concerning AMPH – immune interactions are still not numerous. To analyze the mechanism of AMPH-induced changes in the function of the immune system, rats were pretreated with ß-adrenergic receptor antagonist propranolol (PROP; 5 mg/kg, i.p.) prior to AMPH (1 mg/kg, i.p.) administration. Natural Killer cells cytotoxicity (NKCC) (51Cr-release assay), the number of LGLs (NK cells) (Timonen method), leukocytes, lymphocytes and monocytes, and plasma corticosterone level (CORT) (RIA) were evaluated in the peripheral blood and spleen. In the peripheral blood increases in NKCC (+331%), as well as in LGL (+33%) and monocyte (+65%) number observed after AMPH were partially inhibited by PROP (respectively by 30%, 19%, and 30%) in contrast to lymphopenia (-19%) and granulocytosis (+65%) which were not affected by ß-blockade. In the spleen AMPH-induced decreases in NKCC (-25%) and in all the leukocyte populations number (approximately -30%) were completely blocked by PROP. Plasma CORT level, highly elevated by AMPH (+337%), was attenuated nearly by 50% under ß-adrenergic blockade. These data indicate that AMPH-induced enhancement of cytotoxic activity of NK cell is related to ß-adrenergic mechanism.
To evaluate a possible mechanism of stress-induced lymphopenic effect we assessed the activity of lymphocyte lysosomal enzymes (LE) under immobilization. The effects of immobilization stress on LE (AP, acid phosphatase, cathepsin D and L, ß-N-acetyl-glucosamidase) activity in lymphocytes, number of lymphocytes and plasma cortisol (COR) level in the peripheral blood were examined in the cross-bred Pietrain pigs showing genotypic (presence or lack of RyR1 gene mutation) and phenotypic (reactivity to halothane) differences. It was found that immobilization stress evoked an increase in LE which was concomitant with lymphopenia and a rise of COR level. The most pronounced enhancement of LE, which may reflect a tendency to lymphocyte cytolysis, was found in the recessive homozygotes RyR1 (nn) phenotypically defined as stress/halothane susceptible as well as in the heterozygotes RyR1 (Nn) included in the group of stress/halothane resistant. Despite this individual variability the stress-induced increase in LE activity was present in all the animals. It seems that a possibility of destruction (lysis) of lymphocyte cells should not be excluded as one of the causes of stress lymphopenia.
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