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        <title>Journal of Neuroimmunology 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 Neuroimmunology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Journal+of+Neuroimmunology&t=Journal+of+Neuroimmunology&s=Search&f=source]]></link>
        <lastBuildDate>Tue, 27 Dec 2011 19:17:08 +0100</lastBuildDate>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5358572&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002803%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358572</comments>
            <pubDate>Fri, 28 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358572</guid>        </item>
        <item>
            <title>Social disruption induced priming of CNS inflammatory response to Theiler's virus is dependent upon stress induced IL-6 release</title>
            <link>http://www.medworm.com/index.php?rid=5358578&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002232%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Chronic social disruption stress (SDR) exacerbates acute and chronic phase Theiler's murine encephalomyelitis virus (TMEV) infection, a mouse model of multiple sclerosis. However, the precise mechanism by which this occurs remains unknown. The present study suggests that SDR exacerbates TMEV disease course by priming virus-induced neuroinflammation. It was demonstrated that IL-1β mRNA expression increases following acute SDR; however, IL-6 mRNA expression, but not IL-1β, is upregulated in response to chronic SDR. Furthermore, this study demonstrated SDR prior to infection increases infection related central IL-6 and IL-1β mRNA expression, and administration of IL-6 neutralizing antibody during SDR reverses this increase in neuroinflammation. (Source: Journal of Neuroimmunology...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358578</comments>
            <pubDate>Mon, 17 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358578</guid>        </item>
        <item>
            <title>The effects of fasudil on the permeability of the rat blood–brain barrier and blood–spinal cord barrier following experimental autoimmune encephalomyelitis</title>
            <link>http://www.medworm.com/index.php?rid=5358580&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002323%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Dysfunction of the blood–brain barrier (BBB) and blood–spinal cord barrier (BSCB) is a primary characteristic of multiple sclerosis (MS). We evaluated the protective effects of fasudil, a selective ROCK inhibitor, in a model of experimental autoimmune encephalomyelitis (EAE) that was induced by guinea-pig spinal cord. In addition, we studied the effects of fasudil on BBB and BSCB permeability. We found that fasudil partly alleviated EAE-dependent damage by decreasing BBB and BSCB permeability. These results provide rationale for the development of selective inhibitors of Rho kinase as a novel therapy for MS. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358580</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358580</guid>        </item>
        <item>
            <title>Immune-mediated myelitis associated with Hepatitis virus infections</title>
            <link>http://www.medworm.com/index.php?rid=5358575&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002542%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Virus-induced spinal cord damage results from a cytolytic effect on anterior horn cells or from predominantly cellular immune-mediated damage of long white matter tracts. Infection with the hepatitis virus group, most notably hepatitis C virus, has infrequently been associated with the occurrence of myelitis. The pathogenesis of hepatitis virus-associated myelitis has not been clarified: virus-induced autoimmunity (humoral or cell-mediated, possibly vasculitic) seems the most likely disease mechanism. Limited available information offers no evidence of direct hepatitis virus infection of the spinal cord. Virus neuropenetration may occur after virus-infected mononuclear cells penetrate the blood–brain barrier, but a true neurolytic effect has not been demonstrated. Attacks of ac...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358575</comments>
            <pubDate>Mon, 26 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358575</guid>        </item>
        <item>
            <title>Neonatal androgenization affects the efficiency of β-adrenoceptor-mediated modulation of thymopoiesis</title>
            <link>http://www.medworm.com/index.php?rid=5358581&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002372%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, the study indicates the importance of the neonatal sex steroid milieu for shaping the immunomodulatory capacity of the thymic NA/β-AR signaling system in adult rats. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358581</comments>
            <pubDate>Fri, 23 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358581</guid>        </item>
        <item>
            <title>Reduction in IL-10 producing B cells (Breg) in multiple sclerosis is accompanied by a reduced naïve/memory Breg ratio during a relapse but not in remission</title>
            <link>http://www.medworm.com/index.php?rid=5358582&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002360%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we assessed B cell subsets, including Bregs, during stable and active disease in relapsing remitting multiple sclerosis (RRMS) patients and related B cell subsets to vitamin D status. We report that RRMS patients have a decreased percentage of both memory B cells and Bregs compared to healthy controls. During a relapse, the reduction in Bregs involved in particular naïve Bregs. We found no correlation between vitamin D status and B cell subsets. An effect of vitamin D on Bregs cannot be ruled out, since it might be the function that is interfered with instead of relative numbers. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358582</comments>
            <pubDate>Thu, 22 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358582</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5224051&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002499%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224051</comments>
            <pubDate>Thu, 15 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224051</guid>        </item>
        <item>
            <title>Antibodies to LM1 and LM1-containing ganglioside complexes in Guillain–Barré syndrome and chronic inflammatory demyelinating polyneuropathy</title>
            <link>http://www.medworm.com/index.php?rid=5358583&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002335%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: LM1 is localized in human peripheral nerve myelin. Antibodies to ganglioside complexes (GSCs) have been reported in Guillain–Barré syndrome (GBS). We investigated IgG antibodies to LM1 and two GSCs (GM1 and LMI, or GD1b and LM1) in the sera of each 40 patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and GBS, using ELISA. We detected anti-LM1 antibody in five with GBS and seven with CIDP; anti-GM1/LM1 antibody in three with GBS and one with CIDP; and anti-GD1b/LM1 antibody in two with CIDP. Antibodies to LM1 and LM1-containing GSCs may be among the targets for autoimmunity in GBS and CIDP. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358583</comments>
            <pubDate>Wed, 14 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358583</guid>        </item>
        <item>
            <title>Infliximab monotherapy in Neuro-Behçet's disease: Four year follow-up in a long-standing case resistant to conventional therapies</title>
            <link>http://www.medworm.com/index.php?rid=5358587&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002311%2Fabstract%3Frss%3Dyes</link>
            <description>Behçet's disease (BD) is a vasculitis characterized by hallmark lesions of oral and genital ulcers (). Involvement of parenchymal central nervous system (neuro-BD) is a serious complication commonly characterized by brainstem and/or basal ganglia lesions (). To date, the treatment of neuro-BD remains largely empirical, and may not adequately control the disease (). Given the well-recognized role played by tumor necrosis factor-α (TNFα) in the pathogenesis of active BD (), infliximab (a monoclonal antibody that binds to and neutralizes the activity of TNFα) has been adopted with favorable results in patients resistant to conventional immunosuppressive therapies and in a small placebo controlled study (). A review of published cases reveals that the follow-up of patients under chronic th...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358587</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358587</guid>        </item>
        <item>
            <title>Mannose binding lectin mediated complement pathway in multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=5358585&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002359%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Role of mannose binding lectin (MBL) complement activation pathway, an arm of innate immunity in multiple sclerosis (MS) was evaluated by analyzing the expression of MBL, MBL-associated serine protease-2 (MASP-2), and functional MBL/MASP-2 mediated C4 cleavage (fMBL) in 87 plasma and cerebrospinal fluid (CSF) samples from MS patients and non-MS controls. Median fMBL and MASP-2 plasma levels were higher in MS vs. non-MS cases. These associations remained in an analysis of subtypes of MS disease. These findings suggest a potential activation of MBL complement pathway in MS that may possibly alter the risk or progression of MS disease. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358585</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358585</guid>        </item>
        <item>
            <title>Prior laparotomy or corticosterone potentiates lipopolysaccharide-induced fever and sickness behaviors</title>
            <link>http://www.medworm.com/index.php?rid=5358579&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002281%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Stimulating sensitized immune cells with a subsequent immune challenge results in potentiated pro-inflammatory responses translating into exacerbated sickness responses (i.e. fever, pain and lethargy). Both corticosterone (CORT) and laparotomy cause sensitization, leading to enhanced sickness-induced neuroinflammation or pain (respectively). However, it is unknown whether this sensitization affects all sickness behaviors and immune cell responses equally. We show that prior CORT and prior laparotomy potentiated LPS-induced fever but not lethargy. Prior CORT, like prior laparotomy, was able to potentiate sickness-induced pain. Release of nitric oxide (NO) from peritoneal macrophages stimulated ex vivo demonstrates that laparotomy, but not CORT sensitizes these cells. (Source: Jour...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358579</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358579</guid>        </item>
        <item>
            <title>Role of α7 nicotinic acetylcholine receptors in regulating tumor necrosis factor-α (TNF-α) as revealed by subtype selective agonists</title>
            <link>http://www.medworm.com/index.php?rid=5358577&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002244%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, the role of α7 nAChRs in the regulation of TNF-α release was investigated using high affinity and selective α7 nAChR agonists in mouse peritoneal macrophage and human whole blood in vitro, and in mouse serum in vivo. In mouse peritoneal macrophages, LPS-induced TNF-α release in vitro was inhibited by a selective α7 nAChR agonist, A-833834 (5-[6-(5-Methyl-hexahydro-pyrrolo[3,4-c]pyrrol-2-yl)-pyridazin-3-yl]-1H-indole), and that effect was attenuated by α7 nAChR antagonist methyllycaconitine. The inhibitory effect of A-833834 on LPS-induced TNF-α release was also observed in human whole blood in vitro. I.v. LPS-induced TNF-α release in mouse serum was attenuated following i.p. administration of A-833834. Similarly, i.v. LPS-induced TNF-α release in mouse serum was als...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358577</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358577</guid>        </item>
        <item>
            <title>Role of glial cells in innate immunity and their role in CNS demyelination</title>
            <link>http://www.medworm.com/index.php?rid=5358574&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002293%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The adaptive and innate arms of the immune system are the two pillars of host defense against environmental pathogens. Multiple sclerosis (MS) is an inflammatory demyelinating disease of the CNS which is considered to be autoimmune and is thought to result from breakdown in the usual checks and balances of the adaptive immune response. The major pathological outcome of the disease is “the MS plaque” a unique feature of CNS demyelination characterized by the destruction of oligodendrocytes with loss of myelin and underlying axons. The MS plaque is not seen in other inflammatory disorders of the CNS. The prevailing opinion suggests that MS is mediated by the activation of an adaptive immune response which targets neural antigens. Currently, the role of an innate immune in the d...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358574</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358574</guid>        </item>
        <item>
            <title>Neuroadaptive changes in cerebellar neurons induced by chronic exposure to IL-6</title>
            <link>http://www.medworm.com/index.php?rid=5358576&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002268%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: IL-6 is an important signaling molecule in the CNS. CNS neurons express IL-6 receptors and their signal transduction molecules, consistent with a role for IL-6 in neuronal physiology. Research indicates that IL-6 levels are low in the normal brain but can be significantly elevated in CNS injury and disease. Relatively little is known about how the elevated levels of IL-6 affect neurons. In the current study we show that under conditions of chronic exposure, IL-6 induces alterations in the level of protein expression in developing CNS cells. Such changes may play a role in the altered CNS function observed in CNS conditions associated with elevated levels of IL-6 in the CNS. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358576</comments>
            <pubDate>Mon, 05 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358576</guid>        </item>
        <item>
            <title>Targeting Toll-like receptors: Emerging therapeutics for multiple sclerosis management</title>
            <link>http://www.medworm.com/index.php?rid=5358573&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS016557281100227X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Toll-like receptors (TLR) are important innate immune proteins for the identification and clearance of invading pathogen. TLR signal through adaptor proteins, most commonly myeloid differentiation primary response gene 88 (MyD88). Inappropriate response of specific TLR has been implicated in certain autoimmune diseases, such as multiple sclerosis (MS). Activation of TLR2, TLR4, TLR7 and TLR9 plays a role in experimental allergic encephalomyelitis (EAE), a murine model of MS, while TLR3 activation protects from disease. Therefore, TLR-modulation could be an important adjuvant to current treatments. Here, we focus on TLR involved in EAE and MS pathogenesis highlighting specific components targeting TLR that might offer further therapeutic possibilities. (Source: Journal of Neuroimm...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358573</comments>
            <pubDate>Mon, 05 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358573</guid>        </item>
        <item>
            <title>IL28B polymorphisms are not associated with the response to interferon-beta in multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=5358586&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002219%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Recent studies have revealed an association between interleukin 28B (IL28B) and response to IFN-alpha treatment in hepatitis C patients. Here we investigated the influence of IL28B polymorphisms in the response to interferon-beta (IFNβ) in multiple sclerosis (MS) patients. We genotyped two SNPs of the IL28B gene (rs8099917 and rs12979860) in 588 MS patients classified into responders (n=281) and non-responders (n=307) to IFNβ. Combined analysis of the study cohorts showed no significant associations between SNPs rs8099917 and rs12979860 and the response to treatment. These findings do not support a role of IL28B polymorphisms in the response to IFNβ in MS patients. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358586</comments>
            <pubDate>Fri, 02 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358586</guid>        </item>
        <item>
            <title>Low and dysregulated production of follistatin in immune cells of relapsing–remitting multiple sclerosis patients</title>
            <link>http://www.medworm.com/index.php?rid=5224063&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002207%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: One of the mechanisms known to play a key role in neuronal and oligodendroglial fate specification of neural stem cells (NSCs) is restriction of bone morphogenic proteins (BMP) signaling by BMP antagonists. Here, we demonstrate that follistatin mRNA and protein secreted levels in peripheral blood mononuclear cells (PBMCs) of relapsing–remitting multiple sclerosis (RR-MS) patients are significantly reduced compared to healthy controls (HC). We also observed a different profile of regulation mechanisms. Follistatin was similarly expressed and secreted by T lymphocytes and monocytes among the PBMCs of HC, and follistatin upregulation of HC was subjected to stimulation with both LPS and TNF-α. Among PBMCs of RR-MS patients, however, follistatin was found to be downregulated in the...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224063</comments>
            <pubDate>Thu, 01 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224063</guid>        </item>
        <item>
            <title>Leukotriene synthesis inhibitor decreases vasopressin release in the early phase of sepsis</title>
            <link>http://www.medworm.com/index.php?rid=5224057&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002153%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The aim was to analyze the effect of leukotriene synthesis inhibitor administered intraperitoneally in vasopressin release during sepsis. Male Wistar rats received injections of MK-886 (1.0, 2.0 or 4.0mg/kg) or vehicle (DMSO 5%) 1h before cecal ligation and puncture. There was some variation on the survival rate depending on the dose used but the drug did not modify the hematocrit, osmolality, serum sodium and nitrate, plasma protein, and neutrophil recruitment, in any dose. Nevertheless, vasopressin (AVP) release decreased in a dose–response manner in the early phase of sepsis. These results support the suggestion that leukotrienes (LTs) are involved in AVP release during sepsis. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224057</comments>
            <pubDate>Thu, 01 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224057</guid>        </item>
        <item>
            <title>Anti-neuronal and stress-induced-phosphoprotein 1 antibodies in neuro-Behçet's disease</title>
            <link>http://www.medworm.com/index.php?rid=5358584&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002256%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: No disease-specific neuronal antibodies have so far been defined in neuro-Behçet's disease (NBD). Immunohistochemistry and immunocytochemistry studies showed antibodies to hippocampal and cerebellar molecular layers and the surface antigens of cultured hippocampal neurons in sera and/or cerebrospinal fluids (CSF) of 13 of 20 NBD and 6 of 20 BD patients but not in multiple sclerosis or headache controls. Screening with a protein macroarray led to identification of stress-induced-phosphoprotein-1 (STIP-1) as an antigenic target. High-titer STIP-1-antibodies were detected in 6 NBD patients' sera but not in controls. These results suggest that neuronal antibodies could be useful as diagnostic biomarkers in NBD. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5358584</comments>
            <pubDate>Mon, 29 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5358584</guid>        </item>
        <item>
