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        <title>Journal of NeuroImmune Pharmacology via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Journal of NeuroImmune Pharmacology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Journal+of+NeuroImmune+Pharmacology&t=Journal+of+NeuroImmune+Pharmacology&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 14:04:20 +0100</lastBuildDate>
        <item>
            <title>Not Just Another Jigsaw Puzzle</title>
            <link>http://www.medworm.com/index.php?rid=5638595&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Flqw545v668313164%2F</link>
            <description>Content Type Journal ArticleCategory News &amp; ViewsPages 1-2DOI 10.1007/s11481-012-9341-8

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5638595</comments>
            <pubDate>Tue, 24 Jan 2012 07:52:32 +0100</pubDate>
            <guid isPermaLink="false">5638595</guid>        </item>
        <item>
            <title>CXCL12 Signaling in the Development of the Nervous System</title>
            <link>http://www.medworm.com/index.php?rid=5638594&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F50137q7357141627%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Chemokines are small, secreted proteins that have been shown to be important regulators of leukocyte trafficking and inflammation.
 All the known effects of chemokines are transduced by action at a family of G protein coupled receptors. Two of these receptors,
 CCR5 and CXCR4, are also known to be the major cellular receptors for HIV-1. Consideration of the evolution of the chemokine
 family has demonstrated that the chemokine Stromal cell Derived Factor-1 or SDF1 (CXCL12) and its receptor CXCR4 are the most
 ancient members of the family and existed in animals prior to the development of a sophisticated immune system. Thus, it appears
 that the original function of chemokine signaling was in the regulation of stem cell trafficking and development. CXCR4 signaling
 is i...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5638594</comments>
            <pubDate>Tue, 24 Jan 2012 07:52:32 +0100</pubDate>
            <guid isPermaLink="false">5638594</guid>        </item>
        <item>
            <title>Neuroinflammation and Cognitive Dysfunction in Chronic Disease and Aging</title>
            <link>http://www.medworm.com/index.php?rid=5620266&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F32x113444753568n%2F</link>
            <description>Content Type Journal ArticleCategory GUEST COMMENTARYPages 1-4DOI 10.1007/s11481-011-9340-1Authors
		Amy M. Hein, Department of Neurobiology &amp; Anatomy, University of Rochester School of Medicine &amp; Dentistry, 601 Elmwood Avenue, Box 603, Rochester, NY 14642, USAM. Kerry O’Banion, Department of Neurobiology &amp; Anatomy, University of Rochester School of Medicine &amp; Dentistry, 601 Elmwood Avenue, Box 603, Rochester, NY 14642, USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620266</comments>
            <pubDate>Wed, 18 Jan 2012 06:48:10 +0100</pubDate>
            <guid isPermaLink="false">5620266</guid>        </item>
        <item>
            <title>Anti-Inflammatory Efficacy of Dexamethasone and Nrf2 Activators in the CNS Using Brain Slices as a Model of Acute Injury</title>
            <link>http://www.medworm.com/index.php?rid=5620267&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F6383506x15570q41%2F</link>
            <description>In conclusion, brain slices were amenable to pharmacological
 modification as demonstrated by anti-inflammatory activity with dexamethasone. The utilization of Nrf2 activators to limit
 inflammatory mediators within the CNS requires further investigation. Inactivity in CNS tissue, however, suggests their safe
 use without neurological side-effects in treating non-CNS disorders. Short-term CNS explants may provide a more accurate model
 of in vivo conditions than microglia cultures since the complex tissue microenvironment is maintained.
 
 
	Content Type Journal ArticleCategory ORIGINAL ARTICLEPages 1-13DOI 10.1007/s11481-011-9338-8Authors
		David J. Graber, Department of Pathology, Dartmouth Medical School, Lebanon, NH 03756, USAWilliam F. Hickey, Department of Pathology, Dartmouth Medica...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620267</comments>
            <pubDate>Tue, 17 Jan 2012 07:12:18 +0100</pubDate>
            <guid isPermaLink="false">5620267</guid>        </item>
        <item>
            <title>Nitric Oxide Decreases the Enzymatic Activity of Insulin Degrading Enzyme in APP/PS1 Mice</title>
            <link>http://www.medworm.com/index.php?rid=5582047&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F021203ng9k320162%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Nitric oxide has been implicated in the regulation of enzyme activity, particularly the activity of metalloproteinases. Since
 the inducible form of the nitric oxide synthase (NOS2), is upregulated in Alzheimer’s disease, we investigated the activity
 of two amyloid β degrading enzymes, IDE and neprilysin. In vitro we demonstrated that the activity of IDE was inhibited by
 *NO donor Sin-1, whereas activity of neprilysin remained unaffected. In vivo the activity of insulin-degrading enzyme was
 lowered in APP/PS1 mice, but not in APP/PS1/NOS2(−/−) mice. These data suggest that NOS2 upregulation impairs amyloid β degradation
 through negative regulation of IDE activity and thus loss of NOS2 activity will positively influence amyloid β clearance.
 
 
	Content Type...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5582047</comments>
            <pubDate>Sat, 07 Jan 2012 06:45:03 +0100</pubDate>
            <guid isPermaLink="false">5582047</guid>        </item>
        <item>
            <title>Can Humanized Mice Reflect the Complex Pathobiology of HIV-Associated Neurocognitive Disorders?</title>
            <link>http://www.medworm.com/index.php?rid=5582048&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp1jv14371234u555%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;There is a rebirth of humanized mouse models in reflecting human immunodeficiency virus (HIV) pathobiology. This has allowed
 new investigations of viral diversity, immunity and developmental therapeutics. In the past, HIV infection and disease were,
 in part, mirrored in immune deficient mice reconstituted with human hematopoietic stem cells. What remained from early studies
 reflected the ability to mirror central nervous system (CNS) disease. As the wide spread use of combination antiretroviral
 therapies has changed the severity, but not prevalence, of HIV-associated neurocognitive disorders (HAND), mimicking such
 virus-induced CNS morbidities in humanized animals is essential for HIV/AIDS research activities. To this end, we now review
 the evidence for how and un...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5582048</comments>
            <pubDate>Fri, 06 Jan 2012 06:43:35 +0100</pubDate>
            <guid isPermaLink="false">5582048</guid>        </item>
        <item>
            <title>Low-Dose Memantine Attenuated Morphine Addictive Behavior Through its Anti-Inflammation and Neurotrophic Effects in Rats</title>
            <link>http://www.medworm.com/index.php?rid=5552452&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fett57x6k67771421%2F</link>
            <description>In this study,
 we evaluated whether a low dose of memantine prevents opioid-induced drug-seeking behavior in rats and analyzed its mechanism.
 A conditioned-place-preference test was used to investigate the morphine-induced drug-seeking behaviors in rats. We found
 that a low-dose (0.2–1&amp;nbsp;mg/kg) of subcutaneous memantine significantly attenuated the chronic morphine-induced place-preference
 in rats. To clarify the effects of chronic morphine and low-dose memantine, serum and brain levels of cytokines and brain-derived
 neurotrophic factor (BDNF) were measured. After 6&amp;nbsp;days of morphine treatment, cytokine (IL-1β, IL-6) levels had significantly
 increased in serum; IL-1β and IL-6 mRNA levels had significantly increased in the nucleus accumbens and medial prefrontal
 cortex, bo...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552452</comments>
            <pubDate>Wed, 28 Dec 2011 16:47:19 +0100</pubDate>
            <guid isPermaLink="false">5552452</guid>        </item>
        <item>
            <title>Early Minocycline Treatment Prevents a Decrease in Striatal Dopamine in an SIV Model of HIV-Associated Neurological Disease</title>
            <link>http://www.medworm.com/index.php?rid=5552454&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy410v539n767q7mv%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;HIV-infected individuals, even with antiretroviral therapy, often display cognitive, behavioral and motor abnormalities and
 have decreased dopamine (DA) levels. Minocycline prevents encephalitis and neurodegeneration in SIV models, suggesting that
 it might also protect against nigrostriatal dopaminergic system dysfunction. Using an SIV/macaque model of HIV-associated
 CNS disease, we demonstrated that striatal levels of DA were significantly lower in macaques late in infection and that levels
 of the metabolite DOPAC also tended to be lower. DA levels declined more than its metabolites, indicating a dysregulation
 of DA production or catabolism. Minocycline treatment beginning at 12 but not 21&amp;nbsp;days postinoculation prevented striatal DA
 loss. DA decline was not d...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552454</comments>
            <pubDate>Mon, 26 Dec 2011 06:32:43 +0100</pubDate>
            <guid isPermaLink="false">5552454</guid>        </item>
        <item>
            <title>Chronological Age Impacts Immunotherapy and Monocyte Uptake Independent of Amyloid Load</title>
            <link>http://www.medworm.com/index.php?rid=5552453&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fyg51316620k1r081%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;One vexing issue in biomedical research is the failure of many therapies to translate from success in animal models to effective
 treatment of human disease. One significant difference between the animal models and the human disease is the age of the subject.
 Cancer, stroke and Alzheimer’s occur mainly in humans beyond the 75% mean survival age, while most mouse models use juvenile
 or young adult animals. Here we compare two mouse models of amyloid deposition, the Tg2576 APP model and the more aggressive
 APP+PS1 model in which a mutant presenilin1 gene is overexpressed with Tg2576. Middle-aged APP+PS1 mice and aged APP mice
 have similar degrees of amyloid pathology with a few differences that may partially explain some of the differences between
 the two age cohor...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552453</comments>
            <pubDate>Mon, 26 Dec 2011 06:32:43 +0100</pubDate>
            <guid isPermaLink="false">5552453</guid>        </item>
        <item>
            <title>Inhibition of TLR Ligand- and Interferon Gamma-Induced Murine Microglial Activation by Panax Notoginseng</title>
            <link>http://www.medworm.com/index.php?rid=5538206&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj14630261t156814%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Among the many products which influence microglial activation and resulting neuroinflammation, herbal medicine has recently
 drawn much attention due to its immunomodulatory and neuroprotective activities. The purpose of the current study was to investigate
 the effects of an extract of Panax notoginseng (NotoG™) on TLR ligand- and IFNγ-induced activation in N9 and EOC20 microglial cells lines. NotoG suppressed microglial activation
 as measured by reduced expression of accessory molecules (CD40 and CD86), decreased production of inflammatory mediators (IL-6
 and TNFα), and diminished release of antibacterial products (nitric oxide). Furthermore, this immunosuppressive activity was
 neither dependent on the glucocorticoid receptor, nor the result of a single ginseno...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538206</comments>
            <pubDate>Tue, 20 Dec 2011 06:43:16 +0100</pubDate>
            <guid isPermaLink="false">5538206</guid>        </item>
        <item>
            <title>Repulsive Guidance Molecule-a and Demyelination: Implications for Multiple Sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=5538207&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr131611h7q66mx73%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Drug development for neurodegenerative and neuroinflammatory diseases such as multiple sclerosis and traumatic brain injury
 is challenging. One promising strategy is to target a molecule with multiple biological actions affecting divergent pathophysiological
 disease phases simultaneously since these diseases arise from multiple pathological phases. In recent years, we pursued this
 strategy with a focus on multiple sclerosis and spinal cord injury and found that repulsive guidance molecule-a (RGMa) inhibits
 regeneration of injured CNS axons following spinal cord injury. We also found that RGMa enhances CD4+ T cell activation facilitating CNS demyelination in an animal model of MS, mouse experimental autoimmune encephalomyelitis
 (EAE), which supports the idea that RG...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538207</comments>
            <pubDate>Tue, 20 Dec 2011 06:43:14 +0100</pubDate>
            <guid isPermaLink="false">5538207</guid>        </item>
        <item>
            <title>Chronic IL-1β-Mediated Neuroinflammation Mitigates Amyloid Pathology in a Mouse Model of Alzheimer’s Disease without Inducing Overt Neurodegeneration</title>
            <link>http://www.medworm.com/index.php?rid=5515588&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fkv820046j6816385%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Neuroinflammation is a local tissue response to injurious stimuli in the central nervous system (CNS) and is characterized
 by glial reactivity, induction of cytokines and chemokines, and vascular permeability. The cytokine interleukin (IL)-1β is
 rapidly induced following CNS insult, and is chronically expressed in neurodegenerative disorders such as Alzheimer’s disease
 (AD). We recently developed a novel method of sustained IL-1β production in the brain to study the link between IL-1β and
 AD pathogenesis. Utilizing this model, we have previously demonstrated reduction of plaque size and frequency accompanied
 by a robust neuroinflammatory response. These observations were limited to a single early time point in the course of AD plaque
 deposition and did not in...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515588</comments>
            <pubDate>Fri, 16 Dec 2011 06:53:07 +0100</pubDate>
            <guid isPermaLink="false">5515588</guid>        </item>
        <item>
            <title>Monocyte Mobilization, Activation Markers, and Unique Macrophage Populations in the Brain: Observations from SIV Infected Monkeys Are Informative with Regard to Pathogenic Mechanisms of HIV Infection in Humans</title>
            <link>http://www.medworm.com/index.php?rid=5515589&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F724k2m387646uw25%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Non-human primate models of AIDS and neuroAIDS have been useful to study AIDS in humans in general and neuroAIDS in particular.
 Important information concerning target cells of infection, mechanisms of immune activation and pathology and cell traffic
 has been made in non-human primate models. To date observations in SIV infected monkey models have predicted or paralleled
 monocyte/macrophage biology with HIV infection and neuroAIDS. In this brief review we discuss a CD8+ T lymphocyte depletion
 model of rapid AIDS which results in a high incidence of SIV encephalitis. Specifically we review recent observations we have
 made using this model concerning monocyte turnover, monocyte/macrophage activation, macrophage derived biomarkers of disease
 and novel therapeutic app...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515589</comments>
            <pubDate>Tue, 13 Dec 2011 17:04:27 +0100</pubDate>
            <guid isPermaLink="false">5515589</guid>        </item>
        <item>
            <title>Suppression of Immunodeficiency Virus-Associated Neural Damage by the p75 Neurotrophin Receptor Ligand, LM11A-31, in an In Vitro Feline Model</title>
            <link>http://www.medworm.com/index.php?rid=5495000&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ftn718j4g247w3246%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Feline immunodeficiency virus (FIV) infection like human immunodeficiency virus (HIV), produces systemic and central nervous
 system disease in its natural host, the domestic cat, that parallels the pathogenesis seen in HIV-infected humans. The ability
 to culture feline nervous system tissue affords the unique opportunity to directly examine interactions of infectious virus
 with CNS cells for the development of models and treatments that can then be translated to a natural infectious model. To
 explore the therapeutic potential of a new p75 neurotrophin receptor ligand, LM11A-31, we evaluated neuronal survival, neuronal
 damage and calcium homeostasis in cultured feline neurons following inoculation with FIV. FIV resulted in the gradual appearance
 of dendritic beadin...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5495000</comments>
            <pubDate>Fri, 09 Dec 2011 17:04:26 +0100</pubDate>
            <guid isPermaLink="false">5495000</guid>        </item>
        <item>
            <title>Genetic Knockouts Suggest a Critical Role for HIV Co-Receptors in Models of HIV gp120-Induced Brain Injury</title>
            <link>http://www.medworm.com/index.php?rid=5457945&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fu320265304548755%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Infection with HIV-1 frequently affects the brain and causes NeuroAIDS prior to the development of overt AIDS. The HIV-1 envelope
 protein gp120 interacts with host CD4 and chemokine co-receptors to initiate infection of macrophages and lymphocytes. In
 addition, the virus or fragments of it, such as gp120, cause macrophages to produce neurotoxins and trigger neuronal injury
 and apoptosis. Moreover, the two major HIV co-receptors, the chemokine receptors CCR5 and CXCR4, serve numerous physiological
 functions and are widely expressed beyond immune cells, including cells in the brain. Therefore, HIV co-receptors are poised
 to play a direct and indirect part in the development of NeuroAIDS. Although rodents are not permissive to infection with
 wild type HIV-1, viral co...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5457945</comments>
            <pubDate>Mon, 28 Nov 2011 16:59:01 +0100</pubDate>
            <guid isPermaLink="false">5457945</guid>        </item>
        <item>
            <title>Amyloid Precursor Protein Expression Modulates Intestine Immune Phenotype</title>
            <link>http://www.medworm.com/index.php?rid=5457946&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F38w8160l367618q0%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Amyloid precursor protein (APP) is widely expressed across many tissue and cell types. Proteolytic processing of the protein
 gives rise to a plethora of protein fragments with varied biological activities. Although a large amount of data has been
 generated describing the metabolism of the protein in neurons, its role in regulating the phenotype of other cells remains
 unclear. Based upon prior work demonstrating that APP regulates the activation phenotype of monocytic lineage cells, we hypothesized
 that APP can regulate macrophage activation phenotype in tissues other than brain. Ileums of the small intestines from C57BL6/J
 wild type and APP−/− mice were compared as a representative tissue normally associated with abundant macrophage infiltration. APP−/− int...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5457946</comments>
            <pubDate>Mon, 28 Nov 2011 16:59:00 +0100</pubDate>
            <guid isPermaLink="false">5457946</guid>        </item>
        <item>
            <title>Morphine and gp120 Toxic Interactions in Striatal Neurons are Dependent on HIV-1 Strain</title>
            <link>http://www.medworm.com/index.php?rid=5431875&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F6020qx40u36uk8lw%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;A rigorously controlled, cell culture paradigm was used to assess the role of HIV-1 gp120 ± morphine in mediating opioid-HIV
 interactive toxicity in striatal neurons. Computerized time-lapse microscopy tracked the fate of individual neurons co-cultured
 with mixed-glia from mouse striata during opioid and gp120 exposure. Subpopulations of neurons and astroglia displayed μ-opioid
 receptor, CXCR4, and CCR5 immunoreactivity. While gp120 alone was or tended to be neurotoxic irrespective of whether X4-tropic
 gp120IIIB, R5-tropic gp120ADA, or dual-tropic gp120MN was administered, interactive toxicity with morphine differed depending on HIV-1 strain. For example, morphine only transiently
 exacerbated gp120IIIB-induced neuronal death; however, in combination with gp120MN,...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5431875</comments>
            <pubDate>Fri, 18 Nov 2011 17:33:18 +0100</pubDate>
            <guid isPermaLink="false">5431875</guid>        </item>
        <item>
            <title>Behavioral and Molecular Evidence for a Feedback Interaction Between Morphine and HIV-1 Viral Proteins</title>
            <link>http://www.medworm.com/index.php?rid=5408394&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd203617871565374%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Morphine use and addiction is common among HIV infected individuals. There is an abundance of research supporting the effects
 of morphine and other mu opioid receptor (MOR) ligands, on the function of HIV-1 viral proteins and progression of HIV-1 viral
 infection to AIDS. On the other hand, there is much less research that investigates the possible effects of the persistent
 presence of HIV-1 viral proteins on the expression of the MOR and the analgesic and rewarding effects of MOR ligands such
 as morphine. While researchers have made a great deal of progress in the past several years, the overall investigation of
 the interaction between opiates such as morphine and HIV-1 viral proteins is largely unilateral. It has become widely accepted
 that drugs of abuse interac...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5408394</comments>
            <pubDate>Mon, 14 Nov 2011 16:52:40 +0100</pubDate>
            <guid isPermaLink="false">5408394</guid>        </item>
        <item>
            <title>MicroRNAs in Opioid Pharmacology</title>
            <link>http://www.medworm.com/index.php?rid=5408395&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F5p3203707h4202p1%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;MicroRNAs (miRNA), a class of ~22-nucleotide RNA molecules, are important gene regulators that bind to the target sites of
 mRNAs to inhibit the gene expressions either through translational inhibition or mRNA destabilization. There are growing evidences
 that miRNAs have played several regulatory roles in opioid pharmacology. Like other research fields such as cancer biology,
 the area where numerous miRNAs are found to be involved in gene regulation, we assume that in opioid studies including research
 fields of drug additions and opioid receptor regulation, there may be more miRNAs waiting to be discovered. This review will
 summarize our current knowledge of miRNA functions on opioids biology and briefly describe future research directions of miRNAs
 related to opio...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5408395</comments>
            <pubDate>Tue, 08 Nov 2011 16:49:41 +0100</pubDate>
            <guid isPermaLink="false">5408395</guid>        </item>
        <item>
            <title>Trace Amine Associated Receptor 1 Signaling in Activated Lymphocytes</title>
            <link>http://www.medworm.com/index.php?rid=5360535&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F436848746477m5l8%2F</link>
            <description>This study reports TAAR1 expression, signaling and functionality in rhesus monkey
 lymphocytes. We detected a high level of TAAR1 protein in immortalized rhesus monkey B cell lines and a significant upregulation
 of TAAR1 protein expression in rhesus monkey lymphocytes following PHA treatment. Through screening a wide range of signaling
 pathways for their upregulation following TAAR1 activation by its potent agonist methamphetamine, we identified two transcription
 factors, CREB and NFAT, which are commonly associated with immune activation. Furthermore, we observed a TAAR1-dependent phosphorylation
 of PKA and PKC following treatment with methamphetamine in transfected HEK293 cells, immortalized rhesus monkey B cells and
 PHA-activated rhesus monkey lymphocytes. Accordingly, the high lev...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5360535</comments>
            <pubDate>Fri, 28 Oct 2011 17:12:31 +0100</pubDate>
            <guid isPermaLink="false">5360535</guid>        </item>
        <item>
            <title>[11C]DAC-PET for Noninvasively Monitoring Neuroinflammation and Immunosuppressive Therapy Efficacy in Rat Experimental Autoimmune Encephalomyelitis Model</title>
            <link>http://www.medworm.com/index.php?rid=5360534&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc4p7413260157777%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Neuroimaging measures have potential for monitoring neuroinflammation to guide treatment before the occurrence of significant
 functional impairment or irreversible neuronal damage in multiple sclerosis (MS). N-Benzyl-N-methyl-2-(7-[11C]methyl-8-oxo-2-phenyl-7,8-dihydro-9H-purin-9-yl) acetamide ([11C]DAC), a new developed positron emission tomography (PET) probe for translocator protein 18&amp;nbsp;kDa (TSPO), has been adopted
 to evaluate the neuroinflammation and treatment effects of experimental autoimmune encephalomyelitis (EAE), an animal model
 of MS. [11C]DAC-PET enabled visualization of neuroinflammation lesion of EAE by tracing TSPO expression in the spinal cords; the maximal
 uptake value reached in day 11 and 20 EAE rats with profound inflammatory cell infiltrati...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5360534</comments>
            <pubDate>Fri, 28 Oct 2011 17:12:31 +0100</pubDate>
            <guid isPermaLink="false">5360534</guid>        </item>
        <item>
            <title>Discrepant Effects of Human Interferon-gamma on Clinical and Immunological Disease Parameters in a Novel Marmoset Model for Multiple Sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=5336063&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F163372653117286h%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The core pathogenic process in the common marmoset model of multiple sclerosis (MS) is the activation of memory-like T cells
 specific for peptide 34 to 56 derived from the extracellular domain of myelin/oligodendrocyte glycoprotein (MOG34-56). Immunization with MOG34-56 in incomplete Freund’s adjuvant is a sufficient stimulus for in vivo activation of these T cells, together with the induction
 of MS-like disease and CNS pathology. Ex vivo functional characteristics of MOG34-56 specific T cells are specific cytolysis of peptide pulsed target cells and high IL-17A production. To indentify possible
 functions in this new model of T helper 1 cells, which play a central pathogenic role in MS models induced with complete Freund’s
 adjuvant, we tested the effect of human...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5336063</comments>
            <pubDate>Wed, 19 Oct 2011 15:52:37 +0100</pubDate>
            <guid isPermaLink="false">5336063</guid>        </item>
        <item>
            <title>Drugs of Abuse Effects on Immunity and Microbial Pathogenesis</title>
            <link>http://www.medworm.com/index.php?rid=5324157&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F82n5806670071878%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Substance abuse remains a serious medical, public health, and social problem. The impact on destructive public health and
 health costs compounded with the negative consequences of drugs abuse poses a significant toll on the economy. Despite significant
 advancement of research in the field treatment of and care of patients with substance abuse has lagged behind because of limited
 education and training of clinicians on substance abuse problems. The goal of the special issue is to provide the current
 status on the mechanisms underlying the increased prevalence of opportunistic infections in the drug abuse population, to
 identify important areas where further research would be beneficial and to open new avenues of investigation for therapeutic
 development. We aimed t...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5324157</comments>
            <pubDate>Thu, 13 Oct 2011 15:48:32 +0100</pubDate>
            <guid isPermaLink="false">5324157</guid>        </item>
        <item>
            <title>Mice Chronically Infected with Chimeric HIV Resist Peripheral and Brain Superinfection: A Model of Protective Immunity to HIV</title>
            <link>http://www.medworm.com/index.php?rid=5314698&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F20j50617665020v5%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Infection by some viruses induces immunity to reinfection, providing a means to identify protective epitopes. To investigate
 resistance to reinfection in an animal model of HIV disease and its control, we employed infection of mice with chimeric HIV,
 EcoHIV. When immunocompetent mice were infected by intraperitoneal (IP) injection of EcoHIV, they resisted subsequent secondary
 infection by IP injection, consistent with a systemic antiviral immune response. To investigate the potential role of these
 responses in restricting neurotropic HIV infection, we established a protocol for efficient EcoHIV expression in the brain
 following intracranial (IC) inoculation of virus. When mice were inoculated by IP injection and secondarily by IC injection,
 they also controlled Ec...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5314698</comments>
            <pubDate>Mon, 10 Oct 2011 15:05:10 +0100</pubDate>
            <guid isPermaLink="false">5314698</guid>        </item>
        <item>
            <title>Drugs of Abuse and the Immune System in Perspective</title>
            <link>http://www.medworm.com/index.php?rid=5304593&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw030416716276k2r%2F</link>
            <description>Content Type Journal ArticleCategory PERSPECTIVEPages 1-3DOI 10.1007/s11481-011-9319-yAuthors
		Phillip K. Peterson, Infectious Diseases and International Medicine Division, Department of Medicine, University of Minnesota Medical School, Minneapolis, MN 55415, USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5304593</comments>
            <pubDate>Thu, 06 Oct 2011 15:42:02 +0100</pubDate>
            <guid isPermaLink="false">5304593</guid>        </item>
        <item>
            <title>IL-23 in Infections, Inflammation, Autoimmunity and Cancer: Possible Role in HIV-1 and AIDS</title>
            <link>http://www.medworm.com/index.php?rid=5260974&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F9358652545530l23%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The growing family of interleukin (IL)-12-like cytokines produced by activated macrophages and dendritic cells became the
 important players in the control of infections, development of inflammation, autoimmunity and cancer. However, the role of
 one of them—heterodimer IL-23, which consists of IL12p40 and the unique p19 subunit in HIV-1 infection pathogenesis and progression
 to AIDS, represent special interest. We overviewed findings of IL-23 involvement in control of peripheral bacterial pathogens
 and opportunistic infection, central nervous system (CNS) viral infections and autoimmune disorders, and tumorogenesis, which
 potentially could be applicable to HIV-1 and AIDS.
 
