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We are analyzing https://link.springer.com/article/10.1007/s11481-005-9000-4.

Title:
Impact of Opiate–HIV-1 Interactions on Neurotoxic Signaling | Journal of Neuroimmune Pharmacology
Description:
Opiate drug abuse exacerbates the pathogenesis of human immunodeficiency virus-1 (HIV-1) in the central nervous system through direct actions on glia and neurons. Opiate abuse causes widespread disruption of astroglial and microglial function, and significant increases in astroglial-derived proinflammatory cytokines and chemokines, which likely contributes to neuronal dysfunction, death, and HIV encephalitis. Neurons are also directly affected by opiate–HIV-1 interactions. HIV-1 and the viral proteins gp120 and Tat activate multiple caspase-dependent and caspase-independent proapoptotic pathways in neurons involving phosphatidylinositol 3-kinase (PI3 kinase)/Akt, as well as p38, c-Jun N-terminal kinase (JNK) and/or other mitogen-activated protein kinases (MAPKs). Opiates appear to decrease the threshold for HIV-1-mediated neurotoxicity by sending convergent signals that exacerbate proapoptotic events induced by viral and cellular toxic products. The synergistic proinflammatory and neurotoxic effects of opiate drugs on glia and neurons are largely mediated through μ opioid receptors, which are expressed by subpopulations of astroglia, microglia, and neurons. Opiate abuse intrinsically modifies the host response to HIV-1. Identification of how this occurs is providing considerable insight toward understanding the mechanisms underlying HIV-1-associated dementia.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
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Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

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Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

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Keywords {🔍}

google, scholar, pubmed, cas, article, hiv, kinase, protein, cell, nath, neurons, apoptosis, hauser, human, tat, biol, activation, dementia, survival, knapp, aids, death, science, signaling, elhage, immunodeficiency, virus, neurotoxicity, regulation, neurosci, abuse, microglial, neuronal, pathways, phosphatidylinositol, morphine, exp, chem, opiate, drug, jnk, mitogenactivated, access, astrocytes, caspase, res, akt, involvement, pathway, privacy,

Topics {✒️}

c-jun n-terminal kinase altering g-protein–effector interactions ifn-gamma-inducible protein-10 expression μ opioid receptors pkb/akt-dependent cell survival month download article/chapter morphine-induced macrophage apoptosis serine/threonine protein kinases monocyte chemoattractant protein-1 mitogen-activated protein kinase mitogen-activated protein kinases protein-coupled opiate receptor fas–fas ligand interaction human microglial cells stress-activated map kinase seizure-induced neuronal death phosphatidylinositol 3-kinase/akt-dependent phosphatidylinositol 3-kinase-akt pathway protein-coupled receptors receptor-regulated mapk scaffold nerve growth factor apoptosis signal-regulating kinase pre-symptomatic hiv infection cell-intrinsic death machinery hiv-1 tat-mediated activation caspase-independent proapoptotic pathways mitogen-activated protein mu-opioid induction full article pdf hiv-1 tat-stimulated astrocytes astroglial-derived proinflammatory cytokines tat-mediated neurotoxicity gp120-induced apoptosis hiv-1-mediated neurotoxicity ca2+-dependent mechanism related subjects induced superoxide production akt protein kinase akt/protein kinase kappa-opioid modulation opioid system diversity morphine enhances interleukin-12 pi3-kinase gamma cxcr4-mediated chemotaxis human immunodeficiency virus-1 human immunodeficiency virus human immunodeficiency virus enhanced morphine analgesia morphine stimulates phagocytosis privacy choices/manage cookies

Questions {❓}

  • Anthony IC, Ramage SN, Carnie FW, Simmonds P, Bell JE (2005) Does drug abuse alter microglial phenotype and cell turnover in the context of advancing HIV infection?
  • Arango JC, Simmonds P, Brettle RP, Bell JE (2004) Does drug abuse influence the microglial response in AIDS and HIV encephalitis?