            <title>Four cases of anti-ganglioside antibody-positive neuralgic amyotrophy with good response to intravenous immunoglobulin infusion therapy</title>
            <link>http://www.medworm.com/index.php?rid=5224065&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002220%2Fabstract%3Frss%3Dyes</link>
            <description>We report the case of four patients with NA who were positive for anti-N-acetylgalactosaminyl GD1a (anti-GalNAc-GD1a) antibodies, had a preceding infection, and showed a good response to intravenous immunoglobulin infusion therapy. Anti-ganglioside antibodies, especially the anti-GalNAc-GD1a antibody, may be a useful marker for predicting response to immune therapy. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224065</comments>
            <pubDate>Mon, 29 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224065</guid>        </item>
        <item>
            <title>Lipid arrays identify myelin-derived lipids and lipid complexes as prominent targets for oligoclonal band antibodies in multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=5224062&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002165%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The presence of oligoclonal bands of IgG (OCB) in cerebrospinal fluid (CSF) is used to establish a diagnosis of multiple sclerosis (MS), but their specificity has remained an enigma since its first description over forty years ago. We now report that the use of lipid arrays identifies heteromeric complexes of myelin derived lipids as a prominent target for this intrathecal B cell response. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224062</comments>
            <pubDate>Mon, 29 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224062</guid>        </item>
        <item>
            <title>Dopamine up-regulates Th17 phenotype from individuals with generalized anxiety disorder</title>
            <link>http://www.medworm.com/index.php?rid=5224058&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS016557281100169X%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, our results show that the T cell functional dysregulation in GAD individuals is significantly amplified by DA. These immune abnormalities can have impact in increasing the susceptibility of individuals with anxiety disorders to infectious diseases and inflammatory/autoimmune disorders. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224058</comments>
            <pubDate>Mon, 29 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224058</guid>        </item>
        <item>
            <title>Immune reconstitution is not a prognostic factor in progressive multifocal leukoencephalopathy</title>
            <link>http://www.medworm.com/index.php?rid=5224061&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001937%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Progressive multifocal leukoencephalopathy (PML) is typically associated with minimal inflammation; however, patients may develop an inflammatory response due to immune reconstitution (IRIS). The authors aimed to determine if characteristics and outcomes of PML are altered in those with IRIS. A retrospective records review was performed on 87 patients diagnosed with PML at Johns Hopkins, 27 of which had a syndrome consistent with IRIS. Gadolinium enhancement on MRI occurred in 44.4% of cases of PML-IRIS versus 5.1% in PML (p (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224061</comments>
            <pubDate>Tue, 16 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224061</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5119450&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811002074%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119450</comments>
            <pubDate>Fri, 12 Aug 2011 13:59:44 +0100</pubDate>
            <guid isPermaLink="false">5119450</guid>        </item>
        <item>
            <title>Inflammation in the early stages of neurodegenerative pathology</title>
            <link>http://www.medworm.com/index.php?rid=5224052&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001925%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Inflammation is secondary to protein accumulation in neurodegenerative diseases, including Alzheimer's, Parkinson's and Amyotrophic Lateral Sclerosis. Emerging evidence indicate sustained inflammatory responses, involving microglia and astrocytes in animal models of neurodegeneration. It is unknown whether inflammation is beneficial or detrimental to disease progression and how inflammatory responses are induced within the CNS. Persistence of an inflammatory stimulus or failure to resolve sustained inflammation can result in pathology, thus, mechanisms that counteract inflammation are indispensable. Here we review studies on inflammation mediated by innate and adaptive immunity in the early stages of neurodegeneration and highlight important areas for future investigation. (Sourc...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224052</comments>
            <pubDate>Mon, 08 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224052</guid>        </item>
        <item>
            <title>Differential effect of clopidogrel and aspirin on the release of BDNF from platelets</title>
            <link>http://www.medworm.com/index.php?rid=5224064&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001883%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Anti-platelet treatment is a key therapeutic intervention in patients with cerebrovascular diseases. However, there is no information on its impact on the release of Brain-derived neurotrophic factor (BDNF), which is stored in large amounts in human platelets and essential for neuronal protection and repair. Here, we show that a single oral dose of clopidogrel, but not aspirin, significantly reduced the release of BDNF from platelets in healthy volunteers. These data point, for the first time, to possible differential effects of anti-platelet regimens on neuronal function in patients with cerebrovascular disorders. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224064</comments>
            <pubDate>Tue, 02 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224064</guid>        </item>
        <item>
            <title>Children with autism spectrum disorders (ASD) who exhibit chronic gastrointestinal (GI) symptoms and marked fluctuation of behavioral symptoms exhibit distinct innate immune abnormalities and transcriptional profiles of peripheral blood (PB) monocytes</title>
            <link>http://www.medworm.com/index.php?rid=5224060&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001913%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Innate/adaptive immune responses and transcript profiles of peripheral blood monocytes were studied in ASD children who exhibit fluctuating behavioral symptoms following infection and other immune insults (ASD/Inf, N=30). The ASD/Inf children with persistent gastrointestinal symptoms (ASD/Inf+GI, N=19), revealed less production of proinflammatory and counter-regulatory cytokines with stimuli of innate immunity and marked changes in transcript profiles of monocytes as compared to ASD/no-Inf (N=28) and normal (N=26) controls. This included a 4–5 fold up-regulation of chemokines (CCL2 and CCL7), consistent with the production of more CCL2 by ASD/Inf+GI cells. These results indicate dysregulated innate immune defense in the ASD/Inf+GI children, rendering them more vulnerable to com...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224060</comments>
            <pubDate>Tue, 02 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224060</guid>        </item>
        <item>
            <title>HIF-1α expression in the hippocampus and peripheral macrophages after glutamate-induced excitotoxicity</title>
            <link>http://www.medworm.com/index.php?rid=5224053&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001615%2Fabstract%3Frss%3Dyes</link>
            <description>This study shows the systemic response of increased HIF-1α, EPO, and VEGF mRNA and protein. In addition, VEGF expression was increased in neurons and over-expressed in glial cells in a model of neuroexcitotoxicity in the hippocampus, in which rats were neonatally exposed to high glutamate concentrations. Simultaneous increases in HIF-1α, EPO and VEGF mRNA in peritoneal macrophages were also observed. Our study is consistent with the hypothesis that these genes exert a protective effect in response to neurotoxicity. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224053</comments>
            <pubDate>Tue, 02 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224053</guid>        </item>
        <item>
            <title>Regional difference in inflammatory response to LPS-injection in the brain: Role of microglia cell density</title>
            <link>http://www.medworm.com/index.php?rid=5224056&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001901%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: To elucidate whether density of cells could contribute to the extent of microglial activation, we performed in vitro assays using three different densities of N13 microglia stimulated with LPS. Our results showed that induction of pro-inflammatory factors as TNF-α and iNOS was directly related to cell density, meanwhile the induction of the anti-inflammatory IL-10 was inversely related to cell density. Accordingly, in vivo assays showed that after LPS-injection, iNOS expression was more intense in substantia nigra, a brain area showing specific susceptibility to neurodegeneration after microglia activation, whereas IL-10 expression was more sustained in striatum, an area resistant to damage. These results support that microglia density is pivotal to control the balance between p...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224056</comments>
            <pubDate>Mon, 01 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224056</guid>        </item>
        <item>
            <title>Inhibition of prostaglandin E2 EP3 receptors improves stroke injury via anti-inflammatory and anti-apoptotic mechanisms</title>
            <link>http://www.medworm.com/index.php?rid=5224055&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001743%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Although deletion of EP3 receptors is known to ameliorate stroke injury in experimental stroke models, the underlying mechanisms and the effects of EP3-specific antagonists remain poorly understood. Here we demonstrate the protective effect of postischemic treatment with an EP3 antagonist, ONO-AE3-240, through anti-inflammatory and anti-apoptotic effects. In transient focal ischemia models, peritoneal injection of an EP3 antagonist after occlusion–reperfusion reduced infarction, edema and neurological dysfunctions to almost the same levels of those in EP3 knockout (KO) mice. Furthermore, neuronal apoptosis in the ischemic cortex investigated by terminal dUTP nick-end labeling (TUNEL) and caspase-3 immunostaining were ameliorated in EP3 antagonist-treated mice or EP3 KO mice as ...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224055</comments>
            <pubDate>Mon, 01 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224055</guid>        </item>
        <item>
            <title>Cytokines regulate neuronal gene expression: Differential effects of Th1, Th2 and monocyte/macrophage cytokines</title>
            <link>http://www.medworm.com/index.php?rid=5224054&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001706%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Inflammatory mediators, including cytokines, contribute to neuronal and axonal dysfunction and cell death. To examine the roles of cytokines in pathogenesis and regeneration in the central nervous system (CNS), we analyzed effects of cytokines on early gene regulation (6h) in neuronal cultures, employing gene arrays. Our hypothesis is that neuronal gene expression is differentially regulated in vitro by cytokine mixtures typical of Th1 and Th2 T cells and monocytes/macrophages (M/M). Th1 and M/M cytokines showed similar patterns for regulation of numerous pathways including cytokine-receptor interactions, MAP kinase, toll like receptors, apoptosis, PPAR signaling, cell adhesion molecules (CAMS), antigen processing, adipocytokine, and JAK-STAT signaling. M/M cytokines uniquely reg...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224054</comments>
            <pubDate>Mon, 01 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224054</guid>        </item>
        <item>
            <title>Detection of elevated antibodies against SR protein kinase 1 in the serum of Alzheimer's disease patients</title>
            <link>http://www.medworm.com/index.php?rid=5224059&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001731%2Fabstract%3Frss%3Dyes</link>
            <description>In this study we identified SR Protein Kinase 1 (SRPK1) as a new autoantigen elevated in AD. SRPK1, the prototype of the serine/arginine family of kinases, has been implicated in the regulation of multiple cellular processes such as pre-mRNA splicing, cell proliferation, chromatin structure, nuclear import and germ cell development. Using an ELISA assay, anti-SRPK1 antibodies, targeting mainly the first catalytic domain of the kinase, were detected in sera of patients with AD, at significantly elevated levels as compared to control subjects. The findings of this study document for the first time the existence of antibodies targeting SRPK1 in human sera and are indicative of a correlation between the levels of a-SRPK1 antibodies and the incidence of AD. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5224059</comments>
            <pubDate>Thu, 28 Jul 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5224059</guid>        </item>
        <item>
            <title>Autoimmunity to endoplasmic reticulum chaperone GRP94 in myasthenia gravis</title>
            <link>http://www.medworm.com/index.php?rid=5119462&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001718%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Immune responses to ER stress have been closely related to the pathogenesis of autoimmune diseases. Using an immunoprecipitation assay, 24 (7.1%) of 336 MG serum samples immunoprecipitated a 90-kDa protein from the muscle cellular extracts, but none of the disease or healthy control sera. The 90-kDa protein was affinity-purified and found to match to ER chaperon GRP94 by matrix-assisted laser desorption/ionization-time of flight mass spectroscopy analysis. The frequency of associated autoimmune diseases was much higher in the anti-GRP94-positive than the -negative patients (71% versus 11%, p (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119462</comments>
            <pubDate>Wed, 20 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119462</guid>        </item>
        <item>
            <title>Corticotropin-releasing hormone receptor-1 and 2 activity produces divergent resistance against stress-induced pulmonary Streptococcus pneumoniae infection</title>
            <link>http://www.medworm.com/index.php?rid=5119458&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001895%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Utilizing a murine model of S. pneumoniae infection and restraint stress, we determined how corticotropin releasing hormone (CRH-R) receptors impacts disease. CRH-R1 (antalarmin) and CRH-R2 (astressin2B) antagonists were administered intraperitoneally prior to restraint stress followed by pulmonary S. pneumoniae infection. CRH-R1 inhibition is not protective against pneumococcal disease induced by stress. Conversely, CRH-R2 inhibition attenuates stress-induced bacterial growth and significantly prevented severe sepsis. Neutrophillic responses were associated with CRH receptor-specific disease outcome providing a potential cellular target for stress-induced susceptibility to the development of severe pneumococcal disease. CRH receptor-mediated effects on immune responses could pro...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119458</comments>
            <pubDate>Wed, 20 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119458</guid>        </item>
        <item>
            <title>Modulation of traumatic brain injury using progesterone and the role of glial cells on its neuroprotective actions</title>
            <link>http://www.medworm.com/index.php?rid=5119452&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001676%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: TBI is a complex disease process caused by a cascade of systemic events. Attention is now turning to drugs that act on multiple pathways to enhance survival and functional outcomes. Progesterone has been found to be beneficial in several animal species, different models of brain injury, and in two preliminary human clinical trials. It holds promise as a treatment for TBI. Progesterone's multiple mechanisms of action may work synergistically to prevent the death of neurons and glia, leading to reduced morbidity and mortality. This review highlights the importance of glial cells as mediators of progesterone's actions on the CNS and describes progesterone's pleiotrophic effects on immune enhancement and neuroprotection in TBI. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119452</comments>
            <pubDate>Wed, 20 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119452</guid>        </item>
        <item>
            <title>Intrathecal human herpesvirus 6 antibodies in multiple sclerosis and other demyelinating diseases presenting as oligoclonal bands in cerebrospinal fluid</title>
            <link>http://www.medworm.com/index.php?rid=5119463&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS016557281100172X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Demyelinating diseases of the central nervous system (CNS) often include elevated IgG production in intrathecal space presenting as oligoclonal bands (OCBs) in cerebrospinal fluid (CSF). In most demyelinating diseases, e.g. in multiple sclerosis (MS), the underlying cause is not known. We used isoelectric focusing and affinity immunoblot to study the specificity of CSF OCBs to human herpesvirus-6 (HHV-6) in patients with demyelinating diseases of the CNS including MS. Eighty patients with positive OCB finding were included in the study. The OCBs reacted with the HHV-6 antigen in 18 cases (23%). Twelve of 46 MS patients (26%), 5 of 24 other demyelinating diseases (21%) and 1 of 10 other neurological disorders (10%) had HHV-6 specific OCBs in CSF. A specific intrathecal HHV-6 A and...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119463</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119463</guid>        </item>
        <item>
            <title>Lymphocyte calcium influx kinetics in multiple sclerosis treated without or with interferon beta</title>
            <link>http://www.medworm.com/index.php?rid=5119461&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001688%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Kv1.3 and IKCa1 potassium channels play an important role in the maintenance of calcium-influx during lymphocyte activation and present a possible target for selective immunomodulation. We investigated the calcium-influx characteristics of Th1, Th2, CD4, CD8 T-lymphocytes isolated from multiple sclerosis patients without or with interferon-beta therapy, and its modulation by Kv1.3 and IKCa1 channel inhibitors using flow cytometry. Specific immunomodulation of the CD8 subset can be reached through inhibition of Kv1.3 channels in multiple sclerosis patients without interferon-beta. However, this effect is not specific enough concerning all lymphocyte subsets influencing the autoimmune response, since it also affects anti-inflammatory Th2 cells. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119461</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119461</guid>        </item>
        <item>
            <title>No influence on disease progression of non-HLA susceptibility genes in MS</title>
            <link>http://www.medworm.com/index.php?rid=5119464&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001329%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Recently, several non-HLA loci have been shown to be convincingly associated with Multiple Sclerosis (MS) susceptibility, assumingly indicating important pathways in the pathogenesis. A genotype influence on disease outcome measures by these genes would support a role of these pathways in ongoing tissue damage. Here, however, we report a consistent dissociation between causation and progression for five non-HLA genotypes (IL7R, IL2RA, CLEC16A, CD226 and SH2B3) in 1776 Scandinavian MS patients. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119464</comments>
