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        <title>Cytokine 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 'Cytokine' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Cytokine&t=Cytokine&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 17 Mar 2010 16:33:49 +0100</lastBuildDate>
        <item>
            <title>Electroacupuncture promotes a decrease in inflammatory response associated with Th1/Th2 cytokines, nitric oxide and leukotriene B4 modulation in experimental asthma.</title>
            <link>http://www.medworm.com/index.php?rid=3372283&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20231101%26dopt%3DAbstract</link>
            <description>Authors: Carneiro ER, Xavier RA, Castro MA, Nascimento CM, Silveira VL
    Previously, we have shown that electroacupuncture (EA) in rats decreased eosinophil infiltration into the pulmonary tissue (PT) and in the bronchoalveolar lavage (BAL) in an experimental model of asthma. Th2 cytokines, leukotriene B4 (LTB4) and nitric oxide (NO) are involved in the asthma inflammatory process. The aim of this study was to verify the effects of EA on these asthma mediators. Male Wistar rats were divided into control (C), immobilized (I), sham acupuncture (SA), and acupuncture (A) groups. All rats were sensitized, and EA treatment using clinical acupuncture points was started 24h after antigen priming. EA was done every other day for 2weeks. Subsequently, animals were challenged by inhalation and sacr...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3372283</comments>
            <pubDate>Sat, 13 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3372283</guid>        </item>
        <item>
            <title>Evidence that cervical cancer cells secrete IL-2, which becomes an autocrine growth factor.</title>
            <link>http://www.medworm.com/index.php?rid=3372285&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20227890%26dopt%3DAbstract</link>
            <description>We present evidence that cervical cancer cells express a functional IL-2 receptor (IL-2R). In fact, by RT-PCR we obtained that the IL-2R is present in CALO, and INBL cells, and that it consisted of the alphaIL-2R, betaIL-2R, and gammaIL-2R chains. We also found that IL-2 is a growth factor for these cell lines, and unexpectedly that CALO and INBL themselves being cancer cells produce, and secrete IL-2. Antibodies against the alpha and beta subunits of the IL-2R inhibited cell proliferation thus hinting to a cell growth dependency on this factor. Our results thus provide evidence that the IL-2R on cervical cancer cells is part of an autocrine mechanism for its growth to the extent that, like lymphocytes, they produce and become partially dependent on this growth factor. We think that in vie...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3372285</comments>
            <pubDate>Fri, 12 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3372285</guid>        </item>
        <item>
            <title>CRP-induced levels of oxidative stress are higher in brain than aortic endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3347296&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20207160%26dopt%3DAbstract</link>
            <description>In conclusion BEC show a higher vulnerability to CRP due to increased levels of CRP receptors and the NAD(P)H-oxidase.
    PMID: 20207160 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3347296</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3347296</guid>        </item>
        <item>
            <title>Transforming growth factor beta-1 and interleukin-17 gene transcription in peripheral blood mononuclear cells and the human response to infection.</title>
            <link>http://www.medworm.com/index.php?rid=3347294&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20207161%26dopt%3DAbstract</link>
            <description>Conclusions: Down regulation of TGFbeta-1 gene transcription was related to the occurrence of infection but not the onset of sepsis. Interleukin-17 production in PBMC may not be significant in the human host response to infection.
    PMID: 20207161 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3347294</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3347294</guid>        </item>
        <item>
            <title>Expression of cytokine genes in the aorta is altered by the deficiency in MCP-1: Effect of a high-fat, high-cholesterol diet.</title>
            <link>http://www.medworm.com/index.php?rid=3347289&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20207162%26dopt%3DAbstract</link>
            <description>Conclusions: There is a complex network of interactions linking MCP-1 and other cytokines. The lack of MCP-1 limits the aortic response to atherogenic stimuli, but does not completely protect against neointima formation. Activation of alternative inflammatory pathways in the vascular wall in response to MCP-1 deficiency should be considered to fully understand the actual role of this chemokine.
    PMID: 20207162 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3347289</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3347289</guid>        </item>
        <item>
            <title>Interleukin-1 beta and interleukin-6 gene polymorphism associations with angiographically assessed coronary artery disease in Brazilians.</title>
            <link>http://www.medworm.com/index.php?rid=3347300&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20206549%26dopt%3DAbstract</link>
            <description>This report analyzed the IL-1B-511C&amp;gt;T and IL-6-174G&amp;gt;C polymorphisms in 667 patients (253 African-Brazilians and 414 Caucasian-Brazilians) who underwent coronary angiography. Patients with a coronary obstructive lesion 50% presented a higher frequency of the IL-1B-511CC genotype (30.4%) compared to lesion-free individuals (16.5%, p=0.032) in African- but not in Caucasian-Brazilians. No significant genotype frequency difference was identified for the IL-6-174G&amp;gt;C polymorphism in either ethnic groups. However, after correction for other CAD risk factors using multivariate logistic regression, both the IL-1B-511CC [Odds ratio (OR)=2.3; p=0.019] and the IL-6-174GG (OR=2.0; p=0.028) genotypes were considered independent CAD risk predictors in African-Brazilians. This report shows that th...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3347300</comments>
            <pubDate>Wed, 03 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3347300</guid>        </item>
        <item>
            <title>The -251A&gt;T polymorphism of interleukin-8 is associated with longer mechanical ventilation and hospital staying after coronary surgery.</title>
            <link>http://www.medworm.com/index.php?rid=3347298&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20206550%26dopt%3DAbstract</link>
            <description>Conclusions: OPCAB results in post-operative inflammatory responses. Genetic backgrounds alter the extent of inflammatory response and might relate to clinical outcome of OPCAB.
    PMID: 20206550 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3347298</comments>
            <pubDate>Wed, 03 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3347298</guid>        </item>
        <item>
            <title>The impacts of continuous veno-venous hemofiltration on plasma cytokines and monocyte human leukocyte antigen-DR expression in septic patients.</title>
            <link>http://www.medworm.com/index.php?rid=3340102&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20202859%26dopt%3DAbstract</link>
            <description>Authors: Peng Z, Pai P, Hong-Bao L, Rong L, Han-Min W, Chen H
    The aim of this study was to investigate the impacts of continuous veno-venous hemofiltration (CVVH) on plasma cytokines and monocyte human leukocyte antigen-DR (HLA-DR) expression and to evaluate the relationship between them during CVVH treatment in septic patients. Forty septic patients were enrolled in this study. They were randomly divided into control group (who received conventional treatment, n=20) and CVVH group (who received conventional treatment and CVVH treatment, n=20). The blood samples were taken to measure the changes of plasma cytokines (IFN-gamma, TNF-alpha, IL-1, IL-2, IL-4, IL-6, IL-10 and IL-13) and HLA-DR expression on monocytes. After CVVH treatment, the plasma levels of IFN-gamma, IL-1, IL-2, IL-4, I...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3340102</comments>
            <pubDate>Tue, 02 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3340102</guid>        </item>
        <item>
            <title>Vascular endothelial growth factor, basic fibroblast growth factor, insulin-like growth factor-I and platelet-derived growth factor levels in human milk of mothers with term and preterm neonates.</title>
            <link>http://www.medworm.com/index.php?rid=3340101&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20202860%26dopt%3DAbstract</link>
            <description>Authors: Ozgurtas T, Aydin I, Turan O, Koc E, Hirfanoglu IM, Acikel CH, Akyol M, Erbil MK
    Human milk is a complex biological fluid. It contains many nutrients, anti-infectious and biologically active substance. Human milk also contains many angiogenic polypeptides. We have determined four of these: Vascular endothelial growth factor (VEGF), basic fibroblast growth factor (b-FGF), insulin-like growth factor- I (IGF-I) and platelet-derived growth factor (PDGF). The aim of this study was to compare the concentrations of VEGF, b-FGF, IGF-I and PDGF in human milk collected from mothers with preterm and term neonates. Human milk samples were collected from 29 mothers of preterm (&amp;lt;37weeks) and from 29 mothers of term (38&amp;gt;weeks) infants at days 3, 7 and 28 postpartum. Milk samples were a...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3340101</comments>
            <pubDate>Tue, 02 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3340101</guid>        </item>
        <item>
            <title>Interleukin-22 is a negative regulator of the allergic response.</title>
            <link>http://www.medworm.com/index.php?rid=3336176&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20194033%26dopt%3DAbstract</link>
            <description>Authors: Schnyder B, Lima C, Schnyder-Candrian S
    A proinflammatory role of T helper (Th)17 cells, producing IL-22 and IL-17A, has been favored although there is evidence for negative immune regulation by IL-17A. Here we show that IL-22 was produced during an allergic response in lungs of mice, immunized and challenged with ovalbumin (OVA), and that IL-22 neutralization further augmented the eosinophil recruitment to the lung. In a second allergy model, transfer of OVA-pulsed dendritic cells (DC) into naive mice conveyed eosinophil recruitment in response to subsequent inhaled OVA challenge, while DC preincubation with recombinant IL-22 abolished this response. Similarly, DC preincubation with IL-17A abolished DC-driven eosinophil recruitment, showing that both Th17 cytokines IL-22 and ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3336176</comments>
            <pubDate>Sat, 27 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3336176</guid>        </item>
        <item>
            <title>Induction of IL-13 production and upregulation of gene expression of protease activated receptors in P815 cells by IL-6.</title>
            <link>http://www.medworm.com/index.php?rid=3320295&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20189822%26dopt%3DAbstract</link>
            <description>In conclusion, IL-6 can stimulate IL-13 release from mast cells through an ERK and Akt cell signaling pathway dependent, but PAR independent mechanism.
    PMID: 20189822 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3320295</comments>
            <pubDate>Fri, 26 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3320295</guid>        </item>
        <item>
            <title>Gingival crevicular fluid levels of oncostatin M in periodontal conditions.</title>
            <link>http://www.medworm.com/index.php?rid=3320296&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20189410%26dopt%3DAbstract</link>
            <description>Conclusions: The greater the amount of periodontal tissue destruction there is substantial increase in GCF OSM concentrations. Since, OSM levels are positively correlated with PPD and CAL, it can be considered as an inflammatory biomarker in periodontal diseases.
    PMID: 20189410 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3320296</comments>
            <pubDate>Thu, 25 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3320296</guid>        </item>
        <item>
            <title>Co-expression of insulin-like growth factor-1 and interleukin-4 in an in vitro inflammatory model.</title>
            <link>http://www.medworm.com/index.php?rid=3320297&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20188584%26dopt%3DAbstract</link>
            <description>In this study, we analyze the expression of IGF-1 and IL-4 from a single plasmid vector, where each gene is expressed through an independent promoter and enhancer sequence. Regenerative and anti-inflammatory effects of IGF-1 alone and of both IGF-1 and IL-4 were analyzed in an in vitro chondrocyte inflammatory model. Co-expression of both transgenes in primary chondrocytes was ascertained by immunoassays. Following stimulation with IL-1beta and TNFalpha, pro-inflammatory mediators as well as IGF-binding proteins were down-regulated more effectively in the presence of both genes to levels comparable to the non-stimulated control. Further, cartilage regeneration proteins type II collagen and proteoglycans were up-regulated in stimulated cells transfected with IGF-1 alone and in combination w...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3320297</comments>
            <pubDate>Wed, 24 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3320297</guid>        </item>
        <item>
            <title>Secretion profile of human bone marrow stromal cells: Donor variability and response to inflammatory stimuli.</title>
            <link>http://www.medworm.com/index.php?rid=3316329&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20185331%26dopt%3DAbstract</link>
            <description>Authors: Zhukareva V, Obrocka M, Houle JD, Fischer I, Neuhuber B
    Mesenchymal stem cells (MSC) derived from bone marrow are ideal transplants for a variety of CNS disorders and appear to support recovery after injury by secreting therapeutic factors. There is considerable variability in the secretion profile of MSC derived from different donors and it is known that MSC secretion changes in response to inflammatory stimuli, but no comprehensive analysis has been performed to address these issues. Here we show that MSC from seven donors secrete chemokines and cytokines in variable ranges, with some factors showing high variability. Treatment of cultured MSC with pro-inflammatory cytokines or tissue extracts from injured spinal cord resulted in up-regulation of selected cytokines, whereas ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3316329</comments>
            <pubDate>Tue, 23 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3316329</guid>        </item>
        <item>
            <title>Sputum biomarker profiles in cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD) and association between pulmonary function.</title>
            <link>http://www.medworm.com/index.php?rid=3312096&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20181491%26dopt%3DAbstract</link>
            <description>Authors: Eickmeier O, Huebner M, Herrmann E, Zissler U, Rosewich M, Baer PC, Buhl R, Schmitt-Groh&amp;#xE9; S, Zielen S, Schubert R
    Lung diseases like cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD) are associated with chronic airway inflammation. The aim of our study was to compare a complex biomarker profile in order to characterize specific inflammatory patterns in sputum of patients with CF and COPD. Induced sputum samples of 19 CF-, 26 COPD patients and 21 healthy controls were analyzed for concentrations of IL-1beta, IL-2, IL-6, IL-8, IL-13, IP-10, MCP-1, IFN-gamma and TNF-alpha using the new cytometric bead array (CBA) technology. Significant differences in airway biomarker profiles of CF and COPD were detected. Patients with CF showed a significant increase in...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3312096</comments>
            <pubDate>Mon, 22 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3312096</guid>        </item>
        <item>
            <title>A role for protein kinase PKR in the mediation of Epstein-Barr virus latent membrane protein-1-induced IL-6 and IL-10 expression.</title>
            <link>http://www.medworm.com/index.php?rid=3312098&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20171114%26dopt%3DAbstract</link>
            <description>Authors: Lin SS, Lee DC, Law AH, Fang JW, Chua DT, Lau AS
    Expression of Epstein-Barr virus-encoded oncogenic latent membrane protein 1 (LMP1) has been substantially associated with tumorigenic transformation in the virus-infected cells. The pathogenic complexity of LMP1 is partly due to the cytokine dysregulation including IL-6 and IL-10 in perturbing the host immune responses. Here we have identified an important signaling event mediated by a dsRNA-dependent serine/threonine protein kinase, PKR, in regulating LMP1-induced IL-6 and IL-10 expression. We first demonstrated that PKR plays a significant role in mediating LMP1-induced cytokine expression by using a PKR inhibitor 2-aminopurine, and the specific role of PKR involved was confirmed by the use of siRNA oligos targeting PKR and/o...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3312098</comments>
            <pubDate>Wed, 17 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3312098</guid>        </item>
        <item>
            <title>Circadian variations of interleukin 6 in coronary circulations of patients with myocardial infarction.</title>
            <link>http://www.medworm.com/index.php?rid=3312097&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20171115%26dopt%3DAbstract</link>
            <description>Conclusions: Coronary concentration of IL-6 in patients with STEMI is significantly higher in the afternoon than in the morning. This might be involved in increased morbidity of those patients.
    PMID: 20171115 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3312097</comments>
            <pubDate>Wed, 17 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3312097</guid>        </item>
        <item>
            <title>Genetic variation at the CCR5/CCR2 gene cluster and risk of psoriasis and psoriatic arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=3276925&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20153665%26dopt%3DAbstract</link>
            <description>Conclusions: Our work suggests that the genetic variation at the CCR2/CCR5 genes did not contribute to the risk for Ps, but CCR2 polymorphisms could modulate the risk for arthritis in patients with psoriasis.
    PMID: 20153665 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3276925</comments>
            <pubDate>Thu, 11 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3276925</guid>        </item>
        <item>
            <title>Association of TGFbeta1 polymorphisms involved in radiation toxicity with TGFbeta1 secretion in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3263166&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20144876%26dopt%3DAbstract</link>
            <description>In conclusion, the effect of genetic polymorphisms in TGFbeta1/TGFbetaR1 on secreted TGFbeta1 levels in vitro could not be clarified. The inter-individual variation in TGFbeta1 levels for individuals with the same genotype was too large to obtain statistically significant differences among genotypes.
    PMID: 20144876 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3263166</comments>
            <pubDate>Sun, 07 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3263166</guid>        </item>
        <item>
            <title>Bioactive products generated by Group V sPLA(2) hydrolysis of LDL activate macrophages to secrete pro-inflammatory cytokines.</title>
            <link>http://www.medworm.com/index.php?rid=3255271&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20138782%26dopt%3DAbstract</link>
            <description>Conclusions: These results indicate that in addition to promoting atherosclerotic lipid accumulation in macrophages, GV sPLA(2) hydrolysis of LDL leads to activation of NFkappaB, a key regulator of inflammation.
