414 research outputs found

    Religion and Ethnic Identity Formation in the Former Yugoslavia

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    The electrical resistance of acupuncture source points as a relevant factor for inner organ status

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    The acupuncture source points have been known in the traditional Chinese medicine for about 5000 years and various therapies and diagnostic methods have been applied using them. Studies indicate that these points also express electrical modifications, depending on the health status of the individual. Aim. The aim of the paper is to study the relevance of electrical resistance measurements in these points in distinguishing inner organ changes. The study was conducted on patients from the gastroenterological department. The electrical resistance of the source points was measured using a Wheatstone bridge, of our own manufacturing, based on certain acupuncture maps. The data was collected using disposable Ag/AgCl electrodes and the results of the measurements were compared with the standard diagnosis test results. The statistical interpretation was performed using Microsoft Excel and GraphPad. The measured electrical resistance was between 23 and 600 kilo ohms, with considerable variations from a patient to another. Patients with organ resections (gall bladder, kidney, stomach) expressed a decreased electrical resistance in the source points corresponding to these organs (the gall bladder point etc.). Also, patients with cardiac failure expressed a modified electrical resistance in the heart source point, but also in the pulmonary point, probably anticipating the pulmonary stasis consecutive to the heart disease. Gall bladder lithiasis, hepatic cirrhosis and rheumatism also expressed altered electrical resistance in the correspondent points. Patients with inner organ diseases expressed modified electrical resistance in corresponding source points. Further studies will be conducted to test the accuracy of this method to distinguish specific inner organ pathologies and to test the applicability of this measurement as a screening instrument

    Experimental ‘Jet Lag’ Inhibits Adult Neurogenesis and Produces Long-Term Cognitive Deficits in Female Hamsters

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    Background: Circadian disruptions through frequent transmeridian travel, rotating shift work, and poor sleep hygiene are associated with an array of physical and mental health maladies, including marked deficits in human cognitive function. Despite anecdotal and correlational reports suggesting a negative impact of circadian disruptions on brain function, this possibility has not been experimentally examined. Methodology/Principal Findings: In the present study, we investigated whether experimental ‘jet lag ’ (i.e., phase advances of the light:dark cycle) negatively impacts learning and memory and whether any deficits observed are associated with reductions in hippocampal cell proliferation and neurogenesis. Because insults to circadian timing alter circulating glucocorticoid and sex steroid concentrations, both of which influence neurogenesis and learning/memory, we assessed the contribution of these endocrine factors to any observed alterations. Circadian disruption resulted in pronounced deficits in learning and memory paralleled by marked reductions in hippocampal cell proliferation and neurogenesis. Significantly, deficits in hippocampal-dependent learning and memory were not only seen during the period of the circadian disruption, but also persisted well after the cessation of jet lag, suggesting long-lasting negative consequences on brain function. Conclusions/Significance: Together, these findings support the view that circadian disruptions suppress hippocampal neurogenesis via a glucocorticoid-independent mechanism, imposing pronounced and persistent impairments on learnin

    Examination of age-dependent effects of fetal ethanol exposure on behavior, hippocampal cell counts, and doublecortin immunoreactivity in rats

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    WOS: 000333998100002PubMed ID: 24302592Ethanol is known as a potent teratogen having adverse effects on brain and behavior. However, some of the behavioral deficits caused by fetal alcohol exposure and well expressed in juveniles ameliorate with maturation may suggest some kind of functional recovery occurring during postnatal development. The aim of this study was to reexamine age-dependent behavioral impairments in fetal-alcohol rats and to investigate the changes in neurogenesis and gross morphology of the hippocampus during a protracted postnatal period searching for developmental deficits and/or delays that would correlate with behavioral impairments in juveniles and for potential compensatory processes responsible for their amelioration in adults. Ethanol was delivered to the pregnant dams by intragastric intubation throughout 7-21 gestation days at daily dose of 6 g/kg. Isocaloric intubation and intact control groups were included. Locomotor activity, anxiety, and spatial learning tasks were applied to juvenile and young-adult rats from all groups. Unbiased stereological estimates of hippocampal volumes, the total number of pyramidal and granular cells, and double cortin expressing neurons were carried out for postnatal days (PDs) PD1, PD10, PD30, and PD60. Alcohol insult during second trimester equivalent caused significant deficits in the spatial learning in juvenile rats; however, its effect on hippocampal morphology was limited to a marginally lower number of granular cells in dentate gyrus (DG) on PD30. Thus, initial behavioral deficits and the following functional recovery in fetal-alcohol subjects may be due to more subtle plastic changes within the hippocampal formation but also in other structures of the extended hippocampal circuit. Further investigation is required. (c) 2013 Wiley Periodicals, Inc. Develop Neurobiol 74: 498-513, 2014METU Scientific Research Fund; Turkish Scientific and Technical Council (TUBITAK) [SBAG-107S069]; TUBITAK PhD scholarshipTurkish Scientific and Technical Council (TUBITAK) [SBAG-107S069]Contract grant sponsor: METU Scientific Research Fund.; Contract grant sponsor: Turkish Scientific and Technical Council (TUBITAK); contract grant number: SBAG-107S069 (to E.J.D.).; Contract grant sponsor: TUBITAK PhD scholarship (to B.E.C.)