            <pubDate>Sun, 10 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119464</guid>        </item>
        <item>
            <title>Differential expression of muscarinic acetylcholine receptor subtypes in Jurkat cells and their signaling</title>
            <link>http://www.medworm.com/index.php?rid=5119453&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001408%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Muscarinic acetylcholine receptors expression and signaling in the human Jurkat T cell line were investigated. Semiquantitative real-time PCR and radioligand binding studies, using a wide set of antagonist compounds, showed the co-existence of M3, M4, and M5 subtypes. Stimulation of these subpopulations caused a concentration and time- dependent activation of second messengers and ERK signaling pathways, with a major contribution of the M3 subtype in a Gq/11-mediated response. In addition, we found that T-cell stimulation leads to increased expression of M3 and M5 both at transcriptional and protein levels in a PLC/PKCθ dependent manner. Our data clarifies the functional role of AChR subtypes in Jurkat cells and pave the way to future studies on the potential cross-talk among th...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119453</comments>
            <pubDate>Sun, 10 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119453</guid>        </item>
        <item>
            <title>John W. Prineas Awarded the Order of Australia</title>
            <link>http://www.medworm.com/index.php?rid=5119451&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001639%2Fabstract%3Frss%3Dyes</link>
            <description>Professor John W. Prineas, a prominent clinical neurologist and researcher in multiple sclerosis (MS), was recognized in the 2011 Australia Day Honours List for his contributions to medicine. Specifically, John was made an Officer of the Order of Australia, the award being conferred at an investiture in Sydney on May 6, 2011. As a close personal friend and proud associate since research training days together in England in the mid-1960's, it gives me enormous pleasure to pen this tribute to celebrate the event in the pages of the Journal of Neuroimmunology, a medium for which John has been a reviewer and a contributor over the years. No one could be more worthy of this award and John earned it through a career dedicated to the understanding of multiple sclerosis spanning almost half a cent...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119451</comments>
            <pubDate>Sun, 10 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119451</guid>        </item>
        <item>
            <title>Myeloid lineage cells inhibit neurite outgrowth through a myosin II-dependent mechanism</title>
            <link>http://www.medworm.com/index.php?rid=5119465&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001640%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The molecular mechanisms that underlie the axonal damage that accompanies CNS inflammation are largely unknown. Here, we investigate the effects of immune cells on neuronal viability and axonal growth and show that conditioned media from myeloid lineage cells inhibit neurite outgrowth without causing apoptosis. Treatment with monocyte conditioned medium enhances myosin light chain phosphorylation in neurons and the neurite outgrowth inhibitory effect of myeloid lineage cells can be attenuated with the myosin II inhibitor blebbistatin. Our results suggest that in the context of CNS inflammation myeloid cells may limit axonal repair in the CNS via a myosin II-dependent mechanism. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119465</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119465</guid>        </item>
        <item>
            <title>Parenchymal accumulation of CD163+ macrophages/microglia in multiple sclerosis brains</title>
            <link>http://www.medworm.com/index.php?rid=5119460&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001664%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Reactive macrophages/microglia exert both protective or damaging effects in multiple sclerosis (MS), which contribute to the relapsing–remitting nature of MS. CD163 is considered a marker of M2 (alternatively activated) macrophages. In the MS brain, CD163+ perivascular macrophages express molecules for antigen recognition and presentation. Here we further investigated the accumulation of CD163+ macrophages/microglia in the parenchyma of MS brains. CD163 expression pattern was investigated in different lesions of brain tissue specimens from five MS brains and five neuropathologically unaffected controls by immunohistochemistry. In the parenchyma of normal brain samples, immunoreactivity (IR) of CD163 was absent. In acute active lesions and at the rim of chronic active lesions of...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119460</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119460</guid>        </item>
        <item>
            <title>Human T-cell responses to botulinum neurotoxin: Proliferative responses in vitro of lymphocytes from botulinum neurotoxin A-treated movement disorder patients</title>
            <link>http://www.medworm.com/index.php?rid=5119459&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001652%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We determined the T-cell responses against botulinum neurotoxin type A (BoNT/A) and tetanus toxin (TeNT) of peripheral blood lymphocytes from 95 BoNT-treated patients and 63 non-treated control subjects. The patient group included 80 cervical dystonia and 15 other movement disorder cases. Positive T-cell responses to BoNT/A were detected in 70% of the treated patients, and in only 3% of controls. T-cell responses of BoNT-treated patients against BoNT/A did not differ between patients who were clinically responsive and those who had become non-responsive to the treatment. BoNT-treated patients gave significantly higher in vitro T-cell responses to TeNT than did the controls. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119459</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119459</guid>        </item>
        <item>
            <title>Time-dependent in-vivo effects of interleukin-2 on neurotransmitters in various cortices: Relationships with depressive-related and anxiety-like behaviour</title>
            <link>http://www.medworm.com/index.php?rid=5119454&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001585%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We investigated the impact of systemically injected IL-2 (2.5μg/kg, i.p.) on serotonergic and dopaminergic neurotransmission in various cortical areas by in-vivo microdialysis. IL-2 lastingly reduced extracellular 5-HT levels in the medial prefrontal (−75%), occipital (−70%), and temporal cortices (−45%), whereas dopamine was only moderately reduced in the medial prefrontal cortex.Based on the serotonergic time profile, we conducted further experiments to test for acute and delayed (2h post injection) depressive-related effects of systemic IL-2 (0–5.0μg/kg) in a forced swim test and delayed effects on anxiety-like behaviour in the elevated plus-maze. IL-2 had dose-dependent effects on depressive-related behaviour after delayed but not acute testing, but no effects on an...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119454</comments>
            <pubDate>Mon, 04 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119454</guid>        </item>
        <item>
            <title>Ventral tegmental area-basolateral amygdala-nucleus accumbens shell neurocircuitry controls the expression of heroin-conditioned immunomodulation</title>
            <link>http://www.medworm.com/index.php?rid=5119457&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001627%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The present investigations sought to determine whether the ventral tegmental area (VTA), basolateral amygdala (BLA), and nucleus accumbens shell (NAC) comprise a circuitry that mediates heroin-induced conditioned immunomodulation. Rats were given conditioning trials in which they received an injection of heroin upon placement into a distinctive environment. Prior to testing, rats received unilateral intra-BLA microinfusion of a D1 antagonist concomitantly with unilateral intra-NAC shell microinfusion of an NMDA antagonist. Disconnection of the VTA–BLA–NAC circuit impaired the ability of the heroin-paired environment to suppress lipopolysaccharide-induced immune responses, defining for the first time a specific neural circuit involved in conditioned neural-immune interactions....</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119457</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119457</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=5029691&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001846%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029691</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029691</guid>        </item>
        <item>
            <title>Trigeminal satellite cells express functional calcitonin gene-related peptide receptors, whose activation enhances interleukin-1β pro-inflammatory effects</title>
            <link>http://www.medworm.com/index.php?rid=5119456&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001603%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Calcitonin gene-related peptide (CGRP) is the main mediator of trigeminal pain signal. Functional CGRP receptors were detected in trigeminal satellite cells, a specialized type of glia found within the sensory ganglia. CGRP displayed modest pro-inflammatory effects per se on trigeminal satellite cells, while it significantly enhanced IL-1β actions, increasing the expression and activity of cycloxygenase 2 as well as the expression of the inducible form of nitric oxide synthase and IL-1β. CGRP effects were reverted by a specific CGRP receptor antagonist and mimicked by elevation of intracellular cAMP levels. CGRP exerted also minor proinflammatory effects on cortical astrocytes. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119456</comments>
            <pubDate>Wed, 29 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119456</guid>        </item>
        <item>
            <title>Comparison of a classical Th1 bacteria versus a Th17 bacteria as adjuvant in the induction of experimental autoimmune encephalomyelitis</title>
            <link>http://www.medworm.com/index.php?rid=5119455&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001597%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The relative contribution of myelin-specific Th1 and Th17 cells in the pathology of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), is controversial. IL-12, the key cytokine necessary for the differentiation of Th1 cells, has been found to be dispensable for EAE induction; while the related cytokine associated with Th17 cells, IL-23, is a critical factor for inducing EAE. Since EAE is induced by immunization with myelin proteins in CFA which contains M. tuberculosis that generates a prototypical Th1-mediated immune response, we sought to determine if replacing the M. tuberculosis in the adjuvant with a bacterium that induces an IL-23-dependent Th17 cell response during infection would induce EAE with a different phenotype. C. rodenti...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5119455</comments>
            <pubDate>Tue, 28 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5119455</guid>        </item>
        <item>
            <title>The human caveolin 1 gene upstream purine complex and neurodegeneration—A common signature</title>
            <link>http://www.medworm.com/index.php?rid=5029706&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001330%2Fabstract%3Frss%3Dyes</link>
            <description>We report two novel extreme homozygote haplotypes at 86-bp and 142-bp in the patients vs. controls. The above haplotypes were also detected in the previously reported cases of late-onset AD. The range of homozygote haplotypes in the controls was detected at between 106-bp to 122-bp.Following pooling of the neurodegenerative (n=486) and non-neurodegenerative (n=610) subjects studied for the human CAV1 purine complex to date, twenty haplotypes were found to be homozygous in the neurodegenerative, and not in the control pool (p (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029706</comments>
            <pubDate>Sun, 19 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029706</guid>        </item>
        <item>
            <title>A role for reactive oxygen species in endotoxin-induced elevation of MOR expression in the nervous and immune systems</title>
            <link>http://www.medworm.com/index.php?rid=5029698&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001391%2Fabstract%3Frss%3Dyes</link>
            <description>This study examined the mechanism by which exposure to lipopolysaccharide (LPS) alters mu-opioid receptor (MOR) expression in immune and neuronal cells using an in vitro conditioned medium model system. We found that LPS stimulated the intracellular accumulation of reactive oxygen species (ROS) and MOR expression in macrophage-like TPA-HL-60 cells. Conditioned medium from the LPS-stimulated TPA-HL-60 cells increased MOR expression in SH-SY5Y cells, a neuronal cell model, through actions mediated by TNF-α and GM-CSF. These data suggest that the endotoxin, LPS, modulates MOR expression in nervous and immune cells via ROS signaling, and demonstrates the crosstalk that exists within the neuroimmune axis. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029698</comments>
            <pubDate>Sun, 19 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029698</guid>        </item>
        <item>
            <title>Concomitant autoimmunity in myasthenia gravis — Lack of association with IgA deficiency</title>
            <link>http://www.medworm.com/index.php?rid=5029708&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS016557281100138X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: A marked increase in concomitant autoimmune diseases has previously been noted in patients with myasthenia gravis (MG). We show that these diseases occur both before and after the onset of MG and that the process is not influenced by thymectomy.IgA deficiency (IgAD), which is strongly associated with the same HLA haplotype as early onset MG, has recently been suggested to be an autoimmune disease. However, there was no increase in the prevalence of IgAD in a large cohort of Swedish MG patients. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029708</comments>
            <pubDate>Mon, 13 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029708</guid>        </item>
        <item>
            <title>Cholinergic modulation of dendritic cell function</title>
            <link>http://www.medworm.com/index.php?rid=5029697&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001378%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Dendritic cells (DCs) are highly specialized antigen-presenting cells with a unique ability to activate resting T lymphocytes. Acetylcholine (ACh) is the primary parasympathetic neurotransmitter and also a non-neural paracrine factor produced by different cells. Here, we analyzed the expression of the cholinergic system in DCs. We found that DCs express the muscarinic receptors M3, M4 and M5, as well as the enzymes responsible for the synthesis and degradation of ACh, choline acetyltransferase (ChAT) and acetylcholinesterase (AChE), respectively. Differentiation of DCs in the presence of the cholinergic agonist carbachol, the synthetic analog of ACh, resulted in an increased expression of HLA-DR and CD86 and the stimulation of TNF-α and IL-8 production. All these effects were pr...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029697</comments>
            <pubDate>Sun, 12 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029697</guid>        </item>
        <item>
            <title>Increase of Ki-67+ natural killer cells in multiple sclerosis patients treated with interferon-β and interferon-β combined with low-dose oral steroids</title>
            <link>http://www.medworm.com/index.php?rid=5029707&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001342%2Fabstract%3Frss%3Dyes</link>
            <description>This study, although limited, shows that treatment with IFN-β affects NK cell cycle without altering NK cell apoptosis in MS patients. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029707</comments>
            <pubDate>Tue, 07 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029707</guid>        </item>
        <item>
            <title>Upregulation of microglial C1q expression has no effects on nigrostriatal dopaminergic injury in the MPTP mouse model of Parkinson disease</title>
            <link>http://www.medworm.com/index.php?rid=5029696&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001354%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, C1q is upregulated and considered to be a marker of microglial activation in the nigrostriatal system after subchronic MPTP, but nigrostriatal dopaminergic injury may be not affected by C1q in this model. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029696</comments>
            <pubDate>Sun, 05 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029696</guid>        </item>
        <item>
            <title>A mimotope peptide of Aβ42 fibril-specific antibodies with Aβ42 fibrillation inhibitory activity induces anti-Aβ42 conformer antibody response by a displayed form on an M13 phage in mice</title>
            <link>http://www.medworm.com/index.php?rid=5029695&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001251%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we determined the mimotopes of these antibodies and found a common mimotope sequence, B6-C15, using the Ph.D.-C7C phage library. The B6-C15 showed weak homology to the C-terminus of Aβ42 containing GXXXG dimerization motifs. We synthesized the peptide of B6-C15 fused with biotinylated TAT at the N-terminus (TAT-B6-C15) and characterized its biochemical features on an Aβ42-fibrillation reaction in vitro. We demonstrated that, first, TAT-B6-C15 inhibited Aβ42 fibril formation; secondly, TAT-B6-C15 bound to prefibril Aβ42 oligomers but not to monomers, trimers, tetramers, fibrils, or ultrasonicated fragments; thirdly, TAT-B6-C15 inhibited Aβ42-induced cytotoxicity against human SH-SY5Y neuroblastoma cells; and, fourthly, when mice were administered B6-C15-phages dissolved ...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029695</comments>
            <pubDate>Sun, 05 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029695</guid>        </item>
        <item>
            <title>Immunosuppressive activity of a novel peptide analog of alpha-melanocyte stimulating hormone (α-MSH) in experimental autoimmune uveitis</title>
            <link>http://www.medworm.com/index.php?rid=5029692&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001366%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Autoimmune uveitis is an inflammatory disorder of the eye that can lead to pain and vision loss. Steroids and immunosuppressive drugs are currently the only therapeutics for uveitis and have serious ocular and systemic toxicities. Therefore, safer alternative therapeutics are desired. Alpha-melanocyte stimulating hormone (α-MSH) is a neuropeptide that suppresses effector T cell functions, induces regulatory T cells and has beneficial effects in certain autoimmune and transplant models. A novel d-amino acid peptide analog of native α-MSH (dRI-α-MSH) was produced that was protected from protease digestion and had increased selectivity for the melanocortin-1 receptor. Systemic delivery of the dRI-α-MSH analog dramatically suppressed disease progression and retained retinal archi...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029692</comments>
            <pubDate>Sun, 05 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029692</guid>        </item>
        <item>
            <title>Title Page/Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=4903370&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001524%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903370</comments>
            <pubDate>Tue, 31 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903370</guid>        </item>
        <item>
            <title>Anti-myelin associated glycoprotein antibodies recognize HNK-1 epitope on CNS</title>