 
	Content Type Journal ArticleCategory INVITED REVIEWPages 1-18DOI 10.1007/s11481-011-9315...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260974</comments>
            <pubDate>Fri, 23 Sep 2011 05:56:10 +0100</pubDate>
            <guid isPermaLink="false">5260974</guid>        </item>
        <item>
            <title>Influence of Endogenous Opioid Systems on T Lymphocytes as Assessed by the Knockout of Mu, Delta and Kappa Opioid Receptors</title>
            <link>http://www.medworm.com/index.php?rid=5260975&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F8k42822258666417%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Here, we evaluated the influence of endogenous opioid activation on immune responses by examining consequences of all three
 opioid receptor gene (mu, delta and kappa) inactivation. In triple-opioid receptor knockout mice, splenocytes and thymocytes
 numbers, lymphocyte subsets as well as proliferation and cytokines induced by in vitro stimulation of T lymphocytes were measured.
 Compared with wild-type mice, similar lymphocyte distribution in thymus and spleen as well as comparable T lymphocyte proliferation
 were observed, while lower levels of IL-2 and IFNγ as well as higher levels of IL-4 and IL-10 were found in triple-opioid
 receptor knockout mice. Together, our results indicate a shift from TH1 to TH2 cytokines in triple-opioid receptor knockout
 animals, sugges...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260975</comments>
            <pubDate>Thu, 22 Sep 2011 05:52:27 +0100</pubDate>
            <guid isPermaLink="false">5260975</guid>        </item>
        <item>
            <title>Non-Steroidal Anti-Inflammatory Drugs and Cognitive Function: Are Prostaglandins at the Heart of Cognitive Impairment in Dementia and Delirium ?</title>
            <link>http://www.medworm.com/index.php?rid=5237988&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fhu45x1q6667q434h%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Studies of non-steroidal anti-inflammatory drugs (NSAIDs) in rheumatoid arthritis imply that inflammation is important in
 the development of Alzheimer’s disease (AD). However, these drugs have not alleviated the symptoms of AD in those who have
 already developed dementia. This suggests that the primary mediator targeted by these drugs, PGE2, is not actively suppressing
 memory function in AD. Amyloid-β oligomers appear to be important for the mild cognitive changes seen in AD transgenic mice,
 yet amyloid immunotherapy has also proven unsuccessful in clinical trials. Collectively, these findings indicate that NSAIDs
 may target a prodromal process in mice that has already passed in those diagnosed with AD, and that synaptic and neuronal
 loss are key determinants o...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5237988</comments>
            <pubDate>Mon, 19 Sep 2011 15:40:31 +0100</pubDate>
            <guid isPermaLink="false">5237988</guid>        </item>
        <item>
            <title>Cognitive and Behavioral Consequences of Impaired Immunoregulation in Aging</title>
            <link>http://www.medworm.com/index.php?rid=5237989&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F0601788212634283%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;A hallmark of the aged immune system is impaired immunoregulation of the innate and adaptive immune system in the periphery
 and also in the central nervous system (CNS). Impaired immunoregulation may predispose older individuals to an increased frequency
 of peripheral infections with concomitant cognitive and behavioral complications. Thus, normal aging is hypothesized to alter
 the highly coordinated interactions between the immune system and the brain. In support of this notion, mounting evidence
 in rodent models indicate that the increased inflammatory status of the brain is associated with increased reactivity of microglia,
 the innate immune cells of the CNS. Understanding how immunity is affected with age is important because CNS immune cells
 play an integral ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5237989</comments>
            <pubDate>Mon, 19 Sep 2011 15:40:30 +0100</pubDate>
            <guid isPermaLink="false">5237989</guid>        </item>
        <item>
            <title>Delineating HIV-Associated Neurocognitive Disorders Using Transgenic Models: The Neuropathogenic Actions of Vpr</title>
            <link>http://www.medworm.com/index.php?rid=5225966&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx75h188857760873%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;HIV-associated neurocognitive disorders (HAND) represent a constellation of neurological disabilities defined by neuropsychological
 impairments, neurobehavioral abnormalities and motor deficits. To gain insights into the mechanisms underlying the development
 of these disabilities, several transgenic models have been developed over the past two decades, which have provided important
 information regarding the cellular and molecular factors contributing to the neuropathogenesis of HAND. Herein, we concentrate
 on the neuropathogenic effects of HIV-1 Vpr expressed under the control of c-fms, resulting transgene expression in myeloid cells in both the central and peripheral nervous systems. Vpr’s actions, possibly
 through its impact on cell cycle machinery, in brain cu...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5225966</comments>
            <pubDate>Wed, 14 Sep 2011 16:08:33 +0100</pubDate>
            <guid isPermaLink="false">5225966</guid>        </item>
        <item>
            <title>Lower Glial Metabolite Levels in Brains of Young Children with Prenatal Nicotine Exposure</title>
            <link>http://www.medworm.com/index.php?rid=5225967&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh14368lhq787n244%2F</link>
            <description>This study aims to determine the effects of prenatal nicotine exposure (PNE) on
 brain metabolite levels in young (3–4&amp;nbsp;years old) children, using proton magnetic resonance spectroscopy (1H MRS). Twenty-six children with PNE and 24 nicotine-unexposed children (controls) were evaluated with a structured examination,
 a battery of neuropsychological tests, and MRI/1H MRS (without sedation). Concentrations of N-acetyl compounds (NA), total creatine (tCR), choline-containing compounds (CHO), myo-inositol (MI), and glutamate+glutamine (GLX) were measured in four brain regions. Children with PNE had similar performance
 to controls on neuropsychological testing. However, compared to controls, the PNE group had lower MI (repeated measures ANOVA—p = 0.03) and tCr levels (repeated measu...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5225967</comments>
            <pubDate>Mon, 12 Sep 2011 15:52:36 +0100</pubDate>
            <guid isPermaLink="false">5225967</guid>        </item>
        <item>
            <title>Morphine Alters M. bovis Infected Microglia’s Ability to Activate γδ T Lymphocytes</title>
            <link>http://www.medworm.com/index.php?rid=5184208&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk1q72634393r8g38%2F</link>
            <description>This study
 was designed to determine if Mycobacterium infected microglia activate γδT lymphocytes and if the opiate morphine alters the capability of microglia to activate γδT
 lymphocytes. γδT lymphocytes proliferated, produced IFN-γ, and demonstrated cytolytic response upon exposure to Mycobacterium bovis infected microglia. IFN-γ, and antigen specific cytotoxicity were both markedly impaired due to morphine treatment.
 
