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991.
Bone morphogenetic proteins have been implicated in the development of oligodendrocytes and astrocytes, however, a role for endogenous BMP signaling in glial development has not been demonstrated in a genetic model. Using mice in which signaling via type I BMP receptors Bmpr1a and Bmpr1b have been inactivated in the neural tube, we demonstrate that BMP signaling contributes to the maturation of glial cells in vivo. At P0, mutant mice exhibited a 25-40% decrease in GFAP+ or S100beta+ astrocytes in the cervical spinal cord. The number of oligodendrocyte precursors and the timing of their emergence was unchanged in the mutant mice compared to the normals, however myelin protein expression and mature oligodendrocyte numbers were significantly reduced. These data indicate that BMP signaling promotes the generation of astrocytes and mature, myelinating oligodendrocytes in vivo but does not affect oligodendrocyte precursor development, thus suggesting tight regulation of BMP signaling to ensure proper gliogenesis.  相似文献   
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IntroductionSleep deprivation (SD) has been used as an alternative approach to treat major depressive disorder (MDD). Caffeine, due to its stimulating effect, could be an alternative to promote sleep deprivation. However, there are no data about its potential influence on the antidepressive effect of SD. The objective of this study is to assess the effect of caffeine on SD in non-psychotic patients with moderate to severe unipolar depression.MethodsRandomized, double-blind, crossover clinical trial comparing caffeine and placebo in moderate to severe depressed patients who underwent total sleep deprivation (SD). The patients were assessed with items of the Bond–Lader scale, the 6-item Hamilton Depression Rating Scale (HAMD-6), and the Clinical Global Impression (CGI)-Severity/Improvement.ResultsTwenty patients participated in this study. The patients who consumed caffeine presented the same level of energy before and after sleep deprivation (lethargic–energetic item of the Bond–Lader scale), while the patients in the placebo group had a reduced level of energy after sleep deprivation (p = 0.0045). There was no difference between the caffeine and placebo groups in the other items of the Bond–Lader scale.ConclusionThe combined use of caffeine and SD can be a useful strategy to keep the patient awake without impairing the effect of SD on depressed outpatients. However, further studies involving patients who have responded to SD are needed in order to verify if caffeine also does not interfere with the results in this group.  相似文献   
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After acute immunoreactive infestation with the Chagas' disease parasite, Trypanosoma cruzi, some patients develop chronic megacolon, whereas others remain asymptomatic. Chronic chagasic patients with gastrointestinal involvement exhibit inflammation and degeneration of enteric neurons. Our hypothesis is that enteric glial cells may be involved in the modulation of enteric inflammatory responses or even control the colon's dilatation. The aims of this study were to characterize the phenotype of enteric glial cells according to the expression of S-100 and glial fibrillary acidic protein and to look for correlation between these data and the neuronal loss in the colon of chagasic patients. We studied both dilated and nondilated portions of chagasic megacolon. We used a pan-enteric glial cell marker (anti-S-100), a subpopulation enteric glial cell marker (anti-glial fibrillary acidic protein), and a pan-neuronal marker (anti-Human protein C and protein D) with double-labeled sheets using a confocal microscope. Our results demonstrate that neuronal loss is similar in dilated and nondilated portions of chagasic megacolon. Moreover, the results indicate that neuronal destruction present in chagasic megacolon is preceded by glial component loss. The nondilated portion of chagasic megacolon exhibited increased expression of glial fibrillary acidic protein comparable with the dilated portion and also to the noninfected group. Our results suggest that glial fibrillary acidic protein enteric glial cells prevent dilatation of the organ and protect the enteric nervous system against the inflammatory process and neuronal destruction, preventing the destruction from expanding to unaffected areas of the colon.  相似文献   
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Understanding the biochemical changes associated with various types of exercises is important, since they affect the function of different systems and the type of energy used. Analyzed separately, the clinical signs of distinct muscular alterations have a limited diagnostic value and require the use of complementary laboratory exams. Such exams are also used to evaluate the animal’s training, clinical state or athletic capacity. This study determined the serum concentrations of proteins, metabolites, minerals and serum enzymes in equines subjected to team penning contests, correlating these data with sex and frequency of physical activity. A puncture was made in the external jugular vein to collect 5 mL of blood from 29 equines, 18 males and 11 females, at rest (Group I) and after exercising (Group II). The biochemical serum analyses were carried out with a Micronal B-280 spectrophotometer using commercial kits and an automatic multichannel analyzer (Abbott Diagnostics—ARCHITECT c8000) using specific kits. The animals were divided into Groups A, B, C and D according to the number of times they participated in the contest. The serum albumin concentrations, A:G ratio and iron declined significantly (p < 0.05) after exercising, unlike the concentrations of total proteins, globulins, total calcium, uric acid, urea, creatinine, aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine kinase (CK), which increased. Females showed a higher increase of creatinine. Moreover, the rise in total protein, globulins, creatinine, AST, LDH and CK levels differed among groups A, B, C, and D. It was concluded that the team penning contest causes alterations in the biochemical serum profile of equines, and that sex and the number of participations in the contest are interferential variables.
Renata Lima de MirandaEmail:
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