            <link>http://www.medworm.com/index.php?rid=5029705&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001317%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Antibodies to myelin-associated glycoprotein (MAG) are associated with demyelinating polyneuropathy and are specific for the HNK-1 epitope. To test if anti-MAG IgM recognize HNK-1 on CNS, sera from 20 patients and 238 controls were tested on rat slices by indirect immunofluorescence (IIF). IgM from anti-MAG positive patients, but not from control sera, stained rat brain with perineuronal or neuropil pattern, depending on the CNS region. IIF titers significantly correlated with ELISA anti-MAG titers. The staining of patients’ sera were inhibited by mouse anti-HNK-1 monoclonal antibody. Our results demonstrate that anti-MAG IgM recognizes HNK-1 outside the peripheral nerve myelin carriers. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029705</comments>
            <pubDate>Sun, 29 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029705</guid>        </item>
        <item>
            <title>Orthogonal array formation by human aquaporin-4: Examination of neuromyelitis optica-associated aquaporin-4 polymorphisms</title>
            <link>http://www.medworm.com/index.php?rid=5029704&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001305%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Pathogenic autoantibodies target aquaporin-4 (AQP4) water channels in individuals with neuromyelitis optica (NMO). Recently, allelic mutations were reported at residue 19 of AQP4 in three cases of NMO, and it was suggested that polymorphisms may influence disease by altering AQP4 supramolecular assembly into orthogonal arrays of particles (OAPs). We analyzed the determinants of OAP formation by human AQP4 to investigate the possible role of polymorphisms in NMO pathogenesis. NMO-associated mutations R19I and R19T in AQP4 did not affect OAP assembly, palmitoylation-dependent regulation of assembly, or NMO autoantibody binding. Residue-19 polymorphisms in AQP4 are thus unlikely to be disease relevant. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029704</comments>
            <pubDate>Sun, 29 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029704</guid>        </item>
        <item>
            <title>Association of IL1A, IL1B, ILRN, IL6, IL10 and TNF-α polymorphisms with risk and clinical course of multiple sclerosis in a Polish population</title>
            <link>http://www.medworm.com/index.php?rid=5029703&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001299%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Single nucleotide polymorphisms in human pro- and anti-inflammatory genes, including IL1RN VNTR (rs315952), IL1A 4845G&gt;T (rs17561), L1B-511C&gt;T (rs16944), IL6-174G&gt;C (rs1800795), IL10-1082 A&gt;G (rs 1800896) and TNFα-308G&gt;A (rs1800629) and their impact on multiple sclerosis risk and disease progression in a Polish population were investigated. Increased risk of MS was found for IL6-174 CC homozygotes (OR, 2.88; p (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029703</comments>
            <pubDate>Sun, 29 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029703</guid>        </item>
        <item>
            <title>Increased serum matrix metalloproteinase-9 in neuromyelitis optica: Implication of disruption of blood–brain barrier</title>
            <link>http://www.medworm.com/index.php?rid=5029702&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS016557281100124X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Matrix metalloproteinase-9 (MMP-9) plays an important role in some neuroinflammatory diseases through the blood–brain barrier (BBB) disruption. To investigate the pathogenicity of MMP-9 in neuromyelitis optica (NMO), serum and CSF MMP-9 concentrations were measured in 13 NMO and 15 multiple sclerosis (MS) patients and 14 healthy controls, and correlated with clinical and laboratorial parameters. Serum MMP-9 concentrations were significantly higher in NMO than MS and controls, and correlated with EDSS score, CSF/serum albumin ratio, and CSF IL-8 concentrations. Our results indicate that MMP-9, promoted by elevated IL-8 activation, plays a crucial role in the pathogenesis of NMO through the BBB disruption. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029702</comments>
            <pubDate>Sun, 29 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029702</guid>        </item>
        <item>
            <title>HLA DRB1*1501 is only modestly associated with lesion burden at the first demyelinating event</title>
            <link>http://www.medworm.com/index.php?rid=5029701&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001263%2Fabstract%3Frss%3Dyes</link>
            <description>The objectives were to assess the associations between HLA DRB1*1501 status and magnetic resonance imaging (MRI) measures in clinically isolated syndromes (CIS) at the first demyelinating event.Methods: We genotyped 205 CIS patients (age: 29.0±7.7years) enrolled in the Observational Study of Early Interferon beta 1-a Treatment in High Risk Subjects after CIS (SET study), a multi-center, clinical study of CIS for rs3135005, a single nucleotide polymorphism associated with HLA DRB1*1501 status. The inclusion criteria required 2 or more brain MRI lesions and the presence of two or more oligoclonal bands in cerebrospinal fluid. Clinical and MRI assessments were obtained within 4months of the initial demyelinating event.Results: The frequency of HLA DRB1*1501 positivity was 102/205 (49.7%). HL...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029701</comments>
            <pubDate>Sun, 29 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029701</guid>        </item>
        <item>
            <title>Identification of peptide targets in neuromyelitis optica</title>
            <link>http://www.medworm.com/index.php?rid=5029699&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001044%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Neuromyelitis optica (NMO) is an inflammatory demyelinating disease that predominantly affects the optic nerves and spinal cord. Recombinant antibodies (rAbs) generated from clonally expanded plasma cells in an NMO patient are specific to AQP4 and pathogenic. We screened phage-displayed peptide libraries with these rAbs, and identified 14 high affinity linear and conformational peptides. The linear peptides shared sequence homologies with NMO autoantigen AQP4 on the extracellular surface. Competitive inhibition ELISA and immunocytochemistry demonstrated that these peptides represent epitopes of NMO autoantigen AQP4. Peptide epitopes/mimotopes may have potential uses for disease prognosis, monitoring, and therapy. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029699</comments>
            <pubDate>Sun, 29 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029699</guid>        </item>
        <item>
            <title>Changes in responsiveness of appetite, leptin and hypothalamic IL-1β and TNF-α to lipopolysaccharide in developing rats</title>
            <link>http://www.medworm.com/index.php?rid=5029693&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001019%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, the absence of a leptin response may act to prevent immune stress-induced anorexia during the early neonatal period. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029693</comments>
            <pubDate>Sun, 29 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029693</guid>        </item>
        <item>
            <title>Role of γδ T cells in antibody production and recovery from SFV demyelinating disease</title>
            <link>http://www.medworm.com/index.php?rid=4903373&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000622%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Semliki Forest Virus (SFV) encephalomyelitis has been used to study the pathogenesis of virus-induced demyelination and serves as a model for multiple sclerosis. SFV-infection of mice invariably leads to clinical weakness accompanied by CNS inflammation, viral clearance and primary demyelination by day 21 postinfection (pi), followed by recovery and remyelination by day 35 pi. We have applied this model to the examination of the effects of γδ T cells in antibody production and the pathogenesis of demyelinating lesions. SFV-infection of γδ T cell KO mice resulted in more severe clinical signs than in wild type (WT) B6 mice. SFV-infected WT and γδ KO mice both cleared virus by day 10 pi and inflammation was comparable. Demyelination also appeared to be similar in both groups ...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903373</comments>
            <pubDate>Wed, 25 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903373</guid>        </item>
        <item>
            <title>Twin study on transplacental-acquired antibodies and attention deficit/hyperactivity disorder — A pilot study</title>
            <link>http://www.medworm.com/index.php?rid=5029700&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001275%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusion: Although the study provides no strong support for the hypothesis, infection or immunological factors may be one among several causes of ADHD. The genetic control obtained in a twin design may reduce the exposure contrast and a larger sample is needed to further explore the role of PnPs14 in the etiology of ADHD. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029700</comments>
            <pubDate>Tue, 24 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029700</guid>        </item>
        <item>
            <title>ADEM as a niche variant of post infectious neurological syndromes</title>
            <link>http://www.medworm.com/index.php?rid=5029709&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001287%2Fabstract%3Frss%3Dyes</link>
            <description>We have read with interest the paper recently published by , reporting a thorough analysis of the most relevant features of ADEM. The author cites 3 papers published by our group in reference to the involvement of PNS (), the existence of recurrent variants () and the cytokines and chemokines profile different from MS (). (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029709</comments>
            <pubDate>Tue, 17 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029709</guid>        </item>
        <item>
            <title>CCR4 contributes to the pathogenesis of experimental autoimmune encephalomyelitis by regulating inflammatory macrophage function</title>
            <link>http://www.medworm.com/index.php?rid=5029694&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001238%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Chemokines and their receptors play a critical role in orchestrating the immune response during experimental autoimmune encephalomyelitis (EAE). Expression of CCR4 and its ligand CCL22 has been observed in ongoing disease. Here we describe a role for CCR4 in EAE, illustrating delayed and decreased disease incidence in CCR4−/− mice corresponding with diminished CNS infiltrate. Peripheral T cell responses were unaltered in CCR4−/− mice; rather, disease reduction was related to reduced CD11b+Ly6Chi inflammatory macrophage (iMϕ) numbers and function. These results provide evidence that CCR4 regulates EAE development and further supports the involvement of CCR4 in iMϕ effector function. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5029694</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5029694</guid>        </item>
        <item>
            <title>A potential link between autoimmunity and neurodegeneration in immune-mediated neurological disease</title>
            <link>http://www.medworm.com/index.php?rid=4903378&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000312%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Multiple sclerosis (MS) patients make antibodies to heterogeneous nuclear ribonuclear protein A1 (hnRNP-A1), a nucleocytoplasmic protein. We hypothesized this autoimmune reaction might contribute to neurodegeneration. Antibodies from MS patients reacted with hnRNP-A1-‘M9’, its nuclear translocation sequence. Transfection of anti-M9 antibodies into neurons resulted in neuronal injury and changes in transcripts related to hnRNP-A1 function. Importantly, RNA levels for the spinal paraplegia genes (SPGs) decreased. Changes in SPG RNA levels were confirmed in neurons purified from MS brains. Also, we show molecular interactions between spastin (the encoded protein of SPG4) and hnRNP-A1. These data suggest a link between autoimmunity, clinical phenotype and neurodegeneration in MS....</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903378</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903378</guid>        </item>
        <item>
            <title>TNFRSF1A coding variants in multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4903385&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001020%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Patients with the autoinflammatory disease Tumour Necrosis Factor receptor-associated periodic syndrome (TRAPS) who suffer from demyelinating disease have been described, and one of the milder TRAPS mutations (R92Q in the TNFRSF1A gene) has been suggested as a risk factor for multiple sclerosis (MS). In a study population of 967 MS patients and 1022 controls, we replicate association [P=5×10−4, 3% in patients versus 1% in controls, OR=2.26 (95% CI 1.41–3.61)], which appears independent of an established common risk variant in the same gene. No other non-synonymous variants in the same allele frequency range influencing risk of MS were observed. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903385</comments>
            <pubDate>Thu, 12 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903385</guid>        </item>
        <item>
            <title>Altered expression and secretion of colonic Interleukin-6 in a stress-sensitive animal model of brain-gut axis dysfunction</title>
            <link>http://www.medworm.com/index.php?rid=4903377&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001007%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Interleukin-6 (IL-6) can activate gastrointestinal submucosal neurons, with associated implications for motility and secretory function. Patients with irritable bowel syndrome (IBS) have elevated levels of circulating IL-6. Colons from the Wistar Kyoto (WKY) rat model of IBS secrete more IL-6 (12.84pg/ml) than control Sprague Dawley (SD) colons (5.55pg/ml) and WKY secretions stimulated calcium responses in naïve submucosal neurons of greater amplitude. Recombinant IL-6 activated more submucosal neurons in WKY tissue preparations (p (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903377</comments>
            <pubDate>Wed, 11 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903377</guid>        </item>
        <item>
            <title>The prospects of minocycline in multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4903371&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001032%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Multiple sclerosis (MS) is the most common inflammatory demyelinating disease of the central nervous system (CNS). Although there are several approved drugs for MS, not all patients respond optimally to these drugs. More effective, well-tolerated therapeutic strategies for MS are necessary, either through the development of new medication or combination of existing ones. Minocycline is a traditional antibiotic with profound anti-inflammatory and neuropropective effects and good tolerance for long-term use. The encouraging results from the animal model and clinical experiments on minocycline make it a promising candidate for MS treatment whether used alone or combined with other drugs. In this review, we summarized the pharmacological actions of minocycline and focused on its ther...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903371</comments>
            <pubDate>Wed, 11 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903371</guid>        </item>
        <item>
            <title>Novel mechanisms of immune modulation of natalizumab in multiple sclerosis patients</title>
            <link>http://www.medworm.com/index.php?rid=4903379&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000592%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The goal of this study was to investigate the effects of natalizumab therapy on the immune cell composition and phenotype in the blood of relapsing MS patients treated over the course of 12months. We collected peripheral blood from 26 RRMS patients before treatment onset, and then 6 and 12months after therapy. PBMC was isolated and then analyzed for phenotypic characteristics by FACS and for cytokine production by ELISA.The results of our studies showed changes in both numbers and activation states of immune cells following therapy. These changes were observed at the 6month timepoint and generally persisted through the 12month timepoint. The proportions of NK cells (CD3−CD56+) and hematopoetic stem cells (CD34+lin−) were increased after natalizumab treatment. Decreases were n...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903379</comments>
            <pubDate>Mon, 09 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903379</guid>        </item>
        <item>
            <title>The effect of live, attenuated measles vaccine and measles infection on measles antibody levels in serum and CSF of patients with multiple sclerosis or clinically isolated syndrome</title>
            <link>http://www.medworm.com/index.php?rid=4903383&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000993%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: High occurrence of measles, rubella and varicella zoster antibodies has been used as a biomarker for MS (the MRZ test). We analyzed measles antibody titres with respect to measles infection/measles vaccination status in 166 patients with MS or clinically isolated syndrome. Fifty blood donors served as controls. Measles vaccination yielded CSF measles antibodies in fewer patients (62%) than measles infection did (87%, p=0.001) and yielded lower measles titres in both serum and CSF (p (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903383</comments>
            <pubDate>Sun, 08 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903383</guid>        </item>
        <item>
            <title>Resident B cells regulate thymic expression of myelin oligodendrocyte glycoprotein</title>
            <link>http://www.medworm.com/index.php?rid=4903375&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS016557281100097X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Thymic B cells represent a numerically minor cell population located primarily at the cortico–medullary junction. Their biological role is unclear. B cell-deficient μMT mice exhibited reduced medullary thymic epithelial cell (mTEC) numbers and reduced MOG and insulin mRNA expression. Lymphotoxin produced by B cells was critical for normal tissue restricted antigen (TRA) expression, suggesting that B cells regulate self-antigens through their production of LT. These results reveal an unexpected role of B cells in mTEC maintenance and expression of TRAs through their production of LT. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903375</comments>
            <pubDate>Sun, 08 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903375</guid>        </item>
        <item>
            <title>Recombination mapping of the susceptibility region for sporadic inclusion body myositis within the major histocompatibility complex</title>
            <link>http://www.medworm.com/index.php?rid=4903380&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000609%2Fabstract%3Frss%3Dyes</link>
            <description>In this study recombination mapping was utilised to further refine the known 8.1AH susceptibility region near HLA-DRB1*0301. Caucasian sIBM patients carrying part of the 8.1AH were genotyped for a selection of 8.1AH-haplotypic polymorphisms. A common 8.1AH-specific susceptibility region was defined, spanning 172kb and encompassing three genes — HLA-DRB3, HLA-DRA and BTNL2. It is thus likely that 8.1AH-derived susceptibility to sIBM originates from at least one of these genes. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903380</comments>
            <pubDate>Tue, 03 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903380</guid>        </item>
        <item>
            <title>An encephalomyelitis-specific locus on chromosome 16 in mouse controls disease development and expression of immune-regulatory genes</title>