    PMID: 20138782 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3255271</comments>
            <pubDate>Fri, 05 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3255271</guid>        </item>
        <item>
            <title>Homocysteine and pro-inflammatory cytokine concentrations in acute heart disease.</title>
            <link>http://www.medworm.com/index.php?rid=3244818&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20129796%26dopt%3DAbstract</link>
            <description>Authors: Gokkusu C, Tulubas F, Unlucerci Y, Ozkok E, Umman B, Aydin M
    Inflammation is involved in development and progression of atherosclerosis. Interleukin-2 (IL-2) and interleukin-6 (IL-6) have been correlated with various cardiovascular diseases. Hyperhomocysteinemia is an important risk factor for atherosclerosis and thrombotic disease. Recent studies have demonstrated that homocysteine (Hcy) enhances productions of several pro-inflammatory cytokines. In the light of these findings, we decided to determine if any relationship exists between IL-2 and IL-6, the pro-inflammatory cytokines, and total homocysteine (tHcy) in acute coronary syndrome (ACS). A total of 102 patients with ACS and 90 healthy subjects were included in the study. The levels of tHcy, IL-2 and IL-6 were higher an...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3244818</comments>
            <pubDate>Mon, 01 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3244818</guid>        </item>
        <item>
            <title>No effect of supplementation with cholecalciferol on cytokines and markers of inflammation in overweight and obese subjects.</title>
            <link>http://www.medworm.com/index.php?rid=3236758&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20122848%26dopt%3DAbstract</link>
            <description>In conclusion, we were not able to demonstrate with certainty any significant relation between serum levels of 25(OH)D levels and a number of cytokines and markers of inflammation.
    PMID: 20122848 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3236758</comments>
            <pubDate>Sat, 30 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3236758</guid>        </item>
        <item>
            <title>Predominant inflammatory cytokine secretion pattern in response to two doses of live rubella vaccine in healthy vaccinees.</title>
            <link>http://www.medworm.com/index.php?rid=3229168&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20117947%26dopt%3DAbstract</link>
            <description>Authors: Dhiman N, Haralambieva IH, Vierkant RA, Pankratz VS, Ryan JE, Jacobson RM, Ovsyannikova IG, Poland GA
    We conducted a population-based study on 738 schoolchildren who received two doses of rubella vaccine in order to determine cytokine secretion patterns and their associations with demographic and clinical variables. The results showed a robust rubella-specific inflammatory cytokine response characterized by high median [inter-quartile range (IQR)] secretion levels (in pg/mL) of IL-6 [3681.0 (3160.0, 4052.0)], GM-CSF [28.0 (23.6, 32.6)], and TNF-alpha [29.7 (-7.0, 89.2)]. We also detected modest levels of rubella-specific secretion of Th1 cytokines IL-2 and IFN-gamma, while IL-12p40 was undetectable. In contrast, rubella-specific Th2 responses were hardly detectable. Age at vac...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3229168</comments>
            <pubDate>Fri, 29 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3229168</guid>        </item>
        <item>
            <title>Detection of neutralizing interleukin-17 antibodies in autoimmune polyendocrinopathy syndrome-1 (APS-1) patients using a novel non-cell based electrochemiluminescence assay.</title>
            <link>http://www.medworm.com/index.php?rid=3229170&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20116277%26dopt%3DAbstract</link>
            <description>Authors: Cludts I, Meager A, Thorpe R, Wadhwa M
    Antibodies that neutralize interleukin-17A (IL-17A) are classically detected and quantified using cell-based assays. However, these assays are cumbersome, inherently variable and often susceptible to interference by the matrix of test samples, such as human sera. Since neutralizing antibodies block binding of IL-17A to its cell surface receptor, IL-17R, we used antibody inhibition of IL-17A binding to recombinant IL-17R/Fc fusion protein in an electrochemiluminescence (ECL) platform to develop a novel, non-cell based ligand binding assay that functionally mimics cell-based neutralization assays. Using specific polyclonal antisera and a panel of sera containing neutralizing anti-IL-17A autoantibodies from patients with autoimmune polyendoc...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3229170</comments>
            <pubDate>Wed, 27 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3229170</guid>        </item>
        <item>
            <title>Differences in cytokine levels due to gender in colorectal cancer patients.</title>
            <link>http://www.medworm.com/index.php?rid=3229169&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20116278%26dopt%3DAbstract</link>
            <description>Conclusion: IL-1beta and IL-6 levels were significantly higher in men than in women. This provides evidence of a possible link between gender and cytokine levels in patients with colorectal cancer.
    PMID: 20116278 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3229169</comments>
            <pubDate>Wed, 27 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3229169</guid>        </item>
        <item>
            <title>CKbeta8/CCL23 and its isoform CKbeta8-1 induce up-regulation of cyclins via the G(i)/G(o) protein/PLC/PKCdelta/ERK leading to cell-cycle progression.</title>
            <link>http://www.medworm.com/index.php?rid=3213074&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20097574%26dopt%3DAbstract</link>
            <description>Authors: Kim J, Kim YS, Ko J
    CKbeta8/CCL23 is a CC chemokine and alternative splicing of the CKbeta8 gene produces two mRNAs that encode CKbeta8 and its isoform CKbeta8-1. Chemokines play a critical role in leukocyte trafficking and development of inflammation and chemokines are also known to be involved in cell proliferation. To investigate participation of CKbeta8 and CKbeta8-1 in cell proliferation, we examined the effects of CKbeta8 and CKbeta8-1 in the cell cycle. Both CKbeta8 and CKbeta8-1 induced cell-cycle progression. We next investigated whether MAPKs are involved in CKbeta8- and CKbeta8-1-induced cell proliferation. CKbeta8- and CKbeta8-1-stimulated cells showed phosphorylation of ERK1/2 and an inhibitor study indicated that CKbeta8- and CKbeta8-1-induced activation of ERK1/...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3213074</comments>
            <pubDate>Fri, 22 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3213074</guid>        </item>
        <item>
            <title>Impact of timing strategy of LIGHT, a new TNF superfamily on immune platform induced by HSV-1 gB DNA vaccine.</title>
            <link>http://www.medworm.com/index.php?rid=3213075&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20097089%26dopt%3DAbstract</link>
            <description>In this study, timing effect of cytokine administration on the resultant immune pattern was evaluated in three different timing groups. The group received LIGHT 3days before DNA vaccine, demonstrated significant increase in cell mediated immunity. So, utilization of an adjuvant to DNA vaccine can significantly influences the induced immune response consequently and this phenomenon could be important to obtain the optimal response in DNA vaccine strategy. Given the growing use of plasmid-based immune adjuvants to improve the immunogenicity and efficacy of DNA vaccines, these findings support the need for further detailed study of this class of agent.
    PMID: 20097089 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3213075</comments>
            <pubDate>Thu, 21 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3213075</guid>        </item>
        <item>
            <title>Does interleukin-18 or tumour necrosis factor-alpha have an independent association with the risk of coronary heart disease? Results from a prospective study in New Zealand.</title>
            <link>http://www.medworm.com/index.php?rid=3213076&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20096599%26dopt%3DAbstract</link>
            <description>Conclusions: IL-18, but not TNFalpha, had a non-negligible association with CHD risk, although the association of IL-18 with risk was weak after full adjustment. These cytokines may play a role in CHD pathology, but may not be robust risk biomarkers.
    PMID: 20096599 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3213076</comments>
            <pubDate>Wed, 20 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3213076</guid>        </item>
        <item>
            <title>Molecular characterization and functional analysis of porcine macrophage migration inhibitory factor (MIF) gene.</title>
            <link>http://www.medworm.com/index.php?rid=3201135&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20093039%26dopt%3DAbstract</link>
            <description>We report here the molecular characterization of porcine MIF gene, which resides on chromosome 14q21.3 and encodes 114 amino acids. Porcine MIF mRNA was found to be highly expressed in stomach, to a lesser extent in spleen, and at the lowest levels in skeletal muscle and heart. To gain further insight into the functional regulation of MIF, we cloned the porcine MIF promoter and verified its functionality using luciferase reporter assay. In NIH 3T3 cells, the endogenous MIF mRNA level was up-regulated by rosiglitazone treatment in a dose-dependent manner, which was accompanied by a concurrent increase in peroxisome proliferator-activated receptor (PPAR)gamma2 transcription. Over-expression of porcine PPARgamma2 in NIH 3T3 cells could also up-regulate the transcription of MIF in the absence ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3201135</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3201135</guid>        </item>
        <item>
            <title>Poly(I:C) induces BLyS-expression of airway fibroblasts through phosphatidylinositol 3-kinase.</title>
            <link>http://www.medworm.com/index.php?rid=3201136&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20089415%26dopt%3DAbstract</link>
            <description>Authors: Yamada T, Lizhong S, Takahashi N, Kubo S, Narita N, Suzuki D, Takabayashi T, Kimura Y, Fujieda S
    B lymphocyte stimulator (BLyS), B cell activating factor (BAFF), a member of the tumor necrosis factor ligand superfamily has potent co-stimulatory activity on B cells, and BLyS-production in the airway mucosa is of potential importance as it triggers innate and adaptive immune responses. To investigate whether airway fibroblast could express BLyS, we examined BLyS-expression in human nasal airway fibroblasts and compared to its expression in tonsillar and skin fibroblasts as well as the effect of the Toll-like receptor (TLR) ligands on that in human nasal airway fibroblasts. The expression of BLyS by nasal fibroblasts in the presence of polyinocinic-polycytidykic acid (poly(I:C)) ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3201136</comments>
            <pubDate>Mon, 18 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3201136</guid>        </item>
        <item>
            <title>IL-7 receptor is expressed on adult pre-B-cell acute lymphoblastic leukemia and other B-cell derived neoplasms and correlates with expression of proliferation and survival markers.</title>
            <link>http://www.medworm.com/index.php?rid=3164451&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20060740%26dopt%3DAbstract</link>
            <description>Authors: Sasson SC, Smith S, Seddiki N, Zaunders JJ, Bryant A, Koelsch KK, Weatherall C, Munier ML, McGinley C, Yeung J, Mulligan SP, Moore J, Cooper DA, Milliken S, Kelleher AD
    The interleukin (IL)-7 receptor (IL-7R) is expressed on human pre-B but not mature B-cells. We hypothesised that aberrant expression of IL-7R contributes to B-cell oncogenesis. Surface expression of IL-7R components CD127 and CD132, and intracellular Ki-67 and Bcl-2 were examined by flow cytometry on peripheral blood or bone marrow mononuclear cells (PBMC; BMMC) from patients with B-cell derived neoplasms, chronic human immunodeficiency virus type-1 (HIV-1) infection alone, or healthy volunteers. Plasma IL-7, IL-2, IL-4, IL-6, IL-10, IL-21, TNF-alpha, IFN-gamma and BAFF were measured by enzyme-linked immuno-sor...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3164451</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3164451</guid>        </item>
        <item>
            <title>Combination cytokine therapy inhibits tumor growth by generation of tumor-specific T-cell responses in a murine melanoma model.</title>
            <link>http://www.medworm.com/index.php?rid=3164450&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20060741%26dopt%3DAbstract</link>
            <description>Authors: Kalaaji AN, Lu J, Markovic SN, Celis E, Pittelkow MR
    Various cytokines, including interferon alpha (IFNalpha), tumor necrosis factor alpha (TNFalpha), and granulocyte-macrophage colony-stimulating factor (GM-CSF), have been used as adjuvant therapy for advanced-stage melanoma with some success but with marked toxicity, which appears to be related to higher doses. We investigated the efficacy of IFNalpha, GM-CSF, and TNFalpha in various combinations to induce antitumor and immune responses in a B16F10 murine melanoma model. These studies showed that GM-CSF, IFNalpha, and TNFalpha, when injected together intratumorally, mediated significant inhibition of tumor growth. Tumor regression correlated with local tumor necrosis and significant infiltration of T cells. In addition, this...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3164450</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3164450</guid>        </item>
        <item>
            <title>Th17/Th1 phenotype in demyelinating disease.</title>
            <link>http://www.medworm.com/index.php?rid=3141878&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20045653%26dopt%3DAbstract</link>
            <description>Conclusion: We suggest a greater tendency to Th17 and Th1/Th17 response to non-specific stimulation in MS patients in relapse compared to controls and non-relapse patients.
    PMID: 20045653 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3141878</comments>
            <pubDate>Thu, 31 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3141878</guid>        </item>
        <item>
            <title>Polymorphisms of signal transducers and activators of transcription 1 and 4 (STAT1 and STAT4) contribute to progression of childhood IgA nephropathy.</title>
            <link>http://www.medworm.com/index.php?rid=3141877&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20045654%26dopt%3DAbstract</link>
            <description>Conclusions: Our results suggest that polymorphisms of STAT1 and STAT4 are associated with increased susceptibility, pathological advancement, and development of proteinuria in childhood IgAN.
    PMID: 20045654 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3141877</comments>
            <pubDate>Thu, 31 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3141877</guid>        </item>
        <item>
            <title>Generation of mouse macrophages expressing membrane-bound TNF variants with selectivity for TNFR1 or TNFR2.</title>
            <link>http://www.medworm.com/index.php?rid=3141882&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20045350%26dopt%3DAbstract</link>
            <description>Authors: Shibata H, Abe Y, Yoshioka Y, Nomura T, Sato M, Kayamuro H, Kawara T, Arita S, Furuya T, Nagano K, Yoshikawa T, Kamada H, Tsunoda SI, Tsutsumi Y
    Tumor necrosis factor-alpha (TNF) is expressed on the cell surface as a transmembrane form (tmTNF), that can be released as a soluble form (solTNF) via proteolytic cleavage. These two types of TNF exert their biological functions by binding to one of two TNF receptors, TNFR1 or TNFR2. However, the biological function of tmTNF through these two receptors remains to be determined. Here, we generated macrophages that expressed tmTNF mutants with selectivity for either TNFR1 or TNRF2 as a tool to evaluate signaling through these receptors. Wild-type TNF (wtTNF), TNFR1-selective mutant TNF (mutTNF-R1) or TNFR2-selective mutant TNF (mutTNF-...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3141882</comments>
            <pubDate>Wed, 30 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3141882</guid>        </item>
        <item>
            <title>Body fat distribution has no effect on serum visfatin levels in healthy female subjects.</title>
            <link>http://www.medworm.com/index.php?rid=3141881&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20045351%26dopt%3DAbstract</link>
            <description>In conclusion, we demonstrated that body fat distribution did not affect serum visfatin levels in healthy female subjects. Further studies are needed to clarify the exact factors influencing and determining serum visfatin levels and its clinical reflections.
    PMID: 20045351 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3141881</comments>
            <pubDate>Wed, 30 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3141881</guid>        </item>
        <item>
            <title>Adiponectin is required for enhancement of CCL2 expression in adipose tissue during Listeria monocytogenes infection.</title>
            <link>http://www.medworm.com/index.php?rid=3141880&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20045352%26dopt%3DAbstract</link>
            <description>Authors: Sashinami H, Nakane A
    Obesity is an important background of metabolic syndrome progression. Our previous study demonstrated that chemokine CCL2 expression was suppressed in liver of obese mice that were highly susceptible to Listeria monocytogenes infection. We investigated the role of adiponectin in CCL2 expression in obese mice after L. monocytogenes infection. When leptin-deficient obese ob/ob mice were infected intraperitoneally with L. monocytogenes, the elimination of bacteria from spleen, liver, mesenteric lymph nodes and adipose tissue was inhibited in ob/ob mice compared with their heterozygote littermates, ob/? mice. CCL2 expression in the adipose tissue of ob/? mice was enhanced by L. monocytogenes infection, different from ob/ob mice. Similarly, adiponectin express...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3141880</comments>
            <pubDate>Wed, 30 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3141880</guid>        </item>
        <item>
            <title>Cytokines in bronchoalveolar lavage fluid and serum of lung cancer patients during radiotherapy - Association of interleukin-8 and VEGF with survival.</title>
            <link>http://www.medworm.com/index.php?rid=3137690&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20044268%26dopt%3DAbstract</link>
            <description>This study aimed at clarifying the role of different cytokines (VEGF, TNFalpha, IL-1beta, IL-6, IL-8, IL-12 and IL-18) in bronchoalveolar lavage (BAL) fluid and in the serum of lung cancer patients at baseline and during RT. Bronchoscopy and BAL were performed on 36 lung cancer patients and 36 controls for diagnosis; patients receiving RT had a second bronchoscopy during RT. Serum samples were obtained during RT and three months after RT. In this study lung cancer patients had higher levels of serum and BAL fluid IL-6 and serum IL-8 compared to controls (p&amp;lt;0.001, p=0.039 and p=0.030, respectively). RT caused a significant increase of BAL fluid IL-6 (p=0.037). There were no significant associations between baseline cytokine levels and adverse events or response to treatment. Higher basel...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3137690</comments>
            <pubDate>Tue, 29 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3137690</guid>        </item>
        <item>
            <title>Varying susceptibility of pulmonary cytokine production to lipopolysaccharide in mice.</title>
            <link>http://www.medworm.com/index.php?rid=3135869&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20042347%26dopt%3DAbstract</link>
            <description>Conclusions: Our data provide information for scientists to consider the proper strain of mice for the measurement of specific inflammatory mediators and to select sensitive or resistant mouse strains for understanding genetic variation in the pathogenesis and for the screening of target-oriented drug development.
