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        <title>Journal of Inflammation via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Journal of Inflammation' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Journal+of+Inflammation&t=Journal+of+Inflammation&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 14:04:19 +0100</lastBuildDate>
        <item>
            <title>Anti-inflammation effects of hydrogen saline in LPS activated macrophages and carrageenan induced paw oedema</title>
            <link>http://www.medworm.com/index.php?rid=5648062&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F9%2F1%2F2</link>
            <description>Conclusion:
As a more convenient way than inhaling H2, hydrogen saline exhibits a protective effect against inflammation and it might provide a novel therapeutic approach for inflammatory diseases. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5648062</comments>
            <pubDate>Thu, 02 Feb 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>LPS induced inflammatory responses in human peripheral blood mononuclear cells is mediated through NOX4 and Gi-alpha dependent PI-3kinase signalling</title>
            <link>http://www.medworm.com/index.php?rid=5582009&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F9%2F1%2F1</link>
            <description>In this study we show in human PBMCs that LPS stimulated proinflammatory cytokine release (CXCL8 and IL6) was inhibited by approximately 50% by the broad specificity phosphatidylinositol 3-kinase (PI3K) inhibitor, wortmannin. Our results also demonstrate that activation of PI3K following LPS stimulation is mediated by a NOX4 dependent mechanism releasing endogenous H2O2, as the NOX4 inhibitor apocynin blocked LPS induced AKT phosphorylation. Moreover, LPS-induced PI3K activation was inhibited by the anti-oxidant N-acetylcysteine in a concentration dependent manner (IC50 ~100M). In addition, our data demonstrated that inhibition of small G proteins, by pre-treatment with pertussis toxin, inhibited LPS-induced AKT phosphorylation. Furthermore, the G-protein inhibitors pertussis toxin and mas...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5582009</comments>
            <pubDate>Thu, 12 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5582009</guid>        </item>
        <item>
            <title>Ageing prolongs inflammatory marker expression in regenerating rat skeletal muscles after injury</title>
            <link>http://www.medworm.com/index.php?rid=5552435&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F41</link>
            <description>Conclusion:
Our findings identify a prolonged inflammatory signature in injured muscles from old compared with young and adult rats together with a blunted expression of key markers of regeneration in muscles of old rats. Importantly, our findings identify potential targets for future therapeutic strategies for improving the regenerative capacity of skeletal muscle during ageing. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552435</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552435</guid>        </item>
        <item>
            <title>Anti-inflammatory and antiproliferative activities of date palm pollen (Phoenix Dactylifera) on experimentally-induced atypical prostatic hyperplasia in rats</title>
            <link>http://www.medworm.com/index.php?rid=5538175&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F40</link>
            <description>Conclusion:
DPP may have a potential protective effect in APH-induced Wistar rats through modulation of cytokine expression and/or upregulation of their autocrine/ paracrine receptors. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538175</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538175</guid>        </item>
        <item>
            <title>Accelerated wound healing phenotype in Interleukin 12/23 deficient mice.</title>
            <link>http://www.medworm.com/index.php?rid=5524942&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F39</link>
            <description>Conclusion:
Overall, the accelerated oral mucosal wound healing seen in IL-12/IL-23p40 KO compared to wildtype mice was associated with the early establishment of an inflammatory response and vascularization. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5524942</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5524942</guid>        </item>
        <item>
            <title>Vitreous inflammatory factors and serous retinal detachment in central retinal vein occlusion: a case control series</title>
            <link>http://www.medworm.com/index.php?rid=5494997&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F38</link>
            <description>This study investigated whether the vitreous fluid levels of soluble vascular endothelial growth factor receptor-2 (sVEGFR-2), pigment epithelium-derived factor (PEDF), and soluble intercellular adhesion molecule 1 (sICAM-1) were associated with the occurrence of serous retinal detachment (SRD) in patients with central retinal vein occlusion (CRVO).MethodS: We recruited 33 patients with CRVO and macular edema, as well as 18 controls with nonischemic ocular diseases. Eighteen of the 33 patients with CRVO showed SRD on optical coherence tomography of the macula (defined as subretinal accumulation of fluid with low reflectivity), while the other 15 patients only had cystoid macular edema (CME, defined as hyporeflective intraretinal cavities). Retinal ischemia was evaluated by measuring the ar...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5494997</comments>
            <pubDate>Mon, 12 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5494997</guid>        </item>
        <item>
            <title>Zinc supplementation alters airway inflammation and airway hyperresponsiveness to a common allergen</title>
            <link>http://www.medworm.com/index.php?rid=5487010&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F36</link>
            <description>Conclusions:
This report suggests that the mechanism by which zinc supplementation alters NF-kappaB activity is via the alteration of A20 activity. In addition, this study provides evidence that supplementation of zinc to asthmatics may alter airway reactivity and serum IgE levels, suggesting zinc supplementation as a potential treatment for asthmatics. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5487010</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5487010</guid>        </item>
        <item>
            <title>Elevated salivary C-reactive protein levels are associated with active and passive smoking in healthy youth: A pilot study</title>
            <link>http://www.medworm.com/index.php?rid=5487009&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F37</link>
            <description>Conclusions:
Our preliminary findings indicate that salivary CRP seems to have a similar relation to TSE as its widely used serum (systemic inflammatory) biomarker counterpart. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5487009</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5487009</guid>        </item>
        <item>
            <title>Ex vivo effects of flavonoids extracted from Artemisia herba alba on cytokines and nitric oxide production in Algerian patients with Adamantiades-Behcet's disease</title>
            <link>http://www.medworm.com/index.php?rid=5431862&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F35</link>
            <description>Conclusion:
This study suggests that in vitro supplementation with flavonoids extracted from Artemisia herba alba could have potential immuno-modulatory effects characterised by a down-regulation and up-regulation of Th1 and Th2 cytokines, respectively. Moreover, flavonoids may prevent nitric oxide induced damages. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5431862</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5431862</guid>        </item>
        <item>
            <title>Insulin augments tumor necrosis factor-alpha stimulated expression of vascular cell adhesion molecule-1 in vascular endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=5422292&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F34</link>
            <description>Conclusions, hyperinsulinemia and insulin resistance appear to augment the inflammatory effects of TN F-alpha on VCAM-1 expression and NF-kappa B translocation, both of which are markers of inflammation in the vasculature. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5422292</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5422292</guid>        </item>
        <item>
            <title>Effect of the Cannabinoid Receptor-1 antagonist SR141716A on human adipocyte inflammatory profile and differentiation</title>
            <link>http://www.medworm.com/index.php?rid=5408333&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F33</link>
            <description>Conclusion:
We show for the first time that some clinical effects of SR141716A are probably directly related to its anti-inflammatory effect on mature adipocytes. This fact reinforces that adipose tissue is an important target in the development of tools to treat the metabolic syndrome. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5408333</comments>
            <pubDate>Wed, 16 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5408333</guid>        </item>
        <item>
            <title>Cytokine &amp; chemokine response in the lungs, pleural fluid and serum in thoracic surgery using one-lung ventilation</title>
            <link>http://www.medworm.com/index.php?rid=5400854&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F32</link>
            <description>Conclusion:
The inflammatory response of cytokines affects both the collapsed, operated and the ventilated, non-operated lungs. The difference in extent of response underlines the complexity of the inflammatory processes during OLV. In contrast to the cytokines, the chemokine GROalpha concentrations did not react in the BAL fluid or in the blood. This indicates that GROalpha might not be useful as marker for the inflammatory reaction in complex surgical procedures. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5400854</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5400854</guid>        </item>