            <link>http://www.medworm.com/index.php?rid=4903376&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000981%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: A locus on mouse chromosome 16 was found to control experimental autoimmune encephalomyelitis (EAE) in studies using congenic mice. Genes within the congenic region control encephalomyelitis but not arthritis, indicating the presence of genes in this region involved in central nervous system (CNS) specific mechanisms. Flow cytometry analyses of expression of two candidate genes within the linked locus, Cd200 and Btla, demonstrated a significantly lower expression of CD200 on CD4+ T cells and higher expression of BTLA on B cells from the congenic mice. These results suggest that genes within this mouse chromosome 16 locus specifically control EAE development possibly through immune-regulatory cell-surface molecules. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903376</comments>
            <pubDate>Tue, 03 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903376</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=4805151&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811001160%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805151</comments>
            <pubDate>Sat, 30 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805151</guid>        </item>
        <item>
            <title>Vitamin D-related gene expression profiles in immune cells of patients with relapsing remitting multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4903382&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000968%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: An impaired vitamin D (vit-D) processing by immune cells of relapsing remitting multiple sclerosis (RRMS) patients may increase their vulnerability for a poor vit-D status. We assessed with qPCR the expression of vit-D related genes in PBMC and CD4+ T-cells. Gene expression profiles of vit-D receptor (VDR), CYP27B1 and CYP24A1 did not differ between RRMS patients and healthy controls. Interestingly, more VDR expression in PBMC correlated with less circulating IFN-γ+ CD4+ T-cells. Our results suggest that vit-D processing by immune cells is not impaired in RRMS, and is potentially relevant for the composition of the peripheral CD4+ T-cell compartment. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903382</comments>
            <pubDate>Wed, 20 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903382</guid>        </item>
        <item>
            <title>Complement upregulation and activation on motor neurons and neuromuscular junction in the SOD1 G93A mouse model of familial amyotrophic lateral sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4903384&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000932%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Complement activation products are elevated in cerebrospinal fluid, spinal cord and motor cortex of patients with amyotrophic lateral sclerosis (ALS) but are untested in models. We determined complement expression and activation in the SOD1 G93A mouse model of familial ALS (fALS). At 126days, C3 mRNA was upregulated in spinal cord and C3 protein accumulated in astrocytes and motor neurons. C3 activation products C3b/iC3b were localized exclusively on motor neurons. At the neuromuscular junction, deposits of C3b/iC3b and C1q were detected at day 47, before the appearance of clinical symptoms, and remained detectable at symptomatic stage (126days). Our findings implicate complement in the denervation of the muscle endplate by day 47 and destruction of the neuromuscular junction and...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903384</comments>
            <pubDate>Mon, 18 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903384</guid>        </item>
        <item>
            <title>Immunoneuroendocrine alterations in patients with progressive forms of chronic Chagas disease</title>
            <link>http://www.medworm.com/index.php?rid=4903381&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000725%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We studied the features of parallel immunoneuroendocrine responses in patients with different degrees of chronic Chagas myocarditis (indeterminate, mild/moderate or severe). A systemic inflammatory scenario was evident in patients with severe myocarditis compared to healthy subjects. This was paralleled by a disrupted activation of the hypothalamus-pituitary-adrenal axis, characterized by decreased concentrations of dehydroepiandrosterone-sulfate (DHEA-s) and an unbalanced cortisol/DHEA-s ratio, reinforcing the view that severe Chagas disease is devoid of an adequate anti-inflammatory milieu, likely involved in pathology. Our study constitutes the first demonstration of neuroendocrine disturbances, in parallel to a systemic inflammatory profile, during progressive human Chagas di...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903381</comments>
            <pubDate>Thu, 14 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903381</guid>        </item>
        <item>
            <title>T cell deficiency does not reduce lesions in mice produced by intracerebral injection of NMO-IgG and complement</title>
            <link>http://www.medworm.com/index.php?rid=4903374&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000695%2Fabstract%3Frss%3Dyes</link>
            <description>We reported recently that intracerebral administration of NMO-IgG with human complement produces neuromyelitis optica (NMO) lesions in mice. We examined the role of T cells in the formation of NMO lesions by comparing brain histopathology in wildtype and nude mice. Brains were co-injected with IgG from NMO patients and human complement. At 24h and 5days, wildtype vs. nude mouse brains had comparable inflammation (CD45 immunoreactivity), loss of myelin (Luxol Fast Blue staining) and loss of AQP4 immunoreactivity. We conclude that T cells are not required for the formation of NMO lesions in this mouse model. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903374</comments>
            <pubDate>Wed, 13 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903374</guid>        </item>
        <item>
            <title>Increased memory Th17 cells in patients with neuromyelitis optica and multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4805170&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000713%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: Memory Th17 is related to the development and relapse of NMO and MS, and IVMP can inhibit memory Th17. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805170</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805170</guid>        </item>
        <item>
            <title>Differential levels of resistance to disease induction and development of relapsing experimental autoimmune encelphalomyelitis in two H-2b-restricted mouse strains</title>
            <link>http://www.medworm.com/index.php?rid=4805164&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000701%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Besides the major histocompatibility complex (MHC) genes, background genes are believed to influence the encephalitogenicity of SJL(H-2s) and B10.S (H-2s) mice responding to myelin basic protein (MBP). A new mouse strain was constructed to study the effects of the SJL genetic background in mice responding to H-2b-restricted neuroantigens. Although the SJL.B (H-2b) mouse remained resistant to MBP in active EAE induction, the disease severity was uniformly higher in MOG-induced active EAE and in MBP-induced adoptive EAE when compared to those of B6 (H-2b) mice. Treatment of mice with anti-CD25 antibodies prior to immunization caused 60% of SJL.B mice to become susceptible to MBP-induced EAE while only 14% of B6 mice were converted. In addition, MOG-induced EAE in SJL.B mice followe...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805164</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805164</guid>        </item>
        <item>
            <title>Genetic deficiency of estrogen receptor alpha fails to influence experimental autoimmune myasthenia gravis pathogenesis</title>
            <link>http://www.medworm.com/index.php?rid=4805172&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000646%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Autoimmune myasthenia gravis (MG) is characterized by T cell and antibody responses to muscle nicotinic acetylcholine receptor (AChR). It is well known that MG as other autoimmune diseases is more prevalent in women than men and estrogen administration enhances experimental autoimmune MG (EAMG) severity. To determine whether estrogen influences EAMG pathogenesis through estrogen receptor alpha (ERα) activation, ERα knockout (KO) and wild-type (WT) C57BL/6 mice were immunized with AChR. ERα KO mice were equally susceptible to EAMG as WT mice and exhibited comparable antibody and immunopathological responses to AChR, suggesting a lack of involvement of ERα in EAMG pathogenesis. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805172</comments>
            <pubDate>Sun, 10 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805172</guid>        </item>
        <item>
            <title>The roles of fractalkine/CX3CR1 system in neuronal death following pilocarpine-induced status epilepticus</title>
            <link>http://www.medworm.com/index.php?rid=4805162&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000671%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Although fractalkine is one of chemokines involved in mediation of neuronal/microglial interaction, it is not known whether fractalkine/CX3CR1-mediated pathogenesis occurs in the rat brain following epileptogenic insults. In order to elucidate the roles of the fractalkine/CX3CR1 system in microglial activation and neurodegeneration induced by status epilepticus (SE), we investigated changes in fractalkine/CX3CR1 system within the rat hippocampus following SE. In non-SE induced animals, fractalkine and CX3CR1 immunoreactivity was detected in neurons and microglia, respectively. Following SE, fractalkine immunoreactivity was transiently increased in neurons and astrocytes. CX3CR1 immunoreactivity was also transiently detected in neurons (particularly in CA1 pyramidal cells). Intrac...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805162</comments>
            <pubDate>Sun, 10 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805162</guid>        </item>
        <item>
            <title>Role of gender in multiple sclerosis: Clinical effects and potential molecular mechanisms</title>
            <link>http://www.medworm.com/index.php?rid=4805153&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000658%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Multiple sclerosis (MS) is more prevalent in females than males, and this female predominance is increasing as time goes by. Additionally, gender appears to play critical roles in development, progression and treatment of MS, and is therefore an aspect that should always be considered in the design and interpretation of research and clinical trials for MS. In this review, factors that could potentially explain the gender-biased observations in MS are discussed. These include sex-specific differences between the male and female immune systems and nervous systems, genetic and epigenetic or environmental-related effects, the effects of gonadal hormones, and materno-fetal interactions. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805153</comments>
            <pubDate>Thu, 07 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805153</guid>        </item>
        <item>
            <title>Tumor necrosis factor alpha (TNF-α), anti-TNF-α and demyelination revisited: An ongoing story</title>
            <link>http://www.medworm.com/index.php?rid=4805152&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS016557281100066X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Tumor necrosis factor alpha (TNF-α) is a cytokine with pleiotropic actions that can be present both as a transmembrane protein and soluble cytokine (sTNF). Both ligands interact with two different receptors, TNFR1 and TNFR2, which mediate their biological effects. TNF-α is involved in the pathogenesis of multiple sclerosis (MS), however, administration of anti-TNF-α agents to MS patients has been associated with increased disease activity. Insomuch as TNFR1 mediates demyelination and TNFR2 remyelination, it could be hypothesized that anti-TNF-α agents which selectively inhibit sTNF or signals from TNFR1 could be effective in treating MS. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805152</comments>
            <pubDate>Thu, 07 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805152</guid>        </item>
        <item>
            <title>CXCL10 expressing hematopoietic-derived cells are requisite in defense against HSV-1 infection in the nervous system of CXCL10 deficient mice</title>
            <link>http://www.medworm.com/index.php?rid=4805163&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000683%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The chemokine CXCL10 is crucial for the control of viral replication through the regulation of mobilization of antigen-specific T cells to sites of infection. CXCL10 is highly expressed both at sites of inflammation as well as constitutively within lymphoid organs by both bone marrow (BM)-derived and non-BM-derived cells. However, the relative immunologic importance of CXCL10 expressed by these divergent sources relative to HSV-1 infection is unknown. Using mouse chimeras reconstituted with either wild type or CXCL10 deficient mouse BM, we show BM-derived, radiation-sensitive cells from wild type mice were solely responsible for resistance to HSV-1 in the trigeminal ganglia and brain stem. The resistance was not reflected by a deficiency in the recruitment of effector cells to si...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805163</comments>
            <pubDate>Wed, 06 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805163</guid>        </item>
        <item>
            <title>Memory cells specific for myelin oligodendrocyte glycoprotein (MOG) govern the transfer of experimental autoimmune encephalomyelitis</title>
            <link>http://www.medworm.com/index.php?rid=4805161&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000324%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Multiple sclerosis (MS) is an inflammatory disease of the CNS mediated by CD4+ T cells directed against myelin antigens. Experimental autoimmune encephalomyelitis (EAE) is induced by immunization with myelin antigens like myelin oligodendrocyte glycoprotein (MOG). We have explored the transfer of EAE using MOG35-55-specific TCR transgenic (2D2) T cells. Unsorted 2D2 Th1 cells reliably transferred EAE. Further, we found that CD44hiCD62Llo effector/memory CD4+ T cells are likely responsible for the disease transfer due to the up-regulation of CD44. Given the importance of MOG in MS pathogenesis, mechanistic insights into adoptively transferred EAE by MOG-specific Th1 cells could prove valuable in MS research. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805161</comments>
            <pubDate>Tue, 05 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805161</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=4685418&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000865%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685418</comments>
            <pubDate>Thu, 31 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685418</guid>        </item>
        <item>
            <title>Natalizumab therapy decreases surface expression of both VLA-heterodimer subunits on peripheral blood mononuclear cells</title>
            <link>http://www.medworm.com/index.php?rid=4805169&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000634%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Natalizumab interferes with immune cell migration into the central nervous system via blocking the alpha-4 subunit of very-late activation antigen-4 (VLA-4). Occurrence of rare but serious progressive multifocal leukoencephalopathy during prolonged natalizumab therapy of multiple sclerosis (MS) calls for a more detailed understanding of potential coeffects. We longitudinally studied alpha-4 and beta-1 surface levels on blood cells from 18 MS patients by flow cytometry. Expectedly, detectability of natalizumab-blocked alpha-4 was diminished on all investigated cell subsets. In addition, we report a concurrent and significant decrease of beta-1 surface levels on T-cells, B-cells, natural killer cells, and natural killer T cells, but not on monocytes. Uncovering secondary effects of...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805169</comments>
            <pubDate>Wed, 30 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805169</guid>        </item>
        <item>
            <title>Toll-like receptor 2 is partially involved in the activation of murine astrocytes by Streptococcus suis, an important zoonotic agent of meningitis</title>
            <link>http://www.medworm.com/index.php?rid=4805160&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000294%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The murine astrocyte response to virulent Streptocuccus suis, a swine and an emerging human meningitis-causing pathogen, is reported. Albeit astrocytes do not internalize S. suis, all S. suis strains studied enhanced Toll-like receptor (TLR)2 expression and the production of pro-inflammatory cytokines and inducible nitric oxide synthase. Cell wall components and hemolysin (suilysin) are shown to be mainly responsible for cell activation. Astrocytes from TLR2 knockout mice presented a partial but significant reduction of S. suis-induced production of pro-inflammatory cytokines. These results contribute to increase the knowledge on mechanisms underlying S. suis inflammation in the brain. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805160</comments>
            <pubDate>Wed, 23 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805160</guid>        </item>
        <item>
            <title>Because it is our journal</title>
            <link>http://www.medworm.com/index.php?rid=4685419&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000610%2Fabstract%3Frss%3Dyes</link>
            <description>When first confronted with the opportunity of becoming Editor-in-Chief of The Journal of Neuroimmunology, my first reaction was “is this another thing that I need on my plate.” Having a family with six children, a very demanding job as a researcher, clinician, and now department chairman, it just seemed like the last thing I needed to do was to become editor of a journal. It would also be a daunting task to try to fill the shoes of the founding Editor-in-Chief (Dr. Cedric S. Raine), who really has been one of the giants in the field of neuroimmunology and really helped form the field from its infancy through his efforts as President of the International Society of Neuroimmunology (ISNI) and as the head of its journal. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685419</comments>
            <pubDate>Wed, 23 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685419</guid>        </item>
        <item>
            <title>Recent insights into the mechanism of action of glatiramer acetate</title>
            <link>http://www.medworm.com/index.php?rid=4903372&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000129%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Glatiramer acetate (GA, Copaxone®, co-polymer 1) is an immunomodulatory therapy approved in 1996 by the United States Food and Drug Administration for treatment of relapsing–remitting multiple sclerosis. GA has a good safety profile, moderate efficacy, and a unique mode of action. Recent evidence in an animal model of MS, experimental autoimmune encephalomyelitis (EAE), suggests that GA effects on NK cells and B cells may contribute to therapeutic efficacy. We review the mechanism of action of GA, with particular focus on recent data suggesting a role for regulatory B cells. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4903372</comments>
            <pubDate>Tue, 15 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4903372</guid>        </item>
        <item>
            <title>Disease-associated inflammatory biomarker profiles in blood in different subtypes of multiple sclerosis: Prospective clinical and MRI follow-up study</title>
            <link>http://www.medworm.com/index.php?rid=4805168&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000580%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: To identify biomarkers of disease activity and progression in multiple sclerosis (MS), we analyzed the serum profiles of cytokines, chemokines and apoptotic molecules in different subtypes of MS including clinically isolated syndrome (CIS) and correlated their levels with clinical and volumetric MRI findings obtained over a one-year follow up. Upregulated levels of apoptotic sFas molecule were found in MS patients with a worsening EDSS score and an accumulation of hypointense lesions in MRI. In such patients, the levels of MIF appeared to be higher than in non-progressing patients. In addition, increased levels of serum TNF-α and CCL2 were found especially in primary progressive MS (PPMS). These observations suggest that serum Fas and MIF are candidate biomarkers of neurological...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805168</comments>