    PMID: 20042347 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3135869</comments>
            <pubDate>Mon, 28 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3135869</guid>        </item>
        <item>
            <title>Thr-114 is an important functional residue of fibroblast growth factor 10 identified by structure-based mutational analysis.</title>
            <link>http://www.medworm.com/index.php?rid=3130097&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20036575%26dopt%3DAbstract</link>
            <description>Authors: Wang JF, Cai X, Zou MJ, Wang YY, Wang JX, Xu DG
    Fibroblast growth factor 10 (FGF10) plays important roles in vertebrate limb development, lung branching morphogenesis, and epidermis regeneration. The receptor (FGFR2b) binding specificity is an essential element in regulating the diverse functions of FGF10. Analyzing the FGF10:FGFR2b complex we found that Thr-114 in beta4 of FGF10 could form specific interactions with D3 of FGFR2b. To investigate the role of Thr-114 played on functions of FGF10, two mutants of FGF10 were constructed, named TA (Thr-114--&amp;gt;Ala) and TR (Thr-114--&amp;gt;Arg), respectively. The biological activity assays showed that the receptor-binding affinity, the stimulating growth effect on rat tracheal epithelium (RTE) cells, and the inducing ability in recepto...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130097</comments>
            <pubDate>Thu, 24 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3130097</guid>        </item>
        <item>
            <title>Cytokine profiles of seventeen cytokines, growth factors and chemokines in cord blood and its relation to perinatal clinical findings.</title>
            <link>http://www.medworm.com/index.php?rid=3130096&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20036576%26dopt%3DAbstract</link>
            <description>Authors: Takahashi N, Uehara R, Kobayashi M, Yada Y, Koike Y, Kawamata R, Odaka J, Honma Y, Momoi MY
    Few papers have investigated the cytokine profiles of multiple cytokines in cord blood. We obtained cord blood samples from 224 infants admitted to our neonatal intensive care unit. Cytokine profiles of 17 cytokines were investigated using cytometric bead array technology. We found a wide variety of cytokines of various levels which ranged from 0.59pg/ml (in Interleukin (IL)-4) to 222.0pg/ml (in macrophage inflammatory protein-1beta. Pro-inflammatory cytokines were highly correlated with each other and with granulocyte-colony stimulating factor and IL-8. On the contrary, IL-5, IL-13, and IL-17 did not show any significant correlation with other cytokines. Several maternal factors were s...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130096</comments>
            <pubDate>Thu, 24 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3130096</guid>        </item>
        <item>
            <title>Gene modulation and immunoregulatory roles of Interferongamma.</title>
            <link>http://www.medworm.com/index.php?rid=3130095&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20036577%26dopt%3DAbstract</link>
            <description>Authors: Saha B, Jyothi Prasanna S, Chandrasekar B, Nandi D
    Interferon-gamma (IFNgamma) is a central regulator of the immune response and signals via the Janus Activated Kinase (JAK)-Signal Transducer and Activator of Transcription (STAT) pathway. Phosphorylated STAT1 homodimers translocate to the nucleus, bind to Gamma Activating Sequence (GAS) and recruit additional factors to modulate gene expression. A bioinformatics analysis revealed that greater number of putative promoters of immune related genes and also those not directly involved in immunity contain GAS compared to response elements (RE) for Interferon Regulatory Factor (IRF)1, Nuclear factor kappa B (NFkappaB) and Activator Protein (AP)1. GAS is present in putative promoters of well known IFNgamma-induced genes, IRF1, GBP1, ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130095</comments>
            <pubDate>Thu, 24 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3130095</guid>        </item>
        <item>
            <title>An extract based on the medicinal mushroom Agaricus blazei Murill stimulates monocyte-derived dendritic cells to cytokine and chemokine production in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3130099&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20036142%26dopt%3DAbstract</link>
            <description>Authors: F&amp;#xF8;rland DT, Johnson E, Tryggestad AM, Lyberg T, Hetland G
    The edible mushroom Agaricus blazei Murill (AbM), which has been used in traditional medicine against a range of diseases and possess immunomodulating properties, probably due to its high content of beta-glucans. Others and we have demonstrated stimulatory effects of extracts of this mushroom on different immune cells. Dendritic cells are major directors of immune function. We wanted to examine the effect of AbM stimulation on signal substance release from monocyte-derived dendritic cells (MDDC). After 6d incubation with IL-4 and GM-CSF, the cells were true MDDC. Then the cells were further incubated with up to 10% of the AbM-based extract, AndoSan, LPS (0.5mug/ml) or PBS control. We found that the AbM extract prom...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130099</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3130099</guid>        </item>
        <item>
            <title>Signaling pathway underlying the up-regulatory effect of TNF-alpha on the Na(+)/K(+) ATPase in HepG2 cells.</title>
            <link>http://www.medworm.com/index.php?rid=3130098&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20036143%26dopt%3DAbstract</link>
            <description>Authors: Kassardjian A, Dakroub Z, Zein OE, Kreydiyyeh SI
    The activity of the Na(+)/K(+) ATPase was shown to be reduced during apoptosis and enhanced during cell proliferation. This work investigated whether TNF-alpha exerts also opposite effects on the Na(+)/K(+) ATPase in HepG2 cells and whether these effects are time-dependent. A time response study demonstrated that the activity and protein expression of the ATPase are decreased at 1h and increased at 4, 6 and 8h. This work focused on the up-regulatory 4h-response. TNF-alpha was shown to exert a stimulatory effect on cJNK and NF-kappaB and an inhibitory effect on caspases which, in the basal state, down-regulate the ATPase. The cytokine was found to target the caspases by activating JNK which in turn activates NF-kappaB. The activa...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130098</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3130098</guid>        </item>
        <item>
            <title>IL-10 promotes resistance to apoptosis and metastatic potential in lung tumor cell lines.</title>
            <link>http://www.medworm.com/index.php?rid=3122616&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20034810%26dopt%3DAbstract</link>
            <description>Authors: Zeng L, O'Connor C, Zhang J, Kaplan AM, Cohen DA
    Treatment of non-small cell lung carcinoma (NSCLC) remains at a disappointingly low success rate. Not only is metastatic spread common in NSCLC, but therapeutic success decreases dramatically once metastases are present. Understanding factors which contribute to poor prognosis in NSCLC is critical for development of more successful therapeutic approaches. Interleukin-10 (IL-10) expression has been shown in several studies to correlate with a poorer prognosis in NSCLC; however, the mechanisms by which IL-10 affects lung tumor growth and metastases are unclear. The goal of this study was to evaluate the effects of tumor-derived IL-10 on the growth and metastasis of lung cancer cells in a murine model. Lewis lung carcinoma cells we...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3122616</comments>
            <pubDate>Tue, 22 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3122616</guid>        </item>
        <item>
            <title>High glucose and interleukin-1beta downregulate interleukin-1 type I receptor (IL-1RI) in retinal endothelial cells by enhancing its degradation by a lysosome-dependent mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=3122615&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20034811%26dopt%3DAbstract</link>
            <description>In conclusion, our results indicate that high glucose, probably due to osmotic stress, and IL-1beta downregulate IL-1RI in retinal endothelial cells. The downregulation of IL-1RI is triggered by its activation and is due, at least partially, to lysosomal degradation. High glucose and IL-1beta also enhance the translocation of IL-1RI to the nucleus.
    PMID: 20034811 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3122615</comments>
            <pubDate>Tue, 22 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3122615</guid>        </item>
        <item>
            <title>Vipera aspis venom reduces lethality and down-regulates tumor necrosis factor-alpha in a rat model of LPS-induced sepsis.</title>
            <link>http://www.medworm.com/index.php?rid=3122614&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20034812%26dopt%3DAbstract</link>
            <description>Conclusions: Our data suggest that sub-toxic doses of VAV have a protective effect against LPS-induced septic shock that may be mediated, at least partially, by the modulated TNF-alpha activity. This study thus offers a novel therapeutic approach for the attenuation of bacteremia-induced septic shock through the modulation of a central pro-inflammatory cytokine by VAV vaccination in mammals.
    PMID: 20034812 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3122614</comments>
            <pubDate>Tue, 22 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3122614</guid>        </item>
        <item>
            <title>Increased plasma levels of osteopontin are associated with activation of the renin-aldosterone system and with myocardial and coronary microvascular damage in dilated cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=3119511&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20031444%26dopt%3DAbstract</link>
            <description>Authors: Del Ry S, Giannessi D, Maltinti M, Cabiati M, Prontera C, Iervasi A, Caselli C, Mazzone AM, Neglia D
    In patients with dilated cardiomyopathy (DCM) abnormal myocardial blood flow (MBF) has been associated with coronary microvascular dysfunction. The aim of this study was to test the hypothesis that osteopontin (OPN) plasma levels could be associated with the activation of the renin-aldosterone system (RAS) in these patients and be involved in mediating myocardial and coronary damage. In 66 patients with idiopathic left ventricular dysfunction of variable severity the plasma levels of OPN were correlated with biomarkers of systemic metabolism, RAS activation, myocardial dysfunction and with clinical indexes of left ventricle (LV) function and perfusion obtained by 2D-echocardiog...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3119511</comments>
            <pubDate>Mon, 21 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3119511</guid>        </item>
        <item>
            <title>Local serum levels of vascular endothelial growth factor in infantile hemangioma: Intriguing mechanism of endothelial growth.</title>
            <link>http://www.medworm.com/index.php?rid=3105571&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015661%26dopt%3DAbstract</link>
            <description>Conclusions: (1) VEGF serum levels vary in the different phases of hemangioma growth and may help to distinguish hemangiomas from vascular malformations; (2) obtained local results may support the intrinsic theory of endothelial cell proliferation in hemangiomas.
    PMID: 20015661 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105571</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105571</guid>        </item>
        <item>
            <title>Transcriptional regulation of cytokines and oxidative stress by gallic acid in human THP-1 monocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3105570&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015662%26dopt%3DAbstract</link>
            <description>In this study we investigated hyperglycemia-mediated proinflammatory/prooxidant effects in THP-1 monocytes and tested whether gallic acid could attenuate changes in gene expression induced by high-glucose. Cells were treated either with 5.5mM glucose or 25mM glucose in the absence and presence of gallic acid. While oxidative DNA damage was assessed by COMET assay, GSH and GSSG levels were estimated fluorimetrically. Gene expression patterns were determined by RT-PCR. Cells treated with high-glucose showed increased DNA damage and glutathione depletion and this was attenuated in the presence of gallic acid. High-glucose treated cells exhibited increased mRNA expression of TNF-alpha, IL-6, NADPH oxidase and TXNIP and gallic acid attenuated these proinflammatory and prooxidant effects. Cells ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105570</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105570</guid>        </item>
        <item>
            <title>Roles of endothelin-1 and selected proinflammatory cytokines in the pathogenesis of proliferative diabetic retinopathy: Analysis of vitreous samples.</title>
            <link>http://www.medworm.com/index.php?rid=3105569&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20015663%26dopt%3DAbstract</link>
            <description>CONCLUSION: These data provide evidence of the activation of the local synthesis of ET-1, TNF-alpha, IL-6 in PDR. The relationship between the increase in vitreous ET-1, TNF-alpha concentrations and HbA(1)c concentration is a important confirmation of the necessity to optimise diabetes treatment.
    PMID: 20015663 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105569</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105569</guid>        </item>
        <item>
            <title>Interleukin-21 restrains tumor growth and induces a substantial increase in the number of circulating tumor-specific T cells in a murine model of malignant melanoma.</title>
            <link>http://www.medworm.com/index.php?rid=3067495&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19962321%26dopt%3DAbstract</link>
            <description>Authors: Petersen CC, Diernaes JE, Skovbo A, Hvid M, Deleuran B, Hokland M
    New strategies of immunotherapy are currently being evaluated, and the combination of chemo- and immunotherapy has shown promising results. The cytokine interleukin-21 (IL-21) is known to enhance immune function, and in this study we have investigated its ability to boost the efficacy of chemoimmunotherapy-cyclophosphamide and adoptive cell transfer (ACT)-in the B16-OVA/OT-I murine model of malignant melanoma. Subcutaneous B16-OVA tumors were established in C57BL/6J mice 8days before adoptive transfer of tumor-specific OT-I T cells. In addition to cyclophosphamide and ACT, one group of mice received daily injections of murine IL-21 (mIL-21). Mice treated with mIL-21 had more tumor-specific T cells in the circula...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3067495</comments>
            <pubDate>Wed, 02 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3067495</guid>        </item>
        <item>
            <title>Effects of the new adiponectin paralogous protein CTRP-3 and of LPS on cytokine release from monocytes of patients with type 2 diabetes mellitus.</title>
            <link>http://www.medworm.com/index.php?rid=3057325&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19955001%26dopt%3DAbstract</link>
            <description>Conclusions: CTRP-3 inhibits LPS-induced IL-6 and TNF release. This anti-inflammatory effect is lost in T2D. Serum cholesterol concentration affects the pro-inflammatory potential of LPS to induce TNF release from T2D monocytes in the presence or absence of CTRP-3. CTRP-3 might partly account for the pro-inflammatory state in T2D.
