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http://dally.nimh.nih.gov/index.html

A program developed by the NIMH Laboratory of Neuropsychology for data acquisition and experimental control of neurophysiological experiments. The purpose of this website is to make it easier to access new versions of NIMH CORTEX and its supporting documents. Ultimately, it is also hoped that these pages will make it easier for users to report bugs, request enhancements, and obtain help. Download the latest version and unzip it into a new sub-directory. Then read the on-line documentation. For the new user, the User''s Manuals are invaluable in specifying system requirements and giving an overview of the features and necessary hardware. The Function reference goes into more detail about how to write experiments using NIMH CORTEX. The Demos reference is a good place for new and experienced users to start to get an idea of what NIMH CORTEX can do these days.

Proper citation: NIMH CORTEX (RRID:SCR_006837) Copy   

•   Source: SciCrunch Registry

http://cbdb.nimh.nih.gov/

THIS RESOURCE IS NO LONGER IN SERVICE, documented on February 07, 2013. A multidisciplinary neuroscience laboratory in which basic and clinical scientists work side by side exploring neural mechanisms and models of mental and cognitive function and of neuropsychiatric illness. Experiments are performed at many levels of inquiry, from basic molecular biology of the gene to clinical examinations of patients. A major area of investigation of this laboratory is the genetic mechanisms implicated in the pathogenesis of schizophrenia and its treatment. The laboratory is organized as a multi-disciplinary team of investigators with a common mission: to identify and fully characterize basic genetic and neurobiological mechanisms of schizophrenia and related cognitive and emotional disorders. The various components of this effort are centered various different units or divisions represented by groups of investigators, at various levels of training and experience, working on related experiments. The Director of the Branch and of the Genes, Cognition and Psychosis Program (GCAP) is Daniel R. Weinberger, M.D. The CBDB is the principle research laboratory in the created (2003) Genes, Cognition, and Psychosis Program (GCAP) of the NIMH. After twelve years of residing on the pastoral grounds of St. Elizabeths Hospital, in Southeast Washington, CBDB moved back to the main NIH campus in Bethesda, Maryland in 1998. While the unique setting of St. Elizabeths is irreplaceable, we have occupied beautiful new laboratories and clinic spaces that were created for us, and we are in the mainstream of NIH life.

Proper citation: NIMH Intramural Research Program Clinical Brain Disorders Branch (RRID:SCR_008728) Copy   

•   Source: SciCrunch Registry

http://intramural.nimh.nih.gov/sscc/index.html

Scientific and Statistical Computing Core of the NIMH Intramural Research Program supporting functional neuroimaging research at the NIH. This includes development of new data analysis techniques, their implementation in the AFNI software, advising researchers on the analysis methods, and instructing them in the use of software tools. Support methods: A. Provision of software for analysis for FMRI data (AFNI package: http://afni.nimh.nih.gov) * AFNI has been developed for the last 10 years by Dr Cox, et al. (6 years in Milwaukee, 4 years at NIMH) * Formal and informal instruction in the use of AFNI, including outlines of the statistical methods used in the programs * Installation of AFNI on NIH computers (Mac OS X, Unix, Linux) approximately 120 NIH systems have used AFNI in the last month (80 NIMH, 20 NINDS, 20 other) * Realtime monitoring of FMRI data at scanners * Continuing development of new modules for AFNI to meet needs of NIH researchers B. Consulting with NIH researchers about FMRI data analysis issues, concerns, and methods

Proper citation: NIMH DIRP Scientific and Statistical Computing Core (RRID:SCR_006958) Copy   

•   Source: SciCrunch Registry

http://intramural.nimh.nih.gov/gcap/index.htm

Schizophrenia related portal that aims to solve the mystery of genetic predisposition to psychosis, develop new methods for early diagnosis and prevention, and discover new treatments that will cure people suffering from it. Our objectives are to fully characterize: # neurobiological mechanisms related to susceptibility genes for schizophrenia and related clinical disorders; # genetic variation in aspects of cognition and emotionality associated with schizophrenia; and # small molecular targets for novel therapies. A unique feature of this Program is that its diverse scientific resources will be focused on a highly specific scientific agenda, that is to acquire the critical biological information about the susceptibility genes associated with schizophrenia and related illnesses. Our mission and goal, to understand the basic mechanisms of serious mental illness, has again guided us into new areas of research and to new insights. We have found evidence of new genes implicated in the cause of schizophrenia and involved in brain functions related to cognition and emotion and we have begun to explore how genes interact with each other and with the environment to individualize risk for these conditions. We are working now with over 20 genes related to schizophrenia. One of the key developments in our research over the past year has been the emergence of some targets for the development of novel therapeutics. We have discovered a new schizophrenia susceptibility gene, KCNH2, which represents the first clear target for the development of novel treatments. Just in this past year, for example, we published the first extensive statistical analysis of how schizophrenia genes may vary in their risk effects based on different genetic background (Nicodemus et al Hum Gen 2006), the first studies of schizophrenia genes interacting in effecting gene expression in brain (Lipska et al Hum Mol Genetics 2006a, Lipska et al Hum Mol Gen 2006 b); the first evidence that the mechanism of genetic association of NRG1 with schizophrenia involves a novel isoform of the gene in human brain (Law et al PNAS 2006), and the first evidence that MAOA may be linked to mood and impulse control because it effects critical mood regulatory neural networks (Meyer-Lindenberg et al PNAS 2006).

Proper citation: Genes Cognition and Psychosis Program (RRID:SCR_006292) Copy   

•   Source: SciCrunch Registry