            <pubDate>Mon, 14 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805168</guid>        </item>
        <item>
            <title>Clonal composition of neuroantigen-specific CD8+ and CD4+ T-cells in multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4805167&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000257%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Patients with multiple sclerosis (MS) show a high prevalence of myelin-reactive CD8+ and CD4+ T-cell responses, which are the putative effectors/modulators of CNS neuropathology. Utilizing a novel combination of short-term culture, CFSE-based sorting and anchored PCR, we evaluated clonal compositions of neuroantigen-targeting T-cells from RRMS patients and controls. CDR3 region analysis of TCRβ chains revealed biased use of specific TCRBV-bearing CD4+ clones. CD8+ clones showed homology to published TCR from CNS-infiltrating T-cells in MS lesions. These studies are the first description of TCR usage of CNS-specific CD8+ T-cells and provide insights into their potential regulatory role in disease. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805167</comments>
            <pubDate>Mon, 14 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805167</guid>        </item>
        <item>
            <title>A natural anti-T-cell receptor monoclonal antibody protects against experimental autoimmune encephalomyelitis</title>
            <link>http://www.medworm.com/index.php?rid=4805159&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000300%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The therapeutic potential of natural anti-T-cell receptor (TCR) antibodies is largely unknown. We investigated whether passive administration of C1-19, a novel natural anti-TCRVβ8 monoclonal antibody, could interfere with the development of EAE. Treatment with C1-19 prevented myelin basic protein (MBP)-induced EAE in Vβ8-sufficient B10.PL but not in Vβ8-deficient SJL mice. Furthermore, C1-19 reduced disease severity when administrated shortly after disease onset. These protective effects of C1-19 correlated with a Th2 bias of the cytokine response, in the absence of T-cell deletion or anergy. Together, these findings indicate that natural anti-TCR antibodies could function as therapeutic tools in autoimmune inflammatory diseases. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805159</comments>
            <pubDate>Mon, 14 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805159</guid>        </item>
        <item>
            <title>Interleukin-13 reduces hyperalgesia and the level of interleukin-1β in BALB/c mice infected with Leishmania major with an up-regulation of interleukin-6</title>
            <link>http://www.medworm.com/index.php?rid=4805157&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000270%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we injected BALB/c mice with a high dose of L. major and treated them with IL-13 (15ng/animal) for twelve days (excluding the weekends) and hyperalgesia was assessed using thermal pain tests. Furthermore, the levels of IL-1β and IL-6 were also assessed at different post-infection days. Our results show that IL-6 and more importantly IL-1β don't play a direct role in the L. major-induced hyperalgesia and that IL-13 induces this hyperalgesia through the down-regulation of IL-1β and another proinflammatory cytokine (most probably TNF-α). Furthermore, our data show that IL-13 leads to the upregulation of the level IL-6 which initially seems to have no direct role in the induced hyperalgesia. Therefore, we suggest that the L. major-induced hyperalgesia is mainly mediated by t...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805157</comments>
            <pubDate>Mon, 14 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805157</guid>        </item>
        <item>
            <title>Preconditioning effects of tumor necrosis factor-α and glutamate on calcium dynamics in rat organotypic hippocampal cultures</title>
            <link>http://www.medworm.com/index.php?rid=4805155&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000117%2Fabstract%3Frss%3Dyes</link>
            <description>In this study we have investigated the individual contribution of pre-exposure to TNF-α or glutamate in the development of ‘ischemic tolerance’ to a subsequent insult, using organotypic hippocampal cultures. At 6days in vitro (DIV), cultures were exposed to an acute concentration of glutamate (30μM) or TNF-α (5ng/ml) for 30min, followed by 24h recovery period. We then examined the effect of the pretreatments on calcium dynamics of the cells within the CA region. We found that pretreatment with TNF-α or glutamate caused in a significant reduction in subsequent glutamate-induced Ca2+ influx 24h later (control: 100.0±0.8%, n=7769 cells; TNF-α: 76.8±1.0%, n=5543 cells; glutamate: 75.3±1.4%, n=3859 cells; p0.0001, D=0.0534). Our results suggest that attenuation in resting Ca2+ activ...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805155</comments>
            <pubDate>Mon, 14 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805155</guid>        </item>
        <item>
            <title>Vasoactive intestinal peptide receptor 1 is downregulated during expansion of antigen-specific CD8 T cells following primary and secondary Listeria monocytogenes infections</title>
            <link>http://www.medworm.com/index.php?rid=4805156&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000269%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: As regulation of CD8 T cell homeostasis is incompletely understood, we investigated the expression profile of the vasoactive intestinal peptide (VIP) receptors, VPAC1 and VPAC2, on CD8 T cells throughout an in vivo immune response. Herein, we show that adoptively transferred CD8 T cells responding to a Listeria monocytogenes infection significantly downregulated, functionally active VPAC1 protein expression during primary and secondary expansion. VPAC1 mRNA expression was restored during contraction and regained naïve levels in primary, but remained low during secondary, memory generation. VIP co-administration with primary infection suppressed CD8 T cell expansion (≈50%). VPAC2 was not detected at any time points throughout primary and secondary infections. Collectively, our ...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805156</comments>
            <pubDate>Fri, 11 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805156</guid>        </item>
        <item>
            <title>Interferon-β but not Glatiramer acetate stimulates CXCL10 secretion in primary cultures of thyrocytes: A clue for understanding the different risks of thyroid dysfunctions in patients with multiple sclerosis treated with either of the two drugs</title>
            <link>http://www.medworm.com/index.php?rid=4805171&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000245%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Autoimmune thyroid disease (AITD) has been reported in patients with multiple sclerosis (MS) receiving interferon-beta (IFN-β), but not in those receiving Glatiramer acetate (GA). CXCL10 is a chemokine playing a pathogenetic role in AITD and MS. Our aim was to evaluate the effects on CXCL10 secretion of IFN-β and GA, alone and in combination with TNF-α, in primary cultures of thyrocytes (PCT). Significant and dose-dependent secretions of CXCL10 were induced by IFN-β but not GA. TNF-α synergistically increased IFN-β induced CXCL10 secretion.These results may provide an explanation for the occurrence of AITD during IFN-β, but not during GA, treatment for MS. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805171</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805171</guid>        </item>
        <item>
            <title>RORC and Foxp3 axis in cerebrospinal fluid of patients with Neuro-Behçet's Disease</title>
            <link>http://www.medworm.com/index.php?rid=4685453&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000233%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Neurological manifestations are present in 5% to 30% of patients with Behçet's disease (BD). Neuro-Behçet's Disease (NBD) is hypothetically caused by T helper (Th) cells, which development is dependent on the expression of lineage-specific transcription factors. Cerebrospinal fluid (CSF) mRNA expression of TBX21, GATA3, RORC, FOXP3 and EBI3 were assessed in 18 NBD patients and 26 controls disease [16 noninflammatory neurological disease (NIND) and 10 headache attributed to Behçet's disease (HaBD)]. Expression of TBX21 (Th1), RORC (Th17) and Foxp3 (Treg) were increased in NBD patients compared to HaBD and NIND patients. EBI3 and Th2-associated GATA3 expressions were found to be decreased (P (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685453</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685453</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=4593446&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS016557281100052X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593446</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593446</guid>        </item>
        <item>
            <title>Nicotine treatment reduces LPS-induced sickness responses in telemetry monitoring rats</title>
            <link>http://www.medworm.com/index.php?rid=4805158&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000282%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cholinergic anti-inflammatory pathway (CAP) inhibits unrestrained inflammatory response in a variety of experimental models. Limited research has been done yet to examine the mechanisms of activating CAP on bio-behavioral changes such as heart rate (HR), blood pressure (BP), body temperature (BT), locomotor activity (LA), and autonomic nervous activity (ANA). We observed these parameters using telemetry to clarify pathophysiological mechanisms of CAP. Nicotine significantly attenuated LPS-induced changes in HR, BP, LA, and ANA. These changes were accompanied by significant inhibition of TNF-α and IL-1β syntheses. However the LPS-induced physiological responses persisted much longer than the cytokines production. These results indicate that systemic nicotine treatment inhibits L...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805158</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805158</guid>        </item>
        <item>
            <title>Immunoregulatory function of bone marrow mesenchymal stem cells in EAE depends on their differentiation state and secretion of PGE2</title>
            <link>http://www.medworm.com/index.php?rid=4685433&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS016557281000531X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Bone marrow mesenchymal stem cells (BMSC)-induced amelioration of experimental autoimmune encephalomyelitis (EAE) was diminished with neuronal differentiantion of BMSC (nBMSC). BMSC secreted large amounts of PGE2, compared to nBMSC, which correlated with higher efficacy to EAE inhibition. EAE mice treated with PGE2 inhibitor, meloxicam showed decreased serum levels of PGE2 and in parallel decreased inhibitory effect on EAE course. In addition, high levels of PGE2 secretion correlated with high expression of indoleamine-2,3-dioxygenase (IDO). Meloxicam blocked IDO expression in BMSC transferred mice indicating functional relation between PGE2 and IDO induction. The current findings demonstrates PGE2 involvement in BMSC-induced inhibition of EAE and provides a mechanistic link betw...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685433</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685433</guid>        </item>
        <item>
            <title>Related B cell clones that populate the CSF and CNS of patients with multiple sclerosis produce CSF immunoglobulin</title>
            <link>http://www.medworm.com/index.php?rid=4685452&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000130%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We investigated the overlap shared between the immunoglobulin (Ig) proteome of the cerebrospinal fluid (CSF) and the B cell Ig-transcriptome of CSF and the central nervous system (CNS) tissue of three patients with multiple sclerosis. We determined the IgG-proteomes of CSF by mass spectrometry, and compared them to the IgG-transcriptomes from CSF and brain lesions, which were analyzed by cDNA cloning. Characteristic peptides that were identified in the CSF-proteome could also be detected in the transcriptomes of both, brain lesions and CSF, providing evidence for a strong overlap of the IgG repertoires in brain lesions and in the CSF. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685452</comments>
            <pubDate>Fri, 25 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685452</guid>        </item>
        <item>
            <title>Transcription factor Nrf2 suppresses LPS-induced hyperactivation of BV-2 microglial cells</title>
            <link>http://www.medworm.com/index.php?rid=4685439&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000075%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Microglial hyperactivation is a hallmark of neurodegenerative diseases and the suppression of microglial hyperactivation is being investigated as a means to treat inflammation-mediated neurodegenerative disorders. Here we report that transcription factor Nrf2 in BV-2 microglia, which regulates the expression of phase II antioxidant enzyme genes, decreased the levels of LPS-induced inflammatory cytokines and mediators. These anti-inflammatory effects were not due to Nrf2-mediated up-regulation of phase II enzymes, since over-expression of these enzymes failed to suppress LPS-mediated microglial hyperactivation. However, Nrf2 inhibited LPS-derived increases in p38 MAPK phosphorylation and NF-κB activation. This suggests that Nrf2 inhibits microglial hyperactivation by suppressing ...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685439</comments>
            <pubDate>Thu, 24 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685439</guid>        </item>
        <item>
            <title>Temporal dynamics of cerebrospinal fluid anti-aquaporin-4 antibodies in patients with neuromyelitis optica spectrum disorders</title>
            <link>http://www.medworm.com/index.php?rid=4805166&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000105%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Neuromyelitis optica spectrum disorders (NMOSD) are associated with anti-aquaporin-4 autoantibodies (AQP4-IgG). Limited data is available on longitudinal cerebrospinal fluid (CSF) AQP4-IgG and their relation to disease activity and inflammatory parameters. AQP4-IgG titers were measured in matched longitudinal serum and CSF samples of 12 patients with NMOSD by an immunofluorescence assay and correlated with clinical parameters. CSF AQP4-IgG were present in patients with high serum titers and correlated with spinal MRI lesion length and CSF parameters. Clinical improvement was associated with a decrease in CSF, but not serum, AQP4-IgG titers. Thus, CSF AQP4-IgG were associated with clinical activity and neuroinflammation. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805166</comments>
            <pubDate>Mon, 14 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805166</guid>        </item>
        <item>
            <title>Expression of CXCR7 chemokine receptor in human meningioma cells and in intratumoral microvasculature</title>
            <link>http://www.medworm.com/index.php?rid=4805165&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000099%2Fabstract%3Frss%3Dyes</link>
            <description>We report the expression pattern of these ligand/receptor pairs in 22 human meningiomas. High CXCR7 and CXCL12 expression was associated with high-proliferative tumors. CXCR7 levels were correlated to the content of both ligands, suggesting a possible autocrine regulation. CXCR4 and CXCL12 were homogeneously expressed within tumor cells, while CXCR7 was mainly detected in tumor endothelial cells and CXCL11 in pericytes. Our results highlight the preferential CXCR7 and CXCL12 expression within more aggressive tumors and the possible role of CXCR7 in meningioma vascularization. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805165</comments>
            <pubDate>Mon, 14 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805165</guid>        </item>
        <item>
            <title>Glatiramer acetate attenuates neuropathic allodynia through modulation of adaptive immune cells</title>
            <link>http://www.medworm.com/index.php?rid=4805154&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000087%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Immune-neuronal interactions contribute to neuropathic pain. Thus, immune-competent cells such as microglia may provide targets for pain relief, as may infiltrating lymphocytes. We evaluated the nature of the lymphocyte response in the spinal cord in association with the maintenance of neuropathic allodynia. We assessed T cell contribution to pain processing by targeting these cells with Glatiramer acetate (GA) which when administered systemically reversed neuropathic allodynia, inhibited microglia response and increased IL-10 and IL-4 expressing T cells in neuropathic dorsal horns. These studies advance understanding of lymphocyte contribution to chronic pain and reveal a new mechanism of T cell intervention. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4805154</comments>
            <pubDate>Tue, 08 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4805154</guid>        </item>
        <item>
            <title>Helminths and multiple sclerosis: Will old friends give us new treatments for MS?</title>
            <link>http://www.medworm.com/index.php?rid=4685420&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000063%2Fabstract%3Frss%3Dyes</link>
            <description>Humans instinctively have a strong aversion to spiders, snakes, and parasitic worms. Even young children immediately recoil from images of these animals, describing them as “scary” or “yucky.” These reactions presumably evolved to protect us from harmful pathogens, and neuroscience reveals that the fear and disgust they evoke are hardwired in the amygdala and insula (). And for good reason: pathogenic helminths (roundworms and flatworms) remain a major scourge in the developing world. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685420</comments>
            <pubDate>Tue, 08 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685420</guid>        </item>
        <item>
            <title>Identification of astrocyte-derived immune suppressor factor that induces apoptosis of autoreactive T cells</title>
            <link>http://www.medworm.com/index.php?rid=4685437&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000038%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we have identified and cloned the genes derived from the IFN-γ-treated astrocyte cell line that induce apoptosis of autoreactive T cells. We created subtraction cDNA libraries from the IFN-γ-treated astrocyte cell line and obtained 100 positive clones. After screening of subtracted cDNAs, we found two candidate genes that induced apoptosis of the PLP-reactive T cell line. The first is a previously unknown gene of 726 base pairs that we named astrocyte-derived immune suppressor factor (AdIF). It contained an open reading frame encoding a polypeptide of 228 amino acids. The second was SPARC/osteonectin, a multifunctional glycoprotein secreted in the extracellular matrix. AdIF protein was found at the inflammatory sites of the EAE brain, and bound to the surface of CD4+ T cel...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685437</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685437</guid>        </item>
        <item>
            <title>The impact of parasite infections on the course of multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4685421&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000051%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Previously, we demonstrated that helminth-infected MS patients showed significantly lower number of relapses, reduced disability scores, and lower MRI activity compared to uninfected MS subjects. In the current study, 12 patients with diagnosis of relapsing remitting MS presenting parasite infections were prospectively followed during 90months; due to exacerbation of helminth-infection symptoms after 63months of follow-up, 4 patients received anti-parasite treatment. Helminth-infection control was associated with significant increase in clinical and radiological MS activities. Moreover, these patients showed significant increase in the number of IFN-γ and IL-12 producing cells, and a fall in the number of TGF-β and IL-10 secreting cells, as well as CD4+CD25+FoxP3+ Treg cells ev...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685421</comments>