    PMID: 19955001 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057325</comments>
            <pubDate>Mon, 30 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3057325</guid>        </item>
        <item>
            <title>Exercise training changes IL-10/TNF-alpha ratio in the skeletal muscle of post-MI rats.</title>
            <link>http://www.medworm.com/index.php?rid=3049169&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19948415%26dopt%3DAbstract</link>
            <description>Authors: Batista ML, Rosa JC, Lopes RD, Lira FS, Martins E, Yamashita AS, Brum PC, Lancha AH, Lopes AC, Seelaender M
    Heart failure (HF) is associated with changes in the skeletal muscle (SM) which might be a consequence of the unbalanced local expression of pro- (TNF-alpha) and anti- (IL-10) inflammatory cytokines, leading to inflammation-induced myopathy, and SM wasting. This local effect of HF on SM may, on the other hand, contribute to systemic inflammation, as this tissue actively secretes cytokines. Since increasing evidence points out to an anti-inflammatory effect of exercise training, the goal of the present study was to investigate its effect in rats with HF after post-myocardial infarction (MI), with special regard to the expression of TNF-alpha and IL-10 in the soleus and ex...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3049169</comments>
            <pubDate>Sat, 28 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3049169</guid>        </item>
        <item>
            <title>Expression of MDC/CCL22 and its receptor CCR4 in rheumatoid arthritis, psoriatic arthritis and osteoarthritis.</title>
            <link>http://www.medworm.com/index.php?rid=3036524&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19942450%26dopt%3DAbstract</link>
            <description>Authors: Flytlie HA, Hvid M, Lindgreen E, Kofod-Olsen E, Petersen EL, J&amp;#xF8;rgensen A, Deleuran M, Vestergaard C, Deleuran B
    The pathogenesis of rheumatoid arthritis (RA) and psoriatic arthritis (PsA) involves an abnormal chemokine regulation. The chemokine receptor CCR4 is necessary for T cell migration to the skin. We, therefore, studied if CCR4 and its ligand macrophage-derived chemokine (MDC/CCL22) could participate in spreading the disease between skin and joints by examining RA, PsA and osteoarthritis (OA) patients. In synovial fluid from RA and PsA patients we observed a significantly higher MDC/CCL22 level compared to OA patients. Additionally, the MDC/CCL22 protein was found to be elevated in RA and PsA plasma compared to OA and healthy volunteers. Flow cytometry revealed tha...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3036524</comments>
            <pubDate>Tue, 24 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3036524</guid>        </item>
        <item>
            <title>Effect of simvastatin on endothelial cell apoptosis mediated by Fas and TNF-alpha.</title>
            <link>http://www.medworm.com/index.php?rid=3033848&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19932975%26dopt%3DAbstract</link>
            <description>Authors: Acquavella N, Quiroga MF, Wittig O, Cardier JE
    Although there is evidence suggesting that statins may exert an endothelial protecting effect, recent in vitro data have shown that these compounds may induce endothelial cells (EC) apoptosis. We previously reported that the Fas-death receptor may induce apoptosis of the liver sinusoid endothelial cells (LSEC), and that TNF-alpha increases the susceptibility of these cells to suffer Fas-mediated apoptosis. Based on this evidence, in this study, we investigated the effect of simvastatin on Fas-mediated LSEC apoptosis. Simvastatin induced a significant reduction in LSEC viability, in a dose dependent manner, under serum-containing or serum-free conditions. This effect was prevented by mevalonate and GGPP, indicating the role of hydr...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3033848</comments>
            <pubDate>Mon, 23 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3033848</guid>        </item>
        <item>
            <title>Blockade of multiple but not single cytokines abrogates downregulation of angiotensin II type-I receptors and anticipates septic shock.</title>
            <link>http://www.medworm.com/index.php?rid=3000769&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19914088%26dopt%3DAbstract</link>
            <description>Authors: Schmidt C, H&amp;#xF6;cherl K, Kurt B, Moritz S, Kurtz A, Bucher M
    In this prospective, randomized animal study, the role of proinflammatory cytokines in the pathogenesis sepsis-induced circulatory failure with downregulation of angiotensin-II-type-I-(AT(1))-receptors was investigated. Sepsis in wild-type mice and in mice with deficiencies for TNF-alpha, IL-1beta, IFN-gamma or IL-6 was induced by cecal ligation and puncture (CLP) and wild-type mice were injected with cytokines. Animals were treated with glucocorticoids or small interfering RNA (siRNA) targeting single or multiple cytokines or NF-kappaB. Vascular smooth muscle cells (VSMCs) were incubated with cytokines. CLP resulted in circulatory failure and a significant downregulation of AT(1)-receptors. Injection of single pro...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3000769</comments>
            <pubDate>Thu, 12 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3000769</guid>        </item>
        <item>
            <title>Suppression of tumor necrosis factor receptor associated factor (TRAF)-2 attenuates the proinflammatory and proliferative effect of aggregated IgG on rat renal mesangial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3000770&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19910209%26dopt%3DAbstract</link>
            <description>Authors: Zhu LJ, Yang X, Li XY, Liu QH, Tang XQ, Zhou SF, Kong QY, Axelsson J, Yu XQ
    Immune-complex (IC) mediated glomerulonephritis (GN) is a common cause of chronic kidney disease associated with increased levels of tumor necrosis factor (TNF)-alpha in renal cells. TNF-alpha signaling pathways involve complicated interactions between multiple proteins including TNF-receptor-associated factor (TRAF)-2. We have previously found markedly up-regulated expression of TRAF-2 in renal tissues from IC mediated lupus nephritis patients. Here we investigated the effect of TRAF-2 on inflammatory response in rat mesangial cells (MCs). The results showed that treatment with soluble aggregated IgG (AIgG) resulted in a time- and dose-dependent increase in the expression of interleukin (IL)-1beta and...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3000770</comments>
            <pubDate>Tue, 10 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3000770</guid>        </item>
        <item>
            <title>Plasma interleukin-1beta concentration is associated with stroke in sickle cell disease.</title>
            <link>http://www.medworm.com/index.php?rid=2992892&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19900820%26dopt%3DAbstract</link>
            <description>Authors: Asare K, Gee BE, Stiles JK, Wilson NO, Driss A, Quarshie A, Adams RJ, Kutlar A, Hibbert JM
    The pathogenesis of sickle cell disease (HbSS), which has numerous complications including stroke, involves inflammation resulting in alteration of plasma inflammatory protein concentration. We investigated HbSS children with abnormal cerebral blood flow detected by trans-cranial Doppler ultrasound (TCD) who participated in the multi-center stroke prevention (STOP) study, to determine if plasma inflammatory protein concentration is associated with the outcome of stroke. Thirty-nine plasma samples from HbSS participants with elevated TCD who had no stroke, HbSS-NS (n=13) or had stroke, HbSS-S (n=13), HbSS steady-state controls (n=7) and controls with normal hemoglobin, HbAA (n=6), were an...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2992892</comments>
            <pubDate>Sat, 07 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2992892</guid>        </item>
        <item>
            <title>Effects of carbon monoxide releasing molecule-liberated CO on severe acute pancreatitis in rats.</title>
            <link>http://www.medworm.com/index.php?rid=2992891&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19900821%26dopt%3DAbstract</link>
            <description>In this study, we investigated the role of CO liberated from carbon monoxide releasing molecule-2 (CORM-2) in rats with SAP. SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatobiliary duct. Forty Wistar rats were randomly divided into four groups. Sham group was given normal saline after the sham operation. SAP group was treated with normal saline after the induction of SAP. CORM-2 group was injected with CORM-2 (8mg/kg, i.v.) after the onset of SAP. iCORM-2 group was given iCORM-2 (an inactive compound used as negative control) after SAP induction. All animals were sacrificed at 12h after the operation. Eighty rats (n=20 for each group) were monitored for 7days to observe their survival rates. In another set of experiments, the former three groups received ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2992891</comments>
            <pubDate>Sat, 07 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2992891</guid>        </item>
        <item>
            <title>Tumor necrosis factor alpha induced by Trypanosoma cruzi infection mediates inflammation and cell death in the liver of infected mice.</title>
            <link>http://www.medworm.com/index.php?rid=2972246&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19892564%26dopt%3DAbstract</link>
            <description>Authors: Ronco MT, Franc&amp;#xE9;s DE, Ingaramo PI, Quiroga AD, Alvarez ML, Pisani GB, Revelli SS, Carnovale CE
    Trypanosoma cruzi (T. cruzi) infected C57BL/6 mice developed a progressive fatal disease due to an imbalance in the profile of circulating related compounds accompanying infection like tumor necrosis factor alpha (TNFalpha). TNFalpha has been proposed as an important effector molecule in apoptosis. In this work, we evaluate inflammation and the proteins involved in apoptotic process in liver of infected mice and the role of TNFalpha. C57BL6/mice were infected subcutaneously with 100 viable trypomastigotes of Tulahu&amp;#xE9;n strain of T cruzi. One set of these animals were treated with 375mug of antihuman TNFalpha blocking antibody. Animals were sacrificed at 14days post-infection ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2972246</comments>
            <pubDate>Tue, 03 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2972246</guid>        </item>
        <item>
            <title>Impaired IL-7 signaling may explain a case of atypical JAK3-SCID.</title>
            <link>http://www.medworm.com/index.php?rid=2968175&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19889552%26dopt%3DAbstract</link>
            <description>We report here that the JAK3-E481G mutant transduced IL-2-, IL-4-, IL-15-, and IL-21-induced signals as efficiently as wild-type JAK3. However, this mutant failed to respond to IL-7 by phosphorylating JAK1, JAK3, or STAT5. The other mutant JAK3, JAK3-del482-596, was non-functional. Thus, an impaired IL-7 signal may cause SCID and compromise T-cell differentiation, even if the IL-15 signal is preserved and supports NK-cell development, as in this patient.
    PMID: 19889552 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2968175</comments>
            <pubDate>Mon, 02 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2968175</guid>        </item>
        <item>
            <title>Suppressing IL-32 in monocytes impairs the induction of the proinflammatory cytokines TNFalpha and IL-1beta.</title>
            <link>http://www.medworm.com/index.php?rid=2953625&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19880327%26dopt%3DAbstract</link>
            <description>Authors: Hong J, Bae S, Kang Y, Yoon D, Bai X, Chan ED, Azam T, Dinarello CA, Lee S, Her E, Rho G, Kim S
    Targeting major proinflammatory cytokines such as IL-1beta and TNFalpha is of great interest in patients with chronic inflammatory diseases, including rheumatoid arthritis, colitis, and psoriasis. The cytokine Interleukin (IL)-32 induces proinflammatory cytokines such as TNFalpha, IL-1beta, IL-6, and chemokines. We previously used an IL-32 ligand-affinity column to purify proteinase 3, which is abundantly expressed in neutrophil and monocytic leukocytes but not in other cell types, and found that IL-32 is mainly produced by monocytic leukocytes. This evidence suggested that silencing endogenous IL-32 by short hairpin RNA (shRNA) in monocytic cells might reveal the precise function o...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2953625</comments>
            <pubDate>Fri, 30 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2953625</guid>        </item>
        <item>
            <title>Regulation of memory T cells by gammac cytokines.</title>
            <link>http://www.medworm.com/index.php?rid=2953628&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19879771%26dopt%3DAbstract</link>
            <description>Authors: Osborne LC, Abraham N
    T cells rely on a duality of TCR and gammac cytokine signals for development, activation and peripheral T cell homeostasis. Previous data had suggested that the requirements for CD4 and CD8 memory T cell regulation were qualitatively distinct, but emerging data has shown that the requirements for true antigen specific memory T cells are very similar between these two cell types. This review will focus on contributions made by members of the gammac cytokine family (IL-2, IL-4, IL-7, IL-15 and IL-21) to homeostasis of na&amp;#xEF;ve, memory phenotype and antigen experienced memory T cells.
    PMID: 19879771 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2953628</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2953628</guid>        </item>
        <item>
            <title>TNFalpha and TGF-beta1 influence IL-18-induced IFNgamma production through regulation of IL-18 receptor and T-bet expression.</title>
            <link>http://www.medworm.com/index.php?rid=2953627&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19879772%26dopt%3DAbstract</link>
            <description>In this study, we demonstrate that in the dendritic precursor-like cell line KG-1, IFNgamma production induced by IL-18 is potentiated (&amp;gt;5-fold) by TNFalpha and completely suppressed by TGF-beta1. IL-18 stimulation rapidly activates different MAPK signalling pathways but only blocking of p38 activation alleviates IFNgamma production. The mechanism through which TNFalpha enhances IL-18 induced IFNgamma production is by promoting IL-18 receptor alpha-chain expression which results in higher levels of p38 activation and induces expression of T-bet, a transcriptional regulator of the IFNG gene. In contrast, TGF-beta1 rapidly suppresses IFNgamma production by limiting IL-18 receptor numbers at the cell surface and preventing induction of T-bet expression. TGF-beta1 experience by cells leads ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2953627</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2953627</guid>        </item>
        <item>
            <title>Serum evaluation of soluble interferon-alpha/beta receptor and high-sensitivity C-reactive protein for diagnosis of the patients with gastrointestinal and hepatobiliary-pancreatic cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2953626&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19879773%26dopt%3DAbstract</link>
            <description>Authors: Miyake K, Imura S, Nishioka M, Batmunkh E, Sugimoto K, Ohmoto Y, Shimada M
    Serum soluble interferon-alpha/beta receptor (sIFN-alpha/betaR) and high-sensitivity C-reactive protein (hs-CRP) levels were evaluated in the patients with gastrointestinal and hepatobiliary-pancreatic cancer. We compared the sensitivity and specificity of serum sIFN-alpha/betaR with that of serum hs-CRP and evaluated the two diagnostic parameters in combination. Serum sIFN-alpha/betaR levels were measured in 92 patients and 25 healthy individuals by enzyme-linked immunosorbent assay. The diagnoses were 37 cases of hepatocellular carcinoma, 17 cases of pancreatic cancer, 15 cases of colon cancer, 13 cases of biliary tract cancer, and 10 cases of gastric cancer. Serum levels of sIFN-alpha/betaR and hs-CR...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2953626</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2953626</guid>        </item>
        <item>
            <title>Wide-spectrum profile of inflammatory mediators in the plasma and scales of patients with psoriatic disease.</title>
            <link>http://www.medworm.com/index.php?rid=2953629&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19879157%26dopt%3DAbstract</link>
            <description>Authors: Deeva I, Mariani S, De Luca C, Pacifico V, Leoni L, Raskovic D, Kharaeva Z, Korkina L, Pastore S
    Psoriasis is a chronic recurrent inflammatory disorder of the skin. Clinical subtypes include psoriasis vulgaris (PV), psoriatic arthropathy, and erythrodermic psoriasis. Aim of this study was to analyse relevant inflammatory mediators in the plasma of patients with distinct subtypes of active psoriasis, and in the scales of mild-to-moderate PV patients, and correlation to disease severity. Compared to healthy controls (n=10), patients affected by very severe forms of psoriasis (n=30) were characterized by increased plasma levels of IL-4, IL-6, MCP-1, VEGF and in particular PDGFbb. Each group with severe psoriasis had distinct characteristic features of plasma cytokine profile. Mil...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2953629</comments>
            <pubDate>Wed, 28 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2953629</guid>        </item>
        <item>
            <title>The Th17/Treg functional imbalance during atherogenesis in ApoE(-/-) mice Th17/Treg imbalance in atherogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2912611&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19836260%26dopt%3DAbstract</link>
            <description>Conclusions: Th17/Treg functional imbalance exists during atherogenesis in ApoE(-/-) mice, suggesting a potential role of Th17/Treg imbalance in the formation and progression of atherosclerosis.
    PMID: 19836260 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2912611</comments>
            <pubDate>Tue, 13 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2912611</guid>        </item>
        <item>
            <title>Interleukin-1 receptor antagonist gene (IL1RN) polymorphism possibly associated to severity of rheumatic carditis in a Brazilian cohort.</title>
            <link>http://www.medworm.com/index.php?rid=2895387&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19822442%26dopt%3DAbstract</link>
            <description>Conclusion: In the Brazilian population, the polymorphism of the IL-1ra gene is a relevant factor for rheumatic heart disease severity.
    PMID: 19822442 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2895387</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2895387</guid>        </item>
        <item>
            <title>Oxidative mechanisms of IL-4-induced IL-6 expression in vascular endothelium.</title>
            <link>http://www.medworm.com/index.php?rid=2895386&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19822443%26dopt%3DAbstract</link>
            <description>Authors: Lee YW, Lee WH, Kim PH
    The present study is designed to investigate the effects of interleukin-4 (IL-4) on expression of interleukin-6 (IL-6), as well as to examine the role of distinct sources of reactive oxygen species (ROS) in this process. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) showed that IL-4 significantly up-regulated the mRNA and protein expression of IL-6 in human aortic endothelial cells (HAEC) and C57BL/6 mice. Dihydroethidium (DHE) and dichlorofluorescein (DCF) fluorescence staining demonstrated that IL-4 significantly increased ROS generation in HAEC. A significant and dose-dependent inhibition of IL-4-induced IL-6 expression was observed in HAEC pre-treated with antioxidants, such as pyrrol...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2895386</comments>
            <pubDate>Fri, 09 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2895386</guid>        </item>
        <item>
            <title>Cytokine expression in placenta-derived mesenchymal stem cells in patients with pre-eclampsia and normal pregnancies.</title>
            <link>http://www.medworm.com/index.php?rid=2887470&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19819721%26dopt%3DAbstract</link>
            <description>Conclusions: The decreased levels of sICAM and SDF-1 found in the decidua-derived MSCs from pre-eclamptic pregnancies might be associated with some of the immunological alterations in pre-eclampsia.
    PMID: 19819721 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887470</comments>
            <pubDate>Thu, 08 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887470</guid>        </item>
        <item>
            <title>Apolipoprotein A-I inhibits chemotaxis, adhesion, activation of THP-1 cells and improves the plasma HDL inflammatory index.</title>
            <link>http://www.medworm.com/index.php?rid=2887469&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19819722%26dopt%3DAbstract</link>
            <description>Authors: Wang L, Chen WZ, Wu MP
    The anti-inflammatory effects of high density lipoprotein (HDL) are well described, however, such effects of Apolipoprotein A-I (ApoA-I) are less studied. Building on our previous study, we further explored the mechanism of anti-inflammatory effects of ApoA-I, and focused especially on the interaction between monocyte and endothelial cells and plasma HDL inflammatory index in LPS-challenged rabbits. Our results show that ApoA-I significantly decreased LPS-induced MCP-1 release from THP-1 cells and ox-LDL-induced THP-1 migration ratio (P&amp;lt;0.01, respectively). ApoA-I significantly decreased sL-selectin, sICAM-1 and sVCAM-1 release (P&amp;lt;0.01, P&amp;lt;0.01, P&amp;lt;0.05, respectively) from LPS-stimulated THP-1 cells. Furthermore, ApoA-I significantly inhibited ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887469</comments>
            <pubDate>Thu, 08 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887469</guid>        </item>
        <item>
            <title>Activation of foal neutrophils at different ages by CpG oligodeoxynucleotides and Rhodococcus equi.</title>
            <link>http://www.medworm.com/index.php?rid=2887472&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19819162%26dopt%3DAbstract</link>
            <description>This study examined TLR9-mediated neutrophil activation in neonatal foals. Unmethylated CpGs, ligands for TLR9, were used to stimulate equine neutrophils, either purified or in contact with other peripheral blood leukocytes. Rhodococcus equi was used as another stimulus in parallel. TLR9 mRNA was constitutively expressed at a similar level in purified equine neutrophils across different ages from birth to adulthood, and expression was not affected by either CpG or R. equi. Purified foal neutrophils were directly sensitive to CpG stimulation, reflected by enhanced reactive oxygen species generation following fMLP stimulation, and by expressing significantly (P&amp;lt;0.05) greater mRNA of IFN-gamma, IL-8, IL-12p35, and significantly (P&amp;lt;0.05) decreased TNF-alpha mRNA. In comparison, purified ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887472</comments>
            <pubDate>Wed, 07 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887472</guid>        </item>
        <item>
            <title>Modulation of human beta-defensin-2 expression by 17beta-estradiol and progesterone in vaginal epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=2887471&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19819163%26dopt%3DAbstract</link>
            <description>Authors: Han JH, Kim MS, Lee MY, Kim TH, Lee MK, Kim HR, Myung SC
    We investigated the expression of HBD-1 and -2 in vaginal epithelial cells treated with lipopolysaccharide (LPS) and the effects on HBD-2 expressions by 17beta-estradiol and progesterone. Primary vaginal epithelial cells were isolated from a segment of normal anterior vaginal wall obtained during vaginoplasty and were cultured in keratinocyte growth medium and were allowed to undergo their 3rd passage. Expression of HBD-1 and -2 by different stimuli using LPS 0.5mug/ml, 17beta-estradiol 2nM and progesterone 1muM was measured by RT-PCR, ELISA and real-time RT-PCR, respectively. HBD-1 was produced constitutively in vaginal epithelial cells and the production of HBD-1 was not influenced by LPS, 17beta-estradiol and progeste...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2887471</comments>
            <pubDate>Wed, 07 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2887471</guid>        </item>
        <item>
            <title>Involvement of NF-kappa B pathway in TL1A gene expression induced by lipopolysaccharide.</title>
            <link>http://www.medworm.com/index.php?rid=2877310&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19815424%26dopt%3DAbstract</link>
            <description>Conclusion: (1) LPS induces TL1A expression through the transcriptional activation via a NF-kappa B pathway. (2) The NF-kappa B binding site in the 5' flanking region of TL1A was identified.