        <item>
            <title>Arthrogenicity of type II collagen monoclonal antibodies associated with complement activation and antigen affinity</title>
            <link>http://www.medworm.com/index.php?rid=5387138&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F31</link>
            <description>Conclusion:
The combination of 4 mAbs showing strong abilities to activate the complement and bind mouse CII effectively induced arthritis in DBA/1J mice. This in vitro system may be useful for the selection of mAbs associated with the development of arthritis. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5387138</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5387138</guid>        </item>
        <item>
            <title>Initiation but no execution - modulation of peripheral blood lymphocyte apoptosis in rheumatoid arthritis - a potentail role for heat shock protein 70</title>
            <link>http://www.medworm.com/index.php?rid=5387139&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F30</link>
            <description>Conclusion:
The results suggest that while apoptosis may be initiated in RA-PBLs, they may lack commitment to fully executing the apoptotic program. This may be related to inhibition on apoptotic transduction by HSP70. This study provides evidence that abnormalities in RA-PBLs apoptosis may occur whilst still in circulation and may contribute to pathogenesis of the disease. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5387139</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5387139</guid>        </item>
        <item>
            <title>The effect of the CCR5-delta32 deletion on global gene expression considering immune response and inflammation</title>
            <link>http://www.medworm.com/index.php?rid=5360520&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F29</link>
            <description>Conclusions: Our data indicate that the CCR5-delta32 mutation may be associated with differential gene expression. Some of these genes are critical for immune response, in the case of CD30L probably protective in terms of GVHD. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5360520</comments>
            <pubDate>Wed, 26 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5360520</guid>        </item>
        <item>
            <title>Histological and ultrastructural comparison of cauterization and thrombosis stroke models in immune-deficient mice</title>
            <link>http://www.medworm.com/index.php?rid=5336029&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F28</link>
            <description>Conclusions: Our results provide an exhaustive analysis of the histopathological changes (inflammation, necrosis, tissue remodeling, scarring...) that occur after stroke in the ischemic boundary zone, which are of key importance for the final stroke outcome. This analysis would allow evaluating how different therapies would affect wound and regeneration. Moreover, this stroke model in RAG 2-/- gammaC -/- allows cell transplant from different species, even human, to be analyzed. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5336029</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5336029</guid>        </item>
        <item>
            <title>Antioxidant and potential anti-inflammatory activity of extracts and formulations of white tea, rose, and witch hazel on primary human dermal fibroblast cells</title>
            <link>http://www.medworm.com/index.php?rid=5314678&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F27</link>
            <description>Extracts of white tea, rose and witch hazel have been shown to have anti-inflammatory effects on fibroblasts, cells crucial for wound healing, providing a method to evaluate the benefits of plant extracts in therapeutics. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5314678</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5314678</guid>        </item>
        <item>
            <title>Parthenolide inhibits ERK and AP-1 which are dysregulated and contribute to excessive IL-8 expression and secretion in Cystic Fibrosis cells</title>
            <link>http://www.medworm.com/index.php?rid=5314679&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F26</link>
            <description>Conclusions:
In addition to NFkappaB MAPKs ERK, JNK and p38 and the transcription factor AP-1 are also dysregulated in CF epithelial cells. Parthenolide inhibits both NFkappaB and MAPK/AP-1 pathways resulting in net inhibition of IL-8 production. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5314679</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5314679</guid>        </item>
        <item>
            <title>Effects of pro-inflammatory cytokines on expression of kynurenine pathway enzymes in human dermal fibroblasts</title>
            <link>http://www.medworm.com/index.php?rid=5297159&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F25</link>
            <description>Conclusions:
All of the investigated genes encoding KP enzymes were expressed in human fibroblasts. Expression of many of these appeared to be regulated in response to cytokine treatment as previously reported for other cell-types. Fibroblast cultures, thus, appear to be useful for studies of disease-related abnormalities in the kynurenine pathway of tryptophan degradation. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5297159</comments>
            <pubDate>Sat, 08 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5297159</guid>        </item>
        <item>
            <title>Histology of adipose tissue inflammation in Dercum's disease, obesity and normal weight controls: a case control study</title>
            <link>http://www.medworm.com/index.php?rid=5260922&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F24</link>
            <description>Conclusion:
The findings suggest that there is an inflammatory response in the adipose tissue in DD. However, this response is not more pronounced than that in healthy obese controls. This contradicts inflammation as the aetiology of DD. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5260922</comments>
            <pubDate>Wed, 28 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5260922</guid>        </item>
        <item>
            <title>Activation of monocytes and cytokine production in patients with peripheral atherosclerosis obliterans</title>
            <link>http://www.medworm.com/index.php?rid=5170450&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F23</link>
            <description>Conclusions: The results revealed an unresponsiveness of patient monocytes in vitro probably due to the high activation process occurring in vivo as corroborated by high plasma cytokine levels. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5170450</comments>
            <pubDate>Sun, 28 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5170450</guid>        </item>
        <item>
            <title>Role of IL-33 in inflammation and disease</title>
            <link>http://www.medworm.com/index.php?rid=5161955&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F22</link>
            <description>Interleukin (IL)-33 is a new member of the IL-1 superfamily of cytokines that is expressed by mainly stromal cells, such as epithelial and endothelial cells, and its expression is upregulated following pro-inflammatory stimulation. IL-33 can function both as a traditional cytokine and as a nuclear factor regulating gene transcription. It is thought to function as an 'alarmin' released following cell necrosis to alerting the immune system to tissue damage or stress. It mediates its biological effects via interaction with the receptors ST2 (IL-1RL1) and IL-1 receptor accessory protein (IL-1RAcP), both of which are widely expressed, particularly by innate immune cells and T helper 2 (Th2) cells. IL-33 strongly induces Th2 cytokine production from these cells and can promote the pathogenesis o...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5161955</comments>
            <pubDate>Thu, 25 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5161955</guid>        </item>
        <item>
            <title>Tyrosine Kinases in Rheumatoid Arthritis</title>
            <link>http://www.medworm.com/index.php?rid=5161956&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F21</link>
            <description>Rheumatoid arthritis (RA) is an inflammatory, polyarticular joint disease. A number of cellular responses are involved in the pathogenesis of rheumatoid arthritis, including activation of inflammatory cells and cytokine expression. The cellular responses involved in each of these processes depends on the specific signaling pathways that are activated; many of which include protein tyrosine kinases. These pathways include the mitogen-activated protein kinase pathway, Janus kinases /signal transducers and activators transcription pathway, spleen tyrosine kinase signaling, and the nuclear factor kappa-light-chain-enhancer of activated B cells pathway. Many drugs are in development to target tyrosine kinases for the treatment of RA. Based on the number of recently published studies, this manus...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5161956</comments>
            <pubDate>Tue, 23 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5161956</guid>        </item>
        <item>
            <title>Genetic Polymorphism of ACE and the Angiotensin II Type1 Receptor Genes in Children with Chronic Kidney Disease</title>
            <link>http://www.medworm.com/index.php?rid=5161957&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F20</link>
            <description>Conclusion:
ACE DD and AT1R A/C genotypes implicated possible roles in the hypertensive state and in renal damage among children with ESRD. This result might be useful in planning therapeutic strategies for individual patients. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5161957</comments>
            <pubDate>Mon, 22 Aug 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Triple selectin knockout (ELP-/-) mice fail to develop OVA-induced acute asthma phenotype.</title>
            <link>http://www.medworm.com/index.php?rid=5120083&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F19</link>