 
	Content Type Journal ArticleCategory ORIGINAL ARTICLEPages 1-7DOI 10.1007/s11481-011-9308-1Authors
		Michael Olin, Department of Pediatrics, University of Minnesota, Minneapolis, MN 55455, USAKeumhwa Choi, Veterinary Clinical Sciences, College of Veterinary Medicine, University of Minnesota, 1352 Boyd Ave., St. Paul, MN 55108, USAThomas W. Molitor, Veterinary...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5184208</comments>
            <pubDate>Wed, 31 Aug 2011 15:54:51 +0100</pubDate>
            <guid isPermaLink="false">5184208</guid>        </item>
        <item>
            <title>Clozapine Protects Dopaminergic Neurons from Inflammation-Induced Damage by Inhibiting Microglial Overactivation</title>
            <link>http://www.medworm.com/index.php?rid=5170494&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fkmq26746h3h97675%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Increasing evidence suggests a possible involvement of neuroinflammation in some psychiatric disorders, and also pharmacological
 reports indicate that anti-inflammatory effects are associated with therapeutic actions of psychoactive drugs, such as anti-depressants
 and antipsychotics. The purpose of this study was to explore whether clozapine, a widely used antipsychotic drugs, displays
 anti-inflammatory and neuroprotective effects. Using primary cortical and mesencephalic neuron-glia cultures, we found that
 clozapine was protective against inflammation-related neurodegeneration induced by lipopolysaccharide (LPS). Pretreatment
 of cortical or mesencephalic neuron–glia cultures with clozapine (0.1 or 1&amp;nbsp;μM) for 24&amp;nbsp;h attenuated LPS-induced neurotoxicity.
 ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5170494</comments>
            <pubDate>Thu, 25 Aug 2011 15:49:55 +0100</pubDate>
            <guid isPermaLink="false">5170494</guid>        </item>
        <item>
            <title>Morphine Induces Splenocyte Trafficking into the CNS</title>
            <link>http://www.medworm.com/index.php?rid=5161994&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fu8744910407j8220%2F</link>
            <description>The objective of the study was to use in vivo bioluminescent imaging to determine morphine’s effect on the trafficking
 pattern of splenocytes systemically and into the CNS either in a naïve state or following a neuroinflammatory stimulus. A
 neuroinflammatory response was induced by intracerebrally administering a DNA IFN-γ DNA plasmid into morphine-dependent or
 placebo wildtype mice. Mice with or without a neurostimulus received adoptively transferred firefly luciferase transgenic
 splenocytes and imaged. Morphine dependence significantly altered the inherent ability of splenocytes to traffic into the
 spleen, and lead to non-directed chaotic trafficking throughout the animal, including into the CNS. The morphine-mediated
 effects on trafficking were blocked by the antagonist naltre...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5161994</comments>
            <pubDate>Fri, 19 Aug 2011 16:01:48 +0100</pubDate>
            <guid isPermaLink="false">5161994</guid>        </item>
        <item>
            <title>Immunomodulatory Properties of Kappa Opioids and Synthetic Cannabinoids in HIV-1 Neuropathogenesis</title>
            <link>http://www.medworm.com/index.php?rid=5161995&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy046x40nj886r966%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Anti-retroviral therapy (ART) has had a tremendous impact on the clinical outcomes of HIV-1 infected individuals. While ART
 has produced many tangible benefits, chronic, long-term consequences of HIV infection have grown in importance. HIV-1-associated
 neurocognitive disorder (HAND) represents a collection of neurological syndromes that have a wide range of functional cognitive
 impairments. HAND remains a serious threat to AIDS patients, and there currently remains no specific therapy for the neurological
 manifestations of HIV-1. Based upon work in other models of neuroinflammation, kappa opioid receptors (KOR) and synthetic
 cannabinoids have emerged as having neuroprotective properties and the ability to dampen pro-inflammatory responses of glial
 cells; propertie...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5161995</comments>
            <pubDate>Thu, 18 Aug 2011 06:02:53 +0100</pubDate>
            <guid isPermaLink="false">5161995</guid>        </item>
        <item>
            <title>Cannabinoid Neuroimmune Modulation of SIV Disease</title>
            <link>http://www.medworm.com/index.php?rid=5126475&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq74675414277x371%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Marijuana is one of the most commonly used and abused drugs. Δ-9-tetrahydrocannabinol (Δ-9-THC), the primary psychoactive
 component in marijuana, is FDA-approved to ameliorate AIDS-associated wasting. Because cannabinoid receptors are expressed
 on cells of the immune system, it is possible that chronic Δ-9-THC use may impact HIV disease progression. Until recently,
 longitudinal, controlled, systems-approach studies on the effects of cannabinoids on disease progression were lacking. Data
 from our controlled studies in non-human primates show chronic Δ-9-THC administration prior to and during simian immunodeficiency
 virus (SIV) infection ameliorates disease progression, attenuates viral load and tissue inflammation, significantly reducing
 morbidity and mortality...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5126475</comments>
            <pubDate>Wed, 10 Aug 2011 15:44:39 +0100</pubDate>
            <guid isPermaLink="false">5126475</guid>        </item>
        <item>
            <title>Erratum to: Effects of Obovatol on GSH Depleted Glia-Mediated Neurotoxicity and Oxidative Damage</title>
            <link>http://www.medworm.com/index.php?rid=5126476&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F835j4626121t3291%2F</link>
            <description>Content Type Journal ArticlePages 1-1DOI 10.1007/s11481-011-9305-4Authors
		Moonhee Lee, Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, British Columbia, Canada V6T 1Z3Byoung-Mog Kwon, Laboratory of Chemical Biology and Genomics, Korea Research Institute of Bioscience and Biotechnology, University of Science and Technology, Daejeon, KoreaKyoungho Suk, Department of Pharmacology, Kyungpook National University, School of Medicine, Brain Science and Engineering Institute, Daegu, KoreaEdith McGeer, Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, British Columbia, Canada V6T 1Z3Patrick L. McGeer, Kinsmen Laboratory of Neurological Research, University of British Columbia, 2...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5126476</comments>
            <pubDate>Wed, 10 Aug 2011 15:44:38 +0100</pubDate>
            <guid isPermaLink="false">5126476</guid>        </item>
        <item>
            <title>Morphine, but Not Trauma, Sensitizes to Systemic Acinetobacter baumannii Infection</title>
            <link>http://www.medworm.com/index.php?rid=5126478&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F9w28562163441733%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;
 Acinetobacter baumannii is an important nosocomial pathogen in civilian intensive care units. Recently the incidence has increased in wounded military
 personnel. Morphine is documented in numerous animal studies to be immunosuppressive and to sensitize to infection. The hypotheses
 were tested that morphine, administered for analgesia in the battlefield, predisposes to Acinetobacter infection, and that the opioid may have an additive or synergistic effect with trauma. To test these hypotheses, an intraperitoneal
 infection model was established in mice using several Acinetobacter strains. Morphine administered for 48&amp;nbsp;h by implantation of a slow-release morphine pellet increased mortality compared to
 animals receiving a placebo pellet, an effect that was blocked...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5126478</comments>
            <pubDate>Mon, 08 Aug 2011 19:51:29 +0100</pubDate>
            <guid isPermaLink="false">5126478</guid>        </item>
        <item>
            <title>The Effect of HIV Protease Inhibitors on Amyloid-β Peptide Degradation and Synthesis in Human Cells and Alzheimer’s Disease Animal Model</title>
            <link>http://www.medworm.com/index.php?rid=5126477&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F16215755311xqwl0%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Combined antiretroviral therapy (ART) tremendously improved the lifespan and symptoms associated with AIDS-defining illness
 in affected individuals. However, chronic ART-treated patients frequently develop age-dependent complications, including dementia,
 diabetes, and hyperlipidemia: all risk factors of Alzheimer’s disease. Importantly, the effect of ART compounds on amyloid
 generation and clearance has never been systematically examined. Nine prescribed HIV protease inhibitors were tested for their
 effect on amyloid-β peptide (Aβ) clearance in primary cultured human monocyte-derived macrophages. Atazanavir, ritonavir,
 and saquinavir modestly inhibited of Aβ degradation, while lopinavir, nelfinavir, and ritonavir enhanced secretion of undigested
 Aβ after pha...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5126477</comments>
            <pubDate>Mon, 08 Aug 2011 19:51:29 +0100</pubDate>
            <guid isPermaLink="false">5126477</guid>        </item>
        <item>
            <title>Mechanisms of Dendritic Cell Trafficking Across the Blood–brain Barrier</title>
            <link>http://www.medworm.com/index.php?rid=5109643&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F249257g030175g10%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although the central nervous system (CNS) is considered to be an immunoprivileged site, it is susceptible to a host of autoimmune
 as well as neuroinflammatory disorders owing to recruitment of immune cells across the blood–brain barrier into perivascular
 and parenchymal spaces. Dendritic cells (DCs), which are involved in both primary and secondary immune responses, are the
 most potent immune cells in terms of antigen uptake and processing as well as presentation to T cells. In light of the emerging
 importance of DC traficking into the CNS, these cells represent good candidates for targeted immunotherapy against various
 neuroinflammatory diseases. This review focuses on potential physiological events and receptor interactions between DCs and
 the microvascular en...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5109643</comments>
            <pubDate>Sat, 06 Aug 2011 05:59:03 +0100</pubDate>
            <guid isPermaLink="false">5109643</guid>        </item>
        <item>
            <title>A Lifespan Approach to Neuroinflammatory and Cognitive Disorders: A Critical Role for Glia</title>
            <link>http://www.medworm.com/index.php?rid=5109644&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F9q42j86141267773%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Cognitive decline is a common problem of aging. Whereas multiple neural and glial mechanisms may account for these declines,
 microglial sensitization and/or dystrophy has emerged as a leading culprit in brain aging and dysfunction. However, glial
 activation is consistently observed in normal brain aging as well, independent of frank neuroinflammation or functional impairment.
 Such variability suggests the existence of additional vulnerability factors that can impact neuronal-glial interactions and
 thus overall brain and cognitive health. The goal of this review is to elucidate our working hypothesis that an individual’s
 risk or resilience to neuroinflammatory disorders and poor cognitive aging may critically depend on their early life experience, which can change...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5109644</comments>
            <pubDate>Sat, 06 Aug 2011 05:59:01 +0100</pubDate>
            <guid isPermaLink="false">5109644</guid>        </item>
        <item>
            <title>Effects of Obovatol on GSH Depleted Glia-Mediated Neurotoxicity and Oxidative Damage</title>
            <link>http://www.medworm.com/index.php?rid=5079676&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff5176g0k21q76t62%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Earlier studies indicate that obovatol (OBO), isolated from a medicinal herb Magnolia obovata, has anti-inflammatory and anti-oxidative properties. Depletion of glutathione (GSH) in glial cells with the γ-glutamylcysteine
 synthase inhibitor D,L-buthionine-S,R-sulfoximine (BSO) is known to produce oxidative stress which, in turn, induces these cells to secrete inflammatory cytokines
 and other neurotoxic substances. In the present study, we investigated the ability of OBO to protect SH-SY5Y neuroblastoma
 cells from this effect. Human microglia, astrocytes and their surrogate THP-1 and U373 cell lines were activated by treatment
 with BSO. Such treatment depleted their intracellular GSH and increased levels of damage to DNA, lipids and proteins (8-OHdG,
 lipid peroxide...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5079676</comments>
            <pubDate>Wed, 27 Jul 2011 15:49:03 +0100</pubDate>
            <guid isPermaLink="false">5079676</guid>        </item>
        <item>
            <title>Δ9-Tetrahydrocannabinol Suppresses Cytotoxic T Lymphocyte Function Independent of CB1 and CB2, Disrupting Early Activation Events</title>
            <link>http://www.medworm.com/index.php?rid=5070364&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm42086266752u196%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Previously, CD8+ T cells were found to be a sensitive target for suppression by Δ9-tetrahydrocannabinol (Δ9-THC) in a murine model of influenza infection. To study the effect of Δ9-THC on CD8+ cytotoxic T lymphocytes (CTL), an allogeneic model of MHC I mismatch was used to elicit CTL. In addition, to determine the
 requirement for the cannabinoid receptors 1 (CB1) and 2 (CB2) in Δ9-THC-mediated CTL response modulation, mice null for both receptors were used (CB1
 −/−CB2
 −/−). Δ9-THC suppressed CTL function independent of CB1 and CB2 as evidenced by reduction of 51Cr release by CTL generated from CB1
 −/−CB2
 −/− mice. Furthermore, viability in CD4+ and CD8+ cells was reduced in a concentration-dependent manner with Δ9-THC, independent of CB1 and C...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070364</comments>
            <pubDate>Mon, 25 Jul 2011 15:43:44 +0100</pubDate>
            <guid isPermaLink="false">5070364</guid>        </item>
        <item>
            <title>Opioid Drug Abuse and Modulation of Immune Function: Consequences in the Susceptibility to Opportunistic Infections</title>
            <link>http://www.medworm.com/index.php?rid=5070365&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F5j9m88v1l3175u63%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Infection rate among intravenous drug users (IDU) is higher than the general public, and is the major cause of morbidity and
 hospitalization in the IDU population. Epidemiologic studies provide data on increased prevalence of opportunistic bacterial
 infections such as TB and pneumonia, and viral infections such as HIV-1 and hepatitis in the IDU population. An important
 component in the intravenous drug abuse population and in patients receiving medically indicated chronic opioid treatment
 is opioid withdrawal. Data on bacterial virulence in the context of opioid withdrawal suggest that mice undergoing withdrawal
 had shortened survival and increased bacterial load in response to Salmonella infection. As the body of evidence in support of opioid dependency and its im...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070365</comments>
            <pubDate>Mon, 25 Jul 2011 15:43:43 +0100</pubDate>
            <guid isPermaLink="false">5070365</guid>        </item>
        <item>
            <title>Human Immunodeficiency Virus type 1 Endocytic Trafficking Through Macrophage Bridging Conduits Facilitates Spread of Infection</title>
            <link>http://www.medworm.com/index.php?rid=5070366&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F425550627q22u517%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Bridging conduits (BC) sustain communication and homeostasis between distant tethered cells. These are also exploited commonly
 for direct cell-to-cell transfer of microbial agents. Conduits efficiently spread infection, effectively, at speeds faster
 than fluid phase exchange while shielding the microbe against otherwise effective humoral immunity. Our laboratory has sought
 to uncover the mechanism(s) for these events for human immunodeficiency virus type one (HIV-1) infection. Indeed, in our prior
 works HIV-1 Env and Gag antigen and fluorescent virus tracking were shown sequestered into endoplasmic reticulum-Golgi organelles
 but the outcomes for spreading viral infection remained poorly defined. Herein, we show that HIV-1 specifically traffics through
 endocytic co...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070366</comments>
            <pubDate>Mon, 25 Jul 2011 15:43:35 +0100</pubDate>
            <guid isPermaLink="false">5070366</guid>        </item>
        <item>
            <title>Cocaine and HIV-1 Interplay: Molecular Mechanisms of Action and Addiction</title>
            <link>http://www.medworm.com/index.php?rid=5039929&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl06n4510x76t36m3%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Human immunodeficiency virus (HIV) infection is now being driven by drug-abusing populations. Epidemiological studies on drug
 abusers with AIDS link abuse of cocaine, even more than other drugs, to increased incidence of HIV seroprevalence and progression
 to AIDS. Both cell culture and animal studies demonstrate that cocaine can both potentiate HIV replication and can potentiate
 HIV proteins to cause enhanced glial cell activation, neurotoxicity, and breakdown of the blood-brain barrier. Based on the
 ability of both HIV proteins and cocaine to modulate NMDA receptor on neurons, NMDA receptors have been suggested as a common
 link underlying the crosstalk between drug addiction and HIV infection. While the role of dopamine system as a major target
 of cocaine cannot ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5039929</comments>
            <pubDate>Fri, 15 Jul 2011 15:55:41 +0100</pubDate>
            <guid isPermaLink="false">5039929</guid>        </item>
        <item>
            <title>Opioids and HIV/HCV Infection</title>
            <link>http://www.medworm.com/index.php?rid=5039930&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb3q8364602316876%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Since human immunodeficiency virus (HIV) and hepatitis C virus (HCV) share the same modes of transmission and common risk
 factors for infection, co-infections with HIV and HCV are frequently found in injection drug users (IDUs). IDUs represent
 one of the largest reservoirs of HIV as well as HCV in the United States. These two pathogens are also likely to be responsible
 for the highest infectious disease morbidity and mortality rates among IDUs. IDUs frequently involve the abuse of heroin,
 the most common abused opiate. Opiates have been suggested to have a cofactor role in the immunopathogenesis of HIV disease,
 as they have the potential to compromise host immune responses and enhances microbial infections. Although in vitro studies
 have yielded relatively agreeab...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5039930</comments>
            <pubDate>Thu, 14 Jul 2011 05:59:56 +0100</pubDate>
            <guid isPermaLink="false">5039930</guid>        </item>
        <item>
            <title>A Failure to Normalize Biochemical and Metabolic Insults During Morphine Withdrawal Disrupts Synaptic Repair in Mice Transgenic for HIV-gp120</title>
            <link>http://www.medworm.com/index.php?rid=5030615&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F30u615738441q17n%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Drug abuse in HIV-infected individuals accelerates the onset and progression of HIV-associated neurocognitive disorders (HAND).
 Opiates are a class of commonly abused drugs that have interactive effects with neurotoxic HIV proteins that facilitate glial
 dysfunction, neuronal damage and death. While the combined effects of neurotoxic HIV proteins and morphine have been extensively
 studied in the setting of chronic and acute morphine use, very little in known about the effects of HIV proteins during drug
 withdrawal. Since opiate withdrawal can induce considerable neuronal stress, we determined the effects of opiates (morphine)
 on brain redox balance, sphingolipid metabolism and synaptic integrity during both chronic and withdrawal conditions in non-transgenic
 mice (...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5030615</comments>
            <pubDate>Tue, 12 Jul 2011 06:01:45 +0100</pubDate>
            <guid isPermaLink="false">5030615</guid>        </item>
        <item>
            <title>Behavioral, Structural and Molecular Changes following Long-term Hippocampal IL-1β Overexpression in Transgenic Mice</title>
            <link>http://www.medworm.com/index.php?rid=5030616&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj405286738675565%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Chronic neuroinflammation is associated with many neurodegenerative and neurocognitive disorders, yet few animal models exist
 to study the behavioral effects of prolonged neuroinflammation. Therefore, we recently developed a transgenic mouse model
 harboring an interleukin-1β excisional activation transgene (IL-1βXAT). These mice display localized IL-1β overexpression and resultant neuroinflammation for up to 1&amp;nbsp;year following transgene
 induction. Initial behavioral studies demonstrated long-term memory deficits after 2&amp;nbsp;weeks of hippocampal IL-1β overexpression.
 In the present studies, we extend these behavioral studies both in scope and timing. We find long-term contextual but not
 auditory fear memory impairments following 3&amp;nbsp;months of IL-1β overe...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5030616</comments>
            <pubDate>Tue, 12 Jul 2011 06:01:44 +0100</pubDate>
            <guid isPermaLink="false">5030616</guid>        </item>
        <item>
            <title>Methamphetamine and HIV-1 Tat Down Regulate β-catenin Signaling: Implications for Methampetamine Abuse and HIV-1 Co-morbidity</title>
            <link>http://www.medworm.com/index.php?rid=5020959&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F63146057k223x5j4%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Methamphetamine (Meth) abuse exacerbates HIV-1-associated neurocognitive disorders (HAND). The underlying mechanism for this
 effect is not entirely clear but likely involves cooperation between Meth and HIV-1 virotoxins, such as the transactivator
 of transcription, Tat. HIV-1 Tat mediates damage in the CNS by inducing inflammatory processes including astrogliosis. Wnt/β-catenin
 signaling regulates survival processes for both neurons and astrocytes. Here, we evaluated the impact of Meth on the Wnt/β-catenin
 pathway in astrocytes transfected with Tat. Meth and Tat downregulated Wnt/β-catenin signaling by &amp;gt;50%, as measured by TOPflash
 reporter activity in both an astrocytoma cell line and primary human fetal astrocytes. Meth and Tat also downregulated LEF-1
 tra...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020959</comments>
            <pubDate>Sat, 09 Jul 2011 06:21:06 +0100</pubDate>
            <guid isPermaLink="false">5020959</guid>        </item>
        <item>
            <title>Cannabinoids Inhibit Migration of Microglial-like Cells to the HIV Protein Tat</title>
            <link>http://www.medworm.com/index.php?rid=5020960&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F883jx40375u71701%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Microglia are a population of macrophage-like cells in the central nervous system (CNS) which, upon infection by the human
 immunodeficiency virus (HIV), secrete a plethora of inflammatory factors, including the virus-specified trans-activating protein
 Tat. Tat has been implicated in HIV neuropathogenesis since it elicits chemokines, cytokines, and a chemotactic response from
 microglia. It also harbors a β-chemokine receptor binding motif, articulating a mode by which it acts as a migration stimulus.
 Since select cannabinoids have anti-inflammatory properties, cross the blood–brain barrier, and target specific receptors,
 they have potential to serve as agents for dampening untoward neuroimmune responses. The aim of this study was to investigate
 the effect of sel...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5020960</comments>
            <pubDate>Thu, 07 Jul 2011 05:42:27 +0100</pubDate>
            <guid isPermaLink="false">5020960</guid>        </item>
        <item>
            <title>Tumor Necrosis Factor-alpha and the Roles it Plays in Homeostatic and Degenerative Processes Within the Central Nervous System</title>
            <link>http://www.medworm.com/index.php?rid=5010031&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj36416r404840644%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Tumor Necrosis Factor-alpha (TNF-α) is a prototypic pro-inflammatory cytokine involved in the innate immune response. TNF-α
 ligation and downstream signaling with one of its cognate receptors, TNF-RI or TNF-RII, modulates fundamental processes in
 the brain including synapse formation and regulation, neurogenesis, regeneration, and general maintenance of the central nervous
 system (CNS). During states of chronic neuroinflammation, extensive experimental evidence implicates TNF-α as a key mediator
 in disease progression, gliosis, demyelination, inflammation, blood–brain-barrier deterioration, and cell death. This review
 explores the complex roles of TNF-α in the CNS under normal physiologic conditions and during neurodegeneration. We focus
 our discussion on Mu...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5010031</comments>
            <pubDate>Mon, 04 Jul 2011 16:19:44 +0100</pubDate>
            <guid isPermaLink="false">5010031</guid>        </item>
        <item>
            <title>Methamphetamine-Associated Psychosis</title>
            <link>http://www.medworm.com/index.php?rid=5010030&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ftqr04l7m18120988%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Methamphetamine (METH) is a frequent drug of abuse in U.S. populations and commonly associated with psychosis. This may be
 a factor in frequent criminal justice referrals and lengthy treatment required by METH users. Persecutory delusions and auditory
 hallucinations are the most consistent symptoms of METH-associated psychosis (MAP). MAP has largely been studied in Asian
 populations and risk factors have varied across studies. Duration, frequency and amount of use as well as sexual abuse, family
 history, other substance use, and co-occurring personality and mood disorders are risk factors for MAP. MAP may be unique
 with its long duration of psychosis and recurrence without relapse to METH. Seven candidate genes have been identified that
 may be associated with MAP....</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5010030</comments>
            <pubDate>Mon, 04 Jul 2011 16:19:44 +0100</pubDate>
            <guid isPermaLink="false">5010030</guid>        </item>
        <item>
            <title>Immunosuppressive Effects of Opioids—Clinical Relevance</title>
            <link>http://www.medworm.com/index.php?rid=5010032&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F81k3770606l1187r%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Opioid-induced immunosuppression has been demonstrated in cell culture experiments and in animal models. This is in striking
 contrast to the paucity of confirmatory studies in humans. This review describes the basic pharmacokinetics and –dynamics
 of opioid use in patients. It summarizes the major findings on opioid use and infectious complications in intensive care unit
 (ICU) patients, in patients with acute or chronic non-malignant pain, and in intravenous drug users (IDU). The limitations
 of studies in each area are discussed. For example, ethical concerns may complicate randomized placebo-controlled trials (RCT)
 in acute postoperative pain and for a large part of ICU patients. Importantly, most studies in patients with chronic (non-malignant)
 pain only inadeq...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5010032</comments>
            <pubDate>Mon, 04 Jul 2011 16:19:40 +0100</pubDate>
            <guid isPermaLink="false">5010032</guid>        </item>
        <item>
            <title>Sodium Benzoate, a Metabolite of Cinnamon and a Food Additive, Upregulates Neuroprotective Parkinson Disease Protein DJ-1 in Astrocytes and Neurons</title>
            <link>http://www.medworm.com/index.php?rid=4970513&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff618743725218070%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;DJ-1 (PARK7) is a neuroprotective protein that protects cells from oxidative stress. Accordingly, loss-of-function DJ-1 mutations
 have been linked with a familial form of early onset Parkinson disease. Mechanisms by which DJ-1 level could be enriched in
 the CNS are poorly understood. Recently we have discovered anti-inflammatory activity of sodium benzoate (NaB), a metabolite
 of cinnamon and a widely-used food additive. Here we delineate that NaB is also capable of increasing the level of DJ-1 in
 primary mouse and human astrocytes and human neurons highlighting another novel neuroprotective effect of this compound. Reversal
 of DJ-1-inducing effect of NaB by mevalonate, farnesyl phosphate, but not cholesterol and ubiquinone, suggests that depletion
 of intermediates...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4970513</comments>
            <pubDate>Thu, 23 Jun 2011 16:25:53 +0100</pubDate>
            <guid isPermaLink="false">4970513</guid>        </item>
        <item>
            <title>The Role of IL-1β in Nicotine-Induced Immunosuppression and Neuroimmune Communication</title>
            <link>http://www.medworm.com/index.php?rid=4946658&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh14670561p234151%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Although a number of inflammatory cytokines are increased during sepsis, the clinical trials aimed at down-regulating these
 mediators have not improved the outcome. These paradoxical results are attributed to loss of the “tolerance” phase that normally
 follows the proinflammatory response. Chronic nicotine (NT) suppresses both adaptive and innate immune responses, and the
 effects are partly mediated by the nicotinic acetylcholine receptors in the brain; however, the mechanism of neuroimmune communication
 is not clear. Here, we present evidence that, in rats and mice, NT initially increases IL-1β in the brain, but the expression
 is downregulated within 1–2&amp;nbsp;week of chronic exposure, and the animals become resistant to proinflammatory/pyrogenic stimuli.
 T...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4946658</comments>
            <pubDate>Tue, 14 Jun 2011 05:55:50 +0100</pubDate>
            <guid isPermaLink="false">4946658</guid>        </item>
        <item>
            <title>Nociceptin/Orphanin FQ Receptor-Driven Heterologous Desensitization of the Major HIV-1 Co-receptor CXCR4</title>
            <link>http://www.medworm.com/index.php?rid=4923339&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj066755023k80702%2F</link>
            <description>Content Type Journal ArticlePages 1-5DOI 10.1007/s11481-011-9285-4Authors
		David E. Kaminsky, Department of Microbiology and Immunology, Temple University School of Medicine, 3400 N. Broad Street, Philadelphia, PA 19140, USAThomas J. Rogers, Fels Institute for Cancer Research and Molecular Biology, Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine, 3307 N. Broad Street, Philadelphia, PA 19140, USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4923339</comments>
            <pubDate>Wed, 08 Jun 2011 15:46:53 +0100</pubDate>
            <guid isPermaLink="false">4923339</guid>        </item>
        <item>
            <title>A LC-MS/MS Method for Concurrent Determination of Nicotine Metabolites and Role of CYP2A6 in Nicotine Metabolism in U937 Macrophages: Implications in Oxidative Stress in HIV + Smokers</title>
            <link>http://www.medworm.com/index.php?rid=4913841&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F3720m82004075718%2F</link>
            <description>In conclusion, we have developed a new LCMS/MS method for concurrent determination
 of nicotine metabolites and analyzed the role of CYP2A6 in nicotine metabolism and oxidative stress in U937 macrophages, which
 may have implications in viral replication among HIV + smokers.
 