    PMID: 19815424 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2877310</comments>
            <pubDate>Mon, 05 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2877310</guid>        </item>
        <item>
            <title>Influences of genetic variants in interleukin-15 gene and serum interleukin-15 levels on coronary heart disease.</title>
            <link>http://www.medworm.com/index.php?rid=2859208&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19796965%26dopt%3DAbstract</link>
            <description>In conclusion, our study supports the hypothesis that genetic variation in IL-15 gene and IL-15 levels influence the risk of CHD. Further studies are needed to confirm our hypothesis.
    PMID: 19796965 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2859208</comments>
            <pubDate>Mon, 28 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2859208</guid>        </item>
        <item>
            <title>Mid-trimester maternal plasma cytokines and CRP as predictors of spontaneous preterm birth.</title>
            <link>http://www.medworm.com/index.php?rid=2847298&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783155%26dopt%3DAbstract</link>
            <description>Authors: Kramer MS, Kahn SR, Platt RW, Genest J, Chen MF, Goulet L, S&amp;#xE9;guin L, Lydon J, McNamara H, Libman M, Dahhou M, Lamoureux J, Skogstrand K, Thorsen P
    Most previous studies of maternal cytokines and preterm birth have analyzed immunologic biomarkers after the onset of labor or membrane rupture; fewer have examined the systemic (blood) immune response prior to labor onset. We carried out a case-control study nested in a large (n=5337) prospective, multi-center cohort. Cohort women had an interview, examination, and venipuncture at 24-26weeks. Frozen plasma samples in women with spontaneous preterm birth (n=207) and approximately 2 term controls per case (n=444) were analyzed using Luminex multianalyte profiling technology. Fresh placentas were fixed, stained, and blindly asses...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847298</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847298</guid>        </item>
        <item>
            <title>Modulation of Th1/Th2 cytokines and inflammatory mediators by hydroxychavicol in adjuvant induced arthritic tissues.</title>
            <link>http://www.medworm.com/index.php?rid=2847300&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19782577%26dopt%3DAbstract</link>
            <description>Authors: Pandey A, Bani S, Dutt P, Suri KA
    The present study was undertaken to investigate the anti-arthritic activity of hydroxychavicol (HC) a major phenolic compound isolated from the aqueous extract leaves of plant Piper betle (Piperaceae). The compound showed significant lowering of pro-inflammatory (Th1) cytokine levels in arthritic paw tissue homogenate supernatant viz. IL-2, IFN-gamma, and TNF-alpha with maximum inhibition at higher dose levels of 2 and 4mg/kg p.o. and enhanced the production of anti-inflammatory (Th2) cytokines IL-4 and IL-5 estimated by cytometric bead array immunoassay. Cytometric bead array uses the sensitivity of amplified fluorescence detection by flowcytometer to measure soluble analytes in a particle based immune assay. This assay can accurately quantit...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847300</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847300</guid>        </item>
        <item>
            <title>Dose-dependent effect of radiation on angiogenic and angiostatic CXC chemokine expression in human endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=2847299&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19782578%26dopt%3DAbstract</link>
            <description>Authors: Chang CC, Lerman OZ, Thanik VD, Scharf CL, Greives MR, Schneider RJ, Formenti SC, Saadeh PB, Warren SM, Levine JP
    Blood vessel growth is regulated by angiogenic and angiostatic CXC chemokines, and radiation is a vasculogenic stimulus. We investigated the effect of radiation on endothelial cell chemokine signaling, receptor expression, and migration and apoptosis. Human umbilical vein endothelial cells were exposed to a single fraction of 0, 5, or 20Gy of ionizing radiation (IR). All vasculogenic chemokines (CXCL1-3/5-8) increased 3-13-fold after 5 or 20Gy IR. 20Gy induced a marked increase (1.6-4-fold) in angiostatic CXC chemokines. CXCR4 expression increased 3.5 and 7-fold at 48h after 5 and 20Gy, respectively. Bone marrow progenitor cell chemotaxis was augmented by condition...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847299</comments>
            <pubDate>Wed, 23 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847299</guid>        </item>
        <item>
            <title>Epsilonx-vivo effect of dexamethasone on cytokine production from whole blood of septic patients: Correlation with disease severity.</title>
            <link>http://www.medworm.com/index.php?rid=2847297&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19783455%26dopt%3DAbstract</link>
            <description>Conclusions: Part of the beneficiary effect of corticosteroids in sepsis may be due to an effect on the release of IL-1beta and of sTREM-1. This effect does not seem to be homogeneous for all septic patients.
    PMID: 19783455 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847297</comments>
            <pubDate>Mon, 21 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2847297</guid>        </item>
        <item>
            <title>Toll-like receptor signaling in cell proliferation and survival.</title>
            <link>http://www.medworm.com/index.php?rid=2830773&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19775907%26dopt%3DAbstract</link>
            <description>Authors: Li X, Jiang S, Tapping RI
    Toll-like receptors (TLRs) are important sensors of foreign microbial components as well as products of damaged or inflamed self tissues. Upon sensing these molecules, TLRs initiate a series of downstream signaling events that drive cellular responses including the production of cytokines, chemokines, and other inflammatory mediators. This outcome results from the intracellular assembly of protein complexes that drive phosphorylation and other signaling cascades ultimately leading to chromatin remodeling and transcription factor activation. In addition to driving inflammatory responses, TLRs also regulate cell proliferation and survival which serves to expand useful immune cells and integrate inflammatory responses and tissue repair processes. In this...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2830773</comments>
            <pubDate>Sun, 20 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2830773</guid>        </item>
        <item>
            <title>Increased circulating IL-8 is associated with reduced IGF-1 and related to poor metabolic control in adolescents with type 1 diabetes mellitus.</title>
            <link>http://www.medworm.com/index.php?rid=2830774&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19773182%26dopt%3DAbstract</link>
            <description>Conclusions: In adolescents with T1DM and chronic, poor glucose control, increased serum IL-8 is associated with reduced IGF-1 suggesting a pro-inflammatory milieu that may contribute to alterations in the GH/IGF-1 axis.
    PMID: 19773182 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2830774</comments>
            <pubDate>Fri, 18 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2830774</guid>        </item>
        <item>
            <title>Association of serum amyloid A levels with adipocyte size and serum levels of adipokines: Differences between men and women.</title>
            <link>http://www.medworm.com/index.php?rid=2810253&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19758820%26dopt%3DAbstract</link>
            <description>In conclusion, serum levels of SAA are strongly correlated with serum levels of inflammatory markers as well as measures of glycemic control. There seems to be large sex differences in these associations suggesting that sex-specific factors need to be considered when analyzing SAA levels in relation to metabolic disease.
    PMID: 19758820 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2810253</comments>
            <pubDate>Sun, 13 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2810253</guid>        </item>
        <item>
            <title>Angiotensin II type-1 receptor antagonist attenuates LPS-induced acute lung injury.</title>
            <link>http://www.medworm.com/index.php?rid=2797533&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19748795%26dopt%3DAbstract</link>
            <description>Authors: Wang F, Xia ZF, Chen XL, Jia YT, Wang YJ, Ma B
    Angiotensin II is able to trigger inflammatory responses through an angiotensin II type 1 (AT1) receptor. The role of AT1 receptor in acute lung injury (ALI) is poorly understood. Mice were randomly divided into three groups (n=40 each groups): NS group; LPS group (2mg/kg LPS intratracheally); and LPS+ZD 7155 group, 10mg/kg ZD 7155 (an AT1 receptor antagonist) intraperitoneally 30min prior to LPS exposure. Samples from the lung were isolated and assayed for histopathology analyses or proinflammatory gene expressions, angiotensin II receptors expressions and nuclear factors activities. LPS exposure resulted in severe ALI, elevated levels of TNF-alpha and IL-1beta mRNA expressions, and increased activities of NF-kappaB and activated...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2797533</comments>
            <pubDate>Thu, 10 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2797533</guid>        </item>
        <item>
            <title>Hepatic monocyte chemoattractant protein-1 is upregulated by dietary cholesterol and contributes to liver steatosis.</title>
            <link>http://www.medworm.com/index.php?rid=2797532&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19748796%26dopt%3DAbstract</link>
            <description>Authors: Rull A, Rodr&amp;#xED;guez F, Aragon&amp;#xE8;s G, Marsillach J, Beltr&amp;#xE1;n R, Alonso-Villaverde C, Camps J, Joven J
    To assess the role of monocyte chemoattractant protein-1 (MCP-1/CCL2) in the development of fatty liver, we have used LDLr(-/-) mice as an animal model of high-fat, high-cholesterol diet-induced liver steatosis. The rapid dietary induction of hepatic mRNA MCP-1 expression was paralleled by a concomitant increase in plasma MCP-1 that was strongly associated with the degree of liver steatosis. Hepatocytes showed an intense immunoreactivity for MCP-1 that was mainly located surrounding the hepatic lipid droplets. The intake of cholesterol also increased the concentration of MCP-1 in liver homogenates. This was accompanied by a differential expression of members of the PP...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2797532</comments>
            <pubDate>Thu, 10 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2797532</guid>        </item>
        <item>
            <title>Bioactive TGF-beta levels can be preserved in plasma samples collected into heparin but not EDTA.</title>
            <link>http://www.medworm.com/index.php?rid=2797534&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19748283%26dopt%3DAbstract</link>
            <description>Authors: Walther M, Jallow IK, Jeffries D, Walther B
    Quantifying TGF-beta is important for many research areas since its effects often are dose-dependently bidirectional. The post-transcriptional control of TGF-beta bioavailability points out the need to determine TGF-beta at the protein level. Studies measuring TGF-beta in peripheral blood have to avoid contamination with platelet-derived TGF-beta. Techniques to obtain platelet-poor plasma have been suggested, however, the impact of different anti-coagulants on artificial TGF-beta contamination has not been studied in detail. Here, we compare TGF-beta levels in blood samples collected into heparin and EDTA tubes, stored for 0.5-18h at various temperatures. We show that contamination with latent TGF-beta can only be prevented by collec...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2797534</comments>
            <pubDate>Wed, 09 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2797534</guid>        </item>
        <item>
            <title>Regulation of JNK and p38 MAPK in the immune system: Signal integration, propagation and termination.</title>
            <link>http://www.medworm.com/index.php?rid=2789284&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19740675%26dopt%3DAbstract</link>
            <description>Authors: Huang G, Shi LZ, Chi H
    Stress-activated MAP kinases (MAPKs), comprised of JNK and p38, play prominent roles in the innate and adaptive immune systems. Activation of MAPKs is mediated by a three-tiered kinase module comprised of MAPK kinase kinases (MAP3Ks), MAPK kinases (MAP2Ks) and MAPKs through sequential protein phosphorylation. Activated MAPKs, in turn, phosphorylate transcription factors and other targets to regulate gene transcription and immune responses. Recent studies have provided new insight into the upstream and downstream components of the MAPK pathway that facilitate the activation and propagation of MAPK signaling in immune responses. Moreover, MAPK activity is negatively regulated by MAPK phosphatases (MKPs), a group of dual-specificity phosphatases that dephos...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2789284</comments>
            <pubDate>Sun, 06 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2789284</guid>        </item>
        <item>
            <title>Modulation of the immune response by probiotic strains in a mouse model of gluten sensitivity.</title>
            <link>http://www.medworm.com/index.php?rid=2782576&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19736022%26dopt%3DAbstract</link>
            <description>In this study, we explored the effect of different Lactobacillus spp. and Bifidobacterium lactis in transgenic mice expressing the human DQ8 heterodimer, a HLA molecule linked to Celiac Disease (CD). In vitro analysis on immature bone marrow-derived dendritic cells (iBMDCs) showed that all strains up-regulated surface B7-2 (CD86), indicative of DC maturation, however, with different intensity. No strain induced appreciable levels of IL-10 or IL-12 in iBMDCs, whereas TNF-alpha expression was essentially elicited by Lactobacillus paracasei and Lactobacillus fermentum. Interestingly, these strains were found also to increase the antigen-specific TNF-alpha secretion in vivo, following co-administration of probiotic bacteria in mice mucosally immunized with the gluten component gliadin. Togethe...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2782576</comments>
            <pubDate>Fri, 04 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2782576</guid>        </item>
        <item>
            <title>G to C transition at position -173 of MIF gene of the recipient is associated with reduced relapse rates after allogeneic stem cell transplantation.</title>
            <link>http://www.medworm.com/index.php?rid=2759353&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19720544%26dopt%3DAbstract</link>
            <description>Authors: Chang YY, Greinix HT, Dickinson AM, Wolff D, Jackson GH, Andreesen R, Holler E, Hildebrandt GC
    Pro-inflammatory and dendritic cell-activating properties of macrophage migration inhibitory factor (MIF) suggest a potentially important role for MIF in alloantigen-specific immune responses after allogeneic stem cell transplantation (allo-SCT). We tested whether MIF -173 G/C gene polymorphism of donor or patient had impacts on the outcomes after allo-SCT. Four hundred and fifty-four donor-patient pairs were genotyped and mortality, relapse, and development of complications were analyzed. Patient but not donor MIF -173 *C allele was associated with improved overall survival (OS) (5years: 60.8% versus 46.3%, p=0.042) and disease free survival (DFS) (5years: 55.4% versus 39.5%; p=0.01...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2759353</comments>
            <pubDate>Fri, 28 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2759353</guid>        </item>
        <item>
            <title>Transforming growth factor-beta and Th17 responses in resistance to primary murine schistosomiasis mansoni.</title>
            <link>http://www.medworm.com/index.php?rid=2752470&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19717308%26dopt%3DAbstract</link>
            <description>Authors: Tallima H, Salah M, Guirguis FR, El Ridi R
    Discovery of the T-helper (Th) 17 cell lineage and functions in immune responses of mouse and man prompted us to investigate the role of transforming growth factor-beta (TGF-beta) and interleukin (IL)-17 in innate resistance to murine schistosomiasis mansoni. Schistosoma mansoni-infected BALB/c and C57BL/6 mice were administered with recombinant TGF-beta or mouse monoclonal antibody to TGF-beta to evaluate the impact of this cytokine on host immune responses against lung-stage schistosomula, and subsequent effects on adult worm parameters. Developing schistosomula elicited increase in peripheral blood mononuclear cells (PBMC) mRNA expression and/or plasma levels of IL-4, IL-17, and interferon-gamma (IFN-gamma), cytokines known to anta...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2752470</comments>
            <pubDate>Thu, 27 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2752470</guid>        </item>
        <item>
            <title>In vivo antitumor efficacy of interleukin-21 in combination with chemotherapeutics.</title>
            <link>http://www.medworm.com/index.php?rid=2742142&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19709902%26dopt%3DAbstract</link>
            <description>Authors: Skak K, S&amp;#xF8;ndergaard H, Frederiksen KS, Ehrnrooth E
    Interleukin-21 (IL-21) is a class I cytokine with antitumor properties due to enhanced proliferation and effector function of CD8(+) T cells and natural killer (NK) cells. Here we have explored the magnitude and time-course of cytostatics-induced lymphopenia in mice and investigated whether treatment with cytostatics influences the antitumor effect of IL-21 in mouse tumor models. We show that pegylated liposomal doxorubicin (PLD), irinotecan and oxaliplatin induced transient lymphopenia, whereas 5-fluorouracil (5-FU) transiently increased lymphocyte counts. B cells were more sensitive than T cells towards irinotecan and oxaliplatin. Additive antitumor effects were observed after combining IL-21 with PLD, oxaliplatin and t...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2742142</comments>
            <pubDate>Sun, 23 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2742142</guid>        </item>
        <item>
            <title>IL-17 inhibits human Th1 differentiation through IL-12Rbeta2 downregulation.</title>
            <link>http://www.medworm.com/index.php?rid=2720458&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19692269%26dopt%3DAbstract</link>
            <description>We report a novel negative regulatory role of IL-17 on IL-12Rbeta2 expression associated with reduced IL-12 responsiveness. IL-17 decreased IL-12-induced IFN-gamma expression in PBMC and developing Th1 cells, associated with a selective reduction in IL-12Rbeta2, and not IL-23R, IL-12Rbeta1 or T-bet. Counterregulatory effects of human Th17 on Th1 lineage cytokines may contribute to lineage divergence. In autoimmune disease, IL-17 may reinforce its own developmental programme by reducing IL-12 responsiveness, thus limiting inhibitory effects of IFN-gamma on Th17 development.