            <description>${item.shortDescription} (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5120083</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>The effect of substance P on asthmatic rat airway smooth muscle cell proliferation, migration, and cytoplasmic calcium concentration in vitro</title>
            <link>http://www.medworm.com/index.php?rid=5052876&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F18</link>
            <description>${item.shortDescription} (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5052876</comments>
            <pubDate>Wed, 20 Jul 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Anti-inflammatory function of arctiin by inhibiting COX-2 expression via NF-kappaB pathways</title>
            <link>http://www.medworm.com/index.php?rid=5010015&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F16</link>
            <description>Conclusion:
Taken together these results provide evidence of the bioactivity of arctiin in inflammatory diseases and suggest that arctiin may exert anti-inflammatory effect by inhibiting the pro-inflammatory mediators through the inactivation of NF-kB. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5010015</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5010015</guid>        </item>
        <item>
            <title>In vitro anti-inflammatory and anti-coagulant effects of Antibiotics towards Platelet Activating Factor and Thrombin</title>
            <link>http://www.medworm.com/index.php?rid=5010014&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F17</link>
            <description>Conclusions:
These newly found properties of antibiotics used in sepsis suggest that apart from their general actions, these drugs may present additional beneficial anti-inflammatory and anti-coagulant effects against the onset and establishment of sepsis by inhibiting the PAF/PAF-receptor and/or the thrombin/protease-activated-receptor-1 systems, and/or by reducing PAF-levels through both PAF-biosynthesis inhibition and PAF-catabolism induction. These promising in vitro results need to be further studied and confirmed by in vivo tests, in order to optimize the efficacy of antibiotic treatment in sepsis. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5010014</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5010014</guid>        </item>
        <item>
            <title>T-bet controls severity of hypersensitivity pneumonitis</title>
            <link>http://www.medworm.com/index.php?rid=4960956&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F15</link>
            <description>In this study, we report that initially IFNgamma production is dependent on IL-18 and the transcription factor T-bet, however as the disease continues IFNgamma production is IL-18-independent and partially T-bet dependent. Although IFNgamma production is required for granuloma formation its role is distinct from that of T-bet. Mice that are deficient in T-bet and exposed to S. rectivirgula develop more severe disease characterized by an exacerbated Th17 cell response, decreased Th1 cell response, and increased collagen production in the lung. T-bet-mediated protection does not appear to be due to the development of a protective Th1 response; shifting the balance from a Th17 predominant response to a Th1 response by inhibition of IL-6 also results in lung pathology. The results from this st...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4960956</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4960956</guid>        </item>
        <item>
            <title>Gender difference and sex hormone production in rodent renal ischemia reperfusion injury and repair.</title>
            <link>http://www.medworm.com/index.php?rid=4913819&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F14</link>
            <description>Conclusions:
After ischemia, renal function recovery and tissue injury is gender-dependent. These differences are associated with a modulation of sex hormone production and a modification of tissue remodeling and proliferative cell processes. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4913819</comments>
            <pubDate>Wed, 08 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4913819</guid>        </item>
        <item>
            <title>Insulin alleviates degradation of skeletal muscle protein by inhibiting the ubiquitin-proteasome system in septic rats</title>
            <link>http://www.medworm.com/index.php?rid=4895452&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F13</link>
            <description>Hypercatabolism is common under septic conditions. Skeletal muscle is the main target organ for hypercatabolism, and this phenomenon is a vital factor in the deterioration of recovery in septic patients. In skeletal muscle, activation of the ubiquitin-proteasome system plays an important role in hypercatabolism under septic status. Insulin is a vital anticatabolic hormone and previous evidence suggests that insulin administration inhibits various steps in the ubiquitin-proteasome system. However, whether insulin can alleviate the degradation of skeletal muscle protein by inhibiting the ubiquitin-proteasome system under septic condition is unclear. This paper confirmed that mRNA and protein levels of the ubiquitin-proteasome system were upregulated and molecular markers of skeletal muscle p...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4895452</comments>
            <pubDate>Thu, 02 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4895452</guid>        </item>
        <item>
            <title>Adipokine resistin predicts anti-inflammatory effect of glucocorticoids in asthma</title>
            <link>http://www.medworm.com/index.php?rid=4873341&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F12</link>
            <description>Conclusions:
High resistin levels predicted favourable anti-inflammatory effect of inhaled glucocorticoids suggesting that resistin may be a marker of steroid-sensitive phenotype in asthma. High leptin levels were associated with a more severe disease suggesting that the link between leptin and asthma is not restricted to obesity. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4873341</comments>
            <pubDate>Wed, 25 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4873341</guid>        </item>
        <item>
            <title>Always one step ahead: How pathogenic bacteria use the type III secretion system to manipulate the intestinal mucosal immune system</title>
            <link>http://www.medworm.com/index.php?rid=4776447&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F11</link>
            <description>The intestinal immune system and the epithelium are the first line of defense in the gut. Constantly exposed to microorganisms from the environment, the gut has complex defense mechanisms to prevent infections, as well as regulatory pathways to tolerate commensal bacteria and food antigens. Intestinal pathogens have developed strategies to regulate intestinal immunity and inflammation in order to establish or prolong infection. The organisms that employ a type III secretion system use a molecular syringe to deliver effector proteins into the cytoplasm of host cells. These effectors target the host cell cytoskeleton, cell organelles and signaling pathways. This review addresses the multiple mechanisms by which the type III secretion system targets the intestinal immune response, with a spec...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4776447</comments>
            <pubDate>Mon, 02 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4776447</guid>        </item>
        <item>
            <title>Attenuating effect of pretreatment with Yiqifumai on lipopolysaccharide-induced intestine injury and survival rate in rat</title>
            <link>http://www.medworm.com/index.php?rid=4771991&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F10</link>
            <description>Conclusions:
The results demonstrated the potential of pretreatment with Yiqifumai to ameliorate rat intestine injury, inflammatory response to LPS and the decrease in survival rate caused by LPS challenge. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4771991</comments>
            <pubDate>Sun, 01 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4771991</guid>        </item>
        <item>
            <title>Innate Immunity and Monocyte-Macrophage Activation in Atherosclerosis</title>
            <link>http://www.medworm.com/index.php?rid=4759513&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F9</link>
            <description>Innate inflammation is a hallmark of both experimental and human atherosclerosis. The predominant innate immune cell in the atherosclerotic plaque is the monocyte-macrophage. The behaviour of this cell type within the plaque is heterogeneous and depends on the recruitment of diverse monocyte subsets. Furthermore, the plaque microenvironment offers polarisation and activation signals which impact on phenotype. Microenvironmental signals are sensed through pattern recognition receptors, including toll-like and NOD-like receptors - the latter of which are components of the inflammasome - thus dictating macrophage behaviour and outcome in atherosclerosis. Recently cholesterol crystals and modified lipoproteins have been recognised as able to directly engage these pattern recognition receptors....</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759513</comments>
            <pubDate>Wed, 27 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4759513</guid>        </item>
        <item>
            <title>Inflammatory Signals shift from adipose to liver during high fat feeding and influence the development of steatohepatitis in mice</title>
            <link>http://www.medworm.com/index.php?rid=4595271&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F8</link>
            <description>Conclusions:
Macrophage infiltration accompanied by severe inflammation and metabolic changes occurred in both adipose and liver tissues with a temporal shift in these signals depending upon the duration of HFC feeding. The evidences of gene expression profile, elevated serum alanine aminotransferase, and histological data support a progression towards nonalcoholic fatty liver disease and steatohepatitis in these HFC-fed mice within the time frame of 26 weeks. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4595271</comments>