 
	Content Type Journal ArticlePages 1-11DOI 10.1007/s11481-011-9283-6Authors
		Mengyao Jin, Division of Pharmacology and Toxicology, School of Pharmacy, University of Missouri-Kansas City, 2464 Charlotte Street, Kansas, MO 64108, USARavinder Earla, Division of Pharmacology and Toxicology, School of Pharmacy, University of Missouri-Kansas City, 2464 Charlotte Street, Kansas, MO 64108, USAAnkit Shah, Division of Pharmacology and Toxicology, School of Pharmacy, University of Missouri-Kansas City, 2464 Charlotte Str...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4913841</comments>
            <pubDate>Tue, 07 Jun 2011 09:39:34 +0100</pubDate>
            <guid isPermaLink="false">4913841</guid>        </item>
        <item>
            <title>SIV/Macaque Model of HIV Infection in Cocaine Users: Minimal Effects of Cocaine on Behavior, Virus Replication, and CNS Inflammation</title>
            <link>http://www.medworm.com/index.php?rid=4904290&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl3rx2v10678n6161%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Studies of the effects of drugs of abuse on HIV immune status, disease progression, and neuroAIDS have produced conflicting
 data and have not definitively shown whether this combination promotes cognitive impairment or disease progression. Using
 a consistent SIV–macaque model, we investigated the effects of cocaine on behavior, virologic parameters, and CNS inflammation.
 Macaques received either vehicle or chronic administration of behaviorally active doses of cocaine (1.7 or 3.2&amp;nbsp;mg/kg/day).
 Chronic cocaine administration reduced CD8+ T cell counts during acute and late stage infection but had no effect on CD4+
 T cell counts. Low-dose cocaine-treated animals had lower CSF vRNA levels late in infection, but cocaine did not alter plasma
 viral load or vRNA or ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4904290</comments>
            <pubDate>Fri, 27 May 2011 18:13:30 +0100</pubDate>
            <guid isPermaLink="false">4904290</guid>        </item>
        <item>
            <title>Rosiglitazone Improves Spatial Memory and Decreases Insoluble Aβ1–42 in APP/PS1 Mice</title>
            <link>http://www.medworm.com/index.php?rid=4904291&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fhrwn5556k6603k41%2F</link>
            <description>Content Type Journal ArticlePages 1-5DOI 10.1007/s11481-011-9282-7Authors
		Julie-Ann O’Reilly, Trinity College Institute for Neuroscience, Trinity College, Dublin 2, IrelandMarina Lynch, Trinity College Institute for Neuroscience, Trinity College, Dublin 2, Ireland
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4904291</comments>
            <pubDate>Thu, 26 May 2011 16:07:37 +0100</pubDate>
            <guid isPermaLink="false">4904291</guid>        </item>
        <item>
            <title>Activated Immune Cells in Parkinson's Disease</title>
            <link>http://www.medworm.com/index.php?rid=4822199&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw967k541028l5125%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Recently, an interaction between neurodegenerative processes and the innate and adaptive immune responses has been increasingly
 recognized. Activation of microglia, infiltration of peripheral T lymphocytes, and T-cell interaction with microglia may strongly
 affect the progression of Parkinson's disease (PD) both in patients and in animal models of the disease. Here, we summarize
 the current knowledge regarding the role of microglia in the progression of PD. The plasticity of the microglial response
 is also discussed in the context of PD. In addition, we also focus on the influence of several peripheral T-cell subsets on
 PD progression as well as on possible pathways by which they might act. This review should help increase our understanding
 of the effects of innat...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4822199</comments>
            <pubDate>Mon, 09 May 2011 05:34:56 +0100</pubDate>
            <guid isPermaLink="false">4822199</guid>        </item>
        <item>
            <title>Orphanin FQ/Nociceptin Activates Nuclear Factor Kappa B</title>
            <link>http://www.medworm.com/index.php?rid=4806127&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F0739182m40kk2023%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Endogenous neuropeptide orphanin FQ/nociceptin (OFQ/N) and its receptor, nociceptin orphanin FQ peptide receptor (NOPr), play
 a modulatory role throughout the body including nociceptive sensitivity, motor function, spatial learning, and the immune
 system. NOPr is an inhibitory G protein coupled receptor (GPCR) that modulates expression and release of inflammatory mediators
 from immune cells and in the CNS. Inhibitory GPCRs have been shown to activate the immune and central nervous system regulator,
 nuclear factor kappa B (NFκB), whose family consists of several subunits. When activated, NFκB translocates to the nucleus
 and can modify transcription. To determine if OFQ/N modulates NFκB activity, SH-SY5Y human neuroblastoma cells were treated
 with OFQ/N and asses...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4806127</comments>
            <pubDate>Thu, 05 May 2011 15:48:31 +0100</pubDate>
            <guid isPermaLink="false">4806127</guid>        </item>
        <item>
            <title>Identification of SNF2h, a Chromatin-Remodeling Factor, as a Novel Binding Protein of Vpr of Human Immunodeficiency Virus Type 1</title>
            <link>http://www.medworm.com/index.php?rid=4771992&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx3p6302567311872%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;
 Vpr, an accessory gene of human immunodeficiency virus type 1, encodes a virion-associated nuclear protein that plays an important
 role in the primary viral infection of resting macrophages. It has a variety of biological functions, including roles in a
 cell cycle abnormality at G2/M phase, apoptosis, nuclear transfer of preintegration complex, and DNA double-strand breaks (DSBs), some of which depend
 on its association with the chromatin of the host cells. Given that DSB signals are postulated to be a positive factor in
 the viral infection, understanding the mode of chromatin recruitment of Vpr is important. Here, we identified SNF2h, a chromatin-remodeling
 factor, as a novel binding partner of Vpr involved in its chromatin recruitment. When endogenous SNF2h pro...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4771992</comments>
            <pubDate>Mon, 25 Apr 2011 16:42:01 +0100</pubDate>
            <guid isPermaLink="false">4771992</guid>        </item>
        <item>
            <title>Erratum to: Translocator Protein PET Imaging for Glial Activation in Multiple Sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4745144&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fwpp782n53v3117n8%2F</link>
            <description>Content Type Journal ArticlePages 1-1DOI 10.1007/s11481-011-9273-8Authors
		Unsong Oh, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institute of Health, 10 Center Drive, Bldg 10 Rm 5C103, Bethesda, MD 20892, USAMasahiro Fujita, Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USAVasiliki N. Ikonomidou, Department of Electrical and Computer Engineering, The Volgenau School of Information Technology and Engineering, George Mason University, Fairfax, VA, USAIordanis E. Evangelou, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institute of Health, 10 Center Drive, Bldg 10 Rm 5C103, Bethesda, MD 20892, USAEiji Matsuura, Department of Neurology and ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4745144</comments>
            <pubDate>Wed, 20 Apr 2011 06:05:13 +0100</pubDate>
            <guid isPermaLink="false">4745144</guid>        </item>
        <item>
            <title>Chronic Δ-9-tetrahydrocannabinol Administration Increases Lymphocyte CXCR4 Expression in Rhesus Macaques</title>
            <link>http://www.medworm.com/index.php?rid=4710333&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Flv0u68756u149565%2F</link>
            <description>We examined expression of proliferative and phenotypic markers in circulating lymphocytes of male young adult rhesus macaques
 chronically-treated with THC (i.m. twice daily 0.32&amp;nbsp;mg/kg) for 12&amp;nbsp;months. Chronic THC administration did not alter lymphocyte
 subtypes, naïve and memory subsets, proliferation, or apoptosis of T lymphocytes when compared to time-matched vehicle-treated
 controls. However, chronic THC increased T lymphocyte CXCR4 expression on both CD4+ and CD8+ T lymphocytes compared to control.
 These results show that chronic THC administration produces changes in T cell phenotype, which can potentially contribute
 to host immunomodulation to infectious challenges.
 
 
	Content Type Journal ArticlePages 1-6DOI 10.1007/s11481-011-9277-4Authors
		Nicole J. LeCapitaine, ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4710333</comments>
            <pubDate>Mon, 11 Apr 2011 15:50:07 +0100</pubDate>
            <guid isPermaLink="false">4710333</guid>        </item>
        <item>
            <title>Regulation of Neuronal Ferritin Heavy Chain, A New Player in Opiate-Induced Chemokine Dysfunction</title>
            <link>http://www.medworm.com/index.php?rid=4686592&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk6168k86754p8j45%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The heavy chain subunit of ferritin (FHC), a ubiquitous protein best known for its iron-sequestering activity as part of the
 ferritin complex, has recently been described as a novel inhibitor of signaling through the chemokine receptor CXCR4. Levels
 of FHC as well as its effects on CXCR4 activation increase in cortical neurons exposed to mu-opioid receptor agonists such
 as morphine, an effect likely specific to neurons. Major actions of CXCR4 signaling in the mature brain include a promotion
 of neurogenesis, activation of pro-survival signals, and modulation of excitotoxic pathways; thus, FHC up-regulation may contribute
 to the neuronal dysfunction often associated with opiate drug abuse. This review summarizes our knowledge of neuronal CXCR4
 function, its regulat...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4686592</comments>
            <pubDate>Tue, 05 Apr 2011 09:59:36 +0100</pubDate>
            <guid isPermaLink="false">4686592</guid>        </item>
        <item>
            <title>Cell Signaling Pathways and HIV-1 Therapeutics</title>
            <link>http://www.medworm.com/index.php?rid=4665178&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fjk05757325215162%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Host–virus interactions permeate every aspect of both virus life cycle and host response and involve host cell macromolecular
 machinery and viral elements. It is these intimate interactions that mandate the outcomes of the infection and pathogenesis.
 It is also these intimate interactions that lay the foundation for the development of pharmaceutical interventions. HIV-1
 is no exception in these regards. In the first two decades, HIV/AIDS research has led to the successful development of a number
 of antiviral inhibitors and the landmark formulation of the suppressive therapy. It has become apparent that this therapy
 does not offer a complete solution to cure and eradicate the virus. Meanwhile, this therapy has changed the overall landscape
 of HIV-associated neuro...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4665178</comments>
            <pubDate>Tue, 29 Mar 2011 17:32:35 +0100</pubDate>
            <guid isPermaLink="false">4665178</guid>        </item>
        <item>
            <title>Roles for Biological Membranes in Regulating Human Immunodeficiency Virus Replication and Progress in the Development of HIV Therapeutics that Target Lipid Metabolism</title>
            <link>http://www.medworm.com/index.php?rid=4665179&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw330323470uq2195%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Infection by the human immunodeficiency virus (HIV) involves a number of important interactions with lipid components in host
 membranes that regulate binding, fusion, internalization, and viral assembly. Available data suggests that HIV actively modifies
 the sphingolipid content of cellular membranes to create focal environments that are favorable for infection. In this review,
 we summarize the roles that membrane lipids play in HIV infection and discuss the current status of therapeutics that attempt
 to modify biological membranes to inhibit HIV.
 
 
	Content Type Journal ArticlePages 1-12DOI 10.1007/s11481-011-9274-7Authors
		Norman J. Haughey, Departments of Neurology, Richard T. Johnson Division of Neuroimmunology and Neurological Infections, The Johns Hopkins U...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4665179</comments>
            <pubDate>Tue, 29 Mar 2011 07:06:53 +0100</pubDate>
            <guid isPermaLink="false">4665179</guid>        </item>
        <item>
            <title>Morphine Potentiates Neuropathogenesis of SIV Infection in Rhesus Macaques</title>
            <link>http://www.medworm.com/index.php?rid=4637047&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh2k2873240r38004%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Despite the advent of antiretroviral therapy, complications of HIV-1 infection with concurrent drug abuse are an emerging
 problem. Opiates are well known to modulate immune responses by preventing the development of cell-mediated immune responses.
 Their effect on the pathogenesis of HIV-1 infection however remains controversial. Using the simian immunodeficiency virus/macaque
 model of HIV pathogenesis, we sought to explore the impact of morphine on disease progression and pathogenesis. Sixteen rhesus
 macaques were divided into two groups; four were administered saline and 12 others morphine routinely. Both groups of animals
 were then inoculated with SIVmacR71/17E and followed longitudinally for disease pathogenesis. The morphine group (M+V) exhibited
 a trend towar...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637047</comments>
            <pubDate>Wed, 23 Mar 2011 06:09:30 +0100</pubDate>
            <guid isPermaLink="false">4637047</guid>        </item>
        <item>
            <title>HIV and Chronic Methamphetamine Dependence Affect Cerebral Blood Flow</title>
            <link>http://www.medworm.com/index.php?rid=4637048&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F120536k0n2w44614%2F</link>
            <description>We examined the interaction between HIV infection and a previous history of METH dependence on CBF within the
 lenticular nuclei (LN). Twenty-four HIV−/METH−, eight HIV−/METH+, 24 HIV+/METH−, and 15 HIV+/METH+ participants performed
 a finger tapping paradigm. A multiple regression analysis of covariance assessed associations and two-way interactions between
 CBF and HIV serostatus and/or previous history of METH dependence. HIV+ individuals had a trend towards a lower baseline CBF
 (−10%, p = 0.07) and greater CBF changes for the functional task (+32%, p = 0.01) than HIV− subjects. Individuals with a previous history of METH dependence had a lower baseline CBF (−16%, p = 0.007) and greater CBF changes for a functional task (+33%, p = 0.02). However, no intera...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637048</comments>
            <pubDate>Wed, 23 Mar 2011 06:09:29 +0100</pubDate>
            <guid isPermaLink="false">4637048</guid>        </item>
        <item>
            <title>Murine Motor and Behavior Functional Evaluations for Acute 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP) Intoxication</title>
            <link>http://www.medworm.com/index.php?rid=4637049&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg211617n8l21t89m%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Acute intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces nigrostriatal neurodegeneration that reflects
 Parkinson’s disease (PD) pathobiology. The model is commonly used for rodent studies of PD pathogenesis and diagnostics and
 for developmental therapeutics. However, tests of motor function in MPTP-intoxicated mice have yielded mixed results. This
 unmet need reflects, in part, lesion severity, animal variability, and the overall test sensitivity and specificity. In attempts
 to standardize rodent motor function and behavioral tests, mice were trained on the rotarod or habituated in an open field
 test chamber, and baseline performance measurements were collected prior to MPTP intoxication. One week following MPTP intoxication,
 motor func...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637049</comments>
            <pubDate>Wed, 23 Mar 2011 06:09:28 +0100</pubDate>
            <guid isPermaLink="false">4637049</guid>        </item>
        <item>
            <title>Japanese Encephalitis Virus-Infected Macrophages Induce Neuronal Death</title>
            <link>http://www.medworm.com/index.php?rid=4632443&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg211353560816wu7%2F</link>
            <description>In this study, using an in vitro
 macrophage model, we have shown that upon JE virus infection, these cells secrete various soluble factors which may significantly
 add to the existing inflammatory milieu and lead to apoptotic or necrotic death of neurons. However, it is difficult to quantify
 the extent of involvement of either the microglia or infiltrating macrophages in the inflammatory processes.
 
 
	Content Type Journal ArticlePages 1-14DOI 10.1007/s11481-011-9271-xAuthors
		Arshed Nazmi, National Brain Research Centre, Manesar, Haryana 122050, IndiaKallol Dutta, National Brain Research Centre, Manesar, Haryana 122050, IndiaSulagna Das, National Brain Research Centre, Manesar, Haryana 122050, IndiaAnirban Basu, National Brain Research Centre, Manesar, Haryana 122050, India
	

	
		Jou...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4632443</comments>
            <pubDate>Mon, 21 Mar 2011 19:00:32 +0100</pubDate>
            <guid isPermaLink="false">4632443</guid>        </item>
        <item>
            <title>17th SNIP Scientific Conference</title>
            <link>http://www.medworm.com/index.php?rid=4601669&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff16k4054r3m22453%2F</link>
            <description>Content Type Journal ArticlePages 1-56DOI 10.1007/s11481-011-9264-9

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4601669</comments>
            <pubDate>Mon, 14 Mar 2011 16:52:38 +0100</pubDate>
            <guid isPermaLink="false">4601669</guid>        </item>
        <item>
            <title>Role of β-Catenin/TCF-4 Signaling in HIV Replication and Pathogenesis: Insights to Informing Novel Anti-HIV Molecular Therapeutics</title>
            <link>http://www.medworm.com/index.php?rid=4567142&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx6h3g12263880566%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;A greater understanding of the interaction between HIV and host signaling pathways that restrict virus production may lead
 to new methods to purge virus from latent reservoirs and enhance survival/function of cells targeted by HIV. This review highlights
 the role of the Wnt/β-catenin pathway as a host factor that represses HIV replication in multiple targets, especially those
 relevant to HIV in the central nervous system.
 