    PMID: 19692269 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2720458</comments>
            <pubDate>Sun, 16 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2720458</guid>        </item>
        <item>
            <title>Growth suppressive cytokines and the AKT/mTOR pathway.</title>
            <link>http://www.medworm.com/index.php?rid=2713204&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19682919%26dopt%3DAbstract</link>
            <description>Authors: Kroczynska B, Kaur S, Platanias LC
    The mTOR signaling pathway plays a very important role in the transmission of signals for initiation of mRNA translation and protein expression in mammalian cells. mTOR activates various downstream effectors to promote initiation of cap-dependent mRNA translation and mediate pro-mitogenic and pro-survival signals. Recent evidence has implicated effectors of this signaling cascade in mRNA translation for interferon stimulated genes (ISGs). In addition, it was recently shown that AKT/mTOR-mediated signals play important roles in the generation of IFN-dependent antiviral and growth inhibitory responses, suggesting that mTOR and its effectors can mediate diverse biological responses, depending on the cellular context and the triggering stimuli. I...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2713204</comments>
            <pubDate>Tue, 11 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2713204</guid>        </item>
        <item>
            <title>Interferon-gamma and interleukin-4 single nucleotide gene polymorphisms in Paracoccidioidomycosis.</title>
            <link>http://www.medworm.com/index.php?rid=2713203&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19682920%26dopt%3DAbstract</link>
            <description>In conclusion, our results suggest that functional genetic variants in the IL-4 promoter could influence the production of IL-4 in PCM.
    PMID: 19682920 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2713203</comments>
            <pubDate>Tue, 11 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2713203</guid>        </item>
        <item>
            <title>T-bet-/- RAG2-/- ulcerative colitis: The role of T-bet as a peacekeeper of host-commensal relationships.</title>
            <link>http://www.medworm.com/index.php?rid=2691915&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19666230%26dopt%3DAbstract</link>
            <description>Authors: Garrett WS, Glimcher LH
    Inflammatory bowel disease is a disease that reflects a disequilibrium in host-commensal homeostasis. T-bet-/-xRAG2-/- deficient mice develop a spontaneous juvenile ulcerative colitis resulting from a pro-inflammatory response to the commensal microbiota that is dendritic cell and TNF-alpha driven [schematized in Fig. 1]. The TRUC (T-bet-/- RAG2-/- ulcerative colitis) model is discussed in the broader context of the adaptive and innate immune mechanisms that regulate host-commensal relationships within the intestine.
    PMID: 19666230 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2691915</comments>
            <pubDate>Fri, 07 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2691915</guid>        </item>
        <item>
            <title>Th17 cytokines and host-pathogen interactions at the mucosa: Dichotomies of help and harm.</title>
            <link>http://www.medworm.com/index.php?rid=2691918&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19665391%26dopt%3DAbstract</link>
            <description>Authors: Liu JZ, Pezeshki M, Raffatellu M
    The mucosal surfaces are often the first site of interaction between pathogenic microorganisms and the host. Activation of the mucosal immune response has the important function of containing an infection and preventing dissemination of pathogens to systemic sites (barrier function). Numerous lines of evidence suggest that the barrier function is orchestrated by a subset of cytokines (interleukin (IL-)17 and IL-22), which belong to the Th17 family. IL-17 and IL-22 induce expression of antimicrobial peptides and neutrophil chemoattractants at mucosal sites, and thus play an important role in controlling mucosal infections. However, there is increasing evidence that mucosal pathogens achieve greater colonization during inflammation because they a...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2691918</comments>
            <pubDate>Wed, 05 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2691918</guid>        </item>
        <item>
            <title>The Dectin-2 family of C-type lectins in immunity and homeostasis.</title>
            <link>http://www.medworm.com/index.php?rid=2691917&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19665392%26dopt%3DAbstract</link>
            <description>Authors: Graham LM, Brown GD
    C-type lectins are a diverse family of proteins which recognize a wide range of ligands. This review focuses on the Dectin-2 family of C-type lectins that includes Dectin-2, BDCA-2, DCIR, DCAR, Clecsf8 and Mincle whose genes are clustered in the telomeric region of the NK-gene cluster on mouse chromosome 6 and human chromosome 12. These type II receptors are expressed on myeloid and non-myeloid cells and contain a single extracellular carbohydrate recognition domain and have diverse functions in both immunity and homeostasis. DCIR is the only member of the family which contains a cytoplasmic signalling motif and has been shown to act as an inhibitory receptor, while BDCA-2, Dectin-2, DCAR and Mincle all associate with FcRgamma chain to induce cellular activ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2691917</comments>
            <pubDate>Wed, 05 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2691917</guid>        </item>
        <item>
            <title>Expression patterns of leptin receptor (OB-R) isoforms and direct in vitro effects of recombinant leptin on OB-R, leptin expression and cytokine secretion by human hematopoietic malignant cells.</title>
            <link>http://www.medworm.com/index.php?rid=2691916&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19665393%26dopt%3DAbstract</link>
            <description>Authors: Mouzaki A, Panagoulias I, Dervilli Z, Zolota V, Spadidea P, Rodi M, Panitsas FP, Lagadinou E, de Lastic AL, Georgakopoulos T
    Several studies have implicated leptin in the pathophysiology of neoplasias. We investigated the direct effect of leptin on malignant hematopoietic tissue that included: primary acute myeloid leukemia (AML) cells, leukemic cell lines and bone marrow biopsies from multiple myeloma (MM) patients. PBMC, T-cells, B-cells and monocytes from healthy subjects served as controls. We defined the patterns of OB-R isoform expression in AML cells and leukemic cell lines in comparison to control cells by RT-PCR. rLeptin upregulated the expression of OB-R and endogenous leptin in AML blasts and certain cell lines but not in control cells. Cytometric Bead Array analysi...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2691916</comments>
            <pubDate>Wed, 05 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2691916</guid>        </item>
        <item>
            <title>The roles of MCP-1 and protein kinase Cdelta activation in human eosinophilic leukemia EoL-1 cells.</title>
            <link>http://www.medworm.com/index.php?rid=2691919&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19664934%26dopt%3DAbstract</link>
            <description>This study contributes to an understanding of MCP-1 in eosinophil biology and pathogenic mechanism of eosinophilic disorders.
    PMID: 19664934 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2691919</comments>
            <pubDate>Tue, 04 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2691919</guid>        </item>
        <item>
            <title>Anti-inflammatory effect of aldose reductase inhibition in murine polymicrobial sepsis.</title>
            <link>http://www.medworm.com/index.php?rid=2682439&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19660963%26dopt%3DAbstract</link>
            <description>Conclusions: Our results showed that the inhibition of AR significantly prevented the polymicrobial sepsis-induced increase in inflammatory markers and thus indicate the use of AR inhibitors as anti-inflammatory agents.
    PMID: 19660963 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2682439</comments>
            <pubDate>Mon, 03 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2682439</guid>        </item>
        <item>
            <title>Induction of IL-4 release and upregulated expression of protease activated receptors by GM-CSF in P815 cells.</title>
            <link>http://www.medworm.com/index.php?rid=2675236&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19651524%26dopt%3DAbstract</link>
            <description>In conclusion, GM-CSF can stimulate IL-4 release from mast cells through an ERK and Akt cell signaling pathway dependent, but PAR independent mechanism. GM-CSF may serve as a regulator for IL-4 production in mast cells and through which participates in the mast cell related inflammation.
    PMID: 19651524 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2675236</comments>
            <pubDate>Fri, 31 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2675236</guid>        </item>
        <item>
            <title>STAT3 in CD4(+) T helper cell differentiation and inflammatory diseases.</title>
            <link>http://www.medworm.com/index.php?rid=2668511&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19648026%26dopt%3DAbstract</link>
            <description>Authors: Egwuagu CE
    Jak/STAT pathways influence cell-fate decisions made by differentiating na&amp;#xEF;ve T cells, regulate the intensity and duration of inflammatory responses and are implicated in pathogenic mechanisms of a number of chronic inflammatory diseases. Among the STATs, the STAT3 protein has emerged as an important determinant of whether the na&amp;#xEF;ve T cell differentiates into regulatory (Treg) or an inflammatory (Th17) T cell lineage. STAT3 also has potent anti-inflammatory effects and regulates critical cellular processes such as, cell growth, apoptosis and transcription of inflammatory genes. Dysregulation of STAT3 pathway has therefore been implicated in the development of chronic inflammatory diseases, as well as, a number of malignant and neurodegenerative diseases. T...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2668511</comments>
            <pubDate>Thu, 30 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2668511</guid>        </item>
        <item>
            <title>Glucocorticoid-induced MIF expression by human CEM T cells.</title>
            <link>http://www.medworm.com/index.php?rid=2668512&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19646897%26dopt%3DAbstract</link>
            <description>Authors: Leng L, Wang W, Roger T, Merk M, Wuttke M, Calandra T, Bucala R
    Macrophage migration inhibitory factor (MIF) is an upstream activator of the immune response that counter-regulates the immunosuppressive effects of glucocorticoids. While MIF is released by cells in response to diverse microbial and invasive stimuli, evidence that glucocorticoids in low concentrations also induce MIF secretion suggests an additional regulatory relationship between these mediators. We investigated the expression of MIF from the human CEM T cell line, which exists in two well-characterized, glucocorticoid-sensitive (CEM-C7) and glucocorticoid-resistant (CEM-C1) variant clones. Dexamethasone in low concentrations induced MIF secretion from CEM-C7 but not CEM-C1 T cells by a bell-shaped dose response...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2668512</comments>
            <pubDate>Tue, 28 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2668512</guid>        </item>
        <item>
            <title>Molecular screening of interleukin-6 gene promoter and influence of -174G/C polymorphism on breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2660828&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19640729%26dopt%3DAbstract</link>
            <description>Authors: Ch&amp;#xE9;rel M, Campion L, B&amp;#xE9;zieau S, Campone M, Charrier J, Gaschet J, Ricolleau G, Gouraud W, Charbonnel C, J&amp;#xE9;z&amp;#xE9;quel P
    Interleukin-6 (IL-6) is a cytokine involved in different physiologic and pathophysiologic processes including carcinogenesis. In 2003, a single nucleotide polymorphism (-174G/C) of the IL-6 gene promoter has been linked to breast cancer prognosis in node-positive (N+) breast cancer patients. Since, different studies have led to conflicting conclusions about its role as a prognostic and/or diagnostic marker. The primary aim of our study was to investigate the link between -174G/C polymorphism and breast cancer risk on the one hand, and -174G/C polymorphism and prognosis in different groups of patients: sporadic N+breast cancers (n=138), sporadic...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2660828</comments>
            <pubDate>Sun, 26 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2660828</guid>        </item>
        <item>
            <title>Human cancer cells have specifically lost the ability to induce the synergistic state caused by tumor necrosis factor plus interferon-beta.</title>
            <link>http://www.medworm.com/index.php?rid=2660825&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19640730%26dopt%3DAbstract</link>
            <description>Authors: Bartee E, McFadden G
    Tumor necrosis factor (TNF) and the members of the interferon (IFN) family are major inducible cytokines that function to counteract viral infections or cellular transformation. Recently, our lab has characterized a novel antiviral state which is induced in primary human fibroblasts by co-treatment with TNF plus IFNbeta. Here, we demonstrate that this synergistic state is both antiviral and cytostatic for primary human cells. Significantly, we observed that a wide spectrum of transformed human cancer cells have universally lost the ability to induce the TNF/IFNbeta synergistic state, as defined by three separate criteria. We hypothesize that the ability to induce the TNF/IFNbeta synergistic state is a unique feature of primary cells and is incompatible wit...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2660825</comments>
            <pubDate>Sun, 26 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2660825</guid>        </item>
        <item>
            <title>Age-dependent mobilization of circulating endothelial progenitor cells in infants and young children undergoing cardiac surgery with cardiopulmonary bypass.</title>
            <link>http://www.medworm.com/index.php?rid=2646093&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19632131%26dopt%3DAbstract</link>
            <description>This study was designed to find the effects of age on circulating endothelial progenitor cells (EPCs) and their mobilization in infants and young children following surgical correction of congenital heart defects. In 60 consecutive infants and young children (1month to 3years old) undergoing repair of atrial/ventricular septal defect, the numbers of EPCs and plasma levels of IL-6, -8, -10, TNF-alpha, VEGF and G-CSF were determined preoperatively, at the end of cardiopulmonary bypass (CPB), as well as 6, 12, 24, 48, 72 and 96h following surgery. Preoperative EPCs were reduced with increased age, similar to changes in plasma VEGF and G-CSF levels. Rapid mobilizations of EPCs and plasma VEGF, G-CSF were induced by cardiac surgery with CPB in all infants and young children, and the increased v...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2646093</comments>
            <pubDate>Wed, 22 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2646093</guid>        </item>
        <item>
            <title>Association of polymorphisms in the chemokine receptor CX3CR1 gene with coronary artery disease.</title>
            <link>http://www.medworm.com/index.php?rid=2640218&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19628406%26dopt%3DAbstract</link>
            <description>In conclusion, present data of LURIC do not support the hypothesis that common variants of the CX3CR1 gene are associated with the presence of CAD or MI.
    PMID: 19628406 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2640218</comments>
            <pubDate>Mon, 20 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2640218</guid>        </item>
        <item>
            <title>Cytokine expression during chronic versus occult hepatitis B virus infection in HIV co-infected individuals.</title>
            <link>http://www.medworm.com/index.php?rid=2640220&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19625194%26dopt%3DAbstract</link>
            <description>Authors: Martin CM, Welge JA, Shire NJ, Shata MT, Sherman KE, Blackard JT
    Chronic hepatitis B virus infection is characterized by persistent detectable levels of hepatitis B surface antigen (HBsAg) and HBV DNA in the serum. In contrast, HBsAg is not detectable during occult HBV infection, despite the presence of HBV DNA. An altered host immune response could play a role in the development of occult HBV infection; however, potential differences in immune responses among chronic and occult HBV-infected patients have not been evaluated in vivo. In the current study, we evaluated serum levels of regulatory, apoptotic, and fibrotic/anti-fibrotic cytokines/markers as indicators of immune responses in 25 chronic and 12 occult HBV-infected patients. More than half of the patients in both chron...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2640220</comments>
            <pubDate>Sun, 19 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2640220</guid>        </item>
        <item>
            <title>Flow cytometric analysis of phospho-p38 mitogen-activated kinase (MAPK): p38 MAPK does not mediate the effect of adalimumab on peripheral T cell cytokine production in rheumatoid arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=2627458&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19616965%26dopt%3DAbstract</link>
            <description>Conclusion: In rheumatoid arthritis, adalimumab therapy decreases the phosphorylation of p38 MAPK except for its response to TNF/IL-1, while enhancing the production of IFNgamma. This suggests that p38 MAPK is not directly involved in the effect of TNF inhibition on cytokine production.
    PMID: 19616965 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2627458</comments>
            <pubDate>Thu, 16 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2627458</guid>        </item>
        <item>
            <title>Cigarette smoking enhances T cell activation and a Th2 immune response; an aspect of the pathophysiology in periodontal disease.</title>
            <link>http://www.medworm.com/index.php?rid=2627460&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19616447%26dopt%3DAbstract</link>
            <description>Authors: Torres de Heens GL, van der Velden U, Loos BG
    Smoking is a strong risk factor for periodontitis. Treated patients who smoke show increased risk for further periodontal breakdown, despite receiving maintenance care. Previous work indicated that such patients have a monocytic cytokine response favoring Th2 activity. The purpose of this study was to investigate the T lymphocytic cytokine production representing Th1 and Th2 subpopulations in smokers and non-smokers. Venous blood was collected from 30 treated periodontitis patients (12 smokers) and 24 healthy subjects (12 smokers). Whole blood cell cultures were stimulated and interferon (IFN)-gamma and interleukin (IL)-13 were measured in the culture supernatants, representing types 1 and 2 Th subpopulations, respectively. Unadjus...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2627460</comments>
            <pubDate>Wed, 15 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2627460</guid>        </item>
        <item>
            <title>Eviprostat suppresses proinflammatory gene expression in the prostate of rats with partial bladder-outlet obstruction: A genome-wide DNA microarray analysis.</title>
            <link>http://www.medworm.com/index.php?rid=2627459&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19616448%26dopt%3DAbstract</link>
            <description>Authors: Tagaya M, Oka M, Ueda M, Takagaki K, Tanaka M, Ohgi T, Yano J
    Prostatic inflammation plays a role in the progression of benign prostatic hyperplasia (BPH). Eviprostat is an antioxidant, antiinflammatory phytotherapeutic agent widely used to treat lower urinary tract symptoms in BPH. Because Eviprostat is a mixture of compounds from multiple natural sources, however, its mechanism of action has been difficult to investigate. Here, we describe the use of oligonucleotide microarrays to investigate changes in gene expression in the prostate of rats with surgically induced partial bladder-outlet obstruction and the effect of Eviprostat on those changes. Several dozen proinflammatory genes were activated in obstructed rats, including cytokine, arachidonic acid cascade enzyme, Toll-l...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2627459</comments>
            <pubDate>Wed, 15 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2627459</guid>        </item>
        <item>
            <title>Association of tumor necrosis factor alpha, interferon gamma and interleukin 10 gene polymorphisms with peripheral neuropathy in South Indian patients with type 2 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=2615542&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19608431%26dopt%3DAbstract</link>
            <description>Conclusion: Our findings indicate that the tested markers within the IFNgamma and IL-10 genes, but not the TNFalpha gene, are significantly associated with peripheral neuropathy in South Indian type 2 diabetic patients. The study shows that the 'high-producer' IL-10 -1082 G/G genotype and the 'low-producer' IFNgamma +874 A/A genotype may be responsible for the down regulation of immune response leading to inflammation in this setting.