    Prolonged maternal separation induces undernutrition and systemic inflammation with disrupted hippocampal development in mice

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    Objective: Prolonged maternal separation (PMS) in the first 2 wk of life has been associated with poor growth with lasting effects in brain structure and function. This study aimed to investigate whether PMS-induced undernutrition could cause systemic inflammation and changes in nutrition-related hormonal levels, affecting hippocampal structure and neurotransmission in C57BL/6J suckling mice. Methods: This study assessed mouse growth parameters coupled with insulin-like growth factor-1 (IGF-1) serum levels. In addition, leptin, adiponectin, and corticosterone serum levels were measured following PMS. Hippocampal stereology and the amino acid levels were also assessed. Furthermore, we measured myelin basic protein and synapthophysin (SYN) expression in the overall brain tissue and hippocampal SYN immunolabeling. For behavioral tests, we analyzed the ontogeny of selected neonatal reflexes. PMS was induced by separating half the pups in each litter from their lactating dams for defined periods each day (4 h on day 1, 8 h on day 2, and 12 h thereafter). A total of 67 suckling pups were used in this study. Results: PMS induced significant slowdown in weight gain and growth impairment. Significant reductions in serum leptin and IGF-1 levels were found following PMS. Total CA3 area and volume were reduced, specifically affecting the pyramidal layer in PMS mice. CA1 pyramidal layer area was also reduced. Overall hippocampal SYN immunolabeling was lower, especially in CA3 field and dentate gyrus. Furthermore, PMS reduced hippocampal aspartate, glutamate, and gammaaminobutyric acid levels, as compared with unseparated controls. Conclusion: These findings suggest that PMS causes significant growth deficits and alterations in hippocampal morphology and neurotransmission.This work was supported in part by National Institutes of Health (NIH) research grant 5R01HD053131, funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the NIH Office of Dietary Supplements, and Brazilian grants from CNPq and CAPES (Grant # RO1 HD053131). The authors would like to thank Dr. Patricia Foley for veterinarian technical support and Dr. Jose Paulo Andrade for the excellent comments and suggestions to improve this manuscript. N.S. contributed with the stereological studies. I.L.F. and R.B.O. contributed with the behavioral studies. I.L.F., R.B.O., and R.L.G. contributed with the study design, study analysis, and manuscript preparation. G.A.M. and P.B.F. contributed with neurochemical brain analyses. J.I.A.L. and G.M.A. contributed with hormonal and CRP serum analyses. D.G.C., K.M.C., and R.S.R. contributed with animal experimentation and data collection

    Meta-analysis of diffusion tensor imaging studies shows altered fractional anisotropy occurring in distinct brain areas in association with depression

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    Fractional anisotropy anomalies occurring in the white matter tracts in the brains of depressed patients may reflect microstructural changes underlying the pathophysiology of this disorder. We conducted a meta-analysis of fractional anisotropy abnormalities occurring in major depressive disorder using voxel-based diffusion tensor imaging studies. Using the Embase, PubMed and Google Scholar databases, 89 relevant data sets were identified, of which 7 (including 188 patients with major depressive disorder and 221 healthy controls) met our inclusion criteria. Authors were contacted to retrieve any additional data required. Coordinates were extracted from clusters of significant white matter fractional anisotropy differences between patients and controls. Relevant demographic, clinical and methodological variables were extracted from each study or obtained directly from authors. The meta-analysis was carried out using Signed Differential Mapping. Patients with depression showed decreased white matter fractional anisotropy values in the superior longitudinal fasciculus and increased fractional anisotropy values in the fronto-occipital fasciculus compared to controls. Using quartile and jackknife sensitivity analysis, we found that reduced fractional anisotropy in the left superior longitudinal fasciculus was very stable, with increases in the right fronto-occipital fasciculus driven by just one study. In conclusion, our meta-analysis revealed a significant reduction in fractional anisotropy values in the left superior longitudinal fasciculus, which may ultimately play an important role in the pathology of depression

    Hypericum perforatum treatment: effect on behaviour and neurogenesis in a chronic stress model in mice

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    <p>Abstract</p> <p>Background</p> <p>Extracts of <it>Hypericum perforatum </it>(St. John's wort) have been traditionally recommended for a wide range of medical conditions, in particular mild-to-moderate depression. The present study was designed to investigate the effect of Hypericum perforatum treatment in a mouse model of anxiety/depressive-like behavior, induced by chronic corticosterone administration.</p> <p>Methods</p> <p>CD1 mice were submitted to 7 weeks corticosterone administration and then behavioral tests as Open Field (OF), Novelty-Suppressed Feeding (NSF), Forced Swim Test (FST) were performed. Cell proliferation in hippocampal dentate gyrus (DG) was investigated by both 5-bromo-2'-deoxyuridine (BrdU) and doublecortin (DCX) immunohistochemistry techniques and stereological procedure was used to quantify labeled cells. Golgi-impregnation method was used to evaluate changes in dendritic spines in DG. Hypericum perforatum (30 mg/Kg) has been administered for 3 weeks and then neural development in the adult hippocampus and behavioral changes have been examined.</p> <p>Results</p> <p>The anxiety/depressive-like state due to chronic corticosterone treatment was reversed by exogenous administration of Hypericum perforatum; the proliferation of progenitor cells in mice hippocampus was significantly reduced under chronic corticosterone treatment, whereas a long term treatment with Hypericum perforatum prevented the corticosterone-induced decrease in hippocampal cell proliferation. Corticosterone-treated mice exhibited a reduced spine density that was ameliorated by Hypericum perforatum administration.</p> <p>Conclusion</p> <p>These results provide evidence of morphological adaptations occurring in mature hippocampal neurons that might underlie resilient responses to chronic stress and contribute to the therapeutic effects of chronic Hypericum perforatum treatment.</p
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