Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0277787 (stigma)
 13,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurological manifestations of HIV infection and AIDS are being recognized with a frequency that parallels the increasing number of AIDS cases. Next to sub-Saharan Africa, India has the second largest burden of HIV related pathology, essentially caused by HIV-1 clade C in both the geographic locales, in contrast to USA and Europe. But the true prevalence of HIV related neuroinfections and pathology is not available due to inadequate medical facilities, social stigma and ignorance that lead to underdiagnosis. Neurotuberculosis, followed by cryptococcosis and toxoplasmosis in various combinations are the major neuropathologies reflecting the endemicity and manifesting clinically by reactivation of latent infection. Discordance in the clinical prevalence of various infections, when compared to pathological studies highlight similarities in clinical, radiological modalities of diagnosis and inherent problems in establishing definitive diagnosis. Viral infections appear to be relatively rare. Inspite of heavy burden of HIV/AIDS, HIV associated neoplasia is infrequent, including primary CNS lymphomas. HIV encephalitis and HIV associated dementia are considered infrequent, though systematic studies have just been initiated in various centres. Peripheral neuropathy characteristically manifests with vasculitic neuropathy while diffuse infiltrative lymphocytosis syndrome (DILS) involving nerves has not been reported from India. Spinal cord pathology including vacuolar myelopathy is rare, even in asymptomatic cases. Till now the AIDS cases in India were drug naive but a new cohort of cases following initiation of HAART therapy as a national policy is soon emerging, altering the biology and evolution of HIV/AIDS in India. Lacunae in the epidemiology, diagnosis and study of biology of HIV/AIDS are outlined for future research.
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PMID:Neuropathology of HIV/AIDS with an overview of the Indian scene. 1581 57

Now that schizophrenia researchers may be moving from unilateral molecular genetic approaches to models including so-called gene-environment interactions, the question rises which environments may be considered for such research and how a user perspective may inform the field. It is argued that trauma and stigma, or perhaps better structural discrimination, represent 2 important environmental factors that deserve more attention. Experiential evidence, collected by users, suggests that trauma in childhood and/or adulthood, before, during, and after the onset of schizophrenia, as well as stigma/structural discrimination, may play important roles in the onset and course of the disorder. A certain reluctance on the part of the professional schizophrenia research community to take these variables as serious as, eg, interesting but inconclusive etiological signals from prenatal hypoxia, prenatal folate deficiency, and prenatal toxoplasmosis is suggested. This article outlines the concepts of trauma and stigma and their negative consequences for the onset and course of schizophrenia. The importance of research into these factors and their possible relevance for gene-environment interactions is discussed. While gene-environment interaction research using these variables is indicated and may possibly prove productive, it is argued that such efforts may not be useful if no subsequent attempt is made to translate the results to the level of interventions, codeveloped by users, eg, in the area of coping with the vicious circle of environmental adversity that users can become exposed to.
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PMID:Which environments for G x E? A user perspective on the roles of trauma and structural discrimination in the onset and course of schizophrenia. 1879 Oct 78