            <pubDate>Wed, 16 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4595271</guid>        </item>
        <item>
            <title>Endotoxin-activated microglia injure brain derived endothelial cells via NF-&amp;#954;B, JAK-STAT and JNK stress kinase pathways</title>
            <link>http://www.medworm.com/index.php?rid=4623297&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F7</link>
            <description>Conclusions:
We show that LPS-activated microglia promote BBB disruption through injury to endothelial cells, and the specific blockade of JAK-STAT, NF-κB may prove to be especially useful anti-inflammatory strategies to confer cerebrovascular protection. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4623297</comments>
            <pubDate>Mon, 07 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4623297</guid>        </item>
        <item>
            <title>Endotoxin-activated microglia injure brain derived endothelial cells via NF-kappaB, JAK-STAT and JNK stress kinase pathways</title>
            <link>http://www.medworm.com/index.php?rid=4561824&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F7</link>
            <description>Conclusions:
We show that LPS-activated microglia promote BBB disruption through injury to endothelial cells, and the specific blockade of JAK-STAT, NF-kappaB may prove to be especially useful anti-inflammatory strategies to confer cerebrovascular protection. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4561824</comments>
            <pubDate>Mon, 07 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4561824</guid>        </item>
        <item>
            <title>Controlled Meal Frequency Without Caloric Restriction Alters Peripheral Blood Mononuclear Cell Cytokine Production</title>
            <link>http://www.medworm.com/index.php?rid=4555176&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F6</link>
            <description>Conclusions:
PBMCs of subjects on controlled diets exhibit hypersensitivities to cellular stimulation suggesting that stress associated with altered eating behavior might affect cytokine production by immune cells upon stimulation. Moreover, stimulated PBMCs derived from healthy individuals on a reduced meal frequency diet respond with a reduced capability to produce cytokines. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4555176</comments>
            <pubDate>Mon, 07 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4555176</guid>        </item>
        <item>
            <title>Novel anti-inflammatory role of SLPI in adipose tissue and its regulation by high fat diet</title>
            <link>http://www.medworm.com/index.php?rid=4532996&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F5</link>
            <description>Conclusion:
Our results show that SLPI is also expressed in adipocytes and adipose tissue where it could play an important feedback role in the resolution of inflammation. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4532996</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4532996</guid>        </item>
        <item>
            <title>Low Level Bacterial Endotoxin Activates Two Distinct Signaling Pathways in Human Peripheral Blood Mononuclear Cells</title>
            <link>http://www.medworm.com/index.php?rid=4522855&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F4</link>
            <description>Conclusions: These findings suggest that IL-8 release and the respiratory burst are regulated by distinct endotoxin-dependent signaling pathways in PBMC in low level of endotoxin exposure. Selectively modulating these pathways could lead to new approaches to treat chronic inflammatory diseases, such as atherosclerosis, while preserving the capacity of monocytes to respond to acute bacterial infections. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4522855</comments>
            <pubDate>Fri, 25 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4522855</guid>        </item>
        <item>
            <title>Loss of function mutation in toll-like receptor-4 (TLR4) does not offer protection against obesity and insulin resistance induced by a diet high in trans fat in mice</title>
            <link>http://www.medworm.com/index.php?rid=4461045&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F2</link>
            <description>Background:
Toll-like receptor-4 (TLR4) triggers inflammatory signaling in response to microbial lipoploysaccharide. It has been reported that loss of TLR4 protected against saturated fat-induced inflammation and insulin resistance. It is not known whether loss of TLR4 offers protection against trans fat (TF) induced obesity, inflammation, and insulin resistance. We investigated if mice with loss of function mutation in TLR4 were resistant to TF-induced pathologies such as obesity, inflammation, hyperglycemia, and hyperinsulinemia.
Methods:
C57BL/6j and C57BL/10 mice were cross bred to generate TLR4 mutant and wild type (WT). TLR4 mutant (n=12) and WT (n=12) mice were fed either low fat (LF) (13.5% fat energy) or high TF diets (60% fat energy) for 12 weeks. In vitro experiments were conduc...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4461045</comments>
            <pubDate>Fri, 11 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4461045</guid>        </item>
        <item>
            <title>Differential patterns of histone acetylation in inflammatory bowel diseases</title>
            <link>http://www.medworm.com/index.php?rid=4400971&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F8%2F1%2F1</link>
            <description>Post-translational modifications of histones, particularly acetylation, are associated with the regulation of inflammatory gene expression. We used two animal models of inflammation of the bowel and biopsy samples from patients with Crohn's disease (CD) to study the expression of acetylated histones (H) 3 and 4 in inflamed mucosa. Acetylation of histone H4 was significantly elevated in the inflamed mucosa in the trinitrobenzene sulfonic acid model of colitis particularly on lysine residues (K) 8 and K12 in contrast to non-inflamed tissue. In addition, acetylated H4 was localised to inflamed tissue and to Peyer's patches (PP) in dextran sulfate sodium (DSS)-treated rat models. Within the PP, H3 acetylation was detected in the mantle zone whereas H4 acetylation was seen in both the periphery...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4400971</comments>
            <pubDate>Thu, 27 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4400971</guid>        </item>
        <item>
            <title>Anti-inflammatory effects and possible mechanism of action of lupeol acetate isolated from Himatanthus drasticus (Mart.) Plumel</title>
            <link>http://www.medworm.com/index.php?rid=4267594&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F60</link>
            <description>Conclusions:
The anti-inflammatory effect of LA probably involves the opioid system, as indicated by the complete blockade of the opioid antagonist naloxone. Furthermore, the LA effect was potentiated by PTX (a TNF-alpha inhibitor). LA also decreased the number of iNOS cells, suggesting the participation of pro-inflammatory cytokines and the NO system in the drug action. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4267594</comments>
            <pubDate>Fri, 17 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4267594</guid>        </item>
        <item>
            <title>Inflammatory responses in epithelia: endotoxin-induced IL-6 secretion and iNOS/ NO production are differentially regulated in mouse mammary epithelial cells</title>
            <link>http://www.medworm.com/index.php?rid=4215284&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F58</link>
            <description>Conclusions:
The differential regulation of IL-6 and iNOS together with the differential activation of different NFkappaB dimers suggest that IL-6 and iNOS are regulated by different NFkappaB dimers, and differentially regulated by the microenvironment of epithelial cells. The understanding of innate immune responses and inflammation in epithelia and linkage thereof is crucial for understanding the link between chronic inflammation and cancer in epithelial tissues such as the mammary gland. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4215284</comments>
            <pubDate>Tue, 30 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4215284</guid>        </item>
        <item>
            <title>The role of toll-like receptors in acute and chronic lung inflammation</title>
            <link>http://www.medworm.com/index.php?rid=4201127&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F57</link>
            <description>By virtue of its direct contact with the environment, the lung is constantly challenged by infectious and non-infectious stimuli that necessitate a robust yet highly controlled host response coordinated by the innate and adaptive arms of the immune system. Mammalian Toll-like receptors (TLRs) function as crucial sentinels of microbial and non-infectious antigens throughout the respiratory tract and mediate host innate immunity. Selective induction of inflammatory responses to harmful environmental exposures and tolerance to innocuous antigens are required to maintain tissue homeostasis and integrity. Conversely, dysregulated innate immune responses manifest as sustained and self-perpetuating tissue damage rather than controlled tissue repair. In this article we review aspects of Toll-like ...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4201127</comments>
            <pubDate>Thu, 25 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4201127</guid>        </item>
        <item>
            <title>Increased levels of circulating Annexin A5 in Familial Mediterranean fever</title>
            <link>http://www.medworm.com/index.php?rid=4191992&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F55</link>
