105 research outputs found

    MEDICO ETHNOBOTANICAL PERSPECTIVES OF JYOTISMATI(CELASTRUS PANICULATUS. WILLD )- A HERBAL TRANQUILIZER

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    Jyotismati (Celastrus paniculatus)is a woody climber of vedic lore. In several studies seed oil was screened for its sedative and tranquillizing properties. But the tribal claims of other parts of jyotismati are yet to be studied. The plant jyotismati is used throughout the tribal population of India ofr wound healing, cough, insomnia, opium poisoning.The details of medico ethnobotanical aspect of the plant jyotismati and the recent researches carrying out on the plant clearly indicate that jyotismati place a key role in the healthcare system of India

    Study of HLA-Linked Genes in Paranoid Schizophrenia in an Indian Bengalee Population

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    Adaptive Immunity in Schizophrenia: Functional Implications of T Cells in the Etiology, Course and Treatment

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    Recent advances in psychoneuroimmunology relevant to schizophrenia therapeutics

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    Th17 pathway-mediated immunopathogenesis of schizophrenia : mechanisms and implications

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    Schizophrenia is a highly complex and severe neuropsychiatric disorder with an unknown etiopathology. Evidence for a dysregulated immune system in both the risk for and progression of schizophrenia has recently been overwhelming. Importantly, chronic low-grade inflammation both in the periphery and central nervous system has been shown to contribute predominantly to the pathogenesis of schizophrenia in a subset of individuals. Inflammation in the central nervous system is mediated by a range of proinflammatory cytokines, resident immune cells such as microglia, and brain infiltrating peripheral immunocompetent cells, such as T lymphocytes. Recently, Th17 cells, a subset of T helper cells have emerged as crucial players in mucosal defense against infections. It is linked to atopic, inflammatory, and autoimmune disorders. The risk factors/mechanisms leading to low-grade inflammation in schizophrenia are diverse and include infectious agents, stress, trauma, environmental toxins, genetic vulnerability, physical inactivity, obesity, poor diet, and sleep disruption. Herein, we propose that fetal programming of cellular immune components driven by intrauterine adversity can lead to the generation of long-lasting effector/memory Th17 cells. Th17 cells can disrupt the blood-brain barrier, infiltrate the central nervous system, and, along with other cytokines and microglia, lead to neuroprogression through neuroinflammation in schizophrenia

    Neuroimmunological Aberrations and Cerebral Asymmetry Abnormalities in Schizophrenia: Select Perspectives on Pathogenesis

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    Within the wide-ranging gamut of factors that comprise gene-environment interactions postulated to underlie schizophrenia, the crosstalk between environmental factors and feto-maternal immune components has been put forth as one of the important mechanisms that increase the risk towards schizophrenia in the offspring. Interestingly, immune factors have been shown to critically modulate the brain development during the prenatal stages. Moreover the past many decades, influential theoretical propositions and evidence base (albeit not unequivocally) have compellingly linked prenatal sex hormonal status to critically provoke long lasting immunological changes and subsequently affect developmental programming of cerebral asymmetry in schizophrenia. In this review, we summarize the select perspectives emphasizing the role of neuroimmunoendocrine pathways in anomalous cerebral asymmetry in contemporary understanding of schizophrenia pathogenesis

    Functional implications of the IL-23/IL-17 immune axis in schizophrenia

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