            <pubDate>Mon, 31 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685421</guid>        </item>
        <item>
            <title>Reduced thymic output and peripheral naïve CD4 T-cell alterations in primary progressive multiple sclerosis (PPMS)</title>
            <link>http://www.medworm.com/index.php?rid=4685450&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005345%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We compared naïve CD4 and CD8 T-cell homeostasis in primary progressive multiple sclerosis (PPMS), relapsing–remitting MS (RRMS) and controls. Quantitation of signal joint T-cell receptor (TCR) excision circles (sjTRECs) and quantitative estimates of daily thymic export confirm our previous report of reduced thymic output in RRMS and demonstrate reduced thymic output in PPMS. In PPMS, the decreasing % CD31+ naïve CD4 T-cells but constant sjTRECs and constant naïve CD4 T-cell numbers with age, together with increased Bcl-2 expression suggest increased TCR signaling with increased naïve T-cell survival. We conclude PPMS patients have peripheral immune alterations related to reduced thymic output. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685450</comments>
            <pubDate>Thu, 27 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685450</guid>        </item>
        <item>
            <title>IRF-1 signaling in central nervous system glial cells regulates inflammatory demyelination</title>
            <link>http://www.medworm.com/index.php?rid=4685438&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572811000026%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The present study provides evidence that interferon regulatory factor 1 (IRF-1) signaling in glial cells is involved in the pathogenesis of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Using a bone marrow chimera model of EAE, we demonstrated that CNS IRF-1 regulates inflammatory demyelination and disease severity independently of the peripheral immune cells. In addition, we identified Caspase 1, a pro-inflammatory and pro-apoptotic molecule, as an important transcriptional target of IRF-1. The findings of our study indicate that IRF-1 signaling in glial cells serves as a final common pathway of inflammatory demyelination and may have important clinical implications in MS. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685438</comments>
            <pubDate>Tue, 25 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685438</guid>        </item>
        <item>
            <title>The endocannabinoid arachidonylethanolamide attenuates aspects of lipopolysaccharide-induced changes in energy intake, energy expenditure and hypothalamic Fos expression</title>
            <link>http://www.medworm.com/index.php?rid=4685436&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005552%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Arachidonylethanolamide (AEA), an endocannabinoid, regulates both appetite and the immune system. The present study investigated in the rat the ability of AEA (1mg/kg, s.c.) to attenuate the lipopolysaccharide (LPS)-induced (100μg/kg, i.p.) changes in metabolic indices and Fos expression within hypothalamic and mesolimbic systems. AEA attenuated LPS-induced fever and hypophagia, abolished LPS-induced decreases in Fos expression within the arcuate and ventromedial nucleus of the hypothalamus, while both AEA and LPS independently increased Fos expression within the nucleus accumbens. These results highlight the importance of hypothalamic and mesolimbic systems in the regulation of appetite and energy partitioning. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685436</comments>
            <pubDate>Tue, 25 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685436</guid>        </item>
        <item>
            <title>Protein kinases JAK and ERK mediate protective effect of interleukin-2 upon ganglion cells of the developing rat retina</title>
            <link>http://www.medworm.com/index.php?rid=4685435&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005357%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Interleukin-2 (IL-2), a prototypical pro-inflammatory cytokine firstly related to T cells differentiation, exerts pleiotrophic functions in several areas of the central nervous system. Previously we had described the neurotrophic roles of this interleukin upon retinal neurons. Therefore, the aim of this work was to investigate the signaling pathways involved in the neuroprotective effect of IL-2 on axotomized RGC. Herein we demonstrated that at postnatal day 2 IL-2 receptor α subunit (IL-2Rα) is expressed in inner plexiform layer, retinal ganglion cells layer and retinal nerve fibers layer. Moreover, using a model of organotypic retinal explants and rhodamine dextran retrograde labeling for specifically quantify RGC, we showed that IL-2 increased the survival of axotomized RGC ...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685435</comments>
            <pubDate>Tue, 25 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685435</guid>        </item>
        <item>
            <title>Immunoprotection against toxic biomarkers is retained during Parkinson's disease progression</title>
            <link>http://www.medworm.com/index.php?rid=4685448&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS016557281000528X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The aim was to ascertain any possible linkage between humoral immune responses to principal biomarkers (α-synuclein monomers, its toxic oligomers or fibrils, dopamine and S100B) and cellular immunity in Parkinson's disease development. There were elevated autoantibody titers to α-synuclein monomers, oligomers plus fibrils in 72%, 56%, and 17% of Parkinsonian patients respectively with a 5-year disease duration. Additionally, there were increased titers to dopamine and S100B (96% and 89%) in the 5-year patient group. All of these values subsided in 10-year sufferers.Furthermore, CD3+, CD4+, CD8+ T-lymphocyte and B-lymphocyte subsets declined in the patient cohort during Parkinsonism indicating disease associated reductions in these lymphocyte subsets. (Source: Journal of Neuroim...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685448</comments>
            <pubDate>Tue, 18 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685448</guid>        </item>
        <item>
            <title>Phenytoin at optimum doses ameliorates experimental autoimmune encephalomyelitis via modulation of immunoregulatory cells</title>
            <link>http://www.medworm.com/index.php?rid=4685434&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005333%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We investigated the optimum doses of phenytoin for treatment of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE). Oral and intraperitoneal administrations of 0.25 to 1.0mg per mouse (12.5–50mg/kg) 3 times a week improved the clinical course. Intraperitoneal injections of 1.0mg phenytoin were the most effective, as a significant reduction in EAE severity was seen after only 2 administrations with that protocol. Treatment efficacy was associated with amelioration of cellular infiltrates in the CNS, and an increase in CD4+Foxp3+ and CD4+CD25+CD127− regulatory T cells as well as CD8+ suppressor/cytotoxic T cells in blood. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685434</comments>
            <pubDate>Tue, 18 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685434</guid>        </item>
        <item>
            <title>Cellular immune activation markers neopterin and beta 2-microglobulin are not elevated in the cerebrospinal fluid of patients with Creutzfeldt–Jakob disease</title>
            <link>http://www.medworm.com/index.php?rid=4685449&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005308%2Fabstract%3Frss%3Dyes</link>
            <description>In this study we investigated neopterin and beta(β)2-microglobulin, as markers of cellular immune activation, in the cerebrospinal fluid (CSF) of patients with Creutzfeldt–Jakob disease (CJD) and of patients with other neurological and non-neurological diseases.CSF samples from CJD patients were collected in the framework of the German CJD Surveillance study. Concentrations of neopterin and β2-microglobulin were determined in CSF using ELISA. We could not obtain significant changes in CSF levels of neopterin and β2-microglobulin in CJD patients when compared to other neurological and non-neurological controls. In a subanalysis of CJD patients only, we could find significant elevated neopterin levels in patients with MV genotype, potentially reflecting a distinct disease pathology. Sin...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685449</comments>
            <pubDate>Thu, 13 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685449</guid>        </item>
        <item>
            <title>IgG and IgM antibodies to the refolded MOG1–125 extracellular domain in humans</title>
            <link>http://www.medworm.com/index.php?rid=4685447&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005229%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Antibodies to MOG in serum have a dubious prognostic value in multiple sclerosis. The MOG recombinant protein conformational properties relevant to the antigenic activity are unknown. We employed a solid-phase ELISA based on a product (rMOGED(His)6) expressed in E. coli after subcloning the cDNA of the extracellular domain of rat MOG, performing a refolding procedure on column and affinity purification. The far-UV Circular Dichroism (CD) spectra of rMOGED(His)6 showed a β-sheet, a characteristic feature of the Ig-fold. However, in MS sera and controls we failed to detected IgM or IgG antibodies. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685447</comments>
            <pubDate>Mon, 10 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685447</guid>        </item>
        <item>
            <title>Inverse agonism of cannabinoid CB1 receptor blocks the adhesion of encephalitogenic T cells in inflamed brain venules by a protein kinase A-dependent mechanism</title>
            <link>http://www.medworm.com/index.php?rid=4685432&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005321%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: It is well known that the cannabinoid system has a significant role in the regulation of the immune responses. Cannabinoid receptors CB1 and CB2 are expressed on T lymphocytes and mediate the immunomodulatory effects of cannabinoids on T cell functions. Here we show that the treatment of proteolipid protein (PLP)139–151-specific T cells with SR141716A, a CB1 inverse agonist and prototype of the diarylpyrazoles series, induced a strong inhibition of firm adhesion in inflamed brain venules in intravital microscopy experiments. In contrast, SR144528, a potent CB2 inverse agonist, had no significant effect on both rolling and arrest of activated T cells. In addition, two analogs of SR141716A and CB1 inverse agonists, AM251 and AM281 inhibited encephalitogenic T cell adhesion sugges...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685432</comments>
            <pubDate>Mon, 10 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685432</guid>        </item>
        <item>
            <title>Lipoic acid decreases inflammation and confers neuroprotection in experimental autoimmune optic neuritis</title>
            <link>http://www.medworm.com/index.php?rid=4685431&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005291%2Fabstract%3Frss%3Dyes</link>
            <description>This study provides a rationale for investigating the therapeutic efficacy of LA in acute optic neuritis in humans. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685431</comments>
            <pubDate>Mon, 10 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685431</guid>        </item>
        <item>
            <title>Glutamate signaling through the kainate receptor enhances human immunoglobulin production</title>
            <link>http://www.medworm.com/index.php?rid=4685430&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005254%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: CD23 is implicated as a regulator of IgE synthesis. A soluble form of CD23 (sCD23) is released following cleavage by ADAM10 and enhanced sCD23 is correlated with increased IgE. In the CNS, signaling through the kainate receptor (KAR) increases ADAM10. In B cells, activation of KARs produced a significant increase in ADAM10 and sCD23 release as well as an increase in B cell proliferation and immunoglobulin production. In addition, ADAM10 inhibitors reduce IgE synthesis from in vitro cultures of human B cells. Thus, we report for the first time the unique presence of the kainate receptor in B cells and that activation of KARs could serve as a novel mechanism for enhancing B cell activation. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685430</comments>
            <pubDate>Mon, 10 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685430</guid>        </item>
        <item>
            <title>Elsevier Young Investigator Awards</title>
            <link>http://www.medworm.com/index.php?rid=4593447&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810004844%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593447</comments>
            <pubDate>Mon, 10 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593447</guid>        </item>
        <item>
            <title>Enhanced complement consumption in neuromyelitis optica and Behçet's disease patients</title>
            <link>http://www.medworm.com/index.php?rid=4685446&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005217%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The complement system is essential in the pathogenesis of inflammatory central nervous system disorders. To investigate the involvement of complement pathways in neuromyelitis optica (NMO), levels of breakdown products for classical (C4d), alternative (FBb) and common (sC5b-9) pathways were measured in the sera of 28 NMO and control patients (30 Behçet's disease (BD), 29 multiple sclerosis (MS)) and 31 healthy controls by ELISA. Classical and/or alternative pathway consumption was enhanced in NMO and BD patients as compared to MS patients and healthy controls. Our results suggest that NBD and NMO differ from MS by the predominance of complement system involvement. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685446</comments>
            <pubDate>Fri, 07 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685446</guid>        </item>
        <item>
            <title>Selected human leukocyte antigen class II polymorphisms and risk of adult glioma</title>
            <link>http://www.medworm.com/index.php?rid=4685443&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005163%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Few studies have examined the relationship between human leukocyte antigen (HLA) polymorphisms and adult glioma, particularly at class II loci. We evaluated the association between selected HLA class II polymorphisms and adult glioma in a large, hospital-based case-control study, using unconditional logistic regression. DQB1*06 (OR=1.67, 95% CI=1.17–2.39) and DRB1*13 (OR=1.69, 95% CI=1.08–2.64) alleles were associated with an increased risk of glioma, while the DQB1*05 allele showed an inverse association (OR=0.63, 95% CI=0.43–0.93). These results, which were of borderline significance once controlled for the false discovery rate, suggest a potential role for the DQB1*06, DQB1*05, and DRB1*13 alleles in glioma susceptibility. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685443</comments>
            <pubDate>Mon, 03 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685443</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=4372864&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005497%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4372864</comments>
            <pubDate>Sat, 01 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4372864</guid>        </item>
        <item>
            <title>Vitamin D has a direct immunomodulatory effect on CD8+ T cells of patients with early multiple sclerosis and healthy control subjects</title>
            <link>http://www.medworm.com/index.php?rid=4685451&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005199%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Little is known on a putative effect of vitamin D on CD8+ T cells. Yet, these cells are involved in the immmunopathogenesis of MS. We assessed the cytokine profile of EBV-specific CD8+ T cells of 10 early MS patients and 10 healthy control subjects with or without 1,25(OH)2D3 and found that, with 1,25(OH)2D3, these cells secreted less IFN-γ and TNF-α and more IL-5 and TGF-β. CD4+ T cell depletion or even culture with CD8+ T cells only did not abolish the immunomodulatory effect of 1,25(OH)2D3 on CD8+ T cells, suggesting that 1,25(OH)2D3 can act directly on CD8+ T cells. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685451</comments>
            <pubDate>Mon, 27 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685451</guid>        </item>
        <item>
            <title>Moderate increase in temperature may exacerbate neuroinflammatory processes in the brain: Human cell culture studies</title>
            <link>http://www.medworm.com/index.php?rid=4685428&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005278%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The effect of a moderate, physiologically relevant rise in temperature on several neuroinflammatory parameters was investigated in vitro using human cell lines and cultured human astrocytes. A two degree Celsius rise in temperature was found to enhance the neurotoxicity of microglia-like and astrocytic cells, increase the release of monocyte chemotactic protein (MCP)-1 by activated human monocytic THP-1 cells and amplify the generation of reactive oxygen intermediates by differentiated HL-60 myelocytic cells. Moderate increases in body temperature may exacerbate neuroinflammation and neuronal injury in chronic neurodegenerative disorders. Hence, therapies aimed at lowering the body temperature could be used to slow down the progression of such diseases. (Source: Journal of Neuroi...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685428</comments>
            <pubDate>Mon, 27 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685428</guid>        </item>
        <item>
            <title>Age-associated alterations in sympathetic noradrenergic innervation of primary and secondary lymphoid organs in female Fischer 344 rats</title>
            <link>http://www.medworm.com/index.php?rid=4685427&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005230%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Normal aging processes, as well as, psychological stress affect the immune system; each can act alone, or interact with each other, to cause dysregulation of immune function substantially altering physical and mental health. The sympathetic nervous system (SNS), a major mediator of stress effects on immune function, is significantly affected by normal aging process, and stress can affect aging of the SNS. Previously, we have shown age-associated changes in sympathetic noradrenergic (NA) innervation of lymphoid organs in male rodents that affect immune regulation. The purpose of this study was to investigate sympathetic innervation of lymphoid organs and associated alterations in immune responses in young and aging female Fischer 344 (F344) rats. Histofluorescence and immunocytoch...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685427</comments>
            <pubDate>Mon, 27 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685427</guid>        </item>
        <item>
            <title>Role for tumor necrosis factor-alpha in JC virus reactivation and progressive multifocal leukoencephalopathy</title>
