Soluble factors that promote survival and differentiation of glia and neurons during development are likely to play key roles in neurodegeneration and demyelinating diseases such as multiple sclerosis (MS) and have the potential to be important therapeutic targets. We examined the effect of trkB signaling and the expression patterns of neurotrophic and gliotrophic factors in the mouse brain in MOG-induced experimental allergic encephalomyelitis (EAE). With induction of mild disease, trkB heterozygous mice were more severely affected compared to their wild type littermates. However, with more potent disease induction, trkB heterozygotes fared similar to their wild type littermates, suggesting complex modulatory roles for trkB signaling. One possible explanation for this difference is that the expression patterns of neurotrophic factors correlate with disease severity in individual mice with mild disease, but not in more severe disease. With the less potent induction in C57BL/6 mice, we found that BDNF was consistently increased at EAE onset, while the soluble gliotrophic factor neuregulin (NRG1) was increased only in the chronic phase of the disease. Treatment of these animals with glatiramer acetate (GA) to decrease disease severity resulted in lower levels of both BDNF and NRG1 expression in some mice at 35 days after immunization compared to those in untreated EAE mice, but had no direct effect on these factors in the absence of EAE. Our results suggest a complex interplay between neurotrophic and gliotrophic factors in EAE that is dependent on disease stage and severity. While signaling by BDNF through trkB is protective in mild disease, this effect was not seen in more severe disease. The late induction of NRG1 in the chronic stage of disease could also worsen disease severity through its known ability to activate microglial, inflammatory pathways. While complex, these studies begin to define underlying axoglial trophic activities that are likely involved in both disease pathogenesis and repair.
Myelodysplastic syndromes (MDS) are a clonal hematopoietic stem cell (HSC) disorders. Cytogenetics plays a vital role in pathogenesis, diagnosis, prognosis, and determining treatments in MDS. Cytogenetic studies on CD 34 + cells in Asian MDS patients are limited. The aim of conducting this study was to compare the karyotypic features of CD 34 + cells and their bone marrow (BM) karyotypes. BM samples of 20 primary MDS patients were collected. BM-CD 34 + cells were isolated by CD34 positive selection. Conventional karyotyping was performed on primary BM samples and isolated CD 34 + cells. Fluorescence in situ hybridization (FISH) was performed to confirm del(5q) by using XL 5q31/5q33 locusspecific probe. Chromosomal abnormalities were detected in 41 % (7/17) of BM and 40 % (8/20) of HSC karyotypes. BM and HSC karyotypes were similar (94 %) except in one (BM-normal; CD 34+ cells had del(5q)) where the patient showed characteristic del(5q) phenotype. The abnormalities found were del(5q)-10 % (2/20), del(11q)-5 % (1/20), del(12p)-5 % (1/20), 47,XY,+19-5 % (1/20), hypodiploidy-5 % (1/20), and random loss of chromosomes-10 % (2/20). The percentage of abnormal metaphases counted per case was higher for CD 34 + cell cultures than for BM cultures. Culture failure were less for CD 34 + cells when compared to BM. Sample limitation for BM does not apply for CD 34 + cells if cultures can be maintained. Although the abnormal karyotypes counted were greater using CD 34 + cells than BM, there was no statistically significant difference (p > 0.05). Detection of karyotypic abnormalities could be greater when using CD 34 + cells. All the karyotypic abnormalities reported in this study had been previously known in MDS. Further large scale studies are needed to verify our findings.
Regular physical exercises have shown to improve health. Stress can cause great impact on individual's mental health as well as physical health. Plasma cortisol is used as a biomarker to measure stress. This study was carried out to evaluate the effect of long-term physical exercises on cortisol levels in healthy young men. The study was carried out on four study groups; non-exercised control group (NE), exercised for 6 months (E6M), exercised for 18 months (E18M) and exercised for 30 months (E30M). Thirty participants who underwent regular physical exercises for different time periods were included in each exercised group. Thirty controls were also recruited. Plasma cortisol was measured using ELIZA method and compared to the patterns of plasma glucose levels. Plasma cortisol levels of all exercised groups were significantly less than that of control group (p<0.05). A significant reduction of plasma cortisol level was observed in E6M (p<0.001) and E18 M (p<0.001). Plasma cortisol level of E30M was higher than E6M and E18M but less than the control group. Plasma glucose levels followed the same pattern as cortisol. The results of this study suggest that prolong exercises favorably alters the cortisol and glucose levels indicating reduced stress levels in young adults. The study clearly indicates that the prolong exercises have positive effect on the stress marker; plasma cortisol level as well as overall health of an individual.
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