 
	Content Type Journal ArticlePages 1-13DOI 10.1007/s11481-011-9266-7Authors
		Lisa J. Henderson, Department of Immunology/Microbiology and Center for AIDS Research, Rush University Medical Center, Chicago, IL 60607, USALena Al-Harthi, Department of Immunology/Microbiology and Center for AIDS Research, Rush University Medical Center, Chicago, IL...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4567142</comments>
            <pubDate>Mon, 07 Mar 2011 16:59:14 +0100</pubDate>
            <guid isPermaLink="false">4567142</guid>        </item>
        <item>
            <title>Early Events of HIV-1 Infection: Can Signaling be the Next Therapeutic Target?</title>
            <link>http://www.medworm.com/index.php?rid=4561839&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp781045051791572%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Intracellular signaling events are signposts of biological processes, which govern the direction and action of biological
 activities. Through millions of years of evolution, pathogens, such as viruses, have evolved to hijack host cell machinery
 to infect their targets and are therefore dependent on host cell signaling for replication. This review will detail our current
 understanding of the signaling events that are important for the early steps of HIV-1 replication. More specifically, the
 therapeutic potential of signaling events associated with chemokine coreceptors, virus entry, viral synapses, and post-entry
 processes will be discussed. We argue that these pathways may represent novel targets for antiviral therapy.
 
 
	Content Type Journal ArticlePages 1-15DOI...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4561839</comments>
            <pubDate>Fri, 04 Mar 2011 11:05:25 +0100</pubDate>
            <guid isPermaLink="false">4561839</guid>        </item>
        <item>
            <title>New Insights into the Control of HIV-1 Transcription: When Tat Meets the 7SK snRNP and Super Elongation Complex (SEC)</title>
            <link>http://www.medworm.com/index.php?rid=4541563&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fnv7408v6p0688603%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Recent studies aimed at elucidating the mechanism controlling HIV-1 transcription have led to the identification and characterization
 of two multi-subunit complexes that both contain P-TEFb, a human transcription elongation factor and co-factor for activation
 of HIV-1 gene expression by the viral Tat protein. The first complex, termed the 7SK snRNP, acts as a reservoir where active
 P-TEFb can be withdrawn by Tat to stimulate HIV-1 transcription. The second complex, termed the super elongation complex (SEC),
 represents the form of P-TEFb delivered by Tat to the paused RNA polymerase II at the viral long terminal repeat during Tat
 transactivation. Besides P-TEFb, SEC also contains other elongation factors/co-activators, and they cooperatively stimulate
 HIV-1 transcr...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4541563</comments>
            <pubDate>Mon, 28 Feb 2011 16:47:27 +0100</pubDate>
            <guid isPermaLink="false">4541563</guid>        </item>
        <item>
            <title>Translational Regulation of HIV-1 Replication by HIV-1 Rev Cellular Cofactors Sam68, eIF5A, hRIP, and DDX3</title>
            <link>http://www.medworm.com/index.php?rid=4541562&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx3v01801762j4r5x%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Nuclear export and translation of HIV-1 RNA are two important posttranscriptional events for HIV-1 gene expression and replication.
 HIV-1 Rev functions to export unspliced and incompletely spliced HIV-1 RNA from the nucleus to the cytoplasm; it requires
 interaction with several cellular cofactors such as Sam68, eIF5A, hRIP, and DDX3. Meanwhile, some studies have also implicated
 Rev and some of its cofactors such as Sam68 in HIV-1 RNA translation. Thus, in this study, we aimed to characterize the potential
 function of all these four Rev cofactors in HIV-1 RNA translation. Ectopic expression, siRNA knockdown, and trans-complementation assays confirmed that all these cofactors were very important for HIV-1 gene expression and production through
 Rev and, accordingly, R...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4541562</comments>
            <pubDate>Mon, 28 Feb 2011 16:47:27 +0100</pubDate>
            <guid isPermaLink="false">4541562</guid>        </item>
        <item>
            <title>17th Annual Scientific Conference of the Society on NeuroImmune Pharmacology</title>
            <link>http://www.medworm.com/index.php?rid=4513537&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb4434x26849648v2%2F</link>
            <description>Content Type Journal ArticlePages 1-3DOI 10.1007/s11481-011-9263-xAuthors
		Sulie L. Chang, Institute of NeuroImmune Pharmacology, Seton Hall University, 400 South Orange Avenue, South Orange, NJ 07079, USAGuy A. Cabral, Department of Microbiology and Immunology, Virginia Commonwealth University, School of Medicine, Richmond, VA 23298, USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4513537</comments>
            <pubDate>Mon, 21 Feb 2011 17:07:15 +0100</pubDate>
            <guid isPermaLink="false">4513537</guid>        </item>
        <item>
            <title>Mechanisms of HIV-1 Nef Function and Intracellular Signaling</title>
            <link>http://www.medworm.com/index.php?rid=4502970&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F6227876124650615%2F</link>
            <description>We report the results of a PPI-Pred analysis for protein–protein interfaces. There are three predicted patches produced by
 the analysis which describe regions consistent with the currently known mutational analyses of Nef function.
 
 
	Content Type Journal ArticlePages 1-17DOI 10.1007/s11481-011-9262-yAuthors
		John L. Foster, Division of Infectious Diseases, Center for AIDS Research, Chapel Hill, NC 27599-7042, USASarah J. Denial, Division of Infectious Diseases, Center for AIDS Research, Chapel Hill, NC 27599-7042, USABrenda R. S. Temple, Department of Biochemistry and Biophysics, R. L. Juliano Structural Bioinformatics Core, University of North Carolina, Chapel Hill, NC 27599-7042, USAJ. Victor Garcia, Division of Infectious Diseases, Center for AIDS Research, Chapel Hill, NC 27599-...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4502970</comments>
            <pubDate>Fri, 18 Feb 2011 17:24:39 +0100</pubDate>
            <guid isPermaLink="false">4502970</guid>        </item>
        <item>
            <title>Vpr-Host Interactions During HIV-1 Viral Life Cycle</title>
            <link>http://www.medworm.com/index.php?rid=4484386&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F511033724w561430%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) is a multifunctional viral protein that plays important
 role at multiple stages of the HIV-1 viral life cycle. Although the molecular mechanisms underlying these activities are subject
 of ongoing investigations, overall, these activities have been linked to promotion of viral replication and impairment of
 anti-HIV immunity. Importantly, functional defects of Vpr have been correlated with slow disease progression of HIV-infected
 patients. Vpr is required for efficient viral replication in non-dividing cells such as macrophages, and it promotes, to some
 extent, viral replication in proliferating CD4+ T cells. The specific activities of Vpr include modulation of fidelity of
 viral reverse transcription,...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4484386</comments>
            <pubDate>Fri, 11 Feb 2011 11:53:21 +0100</pubDate>
            <guid isPermaLink="false">4484386</guid>        </item>
        <item>
            <title>Mitogen-Activated Protein Kinase p38 in HIV Infection and Associated Brain Injury</title>
            <link>http://www.medworm.com/index.php?rid=4442864&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa030315l244kj15n%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Infection with human immunodeficiency virus-1 (HIV-1) often leads to HIV-associated neurocognitive disorders (HAND) prior
 to the progression to acquired immunodeficiency syndrome (AIDS). At the cellular level, mitogen-activated protein kinases
 (MAPK) provide a family of signal transducers that regulate many processes in response to extracellular stimuli and environmental
 stress, such as viral infection. Recently, evidence has accumulated suggesting that p38 MAPK plays crucial roles in various
 pathological processes associated with HIV infection, ranging from macrophage activation to neurotoxicity and impairment of
 neurogenesis to lymphocyte apoptosis. Thus, p38 MAPK, which has generally been linked to stress-related signal transduction,
 may be an important mediato...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4442864</comments>
            <pubDate>Tue, 01 Feb 2011 15:51:34 +0100</pubDate>
            <guid isPermaLink="false">4442864</guid>        </item>
        <item>
            <title>HIV-1 gp120-Induced Axonal Injury Detected by Accumulation of β-Amyloid Precursor Protein in Adult Rat Corpus Callosum</title>
            <link>http://www.medworm.com/index.php?rid=4442865&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh07652lx3843j6l8%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;HIV-1 brain infection induces neurodegeneration. While most studies focus on HIV-1-mediated neuronal injury, relatively few
 have investigated HIV-1-associated white matter damage. Corpus callosum (CC) is one of frequently involved white matter structures
 in HIV-1-associated white matter damage. Utilizing a model of ex vivo treatment of brain slice containing CC with HIV-1 glycoprotein
 120 (gp120), we examined axonal injury by analyzing β-amyloid precursor protein (β-APP) accumulation in the axon. Incubation
 of CC slice with gp120 produced a significant higher density of β-APP in the CC tissue compared with non-gp120-treated controls,
 suggesting the presence of axonal damage in the CC. The gp120-induced CC axonal damage was blocked by a chemokine CXCR4 receptor
 ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4442865</comments>
            <pubDate>Tue, 01 Feb 2011 15:51:32 +0100</pubDate>
            <guid isPermaLink="false">4442865</guid>        </item>
        <item>
            <title>HIV-1 Vif Interaction with APOBEC3 Deaminases and its Characterization by a New Sensitive Assay</title>
            <link>http://www.medworm.com/index.php?rid=4429733&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb644l105746nl4q2%2F</link>
            <description>In this study, we describe a successful application
 of the Protein Fragment Complementation Assay (PCA) based on the enzyme TEM-1 β-lactamase to study Vif–A3 interactions. PCA
 is based on the interaction between two protein binding partners (e.g., Vif and A3G), which are fused to the two halves of
 a dissected marker protein (β-lactamase). Binding of the two partners reassembles β-lactamase and hence reconstitutes its
 activity. To validate our assay, we studied the effect of well-described Vif (DRMR, YRHHY) and A3G (D128K) mutations on the
 interaction between the two proteins. Additionally, we studied the interaction of human Vif with other members of the A3 family:
 A3F and APOBEC3C (A3C). Our results demonstrate the applicability of PCA as a simple and reliable technique for the...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4429733</comments>
            <pubDate>Fri, 28 Jan 2011 20:43:30 +0100</pubDate>
            <guid isPermaLink="false">4429733</guid>        </item>
        <item>
            <title>HIV-1 Tat-Mediated Neurotoxicity in Retinal Cells</title>
            <link>http://www.medworm.com/index.php?rid=4429734&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ftw500086216367qw%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The current study was aimed at investigating the effect of HIV-1 protein Tat on the retinal neurosensory cell line R28. Exposure
 of Tat resulted in induction of pro-inflammatory mediators such as CXCL10 and TNF-α in addition to the activation marker GFAP
 in these cells. Conditioned media from Tat-treated R28 cells was able to induce monocyte migration, an effect that was blocked
 by CXCR3 antagonist. Complementary studies in the HIV-1 Tat-transgenic mice, showed a complete absence of the nuclear layer
 and the outer photoreceptor segments of the retina with a concomitant increase in glial activation. These findings lend support
 to the observation in post-HAART era of increased incidence of immune response-mediated retinal degeneration. These findings
 have direct re...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4429734</comments>
            <pubDate>Thu, 27 Jan 2011 17:40:35 +0100</pubDate>
            <guid isPermaLink="false">4429734</guid>        </item>
        <item>
            <title>Tetherin and Its Viral Antagonists</title>
            <link>http://www.medworm.com/index.php?rid=4344297&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx67188u8wt4r1865%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Restriction factors comprise an important layer of host defense to fight against viral infection. Some restriction factors
 are constitutively expressed whereas the majority is induced by interferon to elicit innate immunity. In addition to a number
 of well-characterized interferon-inducible antiviral factors such as RNaseL/OAS, ISG15, Mx, PKR, and ADAR, tetherin (BST-2/CD317/HM1.24)
 was recently discovered to block the release of enveloped viruses from the cell surface, which is regarded as a novel antiviral
 mechanism induced by interferon. Here, we briefly review the history of tetherin discovery, discuss how tetherin blocks virus
 production, and highlight the viral countermeasures to evade tetherin restriction.
 
 
	Content Type Journal ArticlePages 1-14DOI 10.10...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4344297</comments>
            <pubDate>Mon, 10 Jan 2011 15:52:55 +0100</pubDate>
            <guid isPermaLink="false">4344297</guid>        </item>
        <item>
            <title>Education Mission for Neuroimmune Pharmacology</title>
            <link>http://www.medworm.com/index.php?rid=4325121&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj578898428277665%2F</link>
            <description>Content Type Journal ArticlePages 1-3DOI 10.1007/s11481-010-9255-2Authors
		Sulie L. Chang, Institute of NeuroImmune Pharmacology, Seton Hall University, 400 South Orange Avenue, South Orange, NJ 07079, USAGuy A. Cabral, Department of Microbiology and Immunology, Virginia Commonwealth University, School of Medicine, Richmond, VA 23298, USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4325121</comments>
            <pubDate>Thu, 06 Jan 2011 06:45:33 +0100</pubDate>
            <guid isPermaLink="false">4325121</guid>        </item>
        <item>
            <title>APOE ε4 allele and CSF APOE on Cognition in HIV-Infected Subjects</title>
            <link>http://www.medworm.com/index.php?rid=4289175&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp74n3w215756jp21%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The significance of the cerebrospinal fluid (CSF) Apolipoprotein E (APOE) level and whether it might have differential effects
 on brain function due to the presence of APOE ε4 allele(s) in HIV-infected patients are unknown. However, APOE ε4 allele has been associated with greater incidence of HIV-associated dementia and accelerated progression of HIV infection.
 Here, we show further evidence for the role of APOE ε4 in promoting cognitive impairment. We measured the APOE levels in the CSF of HIV-infected individuals. HIV+ subjects showed
 lower CSF APOE proteins than SN controls (−19%, p = 0.03). While SN subjects with or without ε4 allele showed no difference in CSF APOE levels, ε4+ HIV+ subjects had similar
 levels to the SN subjects but higher levels than...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4289175</comments>
            <pubDate>Thu, 23 Dec 2010 18:01:34 +0100</pubDate>
            <guid isPermaLink="false">4289175</guid>        </item>
        <item>
            <title>Proteomic Analysis of HIV-Infected Macrophages</title>
            <link>http://www.medworm.com/index.php?rid=4267612&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fmjtgg72x1grl8717%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Mononuclear phagocytes (monocytes, macrophages, and microglia) play an important role in innate immunity against pathogens
 including HIV. These cells are also important viral reservoirs in the central nervous system and secrete inflammatory mediators
 and toxins that affect the tissue environment and function of surrounding cells. In the era of antiretroviral therapy, there
 are fewer of these inflammatory mediators. Proteomic approaches including surface enhancement laser desorption ionization,
 one- and two-dimensional difference in gel electrophoresis, and liquid chromatography tandem mass spectrometry have been used
 to uncover the proteins produced by in vitro HIV-infected monocytes, macrophages, and microglia. These approaches have advanced
 the understanding of ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4267612</comments>
            <pubDate>Tue, 14 Dec 2010 04:20:13 +0100</pubDate>
            <guid isPermaLink="false">4267612</guid>        </item>
        <item>
            <title>Neuroimmune Pharmacology as a Component of Pharmacology in Medical School Curriculum</title>
            <link>http://www.medworm.com/index.php?rid=4206546&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F7m57446h8w454322%2F</link>
            <description>This article introduces a submodule and concomitant syllabus for inclusion of neuroimmune
 pharmacology as a component of a pharmacology curriculum. The introductory lectures of neuroimmune pharmacology will concentrate
 on the role of the immune system in (1) schizophrenia and major depression; (2) neurodegenerative disorders; and (3) drug
 addiction. Emphasis will be placed on the competencies of critical thinking, problem solving, learning interest, and effectiveness
 of medical students. Problem-based learning and case study discussions will also be applied.
 
 
	Content Type Journal ArticleDOI 10.1007/s11481-010-9252-5Authors
		Yuh F. Chen, Department of Pharmacology, School of Medicine, China Medical University, 91 Hsueh-Shih Road, Taichung, 40421 Taiwan
	