            <description>Conclusions: The results obtained indicate elevated rates of apoptosis of subpopulations of leukocytes involved in autoinflammation and recurrent episodes of fever in familial Mediterranean fever. It was also revealed that regular colchicine treatment sufficiently decreases the rate of apoptosis in familial Mediterranean fever patients by affecting the intensity of autoinflammatory reactions. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4191992</comments>
            <pubDate>Tue, 23 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4191992</guid>        </item>
        <item>
            <title>Suppression of nitric oxide production from nasal fibroblasts by metabolized clarithromycin in vitro</title>
            <link>http://www.medworm.com/index.php?rid=4191991&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F56</link>
            <description>Conclusion:
The present results may suggest that M-4 will be a good candidate for the agent in the treatment of chronic airway inflammatory diseases, since M-4 did not have antimicribiological effects on gram positive and negative bacteria. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4191991</comments>
            <pubDate>Tue, 23 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4191991</guid>        </item>
        <item>
            <title>Hypercholesterolemia and Microvascular Dysfunction: 
Interventional Strategies</title>
            <link>http://www.medworm.com/index.php?rid=4180133&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F54</link>
            <description>Hypercholesterolemia is defined as excessively high plasma cholesterol levels, and is a strong risk factor for many negative cardiovascular events. Total cholesterol levels above 200 mg/dl have repeatedly been correlated as an independent risk factor for development of peripheral vascular (PVD) and coronary artery disease (CAD), and considerable attention has been directed toward evaluating mechanisms by which hypercholesterolemia may impact vascular outcomes; these include both results of direct cholesterol lowering therapies and alternative interventions for improving vascular function. With specific relevance to the microcirculation, it has been clearly demonstrated that evolution of hypercholesterolemia is associated with endothelial cell dysfunction, a near-complete abrogation in vasc...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4180133</comments>
            <pubDate>Thu, 18 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4180133</guid>        </item>
        <item>
            <title>Macrophage Pro-Inflammatory Cytokine Secretion is Enhanced Following Interaction with Autologous Platelets</title>
            <link>http://www.medworm.com/index.php?rid=4152824&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F53</link>
            <description>Conclusions:
The interaction of human macrophages with autologous platelets results in scavenger-receptor-mediated platelet uptake and enhancement of LPS-induced cytokines. Therefore, the presence of activated platelets at sites of inflammation may exacerbate pro-inflammatory macrophage activation. The possibility of reversing macrophage activation with dexamethasone-loaded platelets is a promising therapeutic approach to treating unresolved inflammation. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4152824</comments>
            <pubDate>Thu, 11 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4152824</guid>        </item>
        <item>
            <title>HE3286, an oral synthetic steroid, treats lung inflammation in mice without immune suppression</title>
            <link>http://www.medworm.com/index.php?rid=4120550&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F52</link>
            <description>Conclusions:
HE3286 represents a novel, first-in-class anti-inflammatory agent that may translate certain benefits of b-AET observed in rodents into treatments for chronic inflammatory pulmonary disease. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4120550</comments>
            <pubDate>Sat, 30 Oct 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4120550</guid>        </item>
        <item>
            <title>Defining human mesenchymal stem cell efficacy in vivo</title>
            <link>http://www.medworm.com/index.php?rid=4101378&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F51</link>
            <description>Allogeneic human mesenchymal stem cells (hMSCs) can suppress graft versus host disease (GvHD) and have profound anti-inflammatory and regenerative capacity in stroke, infarct, spinal cord injury, meniscus regeneration, tendinitis, acute renal failure, and heart disease in human and animal models of disease. There is significant clinical hMSC variability in efficacy and the ultimate response in vivo. The challenge in hMSC based therapy is defining the efficacy of hMSCs in vivo. Models which may provide insight into hMSC bioactivity in vivo would provide a means to distinguish hMSCs for clinical utility. MSC function has been described as both regenerative and trophic through the production of bioactive factors. The regenerative component involves the multi-potentiality of MSC progenitor dif...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4101378</comments>
            <pubDate>Sun, 24 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4101378</guid>        </item>
        <item>
            <title>TNFRSF11B computational development network construction and analysis between frontal cortex of HIV encephalitis (HIVE) and HIVE-control patients</title>
            <link>http://www.medworm.com/index.php?rid=4014701&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F50</link>
            <description>Conclusions:
We deduced the stronger TNFRSF11B development network in HIVE consistent with our number computation. It would be necessary of the stronger TNFRSF11B development function to inflammation, brain morphology and cognition of HIVE. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4014701</comments>
            <pubDate>Wed, 29 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4014701</guid>        </item>
        <item>
            <title>Salivary gland derived peptides as a new class of anti-inflammatory agents: review of preclinical pharmacology of C-terminal peptides of SMR1 protein</title>
            <link>http://www.medworm.com/index.php?rid=4005365&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F49</link>
            <description>The limitations of steroidal and non steroidal anti-inflammatory drugs have prompted investigation into other biologically based therapeutics, and identification of immune selective anti-inflammatory agents of salivary origin. The traditional view of salivary glands as accessory digestive structures is changing as their importance as sources of systemically active immunoregulatory and anti-inflammatory factors is recognized. Salivary gland involvement in maintenance of whole body homeostasis is regulated by the nervous system and thus constitutes a &quot;neuroendocrine axis&quot;. The potent anti-inflammatory activities, both in vivo and in vitro, of the tripeptide Phe-Glu-Gly (FEG) are reviewed. FEG is a carboxyl terminal peptide of the prohormone SMR1 identified in the rat submandibular salivary g...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4005365</comments>
            <pubDate>Mon, 27 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4005365</guid>        </item>
        <item>
            <title>Suppression of LPS-induced matrix-metalloproteinase responses in macrophages exposed to phenytoin and its metabolite, 
5-(p-hydroxyphenyl-), 5-phenylhydantoin</title>
            <link>http://www.medworm.com/index.php?rid=3970415&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F48</link>
            <description>Conclusion:
The ability of macrophages to mediate turnover of ECM via the production of metalloproteinases is compromised not only by PHT, but its metabolite, HPPH in a dose-dependent fashion. Further, the preferential dysregulation of macrophage-derived TNF-alpha but not IL-6 in response to bacterial challenge may provide an inflammatory environment facilitating collagen accumulation without the counteracting production of MMPs. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3970415</comments>
            <pubDate>Tue, 14 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3970415</guid>        </item>
        <item>
            <title>Antioxidant activity of tuberosin isolated from Pueraria tuberose Linn</title>
            <link>http://www.medworm.com/index.php?rid=3962997&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F47</link>
            <description>Antioxidant activity of Pueraria tuberose DC, (PT) Leguminosae (Fabaceae) has already been reported by us and here the active compound has been isolated and its action on expression of iNOS has been explored by using LPS induced changes in attached rat peritoneal macrophage cell culture. The pure compound was isolated by column chromatography and its structure was characterized by spectral studies, which was identified as tuberosin (5 hydroxy 3,4,7,3',4' pentamethoxy flavone). Its antioxidant capacity was determined and compared with alcoholic extract as EC50 value for scavenging potential towards pre-generated monocation ABTS* radical, superoxide radicals, hydroxyl radicals, metal chelation property and on lipid peroxidation. Further, rat peritoneal macrophages were isolated, cultured and...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3962997</comments>
            <pubDate>Mon, 13 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3962997</guid>        </item>
        <item>
            <title>Protein targets of inflammatory serine proteases and cardiovascular disease</title>
            <link>http://www.medworm.com/index.php?rid=3916872&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F45</link>
            <description>Serine proteases are a key component of the inflammatory response as they are discharged from activated leukocytes and mast cells or generated through the coagulation cascade. Their enzymatic activity plays a major role in the body's defense mechanisms but it has also an impact on vascular homeostasis and tissue remodeling. Here we focus on the biological role of serine proteases in the context of cardiovascular disease and their mechanism(s) of action in determining specific vascular and tissue phenotypes. Protease-activated receptors (PARs) mediate serine protease effects; however, these proteases also exert a number of biological activities independent of PARs as they target specific protein substrates implicated in vascular remodeling and the development of cardiovascular disease thus ...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3916872</comments>