Schema {🗺️}

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         headline:Impact of Opiate–HIV-1 Interactions on Neurotoxic Signaling
         description:Opiate drug abuse exacerbates the pathogenesis of human immunodeficiency virus-1 (HIV-1) in the central nervous system through direct actions on glia and neurons. Opiate abuse causes widespread disruption of astroglial and microglial function, and significant increases in astroglial-derived proinflammatory cytokines and chemokines, which likely contributes to neuronal dysfunction, death, and HIV encephalitis. Neurons are also directly affected by opiate–HIV-1 interactions. HIV-1 and the viral proteins gp120 and Tat activate multiple caspase-dependent and caspase-independent proapoptotic pathways in neurons involving phosphatidylinositol 3-kinase (PI3 kinase)/Akt, as well as p38, c-Jun N-terminal kinase (JNK) and/or other mitogen-activated protein kinases (MAPKs). Opiates appear to decrease the threshold for HIV-1-mediated neurotoxicity by sending convergent signals that exacerbate proapoptotic events induced by viral and cellular toxic products. The synergistic proinflammatory and neurotoxic effects of opiate drugs on glia and neurons are largely mediated through μ opioid receptors, which are expressed by subpopulations of astroglia, microglia, and neurons. Opiate abuse intrinsically modifies the host response to HIV-1. Identification of how this occurs is providing considerable insight toward understanding the mechanisms underlying HIV-1-associated dementia.
         datePublished:2006-02-24T00:00:00Z
         dateModified:2006-02-24T00:00:00Z
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      headline:Impact of Opiate–HIV-1 Interactions on Neurotoxic Signaling
      description:Opiate drug abuse exacerbates the pathogenesis of human immunodeficiency virus-1 (HIV-1) in the central nervous system through direct actions on glia and neurons. Opiate abuse causes widespread disruption of astroglial and microglial function, and significant increases in astroglial-derived proinflammatory cytokines and chemokines, which likely contributes to neuronal dysfunction, death, and HIV encephalitis. Neurons are also directly affected by opiate–HIV-1 interactions. HIV-1 and the viral proteins gp120 and Tat activate multiple caspase-dependent and caspase-independent proapoptotic pathways in neurons involving phosphatidylinositol 3-kinase (PI3 kinase)/Akt, as well as p38, c-Jun N-terminal kinase (JNK) and/or other mitogen-activated protein kinases (MAPKs). Opiates appear to decrease the threshold for HIV-1-mediated neurotoxicity by sending convergent signals that exacerbate proapoptotic events induced by viral and cellular toxic products. The synergistic proinflammatory and neurotoxic effects of opiate drugs on glia and neurons are largely mediated through μ opioid receptors, which are expressed by subpopulations of astroglia, microglia, and neurons. Opiate abuse intrinsically modifies the host response to HIV-1. Identification of how this occurs is providing considerable insight toward understanding the mechanisms underlying HIV-1-associated dementia.
      datePublished:2006-02-24T00:00:00Z
      dateModified:2006-02-24T00:00:00Z
      pageStart:98
      pageEnd:105
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         AIDS
         μ-opioid receptors
         neurons
         astroglia
         microglia
         neuroimmunology
         monocyte chemoattractant protein-1 (MCP-1/CCL2)
         apoptosis
         p38 mitogen-activated protein kinase (MAPK)
         c-Jun N-terminal kinase (JNK)
         caspase-3
         Neurosciences
         Immunology
         Pharmacology/Toxicology
         Virology
         Cell Biology
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         name:Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, USA
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         name:Department of Neurology, Johns Hopkins University, Baltimore, USA
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         name:Department of Neurscience, Medical University of South Carolina, Charleston, USA
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         name:Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, USA
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         name:Spinal Cord and Brain Injury Research Center (SCoBIRC), University of Kentucky Medical Center, Lexington, USA
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            name:University of Kentucky College of Medicine
            address:
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               type:PostalAddress
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            address:
               name:Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, USA
               type:PostalAddress
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      name:Avindra Nath
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            address:
               name:Department of Neurology, Johns Hopkins University, Baltimore, USA
               type:PostalAddress
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      name:William R. Tyor
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               name:Department of Neurscience, Medical University of South Carolina, Charleston, USA
               type:PostalAddress
            type:Organization
      name:Annadora J. Bruce-Keller
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            name:University of Kentucky College of Medicine
            address:
               name:Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, USA
               type:PostalAddress
            type:Organization
            name:University of Kentucky Medical Center
            address:
               name:Spinal Cord and Brain Injury Research Center (SCoBIRC), University of Kentucky Medical Center, Lexington, USA
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      name:Pamela E. Knapp
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            name:University of Kentucky College of Medicine
            address:
               name:Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, USA
               type:PostalAddress
            type:Organization
            name:University of Kentucky Medical Center
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      name:Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, USA
      name:Spinal Cord and Brain Injury Research Center (SCoBIRC), University of Kentucky Medical Center, Lexington, USA
      name:Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, USA
      name:Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, USA
      name:Department of Neurology, Johns Hopkins University, Baltimore, USA
      name:Department of Neurscience, Medical University of South Carolina, Charleston, USA
      name:Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, USA
      name:Spinal Cord and Brain Injury Research Center (SCoBIRC), University of Kentucky Medical Center, Lexington, USA
      name:Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, USA
      name:Spinal Cord and Brain Injury Research Center (SCoBIRC), University of Kentucky Medical Center, Lexington, USA
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