	
		Journal Journal of Neu...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4206546</comments>
            <pubDate>Wed, 24 Nov 2010 20:22:34 +0100</pubDate>
            <guid isPermaLink="false">4206546</guid>        </item>
        <item>
            <title>Neuroimmune Pharmacology: An Elective Course for Molecular and Cellular Bioscience Graduate Programs</title>
            <link>http://www.medworm.com/index.php?rid=4192012&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl7105960v08523u7%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Neuroimmune pharmacology is an interdisciplinary field which integrates neuroscience, immunology, and pharmacology. This new
 discipline has developed over the last two decades in order to study the etiology and treatment of disorders involving both
 the immune and nervous systems. The proposed Neuroimmune Pharmacology course is a semester-long elective course for students
 in molecular and cellular biology graduate programs. It is designed to introduce these students to basic principles and practices
 of neuroimmune pharmacology as well as to the application of molecular and cellular biological techniques in the study of
 neuroimmune disorders. The goal of this elective course is to help prepare future molecular and cellular biologists to undertake
 research initiative...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4192012</comments>
            <pubDate>Fri, 19 Nov 2010 17:05:36 +0100</pubDate>
            <guid isPermaLink="false">4192012</guid>        </item>
        <item>
            <title>Neuroimmune Pharmacology as a Sub-discipline of Medical Neuroscience in the Medical School Curriculum</title>
            <link>http://www.medworm.com/index.php?rid=4192013&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fcx07p26n2324661w%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The emerging field of neuroimmune pharmacology (NIP) is the confluence of three distinct disciplines: neuroscience, immunology,
 and pharmacology (Gendelman and Ikezu 2008). NIP was born from the realization that inflammation within the central nervous system (CNS) plays a crucial role in many
 neurological pathologies and as such offers a rich array of novel pharmacological targets as potential therapeutics. As this
 field is likely to have a major impact in medical science, educating future physicians on this area will help increase awareness
 and may potentially inspire them to pursue careers in the field of NIP. However, a key challenge for medical educators, is
 how best to incorporate new material on emerging fields, such as NIP, into the medical school curriculum...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4192013</comments>
            <pubDate>Fri, 19 Nov 2010 17:05:35 +0100</pubDate>
            <guid isPermaLink="false">4192013</guid>        </item>
        <item>
            <title>Glatiramer Acetate Modulates TNF-α and IL-10 Secretion in Microglia and Promotes Their Phagocytic Activity</title>
            <link>http://www.medworm.com/index.php?rid=4135676&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F98k542p208pr37l7%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Glatiramer acetate (GA) is an approved immunomodulating agent for the treatment of relapsing–remitting multiple sclerosis.
 Its mode of action is attributed to a T helper cell-type 1 (Th1) to Th2 cytokine shift in T cells. Th2-type GA-reactive T
 cells migrate into the brain and act suppressive at the sites of inflammation. However, there is increasing evidence that
 the effect of GA is not confined to T cells. It inhibits broadly the activation of monocytes and induces peritoneal macrophages
 and monocytes to differentiate into a type 2 antigen-presenting cell (APC) secreting anti-inflammatory cytokines. Thus, we
 examined whether GA has also direct effects on microglia cells which are involved in modifying/directing the local microenvironment
 in the central nervous...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4135676</comments>
            <pubDate>Tue, 02 Nov 2010 17:33:50 +0100</pubDate>
            <guid isPermaLink="false">4135676</guid>        </item>
        <item>
            <title>Immunology as it Pertains to Drugs of Abuse, AIDS and the Neuroimmune Axis: Mediators and Traffic</title>
            <link>http://www.medworm.com/index.php?rid=4089817&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fnl92689k377282gk%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The interactions between the immune and nervous systems are very complex, and yet our understanding of these interactions
 is still relatively limited. The neuroinflammatory reaction that can accompany HIV infection occurs because of a cascade of
 events that appears to require the migration of HIV-infected cells across the blood–brain barrier. In susceptible individuals,
 this leads to inflammatory processes which can include substantial changes in neuronal function. It is possible to consider
 the inflammatory events to be composed of two essential processes. The first process is cellular traffic, and the second,
 is the expression and recognition of the various pro-inflammatory and/or toxic mediators. The added complication of drug abuse
 adds complexity to the tra...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4089817</comments>
            <pubDate>Tue, 19 Oct 2010 19:17:37 +0100</pubDate>
            <guid isPermaLink="false">4089817</guid>        </item>
        <item>
            <title>M. tuberculosis H37Rv Infection of Chinese Rhesus Macaques</title>
            <link>http://www.medworm.com/index.php?rid=4068629&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv8g42n274656n286%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;
 Mycobacterium tuberculosis is the most common communicable infectious disease worldwide and the top killer of human immunodeficiency virus (HIV)-infected
 people. Because of common dual HIV and M. tuberculosis infections, the emergence of multidrug-resistant M. tuberculosis strains, the lack of effective vaccination, the morbidity, and the mortality of M. tuberculosis infection are increasing sharply. Therefore, there is an urgent need for vaccine and drug development against M. tuberculosis infection. These require appropriate animal models that closely resemble human disease. To this end, we infected Chinese
 rhesus macaques with the M. tuberculosis H37Rv strain. Bronchoscopy was used to inoculate nine monkeys with different doses of M. tuberculosis H37Rv strain. Re...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4068629</comments>
            <pubDate>Mon, 11 Oct 2010 16:50:22 +0100</pubDate>
            <guid isPermaLink="false">4068629</guid>        </item>
        <item>
            <title>Neurometabolite Abnormalities in Simian Immunodeficiency Virus-Infected Macaques with Chronic Morphine Administration</title>
            <link>http://www.medworm.com/index.php?rid=4068630&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F4101340u87k8817l%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Opiate abuse increases the risk for human immunodeficiency virus (HIV) infection, while both opiates and HIV may impact the
 immune and nervous systems. To model potential interactions between opiate drugs and HIV on the brain, neurometabolite levels
 were evaluated in simian immunodeficiency virus (SIV)-infected macaques with or without chronic morphine administration. Over
 the course of the study, 58% of these SIV-infected animals progressed to acquired immune deficiency syndrome (AIDS). Brain extracts from four brain regions were evaluated with proton magnetic resonance spectroscopy. Animals with AIDS
 had lower N-acetyl-aspartate in all four brain regions (p ≤ 0.05) as well as lower frontal gray matter total creatine (p = 0.03), lower frontal white matter...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4068630</comments>
            <pubDate>Mon, 11 Oct 2010 16:50:21 +0100</pubDate>
            <guid isPermaLink="false">4068630</guid>        </item>
        <item>
            <title>Translocator Protein PET Imaging for Glial Activation in Multiple Sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4001958&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl8x0m7m2j4827812%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Glial activation in the setting of central nervous system inflammation is a key feature of the multiple sclerosis (MS) pathology.
 Monitoring glial activation in subjects with MS, therefore, has the potential to be informative with respect to disease activity.
 The translocator protein 18&amp;nbsp;kDa (TSPO) is a promising biomarker of glial activation that can be imaged by positron emission
 tomography (PET). To characterize the in vivo TSPO expression in MS, we analyzed brain PET scans in subjects with MS and healthy
 volunteers in an observational study using [11C]PBR28, a newly developed translocator protein-specific radioligand. The [11C]PBR28 PET showed altered compartmental distribution of TSPO in the MS brain compared to healthy volunteers (p = 0.019). Focal inc...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4001958</comments>
            <pubDate>Fri, 24 Sep 2010 17:09:02 +0100</pubDate>
            <guid isPermaLink="false">4001958</guid>        </item>
        <item>
            <title>Erratum to: Neuroimmune Pharmacology from a Neuroscience Perspective</title>
            <link>http://www.medworm.com/index.php?rid=3978239&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk62054m7421kp215%2F</link>
            <description>Content Type Journal ArticleDOI 10.1007/s11481-010-9244-5Authors
		Nicole A. Northrop, Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA 02118, USABryan K. Yamamoto, Department of Neurosciences, University of Toledo College of Medicine, 3000 Arlington Avenue, Toledo, OH 43614, USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3978239</comments>
            <pubDate>Mon, 13 Sep 2010 17:06:50 +0100</pubDate>
            <guid isPermaLink="false">3978239</guid>        </item>
        <item>
            <title>Mother-to-Child Transmission (MTCT) of HIV and Drugs of Abuse in Post-Highly Active Antiretroviral Therapy (HAART) Era</title>
            <link>http://www.medworm.com/index.php?rid=3978240&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F35854w7048753t41%2F</link>
            <description>In this report,
 we review and present evidence that supports the hypothesis that drugs of abuse do have the potential to increase MTCT of
 HIV in the presence of HAART. Exposure to drugs of abuse during pregnancy may increase MTCT of HIV through a variety of mechanisms
 that are addressed in detail including possible damage to the placenta, induction of preterm birth, and increasing maternal
 plasma viral load though a variety of putative mechanisms such as: (a) promoting HIV replication in monocyte/macrophages;
 (b) increasing the expression of CCR5 receptors; (c) decreasing the expression of CCR5 receptor ligands; (d) increasing the
 expression of CXCR4 receptors; (e) increasing the expression of DC-SIGN; (f) impairing the efficacy of HAART through drug–drug
 interaction; and (g) prom...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3978240</comments>
            <pubDate>Mon, 13 Sep 2010 17:06:49 +0100</pubDate>
            <guid isPermaLink="false">3978240</guid>        </item>
        <item>
            <title>Neuroimmune Pharmacology of Neurodegenerative and Mental Diseases</title>
            <link>http://www.medworm.com/index.php?rid=3948160&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy782048855738281%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Neuroimmune pharmacology is a newly emerging field that intersects with neuroscience, immunology, and pharmacology and that
 is seeking avenues for translational research and better understanding of disease mechanisms. It focuses on the immunity of
 the central nervous system (CNS) which is greatly influenced by endogenous effectors, such as cytokines and neurotransmitters,
 and by exogenous substances, including therapeutic compounds, infectious pathogens, and drugs of abuse. In this article, we
 attempt to raise awareness of the pivotal discovery of how those mediators affect the immunity of the CNS in both physiological
 conditions and processes of certain mental illnesses, including psychiatric disorders, neurodegenerative diseases, and cerebral
 dysfunctions due to...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3948160</comments>
            <pubDate>Tue, 07 Sep 2010 17:21:45 +0100</pubDate>
            <guid isPermaLink="false">3948160</guid>        </item>
        <item>
            <title>Synthetic Triterpenoid CDDO Derivatives Modulate Cytoprotective or Immunological Properties in Astrocytes, Neurons, and Microglia</title>
            <link>http://www.medworm.com/index.php?rid=3930236&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw5g2506mh7855403%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;2-Cyano-3,12-dioxoolean-1, 9-dien-28-oic acid (CDDO) is a semisynthetic triterpenoid. CDDO derivatives with an amide, butyl
 ester (BE), imidazolide (IM), or trifluoroethyl amide (TFEA) group at position C-28 of CDDO were evaluated in glial and neuronal
 cells, in vitro. Changes in intracellular NADPH:quinone oxidoreductase (NQO1) levels, protection against oxidative toxicity,
 endotoxin-induced free-radical production, and the median lethal concentration (LC50) were assessed. All four CDDO derivatives
 at nanomolar concentrations increased NQO1 levels in astrocytes and moderately in neurons, but not in microglial cells. Pretreatment
 with 100&amp;nbsp;nM of CDDO-amide, CDDO-TFEA, or CDDO-IM protected astrocytes from hydrogen peroxide toxicity. Only CDDO-amide protected
 ne...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3930236</comments>
            <pubDate>Thu, 02 Sep 2010 08:44:28 +0100</pubDate>
            <guid isPermaLink="false">3930236</guid>        </item>
        <item>
            <title>Neuroimmune Pharmacology from a Neuroscience Perspective</title>
            <link>http://www.medworm.com/index.php?rid=3878284&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F55856260387852p2%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The focus of this commentary is to describe how neuroscience, immunology, and pharmacology intersect and how interdisciplinary
 research involving these areas has expanded knowledge in the area of neuroscience, in particular. Examples are presented to
 illustrate that the brain can react to the peripheral immune system and possesses immune function and that resident immune
 molecules play a role in normal brain physiology. In addition, evidence is presented that the brain immune system plays an
 important role in mediating neurodegenerative diseases, the aging process, and neurodevelopment and synaptic plasticity. The
 identification of these mechanisms has been facilitated by pharmacological studies and has opened new possibilities for pharmacotherapeutic
 approaches t...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3878284</comments>
            <pubDate>Tue, 17 Aug 2010 17:22:17 +0100</pubDate>
            <guid isPermaLink="false">3878284</guid>        </item>
        <item>
            <title>Effects of Early IL-17A Neutralization on Disease Induction in a Primate Model of Experimental Autoimmune Encephalomyelitis</title>
            <link>http://www.medworm.com/index.php?rid=3865986&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F714540560013m759%2F</link>
            <description>We report on the effect of antibody-mediated neutralization of interleukin (IL)-17A in a non-human primate experimental autoimmune
 encephalomyelitis (EAE) model induced with recombinant human myelin oligodendrocyte glycoprotein (rhMOG). We tested a human-anti-human
 IL-17A-antibody in two doses (3 and 30&amp;nbsp;mg/kg) against placebo (PBS). The treatment was started 1&amp;nbsp;day before EAE induction
 and continued throughout the experiment. Although all monkeys developed clinically evident EAE, the onset of neurological
 signs was delayed in some monkeys from both treatment groups. Total CNS lesion volumes, demyelination, or inflammation did
 not differ between the different groups. Immune profiling revealed an altered distribution of IL-17A producing cells in the
 lymphoid organs of antibody...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3865986</comments>
            <pubDate>Wed, 11 Aug 2010 14:51:20 +0100</pubDate>
            <guid isPermaLink="false">3865986</guid>        </item>
        <item>
            <title>Neuronal PINCH is Regulated by TNF-α and is Required for Neurite Extension</title>
            <link>http://www.medworm.com/index.php?rid=3832495&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F53h3xu77l5k18731%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;During HIV infection of the CNS, neurons are damaged by viral proteins, such as Tat and gp120, or by inflammatory factors,
 such as TNF-α, that are released from infected and/or activated glial cells. Host responses to this damage may include the
 induction of survival or repair mechanisms. In this context, previous studies report robust expression of a protein called
 particularly interesting new cysteine histidine-rich protein (PINCH), in the neurons of HIV patients’ brains, compared with
 nearly undetectable levels in HIV-negative individuals (Rearden et al., J Neurosci Res 86:2535–2542, 2008), suggesting PINCH’s involvement in neuronal signaling during HIV infection of the brain. To address potential triggers for
 PINCH induction in HIV patients’ brains, an...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3832495</comments>
            <pubDate>Fri, 06 Aug 2010 07:13:25 +0100</pubDate>
            <guid isPermaLink="false">3832495</guid>        </item>
        <item>
            <title>Proper Laboratory Notebook Practices: Protecting Your Intellectual Property</title>
            <link>http://www.medworm.com/index.php?rid=3818227&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc80m561v411q4404%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;A laboratory notebook contains a wealth of knowledge that can be critical for establishing evidence in support of intellectual
 property rights and for refuting claims of research misconduct. The proper type, organization, use, maintenance, and storage
 of laboratory notebooks should be a priority for everyone at research institutions. Failure to properly document research
 activities can lead to serious problems, including the loss of valuable patent rights. Consequences of improper laboratory
 notebook practices can be harsh; numerous examples are described in court cases and journal articles, indicating a need for
 research institutions to develop strict policies on the proper use and storage of research documentation.
 
 
	Content Type Journal ArticleCategory GUEST ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3818227</comments>
            <pubDate>Mon, 02 Aug 2010 20:25:01 +0100</pubDate>
            <guid isPermaLink="false">3818227</guid>        </item>
        <item>
            <title>Mechanism of Neuroinflammation: Enhanced Cytotoxicity and IL-17 Production via CD46 Binding</title>
            <link>http://www.medworm.com/index.php?rid=3796314&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F0567p38281758628%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The membrane co-factor protein CD46 is the cellular receptor for a number of pathogens including the human herpesvirus 6 (HHV-6).
 In addition to its function as an inhibitory complement receptor, engagement of CD46 in the context of T-cell receptor (TCR)
 signaling influences T-cell activation. Simultaneous cross-linking of the CD3/CD46 molecules led to differentiation of a unique
 population of CD4+ T-cell subset characterized by enhanced expressions of IFN-γ, IL-10, granzyme B, adhesion molecule MAdCAM-1
 (alpha-4-beta-7), surface-bound cytokine LIGHT, and chemokine receptor CCR9. Multiple sclerosis is a chronic inflammatory
 neurodegenerative disorder of the central nervous system (CNS) with unknown etiology. The HHV-6 is a candidate pathogen in
 MS and uses the CD...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3796314</comments>
            <pubDate>Mon, 26 Jul 2010 21:53:12 +0100</pubDate>
            <guid isPermaLink="false">3796314</guid>        </item>
        <item>
            <title>Viral Infections of the Central Nervous System: Pathogenesis to Therapeutics</title>
            <link>http://www.medworm.com/index.php?rid=3791948&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh2606365k86514v4%2F</link>
            <description>Content Type Journal ArticleCategory GUEST COMMENTARYDOI 10.1007/s11481-010-9231-xAuthors
		Samantha S. Soldan, University of Pennsylvania Department of Neurology Philadelphia PA 19104-4283 USASteven Jacobson, NIH Viral Immunology Section, Neuroimmunology Branch Building 10, Room 5C-103 Bethesda MD 20892 USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3791948</comments>
            <pubDate>Sat, 24 Jul 2010 13:50:41 +0100</pubDate>
            <guid isPermaLink="false">3791948</guid>        </item>
        <item>
            <title>Web-Based Course in Neuroimmune Pharmacology</title>
            <link>http://www.medworm.com/index.php?rid=3791949&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F8468836v10433836%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Web-based instruction of biomedical sciences courses has increased dramatically during the last decade, and this increase
 has been driven by the need to increase student access to educational programs and by the increasing demand for courses that
 are compatible with distance learning. Here, a blended learning curriculum in neuroimmune pharmacology is described that combines
 web-based learning modules with traditional face-to-face lectures. The course content is appropriate for graduate-level students
 and can be adapted to an entirely web-based course that can be deployed for distance learning. In addition to providing a
 course syllabus, this article describes the process of creating the web-based modules for course construction.
 
 
	Content Type Journal ArticleCat...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3791949</comments>
            <pubDate>Sat, 24 Jul 2010 13:50:39 +0100</pubDate>
            <guid isPermaLink="false">3791949</guid>        </item>
        <item>
            <title>Arboviral Encephalitides: Transmission, Emergence, and Pathogenesis</title>
            <link>http://www.medworm.com/index.php?rid=3785125&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F0171265469p67vh3%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Arthropod-borne viruses (arboviruses) are of paramount concern as a group of pathogens at the forefront of emerging and re-emerging
 diseases. Although some arboviral infections are asymptomatic or present with a mild influenza-like illness, many are important
 human and veterinary pathogens causing serious illness ranging from rash and arthritis to encephalitis and hemorrhagic fever.
 Here, we discuss arboviruses from diverse families (Flaviviruses, Alphaviruses, and the Bunyaviridae) that are causative agents of encephalitis in humans. An understanding of the natural history of these infections as well
 as shared mechanisms of neuroinvasion and neurovirulence is critical to control the spread of these viruses and for the development
 of effective vaccines and treatmen...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3785125</comments>
            <pubDate>Fri, 23 Jul 2010 12:05:47 +0100</pubDate>
            <guid isPermaLink="false">3785125</guid>        </item>
        <item>
            <title>Minocycline Differentially Modulates Viral Infection and Persistence in an Experimental Model of Japanese Encephalitis</title>
            <link>http://www.medworm.com/index.php?rid=3773874&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa07232737m33k825%2F</link>
            <description>In this study we have also investigated the role of minocycline on the peripheral organs that are infected by JEV.
 Levels of IL-12 and MCP-1 in the organs were estimated by cytometric bead array, and immunohistochemical studies were performed
 on cryosections of tissue to detect CD3- or CD11b-positive cells as well as JEV antigen. We found that the levels of T cell-activating
 cytokine IL-12 and MCP-1 levels were significantly elevated in JEV-infected tissue samples in a time-dependent manner. Corresponding
 to this increase was the increase in the number of CD3- and CD11b-positive cells in the tissues of infected animals. Minocycline
 treatment abrogated these changes. Minocycline treatment also resulted in the gradual decrease in the number of CD11b (but
 not CD3) positive cells in the ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3773874</comments>
            <pubDate>Fri, 16 Jul 2010 07:47:44 +0100</pubDate>
            <guid isPermaLink="false">3773874</guid>        </item>
        <item>
            <title>CXCL12-Mediated Regulation of ANP32A/Lanp, A Component of the Inhibitor of Histone Acetyl Transferase (INHAT) Complex, in Cortical Neurons</title>
            <link>http://www.medworm.com/index.php?rid=3741633&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx390267052851372%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The chemokine receptor CXCR4 and its endogenous ligand, CXCL12, are involved in development and homeostasis of the central
 nervous system and in the neuropathology of various neuroinflammatory/infectious disorders, including neuroAIDS. Our previous
 studies have shown that CXCR4 regulates cell cycle proteins that affect neuronal survival, such as the retinoblastoma protein,
 Rb. These studies also suggested that Rb-mediated gene repression might be involved in the neuronal protection against NMDA
 exitotoxicity conferred by stimulation of the CXCL12/CXCR4 axis. In order to further test this hypothesis, we focused on the
 potential interaction of Rb with another protein implicated in regulation of gene expression, leucine-rich acidic nuclear
 protein (Lanp), also known ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3741633</comments>
            <pubDate>Thu, 08 Jul 2010 16:21:51 +0100</pubDate>
            <guid isPermaLink="false">3741633</guid>        </item>
        <item>
            <title>Neuroimmune Pharmacology as an Emerging Curriculum for Pre-Medical Students</title>
            <link>http://www.medworm.com/index.php?rid=3734870&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fqt08g86t3831m760%2F</link>
            <description>This article is focused on developing a curriculum
 for undergraduate pre-medical students in the area of neuroimmune pharmacology (NIP) to empower them with the knowledge of
 neuroscience and its interaction with immune responses and drug interactions. This course is intended to amalgamate and put
 into perspective a large body of knowledge including: (1) brain function in health and disease, (2) cross talk between neural
 and immune responses, and (3) the pharmacology of drugs of abuse in the context of neurodegenerative diseases. The goal of
 this course is to expose pre-medical students to the field of NIP so that they are equipped with a solid foundation in these
 multidisciplinary fields for future clinical/academic careers.
 
