Neuron-Glia Mechanisms & Interactions Underlying Opioid Abuse-HIV-1 Comorbidity

神经元-胶质细胞机制

基本信息

批准号：
8284484
负责人：
Kurt F Hauser
金额：
$ 12.91万
依托单位：
VIRGINIA COMMONWEALTH UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2009
资助国家：
美国
起止时间：
2009-07-01 至 2014-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8284484
关键词：
AIDS Dementia Complex AIDS neuropathy AIDS/HIV problem Acquired Immunodeficiency Syndrome Address Affect Apoptosis Apoptotic Appearance Area Astrocytes Award Brain region Caspase Cause of Death Cessation of life Clinical Coculture Techniques Collaborations Comorbidity Consequences of HIV Corpus striatum structure Drug abuse Epidemic Event Faculty Funding Genetic Vectors Goals Grant HIV HIV Envelope Protein gp120 HIV Infections HIV Seropositivity HIV-1 Hepatitis C virus Heroin Heroin Abuse Hippocampus (Brain)Homeostasis Human In Situ Nick-End Labeling In Vitro Independent Scientist Award Individual Infection Injury International Joints Knock-out Mediating Mentors Microglia Molecular Morphine Mus Narcotic Antagonists National Institute of Drug Abuse Nerve Degeneration Neuraxis Neuroglia Neuronal Dysfunction Neurons Neurovirology Nursing Faculty Oligodendroglia Opiates Opioid Opioid Receptor Opium Oxycodone PTEN gene Papaver Pathogenesis Pathologic Pathology Pharmaceutical Preparations Pharmacology and Toxicology Play Proteins Publishing Recruitment Activity Research Role S-nitro-N-acetylpenicillamine SCID Mice Scientist Self Administration Seminal Signal Pathway Signal Transduction Slice Students Substance abuse problem Synapses Synaptophysin System Testing Therapeutic Intervention Time Toxic effect Training Transfection Transgenic Mice Translational Research Universities Viral Load result Viral Proteins Virginia Virus analog base career caspase-3 density dosage drug abuser drug of abuse endonuclease G humanized SCID mouse in vivo macrophage monocyte mouse model neuroprotection neurotoxic neurotoxicity opioid abuse overexpression pre-doctoral progenitor receptor function responsible research conduct symposium synergism virotoxins

项目摘要

A K02 independent Scientist Award will enable the candidate to obtain maximum protected time at Virginia Commonwealth University (VCU) to pursue NIDA funded research on substance abuse-HIV-1 comorbidity, acquire advanced cross-disciplinary expertise, and to mentor student and faculty scientists in this area. Drug abuse and HIV-1 are interlinked epidemics with horrific consequences. To address this problem, the candidate directs grant P01 DAI 9398, "Opiate drug abuse and CNS vulnerability to HIV", is PI on grant ROI DA18633, "Mechanisms of opiate drug-HIV:lnduced neurodegeneration", is a co-l on a R01 DA024461 "Glial progenitors as targets of HIV/opiate interactions", is a co-l on a pending NIDA ROS grant to study opioid drug-hepatitis C virus (HCV) interactive pathology, and consultant on numerous other projects. The applicant has published seminal studies demonstrating: that opioids can directly affect CNS maturation; the cellular basis of opioid receptor and function in astrocytes and oligodendrocytes; and that opioids intrinsically exacerbate the pathogenesis of neuroAIDS-identifying both intra- and intercellular pathologic mechanisms in neurons and multiple glial types. The applicant has established worldwide collaborations that continue to optimize approaches to opioid abuse-HIV-1 comorbidity, has mentored highly successful pre- and postdoctoral, and basic and clinical faculty; including training in the responsible conduct of research (RCR), has co-directed a NIDA training grant, and organized local and international conferences promoting substance abuse research. A K02 award will enable the candidate to: (1) pursue the goals of current grants, while developing cutting-edge approaches to substance abuse (e.g., self-administration paradigms), HlV-1 (humanized SCID mouse model), and molecular neurovirology; (2) to merge basic and clinical approaches through translational research with the VCU HIV/AIDS Center and joint VCU/Johns Hopkins Univ. NIDA CTN; while continuing to mentor students/early career scientists (including under-represented individuals and an emphasis on RCR). He was recruited to VCU by the Dept. of Pharmacology and Toxicology to pursue these goals and receives tremendous support for this endeavor.

K02独立科学家奖将使候选人能够在弗吉尼亚州联邦大学（VCU）获得最大的受保护时间，以追求NIDA资助的有关滥用药物HIV-HIV-1合并症的研究，获得高级跨学科专业知识，并指导该领域的学生和教职员工。滥用药物和HIV-1是相互联系的流行病，带来了可怕的后果。为了解决这个问题，候选人指示授予P01 DAI 9398，“阿片类药物滥用和CNS易受HIV的脆弱性”，是授予ROI DA18633，“ Opiate Drugiate-HIV的机制：LNDDAGDED神经变性的机制”，是R01 DA024461“ GLIAL”的CO-L 祖细胞作为艾滋病毒/鸦片相互作用的靶标的祖细胞是对未决的NIDA ROS赠款的共同研究，以研究阿片类药物肝炎病毒C病毒（HCV）互动病理学，以及其他许多其他项目的顾问。申请人发表了精液研究，证明了：阿片类药物可以直接影响CNS的成熟； opiod opiod受体和元素的元素和元素的元素;阿片类药物本质上加剧了神经辅导的发病机理，识别神经元和多种神经胶质类型的细胞内病理机制。（RCR）与NIDA培训赠款共同指导，并组织了促进药物滥用研究的本地和国际会议。（2）合并基本和临床方法通过与VCU HIV/AIDS中心和联合VCU/Johns Hopkins Univ的翻译研究。 NIDA CTN;在继续指导学生/早期职业科学家的同时（包括代表性不足的个人和对RCR的重视）。他是由药理学和毒理学系招募到VCU的，以追求这些目标，并为这项工作提供了巨大的支持。