    PMID: 19608431 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2615542</comments>
            <pubDate>Mon, 13 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2615542</guid>        </item>
        <item>
            <title>Day-to-day variation in plasma interleukin-6 concentrations in older adults.</title>
            <link>http://www.medworm.com/index.php?rid=2611662&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19604707%26dopt%3DAbstract</link>
            <description>Authors: Picotte M, Campbell CG, Thorland WG
    Interleukin-6 (IL-6) is a pro-inflammatory cytokine commonly used in studies as a means of assessing chronic inflammatory status. Despite the use of plasma IL-6 as a marker of chronic inflammation few studies exist that examine the variability of plasma IL-6 within and between individuals. The purpose of this study was to assess inter- and intra-variability of plasma IL-6 concentration in men and postmenopausal women. Sixteen healthy postmenopausal women and 5 men completed the 2-week study. Fasted venous blood samples were obtained on three consecutive mornings for two consecutive weeks (six blood draws per participant). Mean plasma IL-6 values were 2.00+/-1.74pg/mL. Intra-variability was not significantly different (p&amp;gt;0.05) however inte...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2611662</comments>
            <pubDate>Sun, 12 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2611662</guid>        </item>
        <item>
            <title>Role of proinflammatory markers and NT-proBNP in patients with an implantable cardioverter-defibrillator and an electrical storm.</title>
            <link>http://www.medworm.com/index.php?rid=2611661&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19604708%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: Electrical storm is associated with significantly elevated IL-6, hs-CRP and NT-proBNP serum concentrations in ICD-patients with structural heart disease. Thus, ES may be triggered by proinflammatory activity. Combined intraindividual elevation of determined markers might help to identify patients at risk of impending electrical storm.
    PMID: 19604708 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2611661</comments>
            <pubDate>Sun, 12 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2611661</guid>        </item>
        <item>
            <title>Associations of circulating TNFalpha and IL-18 with myocardial infarction and cardiovascular risk markers: The Glasgow Myocardial Infarction Study.</title>
            <link>http://www.medworm.com/index.php?rid=2580569&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19581111%26dopt%3DAbstract</link>
            <description>Conclusions: Circulating levels of IL-18 and TNFalpha were elevated in those with previous MI, but only TNFalpha retained an association after adjustment for classical risk factors. Independently elevated TNFalpha among those with previous MI may reflect cardiac expression of TNFalpha in ongoing myocardial remodeling.
    PMID: 19581111 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2580569</comments>
            <pubDate>Fri, 03 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2580569</guid>        </item>
        <item>
            <title>Serum levels of monocyte chemoattractant protein-1 in periodontal health and disease.</title>
            <link>http://www.medworm.com/index.php?rid=2580570&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19576791%26dopt%3DAbstract</link>
            <description>Conclusions: Serum MCP-1 concentration was found to be, approximately one and half folds higher in gingivitis patients (group II) and three folds higher in chronic periodontitis patients (group III) as compared to healthy subjects (group I). Further, the MCP-1 concentration increased proportionally with the severity of disease in group II and III showing positive correlation with clinical parameters. Thus, its role as an inflammatory biomarker in periodontal disease can be proposed.
    PMID: 19576791 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2580570</comments>
            <pubDate>Tue, 30 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2580570</guid>        </item>
        <item>
            <title>Differential cytokine/chemokines and KL-6 profiles in patients with different forms of tuberculosis.</title>
            <link>http://www.medworm.com/index.php?rid=2573344&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19570688%26dopt%3DAbstract</link>
            <description>Authors: Djoba Siawaya JF, Chegou NN, Heuvel MM, Diacon AH, Beyers N, Helden PV, Walzl G
    Cytokines are involved in the mediation and regulation of immunity, inflammation, and haematopoiesis. Secretion patterns may reflect the pathology or etiology of different diseases. In an attempt to increase our understanding of immunopathology during different forms of tuberculosis, and identify potential biological markers that may differentiate between forms of tuberculosis, we investigated the levels of 29 cytokines and KL-6 in the plasma of HIV uninfected patients with active pulmonary tuberculosis (TB) without pleural effusions and in pleural TB with and without HIV-co-infection. Healthy individuals with latent Mycobacterium tuberculosis infection and patients with non-TB pleural effusions we...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2573344</comments>
            <pubDate>Sun, 28 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2573344</guid>        </item>
        <item>
            <title>Grape-seed procyanidins modulate inflammation on human differentiated adipocytes in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=2556793&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19560935%26dopt%3DAbstract</link>
            <description>Authors: Chac&amp;#xF3;n MR, Ceperuelo-Mallafr&amp;#xE9; V, Maym&amp;#xF3;-Masip E, Mateo-Sanz JM, Arola L, Guiti&amp;#xE9;rrez C, Fernandez-Real JM, Ard&amp;#xE8;vol A, Sim&amp;#xF3;n I, Vendrell J
    Flavonoids are functional constituents of many fruits and vegetables. Procyanidins are flavonoids with an oligomeric structure, and it has been shown that they can improve the pathological oxidative state of a diabetic situation. To evaluate whether procyanidins can modulate inflammation, an event strongly associated with obesity, diabetes and insulin resistance states, we used human adipocytes (SGBS) and macrophage-like (THP-1) cell lines and administered an extract of grape-seed procyanidins (GSPE). THP-1 and SGBS cells pre-treated with GSPE showed a reduction of IL-6 and MCP-1 expression after an inflammatory s...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2556793</comments>
            <pubDate>Thu, 25 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2556793</guid>        </item>
        <item>
            <title>Elevated blood interleukin-10 levels and undiminished systemic interleukin-10 production rate prevail throughout acute protein-energy malnutrition in the weanling mouse.</title>
            <link>http://www.medworm.com/index.php?rid=2549115&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19541500%26dopt%3DAbstract</link>
            <description>The objectives were to determine if blood IL-10 levels rise during the early stages of acute (wasting) pre-pubescent malnutrition in metabolically distinct murine models known to depress inflammatory immune competence and whether systemic IL-10 production is affected in these pathologies. Weanling C57BL/6J mice were assigned to dietary protocols that elicited wasting pathologies mimicking the human diseases of marasmus (restricted-intake group) or incipient kwashiorkor (low-protein group). An age-matched control group also was included. Serum IL-10 bioactivities were assessed in the early (day 3) and advanced (day 14) stages of weight loss, and net systemic IL-10 production was assessed at the same stages of pathology by in vivo cytokine capture. Blood IL-10 levels were elevated in both ma...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2549115</comments>
            <pubDate>Thu, 18 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2549115</guid>        </item>
        <item>
            <title>Hypoxemic resuscitation after hemorrhagic shock is accompanied by reduced serum levels of angiopoietin-2.</title>
            <link>http://www.medworm.com/index.php?rid=2549116&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19540132%26dopt%3DAbstract</link>
            <description>Conclusions: Hypoxemic resuscitation from hemorrhagic shock is a process accompanied by reduced serum levels of Ang2. These findings add significantly to our understanding of that experimental treatment strategy of resuscitation.
    PMID: 19540132 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2549116</comments>
            <pubDate>Tue, 16 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2549116</guid>        </item>
        <item>
            <title>The protective action of radix Astragalus membranaceus against hapten-induced colitis through modulation of cytokines.</title>
            <link>http://www.medworm.com/index.php?rid=2549117&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19539495%26dopt%3DAbstract</link>
            <description>This study provides important new insights that may contribute to further development of Am as a novel therapeutic agent for treating colitis diseases.
    PMID: 19539495 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2549117</comments>
            <pubDate>Mon, 15 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2549117</guid>        </item>
        <item>
            <title>CCL20 produced in the cytokine network of rheumatoid arthritis recruits CCR6(+) mononuclear cells and enhances the production of IL-6.</title>
            <link>http://www.medworm.com/index.php?rid=2549119&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19535263%26dopt%3DAbstract</link>
            <description>Authors: Tanida S, Yoshitomi H, Nishitani K, Ishikawa M, Kitaori T, Ito H, Nakamura T
    Although a notable amount of CCL20 is detectable in the synovial fluid of human rheumatoid arthritis (RA), its role in the pathogenesis of RA remains to be determined. IL-1beta vigorously induced the production of CCL20 from FLSs of human RA and the production of CCL20 induced by TNF-alpha was partially attributed to a trace amount of IL-1beta induced by TNF-alpha. Although IL-6 failed to induce CCL20, TNF-alpha-induced IL-6 enhanced the production of CCL20 in an autocrine/paracrine manner. To determine the role of CCL20 and its sole receptor CCR6 in the recruitment of mononuclear cells (MNCs) into the inflamed joint of RA, conditioned medium of IL-1beta-stimulated FLSs was used in migration assays. T...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2549119</comments>
            <pubDate>Sun, 14 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2549119</guid>        </item>
        <item>
            <title>Interleukin-6 inhibits early differentiation of ATDC5 chondrogenic progenitor cells.</title>
            <link>http://www.medworm.com/index.php?rid=2549118&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19535264%26dopt%3DAbstract</link>
            <description>This study evaluates the effects of IL-6 on chondrogenesis by ATDC5 cells, a clonal murine chondrogenic cell line that provides an excellent model for studying endochondral ossification at growth plate. ATDC5 cells were examined for the expression of IL-6 receptor and gp130 by fluorescence-activated cell sorting analysis. Recombinant murine IL-6 was added to ATDC5 cultures to observe cell differentiation, using a quantitative RT-PCR for the chondrogenic differentiation markers type II collagen, aggrecan, and type X collagen. To block IL-6, the anti-mouse IL-6 receptor monoclonal antibody MR16-1 was added. As a result, the cells expressed IL-6 receptor and gp130. The expression of chondrogenic differentiation marker gene was reduced by IL-6, but this was abrogated by MR16-1. We conclude tha...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2549118</comments>
            <pubDate>Sun, 14 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2549118</guid>        </item>
        <item>
            <title>The response of circulating levels of the interleukin-6/interleukin-6 receptor complex to exercise in young men.</title>
            <link>http://www.medworm.com/index.php?rid=2549120&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19527938%26dopt%3DAbstract</link>
            <description>Authors: Gray SR, Clifford M, Lancaster R, Leggate M, Davies M, Nimmo MA
    The formation of an interleukin-6/IL-6 receptor (IL-6/IL-6R) complex increases the biological activity and half-life of IL-6, with its response to exercise currently unknown. The aim of the present study was to determine the response of circulating levels of the IL-6/IL-6R complex to exercise. Nine healthy male participants performed 1h of cycling exercise at a workload required to elicit 90% lactate threshold. Venous blood samples were taken at rest, immediately post-exercise and after 1.5h rest. Hemoglobin concentration and hematocrit were measured to estimate changes in plasma volume during exercise. The concentrations of IL-6, sIL-6R and the IL-6/IL-6R complex were measured via ELISA and corrected for changes ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2549120</comments>
            <pubDate>Fri, 12 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2549120</guid>        </item>
        <item>
            <title>Modulation of human dermal microvascular endothelial cells by Sarcoptes scabiei in combination with proinflammatory cytokines, histamine, and lipid-derived biologic mediators.</title>
            <link>http://www.medworm.com/index.php?rid=2549121&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19523846%26dopt%3DAbstract</link>
            <description>This study was undertaken to determine if the response of HMVEC-D to scabies is altered in the presence of various proinflammatory cytokines (tumor necrosis factor alpha and interleukins 1alpha, 1beta and 6), histamine, and lipid-derived mediators (prostaglandins D2 and E2, leukotriene B4, platelet activation factor) that likely occur in scabietic lesions in vivo. Scabies extract down-regulated the TNFalpha-induced expression of VCAM-1 by HMVEC-D and this down-regulation still occurred in the presence of the other proinflammatory cytokines, histamine or the lipid-derived mediators. Scabies inhibited the IL-1alpha and IL-1beta-induced secretion of IL-6, while a combination of scabies and histamine or LTB4 reduced the TNFalpha-induced secretion of IL-6. Scabies extract inhibited secretion of...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2549121</comments>
            <pubDate>Tue, 09 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2549121</guid>        </item>
        <item>
            <title>Adiponectin deficiency modulates adhesion molecules expression and cytokine production but does not affect disease severity in the transfer model of colitis.</title>
            <link>http://www.medworm.com/index.php?rid=2549122&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19520591%26dopt%3DAbstract</link>
            <description>In conclusion, although APN regulates expression of cytokines and adhesion molecules in the colon, this does not result in alteration of overall colitis severity in the CD4(+)CD45RB(high) transfer model.
    PMID: 19520591 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2549122</comments>
            <pubDate>Mon, 08 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2549122</guid>        </item>
        <item>
            <title>Maternal obesity and markers of inflammation in pregnancy.</title>
            <link>http://www.medworm.com/index.php?rid=2472155&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19505831%26dopt%3DAbstract</link>
            <description>Conclusions: Maternal obesity in pregnancy is associated with changes in cytokines, protein hormones and acute phase proteins in the second trimester, with an increase in MCP-1 in the morbid obesity category, and an increase in Leptin and hsCRP with increasing BMI category.
    PMID: 19505831 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472155</comments>
            <pubDate>Sat, 06 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472155</guid>        </item>
        <item>
            <title>Decreased serum levels of interleukin-2 and interleukin-6 in Indian Bengalee schizophrenic patients.</title>
            <link>http://www.medworm.com/index.php?rid=2472172&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19502081%26dopt%3DAbstract</link>
            <description>Conclusion: This is the first study to describe a decrease serum level of IL-6 in schizophrenic patients. The study provides the evidence that some kind of immune dysregulation is involved in pathophysiology of schizophrenia. The study also provides the evidence for the immunosuppressive effect of antipsychotic drugs.
    PMID: 19502081 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472172</comments>
            <pubDate>Fri, 05 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472172</guid>        </item>
        <item>
            <title>Effect of hypoxia and exogenous IL-10 on the pro-inflammatory cytokine TNF-alpha and the anti-angiogenic molecule soluble Flt-1 in placental villous explants.</title>
            <link>http://www.medworm.com/index.php?rid=2472203&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19501525%26dopt%3DAbstract</link>
            <description>Conclusion: TNF-alpha release can be inhibited in vitro by IL-10 under hypoxic conditions. However, IL-10 has no affect on sFlt-1 in term placentas, suggesting that these molecules act either via different pathways, or if linked, may be so at different stages of placental development.
    PMID: 19501525 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472203</comments>
            <pubDate>Thu, 04 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472203</guid>        </item>
        <item>
            <title>TNFR and LTbetaR agonists induce follicle-associated epithelium and M cell specific genes in rat and human intestinal epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=2472187&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19501526%26dopt%3DAbstract</link>
            <description>Authors: Wang J, Lopez-Fraga M, Rynko A, Lo DD
    M cells assist mucosal immune surveillance by transcytosis of particles to underlying lymphoid tissue, but the mechanisms of M cell differentiation are poorly understood. To develop a better defined cell culture model of M cell differentiation, we treated human (Caco-2BBe) and rat (IEC-6) intestinal epithelial cell lines with lymphotoxin beta receptor (LTbetaR) and TNF receptor (TNFR) agonists. Treated cells were studied for regulation of genes associated with M cell and follicle-associated epithelium (FAE). We found that LTbetaR and TNFR agonists induce transcription of FAE-specific genes (Ccl20 and Lamb3) in Caco2-BBe cells and IEC-6 cells as well as rodent M cell specific genes such as Sgne-1/Scg5, Cldn4, and Gp2. The cytokines have dis...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472187</comments>
            <pubDate>Thu, 04 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472187</guid>        </item>
        <item>
            <title>Differences in serum cytokine levels between influenza virus A and B infections in children.</title>
            <link>http://www.medworm.com/index.php?rid=2472223&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19497758%26dopt%3DAbstract</link>
            <description>Discussion: the production pattern of the inflammatory cytokines - TNF and IL-6 - were the same between influenza A and B. However, a Th2 predominant cytokine pattern was induced after natural influenza virus A infection, notably IL-4 that differed from that to influenza B.