 
	Content Type Journal ArticleCategory INVITED REVIEWDOI...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734870</comments>
            <pubDate>Wed, 07 Jul 2010 05:44:23 +0100</pubDate>
            <guid isPermaLink="false">3734870</guid>        </item>
        <item>
            <title>Neuroimmune Pharmacology as a Sub-discipline of Immunology in the Medical School Curriculum</title>
            <link>http://www.medworm.com/index.php?rid=3734871&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F485707485386070h%2F</link>
            <description>This article provides a description of a proposed sub-module and attendant syllabus for inclusion of neuroimmune pharmacology
 as a sub-discipline of an immunology course that is offered to medical students during the first year of medical school. Neuroimmune
 pharmacology is an area of study that integrates fundamental concepts in pharmacology, immunology, neuroscience, and infectious
 disease. This convergent disciplinary area is of increasing importance to the foundational training of medical students, especially
 in view of the recognition that a variety of neuropathological processes such as demyelinating disease, drug abuse, and viral
 encephalitis has an immunological component. A lecture sub-module that addresses this convergent topic is proposed for inclusion
 as a sub-discipline ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3734871</comments>
            <pubDate>Tue, 06 Jul 2010 17:05:25 +0100</pubDate>
            <guid isPermaLink="false">3734871</guid>        </item>
        <item>
            <title>Overview of Substance Abuse and Hepatitis C Virus Infection and Co-infections in India</title>
            <link>http://www.medworm.com/index.php?rid=3677831&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fhj50707178k55503%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Hepatitis C virus (HCV) infection can have devastating long-term sequelae. It is very common in injecting drug users (IDU)
 worldwide. India has a huge number of substance abusers, with an estimated 1.1 million IDU. Research on HCV prevalence in
 IDU and especially other substance use is sparse. This review identified 15 such studies. Some of these also studied prevalence
 of hepatitis B virus (HBV) and human immunodeficiency virus (HIV) infections and co-infection rates. The summary findings
 indicate that there are pockets of very high HCV seroprevalence (60–90%), otherwise the range is moderate (30–50%), though,
 in real terms, it still indicates the appreciable magnitude of the problem that may emerge as an epidemic if it goes unheeded.
 HCV infection seems to b...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677831</comments>
            <pubDate>Fri, 18 Jun 2010 10:41:28 +0100</pubDate>
            <guid isPermaLink="false">3677831</guid>        </item>
        <item>
            <title>Immunoregulation of a CB2 Receptor Agonist in a Murine Model of NeuroAIDS</title>
            <link>http://www.medworm.com/index.php?rid=3667922&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft128814772l24q37%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Chronic HIV-1 infection commonly affects behavioral, cognitive, and motor functions in the infected human host and is commonly
 referred to as HIV-1-associated neurocognitive disorders (HAND). This occurs, in measure, as a consequence of ingress of leukocytes
 into brain perivascular regions. Such cells facilitate viral infection and disease by eliciting blood–brain barrier and neuronal
 network dysfunctions. Previous works demonstrated that the endocannabinoid system modulates neuroimmunity and as such neuronal
 and glial functions. Herein, we investigated CB2R receptor expression in murine HIV-1 encephalitis (HIVE) and the abilities
 of a highly selective CB2R agonist, Gp1a, to modulate disease. HIV-1-infected human monocyte-derived macrophages were injected
 into t...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3667922</comments>
            <pubDate>Mon, 14 Jun 2010 13:48:40 +0100</pubDate>
            <guid isPermaLink="false">3667922</guid>        </item>
        <item>
            <title>Methamphetamine-Induced Behavioral and Physiological Effects in Adolescent and Adult HIV-1 Transgenic Rats</title>
            <link>http://www.medworm.com/index.php?rid=3653799&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx21132w855825111%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;We recently reported that six consecutive days of treatment with a moderate dose of methamphetamine (METH) induced greater
 behavioral sensitization in adult HIV-1 transgenic (HIV-1 Tg) rats than in adult Fischer 344/NHsd (F344) non-transgenic, wild-type
 control animals. In the present study, we evaluated the effects of a moderate dose of METH on the brains of adolescent versus
 adult HIV-1 Tg male rats using both behavioral (METH-induced, stereotypic head movement) and physiological (rectal body temperature)
 parameters. We found that both the acute and behavior-sensitizing effects of METH were greater in HIV-1 Tg rats compared with
 controls and also in adolescent rats compared with adult animals, regardless of HIV-1 status. We determined that acute hyperthermic
 eff...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3653799</comments>
            <pubDate>Wed, 09 Jun 2010 09:24:15 +0100</pubDate>
            <guid isPermaLink="false">3653799</guid>        </item>
        <item>
            <title>Reconstitution of huPBL-NSG Mice with Donor-Matched Dendritic Cells Enables Antigen-Specific T-cell Activation</title>
            <link>http://www.medworm.com/index.php?rid=3649885&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm46211r59w822521%2F</link>
            <description>In this study,
 immunodeficient NOD/SCID/IL2r-γnull (NSG) mice were engrafted with human peripheral blood lymphocytes alone or in combination with donor-matched monocyte-derived
 dendritic cells (DC) to determine whether antigen-specific T-cell activation could be reconstituted. Over a period of 3&amp;nbsp;weeks,
 transferred peripheral blood lymphocytes reconstituted the spleen and peripheral blood of recipient mice with predominantly
 human CD45-positive lymphocytes. Animals exhibited a relatively normal CD4/CD8 ratio (average 1.63:1) as well as reconstitution
 of CD3/CD56 (averaging 17.8%) and CD20 subsets (averaging 4.0%). Animals reconstituted with donor-matched CD11c+ DC also demonstrated
 a CD11c+ population within their spleen, representing 0.27% to 0.43% of the recovered human cells ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3649885</comments>
            <pubDate>Mon, 07 Jun 2010 17:15:19 +0100</pubDate>
            <guid isPermaLink="false">3649885</guid>        </item>
        <item>
            <title>n-Dodecyl-β-d-Maltoside Inhibits Aggregation of Human Interferon-β-1b and Reduces Its Immunogenicity</title>
            <link>http://www.medworm.com/index.php?rid=3649886&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv46614510n311211%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The development of neutralizing antibodies to the protein drug interferon-β is a significant impediment to its use in the
 treatment of multiple sclerosis. Neutralizing antibodies to interferon-β arise from aggregation of the peptide during manufacturing
 and storage. We tested the ability of dodecylmaltoside, a nontoxic alkylsaccharide surfactant, to reduce aggregation of interferon-β
 in vitro and to reduce its immunogenicity in vivo. Interferon-β, in solution with and without dodecylmaltoside, was periodically
 evaluated for aggregation by light scatter for 1&amp;nbsp;month. Interferon-β, with and without dodecylmaltoside, was given 3&amp;nbsp;days/week
 for 1&amp;nbsp;month to mice; the sera of these mice were analyzed for anti-interferon-β antibodies by ELISA. Dodecylmal...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3649886</comments>
            <pubDate>Mon, 07 Jun 2010 17:15:18 +0100</pubDate>
            <guid isPermaLink="false">3649886</guid>        </item>
        <item>
            <title>Erratum to: Nicotinic Modulation of Innate Immune Pathways Via α7 Nicotinic Acetylcholine Receptor</title>
            <link>http://www.medworm.com/index.php?rid=3642299&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg485664443908477%2F</link>
            <description>Content Type Journal ArticleCategory ErratumDOI 10.1007/s11481-010-9224-9Authors
		Wen-Yan Cui, University of Virginia Department of Psychiatry and Neurobehavioral Sciences 1670 Discovery Drive, Suite 110 Charlottesville VA 22911 USAMing D. Li, University of Virginia Department of Psychiatry and Neurobehavioral Sciences 1670 Discovery Drive, Suite 110 Charlottesville VA 22911 USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3642299</comments>
            <pubDate>Fri, 04 Jun 2010 06:52:39 +0100</pubDate>
            <guid isPermaLink="false">3642299</guid>        </item>
        <item>
            <title>Tumor Necrosis Factor Alpha Gene −376 Polymorphism and Susceptibility to Multiple Sclerosis: An Egyptian Study</title>
            <link>http://www.medworm.com/index.php?rid=3600948&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fgwr517t6804r1882%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Tumor necrosis factor alpha, a proinflammatory cytokine, plays an important role in the clinical activity of relapsing–remitting
 multiple sclerosis and the development of progression. Dysregulation in the expression of tumor necrosis factor gene had been
 suggested in the pathogenesis of multiple sclerosis. Our aim was to investigate the relationship between tumor necrosis factor
 α−376 polymorphism with disease susceptibility and course of multiple sclerosis in Egyptian patients. Polymerase chain reaction
 and restriction fragment length polymorphism were carried out on 36 primary progressive multiple sclerosis patients, 36 age-
 and sex-matched remitting relapsing multiple sclerosis patients (diagnosed according to McDonald’s Diagnostic criteria) and
 30 age- ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3600948</comments>
            <pubDate>Mon, 24 May 2010 16:43:25 +0100</pubDate>
            <guid isPermaLink="false">3600948</guid>        </item>
        <item>
            <title>Translational Research in NeuroAIDS: A Neuroimmune Pharmacology-Related Course</title>
            <link>http://www.medworm.com/index.php?rid=3600949&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fwj62232h2053p466%2F</link>
            <description>We describe how NIP is integrated in the TR-NAMH program in the context
 of HAND.
 
 
	Content Type Journal ArticleCategory ORIGINAL ARTICLEDOI 10.1007/s11481-010-9222-yAuthors
		Amanda Brown, Johns Hopkins University Department of Neurology, Division of Neuroimmunology and Neurological Infections 600 N. Wolfe Street, Pathology 509 Baltimore MD 21287 USABruce Shiramizu, University of Hawaii at Manoa Hawaii Center for AIDS, John A. Burns School of Medicine 3675 Kilauea Avenue, 5th Floor Young Building Honolulu HI 96816 USAAvindra Nath, Johns Hopkins University Department of Neurology, Division of Neuroimmunology and Neurological Infections 600 N. Wolfe Street, Pathology 509 Baltimore MD 21287 USAValerie Wojna, University of Puerto Rico, Medical Sciences Campus Division of Neurology, Departm...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3600949</comments>
            <pubDate>Mon, 24 May 2010 05:42:21 +0100</pubDate>
            <guid isPermaLink="false">3600949</guid>        </item>
        <item>
            <title>Morphine Suppresses MHC-II Expression on Circulating B Lymphocytes via Activation of the HPA</title>
            <link>http://www.medworm.com/index.php?rid=3539749&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc2321v162680147t%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Morphine has been shown to alter gene expression of the major histocompatibility complex, class II (MHC-II) in circulating
 rat immunocytes. Here, we demonstrate that a single morphine injection (10&amp;nbsp;mg/kg) reduces basal MHC-II protein expression
 on circulating B lymphocytes by 33%, while also impairing the ability of B lymphocytes to increase MHC-II upon interleukin-4
 induction. As these data implicate opioids in the regulation of antigen presentation, studies were undertaken to examine the
 potential mechanisms through which morphine exerts this suppressive effect. Central injection studies utilized Tyr-D-Ala-Gly-(me)
 Phe-Gly-ol (DAMGO), an opioid receptor agonist, which mimicked morphine’s effect on MHC-II, while D-Phe-Cys_Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2
 (CTO...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3539749</comments>
            <pubDate>Tue, 04 May 2010 08:18:02 +0100</pubDate>
            <guid isPermaLink="false">3539749</guid>        </item>
        <item>
            <title>Neuroimmunity of HTLV-I Infection</title>
            <link>http://www.medworm.com/index.php?rid=3531480&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv75n0h231v71l425%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Human T-lymphotrophic virus type I (HTLV-I) is an oncogenic retrovirus and its infection is associated with a variety of human
 diseases including HTLV-I-associated myelopathy/tropic spastic paraparesis (HAM/TSP). Large numbers of epidemiological, virological,
 immunological, and clinical studies on HTLV-I- and HTLV-I-associated diseases have been published, although the pathogenesis
 of HAM/TSP remains to be fully understood. In the last several years, researchers have shown that several key factors are
 important in HTLV-I-associated neurologic disease including high HTLV-I proviral load and a strong immune response to HTLV-I.
 Here, we review pathophysiological findings on HAM/TSP and focus on viral-host immune responses to the virus in HTLV-I infected
 individuals. ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3531480</comments>
            <pubDate>Sat, 01 May 2010 07:10:39 +0100</pubDate>
            <guid isPermaLink="false">3531480</guid>        </item>
        <item>
            <title>HERVs in Neuropathogenesis</title>
            <link>http://www.medworm.com/index.php?rid=3512911&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw1473l48l1064848%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In humans, exogenous retroviruses are known to cause immunodeficiency and neurological disease. While endogenous retroviruses
 are firmly established pathogens in other species, the human endogenous retroviruses (HERVs) may well be considered as emerging
 pathogens. HERVs also exhibit complex interactions with exogenous retroviruses and herpesviruses. Two neurological disorders
 in particular are associated with HERVs: multiple sclerosis (MS) and schizophrenia. HERV-H/F and HERV-W are specifically activated
 both in the circulation and the central nervous system (CNS) in a majority of MS patients, and particularly, the envelopes
 (env transcription and Env proteins) appear strongly associated with disease activity. Interferon beta (IFN-β) therapy is well-established
 f...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3512911</comments>
            <pubDate>Tue, 27 Apr 2010 07:02:38 +0100</pubDate>
            <guid isPermaLink="false">3512911</guid>        </item>
        <item>
            <title>Blue Moon Neurovirology: The Merits of Studying Rare CNS Diseases of Viral Origin</title>
            <link>http://www.medworm.com/index.php?rid=3509267&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk01284t220681840%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;While measles virus (MV) continues to have a significant impact on human health, causing 150,000–200,000 deaths worldwide
 each year, the number of fatalities that can be attributed to MV-triggered central nervous system (CNS) diseases are on the
 order of a few hundred individuals annually (World Health Organization 2009). Despite this modest impact, substantial effort has been expended to understand the basis of measles-triggered neuropathogenesis.
 What can be gained by studying such a rare condition? Simply stated, the wealth of studies in this field have revealed core
 principles that are relevant to multiple neurotropic pathogens, and that inform the broader field of viral pathogenesis. In
 recent years, the emergence of powerful in vitro systems, novel animal m...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3509267</comments>
            <pubDate>Sat, 24 Apr 2010 08:09:40 +0100</pubDate>
            <guid isPermaLink="false">3509267</guid>        </item>
        <item>
            <title>Activation of Egr-1 Expression in Astrocytes by HIV-1 Tat: New Insights into Astrocyte-Mediated Tat Neurotoxicity</title>
            <link>http://www.medworm.com/index.php?rid=3502099&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr770747h46215707%2F</link>
            <description>In this study, we further examined the
 relationship between Tat and Egr-1 in astrocytes. We found increased Egr-1 protein expression in Tat-expressing human astrocytoma
 cells and mouse primary astrocytes. Using the Egr-1 promoter-driven firefly luciferase reporter gene assay and the site-directed
 mutagenesis, we demonstrated that Tat increased Egr-1 expression by transactivating the Egr-1 promoter and involving specific
 serum response elements within the promoter. Consistent with these data, we showed that Tat transactivation of the Egr-1 promoter
 was abrogated when astrocytes were cultured in serum-reduced media. Taken together, these results reveal that Tat directly
 transactivates Egr-1 expression and suggest that Tat interaction with Egr-1 is probably one of the very upstream mole...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3502099</comments>
            <pubDate>Fri, 23 Apr 2010 08:29:17 +0100</pubDate>
            <guid isPermaLink="false">3502099</guid>        </item>
        <item>
            <title>Neuroimmune Pharmacological Control of EAE</title>
            <link>http://www.medworm.com/index.php?rid=3502100&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh13632036p810131%2F</link>
            <description>Content Type Journal ArticleCategory GUEST COMMENTARYDOI 10.1007/s11481-010-9219-6Authors
		Kalipada Pahan, Rush University Medical Center Department of Neurological sciences Cohn Research Building, Suite 320, 1735 West Harrison St Chicago IL 60612 USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3502100</comments>
            <pubDate>Fri, 23 Apr 2010 08:29:12 +0100</pubDate>
            <guid isPermaLink="false">3502100</guid>        </item>
        <item>
            <title>Microbial Induction of Vascular Pathology in the CNS</title>
            <link>http://www.medworm.com/index.php?rid=3484065&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg542hr6104v27681%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The central nervous system (CNS) is a finely tuned organ that participates in nearly every aspect of our day-to-day function.
 Neurons lie at the core of this functional unit and maintain an active dialogue with one another as well as their fellow CNS
 residents (e.g. astrocytes, oligodendrocytes, microglia). Because of this complex dialogue, it is essential that the CNS milieu
 be tightly regulated in order to permit uninterrupted and efficient neural chemistry. This is accomplished in part by anatomical
 barriers that segregate vascular components from the cerebral spinal fluid (CSF) and brain parenchyma. These barriers impede
 entry of noxious materials and enable the CNS to maintain requisite protein and ionic balances for constant electrochemical
 signaling. Under ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3484065</comments>
            <pubDate>Sat, 17 Apr 2010 16:50:58 +0100</pubDate>
            <guid isPermaLink="false">3484065</guid>        </item>
        <item>
            <title>Molecular Regulation of JC Virus Tropism: Insights into Potential Therapeutic Targets for Progressive Multifocal Leukoencephalopathy</title>
            <link>http://www.medworm.com/index.php?rid=3481553&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn312060n272l5605%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Progressive multifocal leukoencephalopathy (PML) is a growing concern for patients undergoing immune modulatory therapies
 for treatment of autoimmune diseases such as multiple sclerosis. Currently, there are no drugs approved for the treatment
 of PML that have been demonstrated in the patient to effectively and reproducibly alter the course of disease progression.
 The human polyoma virus JC is the causative agent of PML. JC virus (JCV) dissemination is tightly controlled by regulation
 of viral gene expression from the promoter by cellular transcription factors expressed in cells permissive for infection.
 JCV infection likely occurs during childhood, and latent virus containing PML-associated promoter sequences is maintained
 in lymphoid cells within the bone marrow...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3481553</comments>
            <pubDate>Fri, 16 Apr 2010 16:52:53 +0100</pubDate>
            <guid isPermaLink="false">3481553</guid>        </item>
        <item>
            <title>Studies in the Modulation of Experimental Autoimmune Encephalomyelitis</title>
            <link>http://www.medworm.com/index.php?rid=3481554&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv4x23l11247m4743%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Experimental autoimmune encephalomyelitis (EAE), an experimental model for multiple sclerosis, can be induced through inoculation
 with several different central nervous system (CNS) proteins or peptides. Modulation of EAE, resulting in either protection
 from EAE or enhancement of EAE, can also be accomplished through either vaccination or DNA immunization with molecular mimics
 of self-CNS proteins. Previously published data on this method of EAE modulation will be reviewed. New data is presented,
 which demonstrates that EAE can also be modulated through the administration of the β-(1,3)-d-glucan, curdlan. Dendritic cells stimulated by curdlan are involved in the differentiation of the interleukin-17 producing
 subset of CD4+ T cells that are recognized effector cel...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3481554</comments>
            <pubDate>Fri, 16 Apr 2010 16:52:52 +0100</pubDate>
            <guid isPermaLink="false">3481554</guid>        </item>
        <item>
            <title>A Common Neuronal Response to Alphaherpesvirus Infection</title>
            <link>http://www.medworm.com/index.php?rid=3481555&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F4703108246m04221%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Alphaherpesviruses are a subfamily of the Herpesviridae that can invade the nervous system and establish either lytic or latent infections. The establishment of latent infection
 can occur only in neurons, indicating a unique virus–host interaction in these cells. Here, we compare results from seven
 microarray studies that focused on the host response of either neural tissue or isolated neurons to alphaherpesvirus infection.
 These studies utilized either herpes simplex virus type 1 or pseudorabies virus as the infectious agent. From these data,
 we have found common host responses spanning a variety of infection models in different species, with different herpesvirus
 strains, and during all phases of infection including lytic, latent, and reactivation. The repeated...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3481555</comments>
            <pubDate>Fri, 16 Apr 2010 16:52:51 +0100</pubDate>
            <guid isPermaLink="false">3481555</guid>        </item>
        <item>
            <title>HIV-Associated Neurocognitive Disorder: Pathogenesis and Therapeutic Opportunities</title>
            <link>http://www.medworm.com/index.php?rid=3481556&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq163577018108113%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Human immunodeficiency virus type 1 (HIV) infection presently affects more that 40 million people worldwide, and is associated
 with central nervous system (CNS) disruption in at least 30% of infected individuals. The use of highly active antiretroviral
 therapy has lessened the incidence, but not the prevalence of mild impairment of higher cognitive and cortical functions (HIV-associated
 neurocognitive disorders) as well as substantially reduced a more severe form dementia (HIV-associated dementia). Furthermore,
 improving neurological outcomes will require novel, adjunctive therapies that are targeted towards mechanisms of HIV-induced
 neurodegeneration. Identifying such molecular and pharmacological targets requires an understanding of the events preceding
 irrevers...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3481556</comments>
            <pubDate>Thu, 15 Apr 2010 16:54:59 +0100</pubDate>
            <guid isPermaLink="false">3481556</guid>        </item>
        <item>
            <title>In Vivo Morphine Treatment Synergistically Increases LPS-Induced Caspase Activity in Immune Organs</title>
            <link>http://www.medworm.com/index.php?rid=3481557&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm65057275123h7v5%2F</link>
            <description>The objective of this study was to develop an in vivo detection method
 for assessing caspase activity induced both by morphine directly and by morphine combined with lipopolysaccharide (LPS)–immune
 activation. Mice were administered saline, morphine, LPS, or a combination of morphine and LPS. Prior to sacrifice, mice were
 injected with a poly-caspase-specific apoptosis detection probe to detect internal caspase activity in vivo. Results revealed
 that morphine alone did not directly induce caspase activity. However, morphine significantly enhanced the LPS-induced caspase
 activity in spleen, thymus, and bone marrow-derived immune cells. The use of a poly-caspase detection probe methodology to
 label caspase activity in vivo provides a powerful quantitative tool for the in vivo analysi...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3481557</comments>
            <pubDate>Wed, 14 Apr 2010 06:56:14 +0100</pubDate>
            <guid isPermaLink="false">3481557</guid>        </item>
        <item>
            <title>Innate and Adaptive Factors Regulating Human Immunodeficiency Virus Type 1 Genomic Activation</title>
            <link>http://www.medworm.com/index.php?rid=3469302&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl868w18n3m54757q%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Over the past decade, antiretroviral therapy targeting the viral entry process, reverse transcriptase, integrase, and protease,
 has prolonged the lives of people infected with human immunodeficiency virus type 1 (HIV-1). However, despite the development
 of more effective therapeutic strategies, reservoirs of viral infection remain. This review discusses molecular mechanisms
 surrounding the development of latency from the site of integration to pre- and post-integration maintenance of latency, including
 epigenetic factors. In addition, an overview of innate and adaptive cells important to HIV-1 infection are examined from the
 viewpoint of cytokines released and cytokines that act on these cells to explore an overall understanding of HIV-1 proviral
 genome activation...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3469302</comments>
            <pubDate>Mon, 12 Apr 2010 17:58:25 +0100</pubDate>
            <guid isPermaLink="false">3469302</guid>        </item>
        <item>
            <title>Nicotinic Modulation of Innate Immune Pathways Via α7 Nicotinic Acetylcholine Receptor</title>
            <link>http://www.medworm.com/index.php?rid=3469303&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fu447823k4v246178%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The major addictive component of tobacco, nicotine, exerts anti-inflammatory effects in multiple cell types and may benefit
 neurons in various degenerative disorders, such as Alzheimer’s and Parkinson’s disease, in which an inflammation-related mechanism
 is implicated. Among the various nicotinic acetylcholine receptors, α7, which has been identified in both neurons and immune
 cells and has high permeability to calcium, is believed to contribute significantly to nicotinic anti-inflammatory and neuron-protective
 effects. Although nicotine has been used in clinical trials for the treatment of some inflammatory diseases such as ulcerative
 colitis, the molecular mechanisms of its actions are largely unknown. In this review, we provide current evidence for nicotine...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3469303</comments>
            <pubDate>Mon, 12 Apr 2010 17:58:24 +0100</pubDate>
            <guid isPermaLink="false">3469303</guid>        </item>
        <item>
            <title>Chronic Viral Infection and Primary Central Nervous System Malignancy</title>
            <link>http://www.medworm.com/index.php?rid=3469304&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk251x482g2070584%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Primary central nervous system (CNS) tumors cause significant morbidity and mortality in both adults and children. While some
 of the genetic and molecular mechanisms of neuro-oncogenesis are known, much less is known about possible epigenetic contributions
 to disease pathophysiology. Over the last several decades, chronic viral infections have been associated with a number of
 human malignancies. In primary CNS malignancies, two families of viruses, namely polyomavirus and herpesvirus, have been detected
 with varied frequencies in a number of pediatric and adult histological tumor subtypes. However, establishing a link between
 chronic viral infection and primary CNS malignancy has been an area of considerable controversy, due in part to variations
 in detection freq...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3469304</comments>
            <pubDate>Mon, 12 Apr 2010 17:58:23 +0100</pubDate>
            <guid isPermaLink="false">3469304</guid>        </item>
        <item>
            <title>Alcohol-Induced Interactive Phosphorylation of Src and Toll-like Receptor Regulates the Secretion of Inflammatory Mediators by Human Astrocytes</title>
            <link>http://www.medworm.com/index.php?rid=3469305&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb12mkq6r841g7361%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Secretion of pro-inflammatory molecules by astrocytes after alcohol treatment was shown to be associated with neuroinflammation.
 We hypothesized that activation of cytosolic phospholipase A2 (cPLA2) and cyclooxygenase (COX-2) by ethanol in astrocytes
 enhanced the secretion of inflammatory agents via the interactive tyrosine phosphorylation of toll-like receptor 4 (TLR4)
 and Src kinase. To test this hypothesis, we treated primary human astrocytes with 20&amp;nbsp;mM ethanol for 48&amp;nbsp;h at 37°C. Ethanol
 exposure elevated cytochrome P450-2E1 activity, reactive oxygen species levels, and secretion of prostaglandin E2 (PGE2) in
 these cells. Secretion of PGE2 was associated with induction of cPLA2 activity and protein content as well as COX-2 protein
 level in a Src phosp...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3469305</comments>
            <pubDate>Thu, 08 Apr 2010 18:03:04 +0100</pubDate>
            <guid isPermaLink="false">3469305</guid>        </item>
        <item>
            <title>Epstein–Barr Virus Infection and Multiple Sclerosis: A Review</title>
            <link>http://www.medworm.com/index.php?rid=3450848&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd01314196rg73x47%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Epstein–Barr virus (EBV) infection results in a life-long persistence of the virus in the host’s B-lymphocytes and has been
 associated with numerous cancers including Burkitt’s lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma. There is considerable
 evidence that EBV infection is a strong risk factor for the development of multiple sclerosis. Early age at primary EBV infection
 is typically asymptomatic, but primary infection during adolescence or adulthood often manifests as infectious mononucleosis,
 which has been associated with a two- to threefold increased risk of MS. Most importantly, MS risk is extremely low in individuals
 who are EBV negative, but it increases several folds following EBV infection. Additional evidence supporting a role for EBV
 ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3450848</comments>
            <pubDate>Mon, 05 Apr 2010 21:36:14 +0100</pubDate>
            <guid isPermaLink="false">3450848</guid>        </item>
        <item>
            <title>Pathogenesis of Murine Coronavirus in the Central Nervous System</title>
            <link>http://www.medworm.com/index.php?rid=3450847&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw34464659127vh10%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Murine coronavirus (mouse hepatitis virus, MHV) is a collection of strains that induce disease in several organ systems of
 mice. Infection with neurotropic strains JHM and A59 causes acute encephalitis, and in survivors, chronic demyelination, the
 latter of which serves as an animal model for multiple sclerosis. The MHV receptor is a carcinoembryonic antigen-related cell
 adhesion molecule, CEACAM1a; paradoxically, CEACAM1a is poorly expressed in the central nervous system (CNS), leading to speculation
 of an additional receptor. Comparison of highly neurovirulent JHM isolates with less virulent variants and the weakly neurovirulent
 A59 strain, combined with the use of reverse genetics, has allowed mapping of pathogenic properties to individual viral genes.
 The spik...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3450847</comments>
            <pubDate>Mon, 05 Apr 2010 21:36:14 +0100</pubDate>
            <guid isPermaLink="false">3450847</guid>        </item>
        <item>
            <title>Psychiatric Symptoms and HPA Axis Function in Adolescent Methamphetamine Users</title>
            <link>http://www.medworm.com/index.php?rid=3430698&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F27014100ll8x9771%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Methamphetamine (METH) is a widely abused drug. However, little is known about the effects of chronic METH consumption on
 HPA axis function and psychiatric symptomatology in adolescent METH users. The current study evaluated psychiatric symptoms
 and changes in the stress response of adolescent METH users. Forty-one adolescent METH users and 75 comparison subjects in
 the same age range (ages 12-23&amp;nbsp;years) were recruited. Each subject completed the Symptom Checklist-90R (SCL-90) and was evaluated
 using the Brief Psychiatric Rating Scale. In addition, the subjects completed the Trier Social Stress Test (TSST) and had
 salivary cortisol levels measured 30 min before, immediately after, and 60&amp;nbsp;min after the TSST. Adolescent METH users showed
 greater severity of...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3430698</comments>
            <pubDate>Wed, 31 Mar 2010 16:44:19 +0100</pubDate>
            <guid isPermaLink="false">3430698</guid>        </item>
        <item>
            <title>HIV Neuropathogenesis: a Tight Rope Walk of Innate Immunity</title>
            <link>http://www.medworm.com/index.php?rid=3430699&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fvhl355375368uk12%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;During the course of HIV-1 disease, virus neuroinvasion occurs as an early event, within weeks following infection. Intriguingly,
 subsequent central nervous system (CNS) complications manifest only decades after the initial virus exposure. Although CNS
 is commonly regarded as an immune-privileged site, emerging evidence indicates that innate immunity elicited by the CNS glial
 cells is a critical determinant for the establishment of protective immunity. Sustained expression of these protective immune
 responses, however, can be a double-edged sword. As protective immune mediators, cytokines have the ability to function in
 networks and co-operate with other host/viral mediators to tip the balance from a protective to toxic state in the CNS. Herein,
 we present an over...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3430699</comments>
            <pubDate>Wed, 31 Mar 2010 06:04:40 +0100</pubDate>
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        <item>
            <title>Changes in the NMR Metabolic Profile of Human Microglial Cells Exposed to Lipopolysaccharide or Morphine</title>
            <link>http://www.medworm.com/index.php?rid=3405568&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F320675821054762w%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Microglial cells play a major role in host defense of the central nervous system. Once activated, several functional properties
 are up-regulated including migration, phagocytosis, and secretion of inflammatory mediators such as cytokines and chemokines.
 Little, if anything, is known about the metabolic changes that occur during the activation process. High-resolution 1H nuclear magnetic resonance spectra obtained from perchloric acid extracts of human microglial cell cultures exposed to lipopolysaccharide
 (LPS) or morphine were used to both identify and quantify the metabolites. We found that human microglia exposed to LPS had
 increased concentrations of glutamate and lactate, whereas the cells exposed to morphine had decreased concentrations in creatinine,
 taurine...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3405568</comments>
            <pubDate>Wed, 24 Mar 2010 05:46:52 +0100</pubDate>
            <guid isPermaLink="false">3405568</guid>        </item>
        <item>
            <title>Mycobacteria-Induced Suppression of Autoimmunity in the Central Nervous System</title>
            <link>http://www.medworm.com/index.php?rid=3400654&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft21w8t13748hm8u6%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Mycobacterial suppression of central nervous system (CNS) autoimmunity has been demonstrated in various experimental models,
 epidemiological studies, and clinical trials. Recent studies have led to an increased understanding of the cellular and molecular
 interactions involved in the pathogenesis of autoimmune diseases and of mycobacterial immunity. Here, we review some of the
 mechanisms by which mycobacterial infection might modulate the clinical course of CNS autoimmunity. A more complete understanding
 of these mechanisms may lead to the development of novel immunotherapeutic tools for treating autoimmune diseases.
 