            <link>http://www.medworm.com/index.php?rid=4685426&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005242%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: JCV causes the CNS demyelinating disease progressive multifocal leukoencephalopathy (PML). After primary infection, JCV persists in a latent state, where viral protein expression and replication are not detectable. NF-κB and C/EBPβ regulate the JCV promoter via a control element, κB, suggesting proinflammatory cytokines may reactivate JCV to cause PML, e.g., in HIV-1/AIDS. Since HIV-1 induces cytokines in brain, including TNF-α, we examined a role for TNF-α in JCV regulation. TNF-α stimulated both early and late JCV transcription. Further, the κB element conferred TNF-α response to a heterologous promoter. Immunohistochemistry of HIV+/PML revealed robust labeling for TNF-α and TNFR-1. These data suggest TNF-α stimulation of κB may contribute to JCV reactivation in HIV+...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685426</comments>
            <pubDate>Mon, 27 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685426</guid>        </item>
        <item>
            <title>Chronic stress promotes lymphocyte reduction through TLR2 mediated PI3K signaling in a β-arrestin 2 dependent manner</title>
            <link>http://www.medworm.com/index.php?rid=4685429&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005266%2Fabstract%3Frss%3Dyes</link>
            <description>In this study, we investigated the effects of TLR2 ligands on stress-induced lymphocyte reduction. We also defined whether the phosphoinositide 3-kinases (PI3Ks)/Akt pathway contributes to TLR2-mediated lymphocyte numbers altered by stress. Our data have shown that stimulation of TLR2 by TLR2 ligands peptidoglycan (PGN) or Pam3CSK4 (Pam3) attenuates stress-induced reduction in lymphocyte numbers. However, TLR2 ligand-induced protection from stress-induced lymphocyte reduction is lost in TLR2 deficiency in mice. Furthermore, stimulation of TLR2 by PGN induces protection from stress-induced reduction in the number of splenocytes through PI3K. Moreover, PGN dramatically increases the level of phosphorylation of Akt through a PI3K-dependent manner. Moreover, we found that stimulation of TLR2 b...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685429</comments>
            <pubDate>Thu, 23 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685429</guid>        </item>
        <item>
            <title>Peptide reactivity between multiple sclerosis (MS) CSF IgG and recombinant antibodies generated from clonally expanded plasma cells in MS CSF</title>
            <link>http://www.medworm.com/index.php?rid=4685444&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005187%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We employed 19 recombinant antibodies (rAbs) generated from clonally expanded plasma cells, and native IgG from cerebrospinal fluid (CSF) of three multiple sclerosis (MS) patients for panning with phage displayed random peptide libraries. Specific peptide epitopes/mimotopes were identified and characterized. Importantly, peptide–antibody interactions were shared by rAbs and native IgG from the same patient. Three peptides strongly interacted with at least one other MS CSF, but not to inflammatory CNS controls. Database searches revealed several protein candidates including stress proteins, cell surface proteins, and neuronal proteins. Peptides derived from the candidate proteins were recognized by rAbs. Identification of peptide epitopes/mimotopes in MS may provide clues regard...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685444</comments>
            <pubDate>Wed, 22 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685444</guid>        </item>
        <item>
            <title>Additive effects of orexin B and vasoactive intestinal polypeptide on LL-37-mediated antimicrobial activities</title>
            <link>http://www.medworm.com/index.php?rid=4685425&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005205%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The present study examined the bactericidal effects of orexin B (ORXB) and vasoactive intestinal peptide (VIP) alone or combined with cationic antimicrobial peptides, such as LL-37, on Escherichia coli, Pseudomonas aeruginosa, Streptococcus mutans and Staphylococcus aureus. The bactericidal effect of ORXB or VIP alone was detected in low NaCl concentration, but attenuated in physiological NaCl concentration (150mM). However, such attenuated bactericidal activities of ORXB and VIP in 150mM NaCl were regained by adding LL-37. Therefore, our results indicate that VIP and ORXB appear to mediate bactericidal effects in concert with LL-37 in the physiological context of mucosal tissue. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685425</comments>
            <pubDate>Wed, 22 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685425</guid>        </item>
        <item>
            <title>Reduced thymic expression of ErbB receptors without auto-antibodies against synaptic ErbB in myasthenia gravis</title>
            <link>http://www.medworm.com/index.php?rid=4593468&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810004741%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: In myasthenia gravis (MG), the neuromuscular transmission is impaired mainly by auto-antibodies against the acetylcholine receptor (AChR) or MuSK. In about 5% of the MG patients, however, the auto-antigen is still unknown. We investigated whether these idiopathic MG patients (iMG) have auto-antibodies against ErbB proteins, which influence the AChR density at the NMJ. Our results show reduced mRNA expression levels of ErbB4 in thymus tissue of iMG patients compared to AChR-MG and non-MG patients, but we could not detect anti-ErbB antibodies in sera of iMG patients. Therefore, our results do not support a role for ErbB receptors as auto-antigens in iMG patients. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593468</comments>
            <pubDate>Mon, 20 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593468</guid>        </item>
        <item>
            <title>Plasma cytokine concentrations associated with HIV/hepatitis C coinfection are related to attention, executive and psychomotor functioning</title>
            <link>http://www.medworm.com/index.php?rid=4685445&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005175%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cytokine disturbances have been linked to brain dysfunction among HIV-infected people. Past studies have not simultaneously examined a large set of cytokine measures and their relationships to HIV-associated neurocognitive deficits. We hypothesized that performance on measures of attention and executive and psychomotor functions would be associated with plasma cytokine concentrations in HIV-infected individuals. Plasma samples drawn from 30 HIV-infected and 37 HIV seronegative individuals were analyzed via xMAP multiplexed bead array immunoassay to determine concentrations of 13 cytokines. Performance on Trail Making A/B, Stroop Test, Letter–Number Sequencing, Digit Symbol Coding, Symbol Search, and Grooved Pegboard tests was assessed. Statistical analyses were performed to exa...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685445</comments>
            <pubDate>Mon, 13 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685445</guid>        </item>
        <item>
            <title>A case for regulatory B cells in controlling the severity of autoimmune-mediated inflammation in experimental autoimmune encephalomyelitis and multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4372865&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810004881%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Multiple sclerosis (MS) is considered to be a T cell-mediated autoimmune disease that results in the presence of inflammatory lesions/plaques associated with mononuclear cell infiltrates, demyelination and axonal damage within the central nervous system (CNS). To date, FDA approved therapies in MS are thought to largely function by modulation of the immune response. Since autoimmune responses require many arms of the immune system, the direct cellular mechanisms of action of MS therapeutics are not definitively known. The mouse model of MS, experimental autoimmune encephalomyelitis (EAE), has been instrumental in deciphering the mechanism of action of MS drugs. In addition, EAE has been widely used to study the contribution of individual components of the immune system in CNS aut...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4372865</comments>
            <pubDate>Mon, 13 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4372865</guid>        </item>
        <item>
            <title>HLA-DPB1*0501 is associated with susceptibility to anti-aquaporin-4 antibodies positive neuromyelitis optica in Southern Han Chinese</title>
            <link>http://www.medworm.com/index.php?rid=4685442&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005114%2Fabstract%3Frss%3Dyes</link>
            <description>Conclusions: DPB1*0501 correlates with risk of AQP4-Ab positive NMO in Southern Han Chinese. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685442</comments>
            <pubDate>Mon, 06 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685442</guid>        </item>
        <item>
            <title>Identification of antibodies as biological markers in serum from multiple sclerosis patients by immunoproteomic approach</title>
            <link>http://www.medworm.com/index.php?rid=4685441&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005102%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We identified the antibody against mitochondrial heat shock protein 70 (mtHSP70) in serum from multiple sclerosis (MS) patients by proteomics-based analysis. The prevalence of the anti-mtHSP70 antibody is significantly higher in serum from MS patients than in serum from Parkinson disease patients, multiple cerebral infarction patients, infectious meningoencephalitis patients, and healthy controls (HCs) (68% sensitivity; 74% specificity). We studied the clinical features and magnetic resonance imaging findings of MS patients with the anti-mtHSP70 antibody. As a result, there were no significant differences between the anti-mtHSP70-antibody-positive and -negative MS patients. Additionally, in our comprehensive analysis of the prevalence of both the anti-mtHSP70 antibody and the ant...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685441</comments>
            <pubDate>Mon, 06 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685441</guid>        </item>
        <item>
            <title>Eicosapentaenoic acid decreases TNF-α and protects dystrophic muscles of mdx mice from degeneration</title>
            <link>http://www.medworm.com/index.php?rid=4593466&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810004820%2Fabstract%3Frss%3Dyes</link>
            <description>We examined the effects of eicosapentaenoic acid (EPA) on dystrophic muscle degeneration. Mdx mice (14days old) received EPA for 16days. The sternomastoid, diaphragm and biceps brachii muscles were removed. Control mdx mice received vehicle. EPA decreased creatine kinase and myonecrosis and reduced the levels of TNF-α. These results suggest that EPA plays a protective role in dystrophic muscle degeneration, possibly by reducing TNF-α, and support further investigations of EPA as a potential therapy for dystrophinopathies. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593466</comments>
            <pubDate>Mon, 06 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593466</guid>        </item>
        <item>
            <title>The kinase inhibitory region of SOCS-1 is sufficient to inhibit T-helper 17 and other immune functions in experimental allergic encephalomyelitis</title>
            <link>http://www.medworm.com/index.php?rid=4593462&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810004686%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Suppressors of cytokine signaling (SOCS) negatively regulate the immune response, primarily by interfering with the JAK/STAT pathway. We have developed a small peptide corresponding to the kinase inhibitory region (KIR) sequence of SOCS-1, SOCS1-KIR, which inhibits kinase activity by binding to the activation loop of tyrosine kinases such as JAK2 and TYK2. Treatment of SJL/J mice with SOCS1-KIR beginning 12days post-immunization with myelin basic protein (MBP) resulted in minimal symptoms of EAE, while most control treated mice developed paraplegia. SOCS1-KIR treatment suppressed interleukin-17A (IL-17A) production by MBP-specific lymphocytes, as well as MBP-induced lymphocyte proliferation. When treated with IL-23, a key cytokine in the terminal differentiation of IL-17-producin...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593462</comments>
            <pubDate>Mon, 06 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593462</guid>        </item>
        <item>
            <title>Exogenous granulocyte colony-stimulating factor exacerbate pain-related behaviors after peripheral nerve injury</title>
            <link>http://www.medworm.com/index.php?rid=4593459&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810004649%2Fabstract%3Frss%3Dyes</link>
            <description>This study was designed to test the hypothesis that exogenous administration of recombinant mouse granulocyte-colony-stimulating factor (rmG-CSF) to enhance the recruitment of inflammatory cells to painful inflamed sites could attenuate pain in a chronic neuropathic pain model in mice. Our results indicate that treatment with rmG-CSF increased several cytokines and opioid peptides content; however, it did not attenuate but exacerbate neuropathic pain. Our study highlights the potent pro-inflammatory potential of G-CSF and suggests they may be targets for therapeutic intervention in chronic neuropathic pain. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593459</comments>
            <pubDate>Mon, 06 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593459</guid>        </item>
        <item>
            <title>Novel survivin mutant protects differentiated SK-N-SH human neuroblastoma cells from activated T-cell neurotoxicity</title>
            <link>http://www.medworm.com/index.php?rid=4685423&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS016557281000487X%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Currently, there are no known treatments for protection of axonal loss associated with neuroinflammatory diseases such as multiple sclerosis (MS). Survivin is a member of the inhibitors of the apoptosis (IAP) family of proteins that its neuroprotective effects have not been studied. We demonstrate here that SurR9-C84A, a survivin mutant, exhibits a neuroprotective role against the cytotoxic effects of activated T-cell infiltrates, such as granzyme B (GrB). The activated T-cell supernatants induce toxicity on differentiated SK-N-SH cells, which is associated with the loss of Ca2+ homeostasis, the increased population of dead cells, mitochondrial membrane depolarisation, and the accelerated expression of cyclinD1, caspase3 and Fas, as observed for most apoptotic cells. Alternativel...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685423</comments>
            <pubDate>Fri, 03 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685423</guid>        </item>
        <item>
            <title>Induction of hippocampal neurogenesis by a tolerogenic peptide that ameliorates lupus manifestations</title>
            <link>http://www.medworm.com/index.php?rid=4593467&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810004856%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: To determine the effect of the tolerogenic peptide hCDR1 on hippocampal neurogenesis, we treated SLE-afflicted (NZBxNZW)F1 mice with hCDR1 (once a week for 10weeks). The treatment resulted in the up-regulation of neurogenesis in the dentate gyrus and restored the NeuN immunoreactivity in brain hippocampi of the mice in association with increased gene expression of IGF-1, NGF and BDNF. Furthermore, hCDR1 treatment significantly up-regulated p-ERK and p-Akt that are suggested to be key components in mediating growth factor-induced neurogenesis. The observed effects of hCDR1 on hippocampal-neurogenesis and on associated signaling pathways suggest a potential role for hCDR1 in CNS lupus. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593467</comments>
            <pubDate>Fri, 03 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593467</guid>        </item>
        <item>
            <title>Population structure and HLA DRB1*1501 in the response of subjects with multiple sclerosis to first-line treatments</title>
            <link>http://www.medworm.com/index.php?rid=4685440&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810004893%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Using retrospectively collected outcome data for treatment naïve subjects treated with either glatiramer acetate (GA) (n=332) or interferon beta (IFN β) (n=424), we replicated the lack of a significant difference in efficacy between these treatments. Further, for both treatments, we observed a decline in the hazard of a relapse over time, which may suggest the existence of subsets of subjects with differential responses to each treatment. The HLA DRB1*1501 allele explained some of this variation in event-free survival while on GA, and we found suggestive evidence that an IRF8 polymorphism influences event-free survival in IFN β treated subjects. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685440</comments>
            <pubDate>Mon, 29 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4685440</guid>        </item>
        <item>
            <title>Cold stress induced morphological microglial activation and increased IL-1β expression in astroglial cells in rat brain</title>
            <link>http://www.medworm.com/index.php?rid=4685424&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810005096%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The present study investigated the possible impact of cold stress on the immune functions of the brain. Wistar rats were exposed to 4°C for 2h prior to analysis of immunohistochemical analysis of OX-42 and IL-1β, which are markers of microglia and inflammation, respectively. Exposure to cold stress induced morphological microglial activation in as early as 30min, and the activation lasted up to 2h following the stress. In addition, increased IL-1β-immunoreactivity was detected in the hippocampus and hypothalamus. However, IL-1β was not co-localized with microglia, and was predominantly expressed in astroglia. The present study provides the first evidence that cold stress contributes to neuro-immunomodulation in the brain through microglial activation and expression of IL-1β ...</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4685424</comments>
            <pubDate>Mon, 29 Nov 2010 00:00:00 +0100</pubDate>
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            <title>Cathepsins (S and B) and their inhibitor Cystatin C in immune cells: Modulation by interferon-β and role played in cell migration</title>
            <link>http://www.medworm.com/index.php?rid=4593475&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810004650%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We investigated the modulation of Cathepsin S, Cathepsin B and Cystatin C expression in immune cells by interferon (IFN)-β, and their role in cell migration. Cathepsin levels were increased in monocytic and T line cells upon activation. IFN-β abolished this increase of Cathepsin B in monocytes and of Cathepsin S in T cells, while increased Cystatin C. Neutralizing Cystatin C increased cell migration, while migration of monocytes and T cells was inhibited by IFN-β, by Cystatin C, and T cell migration was suppressed by Cathepsin S and B inhibitors. These findings support further studies in the importance of Cathepsins and Cystatins in immunomodulation. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593475</comments>
            <pubDate>Mon, 29 Nov 2010 00:00:00 +0100</pubDate>
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            <title>Reduced production of noggin by immune cells of patients with relapsing–remitting multiple sclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4593470&amp;cid=s_37053_3_f&amp;fid=37053&amp;url=http%3A%2F%2Fwww.jni-journal.com%2Farticle%2FPIIS0165572810004571%2Fabstract%3Frss%3Dyes</link>
            <description>In conclusion, T cells possess the potential to participate in the induction of neurogeneration by the production of noggin. This potential seems to be defective in immune cells of RR-MS patients as there is reduced mRNA expression and protein secretion levels of noggin, insufficient stimulatory effect of CD3/CD28 stimulation and unresponsiveness to TNF-α in these patients PBMCs. (Source: Journal of Neuroimmunology)</description>
            <author>Journal of Neuroimmunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593470</comments>
            <pubDate>Mon, 29 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4593470</guid>        </item>
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