            <pubDate>Sun, 29 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3916872</guid>        </item>
        <item>
            <title>An ovine tracheal explant culture model for allergic airway inflammation</title>
            <link>http://www.medworm.com/index.php?rid=3916871&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F46</link>
            <description>Conclusions:
Sheep tracheal explants maintain characteristics of the airway mucosa that may not be replicated when studying isolated cell populations in vitro. There were key differences identified in explants from allergic compared to control airways and in their responses in culture for 24 h. Importantly, this study establishes the potential for the application of tracheal explant cultures in relevant ex vivo investigations on the therapeutic and mechanistic modalities of asthmatic disease. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3916871</comments>
            <pubDate>Sun, 29 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3916871</guid>        </item>
        <item>
            <title>Increase of aqueous inflammatory factors in macular edema with branch retinal vein occlusion: a case control study</title>
            <link>http://www.medworm.com/index.php?rid=3900787&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F44</link>
            <description>This study investigated whether intercellular adhesion molecule-1 (ICAM-1) has a role in the pathogenesis of macular edema associated with branch retinal vein occlusion (BRVO) together with vascular endothelial growth factor (VEGF).MethodS: A retrospective case control study was performed in 22 patients with BRVO and macular edema, as well as 10 patients with nonischemic ocular diseases as the control group. Retinal ischemia was evaluated by measuring the area of capillary non-perfusion with Scion Image software, while the severity of macular edema was examined by optical coherence tomography. Aqueous humor samples were obtained during the performance of combined vitrectomy and cataract surgery. ICAM-1 and VEGF levels in aqueous humor and plasma specimens were determined by enzyme-linked i...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3900787</comments>
            <pubDate>Wed, 25 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3900787</guid>        </item>
        <item>
            <title>Inhibition of allogeneic inflammatory responses by the Ribonucleotide Reductase Inhibitors, Didox and Trimidox</title>
            <link>http://www.medworm.com/index.php?rid=3878266&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F43</link>
            <description>Conclusions:
In conclusion, these data provide critical information to justify further investigation into the potential use of these compounds post allogeneic bone marrow transplantation to alleviate graft-versus-host disease thereby achieving better outcomes. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3878266</comments>
            <pubDate>Tue, 17 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3878266</guid>        </item>
        <item>
            <title>The inflammatory cytokine tumor necrosis factor modulates the expressions of Salmonella typhimurium effector proteins</title>
            <link>http://www.medworm.com/index.php?rid=3859517&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F42</link>
            <description>Tumor necrosis factor alpha(TNF-alpha) is a host inflammatory factor. Bacteria increase TNF-alpha expression in a variety of human diseases including infectious diseases, inflammatory bowel diseases, and cancer. It is unknown, however, how TNF-alpha directly modulates bacterial protein expression during intestinal infection and chronic inflammation. In the current study, we hypothesize that Salmonella typhimurium senses TNF-alpha and show that TNF-alpha treatment modulates Salmonella virulent proteins (called effectors), thus changing the host-bacterial interaction in intestinal epithelial cells. We investigated the expression of 23 Salmonella effectors after TNF-alpha exposure. We found that TNF-alpha treatment led to differential effector expression: effector SipA was increased by TNF-al...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3859517</comments>
            <pubDate>Wed, 11 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3859517</guid>        </item>
        <item>
            <title>Anti-inflammatory activity and neutrophil reductions mediated by the JAK1/JAK3 inhibitor, CP-690,550, in rat adjuvant-induced arthritis</title>
            <link>http://www.medworm.com/index.php?rid=3856174&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F41</link>
            <description>Conclusion:
Results from this investigation suggest that CP-690,550 is a potent inhibitor of JAK1 and JAK3 with potentially reduced cellular potency for JAK2. In rat AIA, as in the case of human RA, PBNC were decreased at efficacious exposures of CP-690,550. Inflammatory end points were similarly reduced, as judged by attenuation of paw edema and cytokines IL-6 and IL-17. Plasma concentration at these exposures was consistent with inhibition of JAK1 and JAK3 but not JAK2. Decreases in PBNC following CP-690,550 treatment may thus be related to attenuation of inflammation and are likely not due to suppression of granulopoiesis through JAK2 inhibition. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3856174</comments>
            <pubDate>Tue, 10 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3856174</guid>        </item>
        <item>
            <title>Leukocyte oxygen radical production determines disease severity in the recurrent Guillain-Barre syndrome</title>
            <link>http://www.medworm.com/index.php?rid=3835937&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F40</link>
            <description>Conclusion: We conclude that a lower respiratory burst in leukocytes is strongly associated with a severe course of RGBS. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3835937</comments>
            <pubDate>Sat, 07 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3835937</guid>        </item>
        <item>
            <title>Cetirizine a histamine H1 receptor antagonist improves viral myocarditis</title>
            <link>http://www.medworm.com/index.php?rid=3818225&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F39</link>
            <description>Conclusion:
These results suggest that cetirizine exerts its beneficial effects on viral myocarditis by suppressing expression of pro-inflammatory cytokines, genes related to cardiac remodeling in the hearts of mice. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3818225</comments>
            <pubDate>Tue, 03 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3818225</guid>        </item>
        <item>
            <title>Differential induction of inflammatory cytokines by dendritic cells treated with novel TLR-cytokine based cocktails: targeting dendritic cells in autoimmunity</title>
            <link>http://www.medworm.com/index.php?rid=3791938&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F37</link>
            <description>Conclusions:
The identification of novel Th1-promoting cocktails allows screening of anti-inflammatory drug candidates by assessing the ability to suppress the activation and differentiation of imDCs into inflammatory DCs with a specific Th1-promoting phenotype. The model thus provides a screening tool, which can identify potential anti-inflammatory effects on the natural regulator of the immune response, the dendritic cell. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3791938</comments>
            <pubDate>Mon, 26 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3791938</guid>        </item>
        <item>
            <title>Increased expression of cardiac IL-17 after burn</title>
            <link>http://www.medworm.com/index.php?rid=3791937&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F38</link>
            <description>Conclusion:
These findings indicate that early after burn, cardiac tissue is associated with significantly elevated levels of Th-17 cytokines. The early Th-17 response after burn appears to be specific for cardiac tissue and may promote myocardial inflammation and dysfunction associated with this form of trauma. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3791937</comments>
            <pubDate>Mon, 26 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3791937</guid>        </item>
        <item>
            <title>Waist circumference as the predominant contributor to the micro-inflammatory response in the metabolic syndrome: a cross sectional study</title>
            <link>http://www.medworm.com/index.php?rid=3788064&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F35</link>
            <description>Conclusions:
From amongst the various components of the MetS, waist circumference appears to exert the most influence upon the presence and intensity of the micro-inflammatory response. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3788064</comments>
            <pubDate>Sun, 25 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3788064</guid>        </item>
        <item>
            <title>Prediabetes and prehypertension in disease free obese adults correlate with an exacerbated systemic proinflammatory milieu</title>
            <link>http://www.medworm.com/index.php?rid=3788063&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F36</link>
            <description>Background:
Obesity is a pro-inflammatory state frequently associated with widespread metabolic alterations that include insulin resistance and deregulation of blood pressure (BP). This cascade of events in some measure explains the susceptibility of obese adults for co-morbid conditions like diabetes mellitus and hypertension.Hypothesis: We hypothesized that an elevated systemic proinflammatory burden correlates with dysglycemia and deregulated blood pressure.