 
	Content Type Journal ArticleCategory Invited ReviewDOI 10.1007/s11481-010-9199-6Authors
		JangEun Lee, University of Wisconsin Department of Pathol...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3400654</comments>
            <pubDate>Tue, 23 Mar 2010 18:07:57 +0100</pubDate>
            <guid isPermaLink="false">3400654</guid>        </item>
        <item>
            <title>Nanoformulated Antiretroviral Drug Combinations Extend Drug Release and Antiretroviral Responses in HIV-1-Infected Macrophages: Implications for NeuroAIDS Therapeutics</title>
            <link>http://www.medworm.com/index.php?rid=3375699&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft4285q0318jlp933%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;We posit that improvements in pharmacokinetics and biodistributions of antiretroviral therapies (ART) for human immunodeficiency
 virus type one-infected people can be achieved through nanoformulationed drug delivery systems. To this end, we manufactured
 nanoparticles of atazanavir, efavirenz, and ritonavir (termed nanoART) and treated human monocyte-derived macrophages (MDM)
 in combination therapies to assess antiretroviral responses. This resulted in improved drug uptake, release, and antiretroviral
 efficacy over monotherapy. MDM rapidly, within minutes, ingested nanoART combinations, at equal or similar rates, as individual
 formulations. Combination nanoART ingested by MDM facilitated individual drug release from 15 to &amp;gt;20&amp;nbsp;days. These findings
 are notewo...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3375699</comments>
            <pubDate>Tue, 16 Mar 2010 14:52:20 +0100</pubDate>
            <guid isPermaLink="false">3375699</guid>        </item>
        <item>
            <title>16th Annual Society on NeuroImmune Pharmacology Conference</title>
            <link>http://www.medworm.com/index.php?rid=3328537&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff63195v773126634%2F</link>
            <description>Content Type Journal ArticleCategory BRIEF REPORTDOI 10.1007/s11481-010-9196-9Authors
		Guy A Cabral, Virginia Commonwealth University School of Medicine Richmond VA USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3328537</comments>
            <pubDate>Tue, 02 Mar 2010 10:06:44 +0100</pubDate>
            <guid isPermaLink="false">3328537</guid>        </item>
        <item>
            <title>16th Annual Conference of the Society on Neuroimmune Pharmacology</title>
            <link>http://www.medworm.com/index.php?rid=3304000&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fftv34576875un640%2F</link>
            <description>Content Type Journal ArticleCategory Guest CommentaryDOI 10.1007/s11481-010-9195-xAuthors
		Guy A. Cabral, Virginia Commonwealth University Department of Microbiology and Immunology, School of Medicine Richmond VA USAThomas J. Rogers, Temple University School of Medicine Fels Institute for Cancer Research and Molecular Biology, Center for Substance Abuse Research, Center for Inflammation, Translational and Clinical Lung Research Philadelphia PA USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3304000</comments>
            <pubDate>Tue, 23 Feb 2010 07:59:34 +0100</pubDate>
            <guid isPermaLink="false">3304000</guid>        </item>
        <item>
            <title>Central Nervous System Expression of Interferon Regulatory Factor 1 Regulates Experimental Autoimmune Encephalomyelitis</title>
            <link>http://www.medworm.com/index.php?rid=3304001&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fxk1302g019w19562%2F</link>
            <description>In this study, we examined the role of central nervous system (CNS) expression of IRF-1
 in the natural course of EAE. In an effort to dissect the CNS effects from the peripheral immune effects of IRF-1, we generated
 bone marrow chimera mice that differentially expressed IRF-1 in the CNS and in the immune system. We found that mice lacking
 IRF-1 in the CNS developed significantly milder clinical symptoms and shorter disease duration compared to those with wild-type
 background. Based on these results, we concluded that the CNS expression of IRF-1 regulates the disease process in EAE. Our
 findings are relevant to the inflammatory mechanisms involved in multiple sclerosis and may provide a basis for development
 of novel therapeutic targets of the disease.
 
 
	Content Type Journal Articl...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3304001</comments>
            <pubDate>Tue, 23 Feb 2010 07:59:33 +0100</pubDate>
            <guid isPermaLink="false">3304001</guid>        </item>
        <item>
            <title>Histone Deacetylase Inhibitors Suppress the Expression of Inflammatory and Innate Immune Response Genes in Human Microglia and Astrocytes</title>
            <link>http://www.medworm.com/index.php?rid=3281180&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fcn332j5426268517%2F</link>
            <description>In this study, we examined the effects of two non-selective HDACi, trichostatin A and
 valproic acid, on antiviral and cytokine gene expression in primary human microglia and astrocytes stimulated with TLR3 or
 TLR4 ligand. HDACi potently suppressed the expression of innate antiviral molecules such as IFNβ, interferon-simulated genes,
 and proteins involved in TLR3/TLR4 signaling. HDACi also suppressed microglial and astrocytic cytokine and chemokine gene
 expression, but with different effects on different groups of cytokines. These results have important implications for the
 clinical use of HDACi.
 
 
	Content Type Journal ArticleCategory ORIGINAL ARTICLEDOI 10.1007/s11481-010-9192-0Authors
		Hyeon-Sook Suh, Albert Einstein College of Medicine Department of Pathology 1300 Morris Park A...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3281180</comments>
            <pubDate>Tue, 16 Feb 2010 06:44:51 +0100</pubDate>
            <guid isPermaLink="false">3281180</guid>        </item>
        <item>
            <title>Advances in the “Omics” for Diagnosis, Pathogenesis, and Therapeutic Development</title>
            <link>http://www.medworm.com/index.php?rid=3264146&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F03m497932l486665%2F</link>
            <description>Content Type Journal ArticleCategory Guest CommentaryDOI 10.1007/s11481-010-9194-yAuthors
		Howard S. Fox, University of Nebraska Medical Center Department of Pharmacology and Experimental Neuroscience Omaha NE 68198-5880 USA
	

	
		Journal Journal of Neuroimmune PharmacologyOnline ISSN 1557-1904Print ISSN 1557-1890 (Source: Journal of NeuroImmune Pharmacology)</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3264146</comments>
            <pubDate>Mon, 08 Feb 2010 17:20:23 +0100</pubDate>
            <guid isPermaLink="false">3264146</guid>        </item>
        <item>
            <title>Nociceptin/Orphanin FQ Suppresses Adaptive Immune Responses In Vivo and at Picomolar Levels In Vitro</title>
            <link>http://www.medworm.com/index.php?rid=3232990&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F47274q72l8q2662v%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Nociceptin/orphanin FQ (N/OFQ), added in vitro to murine spleen cells in the picomolar range, suppressed antibody formation
 to sheep red blood cells in a primary and a secondary plaque-forming cell assay. The activity of the peptide was maximal at
 10−12&amp;nbsp;M, with an asymmetric U-shaped dose–response curve that extended activity to 10−14&amp;nbsp;M. Suppression was not blocked by pretreatment with naloxone. Specificity of the suppressive response was shown using affinity-purified
 rabbit antibodies against two N/OFQ peptides and with a pharmacological antagonist. Antisera against both peptides were active,
 in a dose-related manner, in neutralizing N/OFQ-mediated immunosuppression, when the peptide was used at concentrations from
 10−12.3 to 10−11.6&amp;nbsp;M. In...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3232990</comments>
            <pubDate>Mon, 01 Feb 2010 06:47:39 +0100</pubDate>
            <guid isPermaLink="false">3232990</guid>        </item>
        <item>
            <title>Agent-specific Shadoo Responses in Transmissible Encephalopathies</title>
            <link>http://www.medworm.com/index.php?rid=3228929&amp;cid=s_33363_13_f&amp;fid=33363&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F61778108u386746r%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Transmissible spongiform encephalopathies (TSE) are neurodegenerative diseases caused by an infectious agent with viral properties.
 Host prion protein (PrP), a marker of late stage TSE pathology, is linked to a similar protein called Shadoo (Sho). Sho is
 reduced in mice infected with the RML scrapie agent, but has not been investigated in other TSEs. Although PrP is required
 for infection by TSE agents, it is not known if Sho is similarly required. Presumably Sho protects cells from toxic effects
 of misfolded PrP. We compared Sho and PrP changes after infection by very distinct TSE agents including sporadic CJD, Asiatic
 CJD, New Guinea kuru, vCJD (the UK epidemic bovine agent) and 22L sheep scrapie, all passaged in standard mice. We found that
 Sho reductions were ...</description>
            <author>Journal of NeuroImmune Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3228929</comments>
            <pubDate>Fri, 29 Jan 2010 12:06:11 +0100</pubDate>
            <guid isPermaLink="false">3228929</guid>        </item>
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