    PMID: 19497758 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472223</comments>
            <pubDate>Tue, 02 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472223</guid>        </item>
        <item>
            <title>Lack of nuclear translocation of cytoplasmic domains of IL-2/IL-15 receptor subunits.</title>
            <link>http://www.medworm.com/index.php?rid=2472750&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19329337%26dopt%3DAbstract</link>
            <description>Authors: Fujii H, Hoshino A
    Some sensors of extracellular signaling molecules such as Notch and sterol response element binding protein (SREBP) receive ligand-induced intra-membrane proteolysis followed by nuclear translocation of their cytoplasmic domains to regulate gene expression programs in the nucleus. It has not been extensively examined whether ligand-induced intra-membrane proteolysis of type I cytokine receptors and nuclear translocation of cytoplasmic domains occur. Here, by using a sensitive reporter system, we examined this possibility for the interleukin-2 (IL-2) receptor (IL-2R) beta-chain (IL-2R beta) and the IL-15 receptor (IL-15R) alpha-chain (IL-15R alpha). Flowcytometric analysis revealed that ligand stimulation does not induce nuclear translocation of their cytopla...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472750</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472750</guid>        </item>
        <item>
            <title>Upregulated monocytic expression of CXC chemokine ligand 10 (CXCL-10) and its relationship with serum interleukin-6 levels in the syndrome of frailty.</title>
            <link>http://www.medworm.com/index.php?rid=2472731&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19342252%26dopt%3DAbstract</link>
            <description>Authors: Qu T, Yang H, Walston JD, Fedarko NS, Leng SX
    Frailty is an important geriatric syndrome that predicts disability and mortality. Substantial evidence suggests inflammation marked by elevated IL-6 levels as a key pathophysiologic factor that contributes to frailty. CXCL-10, a potent pro-inflammatory chemokine, has increased levels with age and is implicated in several inflammatory conditions. To better understand molecular mechanisms of inflammation activation in frailty, we evaluated monocytic expression of CXCL-10 and other inflammatory pathway genes by pathway-specific gene array analysis and quantitative RT-PCR. Frailty status was determined by the validated criteria. Sixteen pairs of community-dwelling frail and age-, race-, and sex-matched non-frail participants (mean age...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472731</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Role of a LIF antagonist in LIF and OSM induced MMP-1, MMP-3, and TIMP-1 expression by primary articular chondrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2472713&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19342253%26dopt%3DAbstract</link>
            <description>Authors: Upadhyay A, Sharma G, Kivivuori S, Raye WS, Zabihi E, Carroll GJ, Jazayeri JA
    Cartilage degradation is mediated by matrix metalloproteinases (MMPs) and their inhibitors, tissue metalloproteinases (TIMPs), which are transcriptionally regulated by a variety of growth factors and cytokines. The levels of various MMPs as well as TIMPs have been shown to increase in response to certain cytokines. These include leukaemia inhibitory factor (LIF) and Oncostatin M (OSM), both of which have been detected in the synovial fluids of patients with rheumatoid arthritis (RA). However, the role of LIF and OSM in the regulation of various MMPs and TIMPs is still incompletely understood. The aims of this study were to examine the effects of LIF and OSM on MMP-1, MMP-3, and TIMP-1 production. In ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472713</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472713</guid>        </item>
        <item>
            <title>Identification of ADAM10 as a major TNF sheddase in ADAM17-deficient fibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=2472695&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19346138%26dopt%3DAbstract</link>
            <description>Authors: Mezyk-Kope&amp;#x107; R, Bzowska M, Stali&amp;#x144;ska K, Che&amp;#x142;micki T, Podkalicki M, Jucha J, Kowalczyk K, Mak P, Bereta J
    ADAM17 (a disintegrin and metalloprotease)-deficient murine fibroblasts stably transfected with proTNF cDNA release significant amounts of biologically active soluble TNF. The enzyme responsible for this activity is a membrane protein that hydrolyzes the peptide bond Ala(76):Val(77) within proTNF. Its activity is inhibited by 1,10-phenantroline and GM6001, insusceptible to TIMP-2 (tissue inhibitor of metalloproteinases-2), and stimulated by ionomycin. These characteristics match ADAM10. The moderate silencing of ADAM10 by shRNA resulted in a significant inhibition of TNF shedding. There was no correlation between the level of ADAM10 expression and the prese...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472695</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472695</guid>        </item>
        <item>
            <title>Induction of type 1 interferon receptor by zinc in U937 cells.</title>
            <link>http://www.medworm.com/index.php?rid=2472636&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19362011%26dopt%3DAbstract</link>
            <description>This study aims to determine whether zinc enhances interferon (IFN)-alpha activity in U937 cells. Type 1 IFN2 receptor (IFNAR2) protein in U937 cells was measured by flow cytometry. After 24h of exposure to zinc chloride or polaprezinc (a chelate of zinc and L-carnosine) at concentrations ranging from 50 to 200 microM, histograms showing anti-IFNAR2 antibody-positive cells shifted to a higher FITC intensity. Zinc chloride and polaprezinc increased IFNAR2 mRNA levels approximately 30% and 40%, respectively, compared to the control. L-carnosine alone did not alter IFNAR2 mRNA or protein levels. Cellular levels of 2'-5' oligoadenylate synthetases (OAS) were markedly increased by IFN-alpha, and the increase was significantly accelerated by polaprezinc. However, polaprezinc alone did not increa...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472636</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472636</guid>        </item>
        <item>
            <title>Effects of diet and exercise on metabolic disturbances in high-fat diet-fed mice.</title>
            <link>http://www.medworm.com/index.php?rid=2472613&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19362852%26dopt%3DAbstract</link>
            <description>Authors: Vieira VJ, Valentine RJ, Wilund KR, Woods JA
    Consumption of a high-fat diet (HFD) is associated with white adipose tissue (WAT) inflammation, which contributes to key components of the metabolic syndrome, including insulin resistance (IR) and hepatic steatosis (HS). To determine the differential effects of exercise training (EX), low-fat diet (LFD), and their combination on WAT inflammation, Balb/cByJ male mice (n=34) were fed an HFD for 12 wks before they were randomized into one of four intervention groups: HFD-EX, LFD-EX, HFD-sedentary (SED), or LFD-SED. EX mice performed 12 wks of exercise training on a motorized treadmill (1h/d, 5d/wk, 12 m/min, 5% grade, approximately 65% VO(2) max), while SED mice remained sedentary in their home cages. WAT gene expression of adipokines...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472613</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472613</guid>        </item>
        <item>
            <title>Molecular characterization of IL-32 in human endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=2472579&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19364659%26dopt%3DAbstract</link>
            <description>Authors: Kobayashi H, Lin PC
    IL-32 is a newly discovered protein found in human and certain primates, but absent in rodent. Various reports suggest its role as a proinflammatory mediator. Since vascular endothelium is critical in inflammation, we investigate IL-32 in endothelial cells. We found that the gene is expressed in human endothelial cells and Akt strongly induces its expression. Sequence analysis indicates IL-32 beta as the major isoform in endothelial cells. Surprisingly, we did not detect any secretion of IL-32 beta in human endothelial cells; instead we observed co-localization of IL-32 beta with endoplasmic reticulum, suggesting IL-32 beta is an intracellular protein in these cells. Promoter analysis identified a minimum required region for IL-32 transcription at -0.1 to +...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472579</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472579</guid>        </item>
        <item>
            <title>Studies on toll-like receptor stimuli responsiveness in HIV-1 and HIV-2 infections.</title>
            <link>http://www.medworm.com/index.php?rid=2472555&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19375940%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: Innate immunity responsiveness can be monitored by whole blood stimulation. Both advanced HIV-1 and HIV-2 infections may cause innate immunity dysregulation.
    PMID: 19375940 [PubMed - in process] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472555</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472555</guid>        </item>
        <item>
            <title>Tumor necrosis factor (TNF)-alpha-induced IL-8 expression in gastric epithelial cells: role of reactive oxygen species and AP endonuclease-1/redox factor (Ref)-1.</title>
            <link>http://www.medworm.com/index.php?rid=2472535&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19376732%26dopt%3DAbstract</link>
            <description>Authors: O'Hara AM, Bhattacharyya A, Bai J, Mifflin RC, Ernst PB, Mitra S, Crowe SE
    TNF-alpha contributes to oxidative stress via induction of reactive oxygen species (ROS) and pro-inflammatory cytokines. The molecular basis of this is not well understood but it is partly mediated through the inducible expression of IL-8. As redox factor-1 (Ref-1), is an important mediator of redox-regulated gene expression we investigated whether ROS and Ref-1 modulate TNF-alpha-induced IL-8 expression in human gastric epithelial cells. We found that TNF-alpha treatment of AGS cells enhanced nuclear expression of Ref-1 and potently induced IL-8 expression. Overexpression of Ref-1 enhanced IL-8 gene transcription at baseline and after TNF-alpha treatment whereas Ref-1 suppression and antioxidant treatm...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472535</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472535</guid>        </item>
        <item>
            <title>Regulation of costimulation in the era of butyrophilins.</title>
            <link>http://www.medworm.com/index.php?rid=2472515&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19380239%26dopt%3DAbstract</link>
            <description>Authors: Arnett HA, Escobar SS, Viney JL
    The butyrophilin and butyrophilin-like superfamily of molecules has garnered attention in the immunology world in the past few years as a result of the observation that the butyrophilin-like 2 molecule, BTNL2, can alter T cell responsiveness. Additional interest in this superfamily solidified following the discovery that genetic polymorphisms in BTNL2 are associated with predisposition to many human diseases. In this review, we will provide an overview of the members comprising the butyrophilin superfamily of molecules. We will then discuss BTNL2 immunomodulatory function, and BTNL2 structural associations with other costimulatory molecules. We will then draw your attention to some of the lesser-known butyrophilin superfamily members by describi...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472515</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472515</guid>        </item>
        <item>
            <title>Factors regulating circulating vascular endothelial growth factor (VEGF): association with bone mineral density (BMD) in post-menopausal osteoporosis.</title>
            <link>http://www.medworm.com/index.php?rid=2472494&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19394248%26dopt%3DAbstract</link>
            <description>Authors: Costa N, Paramanathan S, Mac Donald D, Wierzbicki AS, Hampson G
    Vascular endothelial growth factor (VEGF) plays an important role in bone health. We investigated the factors which influence circulating VEGF and their association with bone mineral density (BMD). Two hundred and fifty two post-menopausal women aged 64.5 [9.2] years were studied. BMD was determined at the lumbar spine (LS), femoral neck (FN) and total hip (TH). Serum oestradiol and VEGF were measured. Subjects were genotyped for two polymorphic variants in the 5' untranslated region of the VEGF gene; G(634)C and C(936)T. Positive correlations were seen between circulating VEGF and BMI (r=0.2, p&amp;lt;0.02) and oestradiol (r=0.25, p&amp;lt;0.001). Following multi-linear regression analysis, serum VEGF was associated with...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472494</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472494</guid>        </item>
        <item>
            <title>Reciprocal regulation of 17beta-estradiol, interleukin-6 and interleukin-8 during growth and progression of epithelial ovarian cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2472451&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401270%26dopt%3DAbstract</link>
            <description>Authors: Yang J, Wang Y, Gao Y, Shao J, Zhang XJ, Yao Z
    Estrogens have been associated with risk for epithelial ovarian cancer (OVCA). Both IL-6 and IL-8 are also likely involved in the progression of OVCA. In order to discover the underline molecular mechanism, we investigated the modulation of estrogen and two cytokines in the growth and progression of epithelial OVCA. In these studies, the effect of 17beta-estradiol (E(2)) on the expression levels of IL-6, IL-8 and their receptors was investigated. The effect of IL-6 and IL-8 on activation of estrogen-responsive promoter as well as estrogen receptor (ER)alpha and ER beta expression was also analyzed. Gene expression profile analysis revealed that CAOV-3 and OVCAR-3 cells, which express ER, IL-6 and IL-8 receptors, are suitable model...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472451</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472451</guid>        </item>
        <item>
            <title>Pathogenic bacteria and TNF do not induce production of macrophage migration inhibitory factor (MIF) by human monocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2472432&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19406662%26dopt%3DAbstract</link>
            <description>Authors: Temple SE, Cheong KY, Price P, Waterer GW
    Elevated serum macrophage migration inhibitory factor (MIF) is associated with severe sepsis, but it is not clear whether bacteria stimulate synthesis of MIF by blood leukocytes directly or via induction of TNF. Here we assess production of MIF mRNA and protein by blood leukocytes from healthy human subjects (n=28) following exposure to bacteria commonly associated with sepsis (Escherichia coli and Streptococcus pneumoniae). Bacteria did not increase levels of MIF mRNA or secreted protein. CD14(+) monocytes were the main cell type producing MIF before and after stimulation. Exposure of leukocytes to TNF did not induce MIF. Hence elevated levels of serum MIF observed in sepsis may not reflect MIF produced by blood leukocytes stimulated ...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472432</comments>
            <pubDate>Mon, 01 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472432</guid>        </item>
        <item>
            <title>Serum factors potentiate hypoxia-induced hepatotoxicity in vitro through increasing transforming growth factor-beta1 activation and release.</title>
            <link>http://www.medworm.com/index.php?rid=2472265&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19457680%26dopt%3DAbstract</link>
            <description>Conclusion: The results suggest that the mechanism governing TGF-beta activation plays a crucial role in hypoxia-induced hepatotoxicity. Thus, interventions on TGF-beta1 bioavailability and/or its cognate signaling may be of benefit in preventing hypoxia-related liver injuries.
    PMID: 19457680 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472265</comments>
            <pubDate>Mon, 18 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472265</guid>        </item>
        <item>
            <title>No association between CALCA polymorphisms and clinical outcome or serum procalcitonin levels in German polytrauma patients.</title>
            <link>http://www.medworm.com/index.php?rid=2472301&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19447044%26dopt%3DAbstract</link>
            <description>Conclusion:CALCA polymorphisms are unlikely to influence clinical outcome in polytraumatized patients. Effects of microbial and inflammatory mediators, as well as other risk factors (gender, age, etc.) seem to have a more significant influence on the transcriptional regulation of CALCA and on PCT plasma concentrations than CALCA polymorphisms.
    PMID: 19447044 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472301</comments>
            <pubDate>Thu, 14 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472301</guid>        </item>
        <item>
            <title>Increased secretion of IP-10 from monocytes under hyperglycemia is via the TLR2 and TLR4 pathway.</title>
            <link>http://www.medworm.com/index.php?rid=2472282&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19447045%26dopt%3DAbstract</link>
            <description>Authors: Devaraj S, Jialal I
    Among the chemokines, members of the CXC family include IP-10 (interferon-gamma induced protein of 10kDa). Elevated serum IP-10 levels have been shown in diabetes. However, there is a paucity of data examining the sources and regulation of IP-10 under hyperglycemic conditions and this was the overall aim of the study. Type 1 diabetes (T1DM) is a pro-inflammatory state. We previously demonstrated increased toll like receptor (TLR) 2 and 4 activation in monocytes of T1DM patients. Thus, we also examined the role of the TLR pathway in modulating IP-10 release from human monocytes under hyperglycemia. Also, circulating and monocytic levels of IP-10 in patients with T1DM with and without microvascular complications (T1DM-MV and T1DM) and controls (C) was assesse...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472282</comments>
            <pubDate>Thu, 14 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472282</guid>        </item>
        <item>
            <title>IL-4 stimulates mouse macrophages to express APRIL through p38MAPK and two different downstream molecules, CREB and Stat6.</title>
            <link>http://www.medworm.com/index.php?rid=2472377&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19427796%26dopt%3DAbstract</link>
            <description>In this study, we investigated the role of IL-4 in APRIL expression by mouse macrophages and the signaling mechanism involved. IL-4 markedly enhanced APRIL expression in mouse macrophages at the transcriptional and protein level. The p38MAPK inhibitor SB203580 completely abolished the IL-4 effect, whereas overexpression of CREB with IL-4 augmented APRIL expression. This increase was abolished by SB203580 treatment, indicating that p38MAPK may activate CREB. Overexpression of Stat6 also augmented IL-4-induced APRIL expression; this effect was partially abolished by SB203580 but not by the Jak inhibitor AG490, indicating that Stat6 mediates IL-4-induced APRIL expression in a Jak-independent manner and that p38MAPK acts as the intermediate. Our results demonstrate that IL-4 up-regulates APRIL...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472377</comments>
            <pubDate>Thu, 07 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2472377</guid>        </item>
        <item>
            <title>The effects of body temperature control on cytokine production in a rat model of ventilator-induced lung injury.</title>
            <link>http://www.medworm.com/index.php?rid=2472357&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19427797%26dopt%3DAbstract</link>
            <description>Conclusion: The body temperature significantly affects cytokine production in a model of VILI. Body temperature control may be a potentially effective therapeutic modality to regulate cytokine production in VILI.
    PMID: 19427797 [PubMed - as supplied by publisher] (Source: Cytokine)</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472357</comments>
            <pubDate>Thu, 07 May 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Identification and characterization of human ARIP2 and its relation to breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2472675&amp;cid=s_35506_67_f&amp;fid=35506&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19349195%26dopt%3DAbstract</link>
            <description>In this study, we used RT-PCR to obtain a human homologue of mouse ARIP2, human activin receptor-interacting protein 2 (hARIP2). Like murine ARIP2, hARIP2 has a PDZ domain in its NH2-terminal region and can interact specifically with ActRIIs. Overexpression of hARIP2 reduced activin-induced transcriptional activity and enhanced cell proliferation and colony formation in human breast adenocarcinoma MCF-7 cells and MDA-MB-231 cells. However, down-regulation of hARIP2 expression by RNAi enhanced activin-induced transcriptional activity and reduced cell proliferation and colony formation. Immunohistochemistry revealed that hARIP2 was expressed more frequently and much more intensely in malignant breast tissues such as simple carcinoma, invasive ductal carcinoma and mucinous adenocarcinoma than...</description>
            <author>Cytokine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2472675</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
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