Methods:
We analyzed the screening anthropometric and laboratory measures from healthy disease free obese adults (n=35; women (W) 27, men (M) 8) in a weight loss study.
Results:
Healthy obese normoglycemic (fasting serum glucose: FSG (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3788063</comments>
            <pubDate>Sun, 25 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3788063</guid>        </item>
        <item>
            <title>Emphysema is associated with increased inflammation in lungs of atherosclerosis-prone mice by cigarette smoke: implications in comorbidities of COPD</title>
            <link>http://www.medworm.com/index.php?rid=3773868&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F34</link>
            <description>Conclusion: These findings suggest that CS causes premature emphysema and a decline of lung function in mice susceptible to cardiovascular abnormalities via abnormal lung inflammation, increased oxidative stress and alterations in levels of MMPs and eNOS. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3773868</comments>
            <pubDate>Wed, 21 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3773868</guid>        </item>
        <item>
            <title>Cigarette Smoke Exposure Alters mSin3a and Mi-2alpha/beta Expression; implications in the control of pro-inflammatory gene transcription and glucocorticoid function</title>
            <link>http://www.medworm.com/index.php?rid=3759544&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F33</link>
            <description>Conclusions:
Cigarette smoke exposure induced glucocorticoid insensitivity and alters co-repressor activity and expression which is prevented by blockade of PI3Kdelta signaling with glucocorticoid treatment. Inhibition of PI3Kdelta signalling in combination with glucocorticoid treatment may therefore provide a therapeutic strategy for restoring oxidant-induced glucocortiocid unresponsiveness. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3759544</comments>
            <pubDate>Thu, 15 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3759544</guid>        </item>
        <item>
            <title>Regulation of apoptosis and priming of neutrophil oxidative burst by diisopropyl fluorophosphate</title>
            <link>http://www.medworm.com/index.php?rid=3731198&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F32</link>
            <description>Conclusion:
We conclude that DFP has significant biological effects on neutrophil function that may confound the interpretation of studies that use it for its antiprotease activity. We further conclude that endogenous proteases play a role in the biology of constitutive neutrophil apoptosis. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3731198</comments>
            <pubDate>Tue, 06 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3731198</guid>        </item>
        <item>
            <title>The role of Qa-2, the functional homolog of HLA-G, in a Behcet's disease-like mouse model induced by the herpes virus simplex</title>
            <link>http://www.medworm.com/index.php?rid=3688539&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F31</link>
            <description>Conclusions:
Silencing Qa-2 by injecting siRNA into mice resulted in deterioration of symptoms in BD-like mice. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3688539</comments>
            <pubDate>Wed, 23 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3688539</guid>        </item>
        <item>
            <title>Fas (CD95) induces rapid, TLR4/IRAK4-dependent release of pro-inflammatory HMGB1 from macrophages</title>
            <link>http://www.medworm.com/index.php?rid=3667919&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F30</link>
            <description>Although Fas (CD95) is recognized as a death receptor that induces apoptosis, recent studies indicate that the Fas/FasL system can induce pro-inflammatory cytokine production by macrophages independent of conventional caspase-mediated apoptotic signaling. The precise mechanism(s) by which Fas activates macrophage inflammation is unknown. We hypothesized that Fas stimulates rapid release of high mobility group box 1 (HMGB1) that acts in an autocrine and/or paracrine manner to stimulate pro-inflammatory cytokine production via a Toll-like receptor-4 (TLR4)/Interleukin-1 receptor associated kinase-4 (IRAK4)-dependent mechanism. Following Fas activation, HMGB1 was released within 1 hr from viable RAW267.4 cells and primary murine peritoneal macrophages. HMGB1 release was more rapid following F...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3667919</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3667919</guid>        </item>
        <item>
            <title>Smoking status and tumor necrosis factor-alpha mediated systemic inflammation in COPD patients</title>
            <link>http://www.medworm.com/index.php?rid=3646096&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F29</link>
            <description>This study investigated the association between inflammation, smoking status, and disease. Methods: A cross-sectional analysis comparing 53 COPD ex-smokers, 24 COPD current smokers, 24 current smoker controls and 34 never-smoker controls was performed. Assessments included medical history, body composition, spirometry, and plasma concentration of tumor necrosis factor-alpha (TNF-alpha), interleukins (IL)-6, IL-8, and C-reactive protein (CRP). Results: Our exploratory analysis showed that serum TNF-alpha was higher in COPD current smokers [4.8(4.2-5.8)pg/mL] and in current smoker controls [4.8 (4.2-6.1) pg/mL] when compared to COPD ex-smokers [4.3 (3.9-4.9)pg/mL; p=0.02] and to never-smoker controls [3.7 (3.4-4.0)pg/mL; p (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3646096</comments>
            <pubDate>Tue, 08 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3646096</guid>        </item>
        <item>
            <title>Gender differences and inflammation: an in vitro model of blood cells stimulation in prepubescent children</title>
            <link>http://www.medworm.com/index.php?rid=3619176&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F28</link>
            <description>Conclusions:
Persistence of the latter dimorphism throughout life casts doubts on its direct relationship with individual hormonal status, as already documented by others in vitro, and supports the need for alternative hypothesis, such as the influence of X chromosome gene products escaping X inactivation in females and absent in subjects with X monosomy (males, TS). (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3619176</comments>
            <pubDate>Tue, 01 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3619176</guid>        </item>
        <item>
            <title>Anti-inflammatory treatment strategies for ischemia/reperfusion injury in transplantation</title>
            <link>http://www.medworm.com/index.php?rid=3608707&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F27</link>
            <description>Inflammatory reactions in the graft have a pivotal influence on acute as well as long-term graft function. The main reasons for an inflammatory reaction of the graft tissue are rejection episodes, infections as well as ischemia/reperfusion (I/R) injury. The latter is of particular interest as it affects every solid organ during the process of transplantation. I/R injury impairs acute as well as long-term graft function and is associated with an increased number of acute rejection episodes that again affect long-term graft outcome.I/R injury is the result of ATP depletion during prolonged hypoxia. Further tissue damage results from the reperfusion of the tissue after the ischemic insult. Adaptive cellular responses activate the innate immune system with its Toll-like receptors and the compl...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3608707</comments>
            <pubDate>Thu, 27 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3608707</guid>        </item>
        <item>
            <title>Hematopoietic Pyk2 regulates migration of differentiated HL-60 cells</title>
            <link>http://www.medworm.com/index.php?rid=3605059&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F26</link>
            <description>Conclusions:
We conclude that Pyk2 is activated by beta2-integrin adhesion. The activated concentration of Pyk2 and colocalization with F-actin in pseudopodia suggests that Pyk2 may regulate cell spreading and migration in dHL60 cells. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3605059</comments>
            <pubDate>Wed, 26 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3605059</guid>        </item>
        <item>
            <title>Wound trauma mediated inflammatory signaling attenuates a tissue regenerative response in MRL/MpJ mice</title>
            <link>http://www.medworm.com/index.php?rid=3596896&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F25</link>
            <description>Conclusion:
These findings suggest that the observed systemic inflammatory response of a severe thermal injury undoubtedly has an adverse effect on wound healing and tissue regeneration. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3596896</comments>
            <pubDate>Mon, 24 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3596896</guid>        </item>
        <item>
            <title>Differential splicing of the apoptosis-associated speck like protein containing a caspase recruitment domain (ASC) regulates inflammasomes</title>
            <link>http://www.medworm.com/index.php?rid=3574944&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F23</link>
            <description>Conclusions:
Alternative splicing and potentially other editing mechanisms generate ASC isoforms with distinct abilities to function as inflammasome adaptor, which is potentially utilized to regulate inflammasomes during the inflammatory host response. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3574944</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574944</guid>        </item>
        <item>
            <title>Proposed protective mechanism of the pancreas in the rat</title>
            <link>http://www.medworm.com/index.php?rid=3574943&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F24</link>
            <description>Conclusions:
Our data suggests that heparan and LPS both induce host defense reactions, though by using different mechanisms of cell-recruitment. This implies that the etiology of pancreatic inflammation may influence how the subsequent events will develop. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3574943</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574943</guid>        </item>
        <item>
            <title>Pharmacokinetics of Linezolid and Ertapenem in experimental parapneumonic pleural effusion.</title>
            <link>http://www.medworm.com/index.php?rid=3571031&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F22</link>
            <description>Conclusion:
Pleural fluid levels of both antibiotics are inhibitory for common specified pathogens causing empyema. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3571031</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3571031</guid>        </item>
        <item>
            <title>Captopril reduces cardiac inflammatory markers in spontaneously hypertensive rats by inactivation of NF-kappaB</title>
            <link>http://www.medworm.com/index.php?rid=3557721&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F21</link>
            <description>Conclusion:
These findings show that captopril decreases the inflammation process in the left ventricle of hypertensive rats and suggest that NF-KB-driven inflammatory reactivity might be responsible for this effect through an inactivation of NF-KB-dependent pro-inflammatory factors. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3557721</comments>
            <pubDate>Tue, 11 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3557721</guid>        </item>
        <item>
            <title>Molecular imaging of transcriptional regulation during inflammation</title>
            <link>http://www.medworm.com/index.php?rid=3503445&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F20</link>
            <description>Molecular imaging enables non-invasive visualization of the dynamics of molecular processes within living organisms in vivo. Different imaging modalities as MRI, SPECT, PET and optic imaging are used together with molecular probes specific for the biological process of interest. Molecular imaging of transcription factor activity is done in animal models and mostly in transgenic reporter mice, where the transgene essentially consists of a promoter that regulates a reporter gene. During inflammation, the transcription factor NF-kappaB is widely involved in orchestration and regulation of the immune system and almost all imaging studies in this field has revolved around the role and regulation of NF-kappaB. We here present a brief introduction to experimental use and design of transgenic repo...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3503445</comments>
            <pubDate>Sun, 25 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3503445</guid>        </item>
        <item>
            <title>Role of inflammation in tubulo-interstitial damage associated to obstructive nephropathy</title>
            <link>http://www.medworm.com/index.php?rid=3491855&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F19</link>
            <description>Obstructive nephropathy is characterized by an inflammatory state in the kidney, that is promoted by cytokines and growth factors produced by damaged tubular cells, infiltrated macrophages and accumulated myofibroblasts. This inflammatory state contributes to tubular atrophy and interstitial fibrosis characteristic of obstructive nephropathy. Accumulation of leukocytes, especially macrophages and T lymphocytes, in the renal interstitium is strongly associated to the progression of renal injury. Proinflammatory cytokines, NF-kappaB activation, adhesion molecules, chemokines, growth factors, NO and oxidative stress contribute in different ways to progressive renal damage induced by obstructive nephropathy, as they induce leukocytes recruitment, tubular cell apoptosis and interstitial fibrosi...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3491855</comments>
            <pubDate>Wed, 21 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3491855</guid>        </item>
        <item>
            <title>Simvastatin protects bladder and renal functions following spinal cord injury in rats</title>
            <link>http://www.medworm.com/index.php?rid=3484062&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F17</link>
            <description>Conclusion:
Post-injury administration of simvastatin ameliorates bladder and renal dysfunction associated with SCI in rats. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3484062</comments>
            <pubDate>Sun, 18 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3484062</guid>        </item>
        <item>
            <title>Elevated endotoxin levels in non-alcoholic fatty liver disease</title>
            <link>http://www.medworm.com/index.php?rid=3422109&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F15</link>
            <description>This study aimed to examine the importance of serum endotoxin and inflammatory markers in non-alcoholic fatty liver disease (NAFLD) patients, with and without type 2 diabetes mellitus (T2DM), and to explore the effect of treatment with a lipase inhibitor, Orlistat, on their inflammatory status.
Methods:
Fasted serum from 155 patients with biopsy proven NAFLD and 23 control subjects were analysed for endotoxin, soluble CD14 (sCD14), soluble tumour necrosis factor receptor II (sTNFRII) and various metabolic parameters. A subgroup of NAFLD patients were re-assessed 6 and 12 months after treatment with diet alone (n=6) or diet plus Orlistat (n=8).
Results:
Endotoxin levels were significantly higher in patients with NAFLD compared with controls (NAFLD: 10.6(7.8, 14.8) EU/mL; controls: 3.9(3.2, ...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3422109</comments>
            <pubDate>Mon, 29 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3422109</guid>        </item>
        <item>
            <title>Characterization of protein tyrosine phosphatase H1 knockout mice in animal models of local and systemic inflammation</title>
            <link>http://www.medworm.com/index.php?rid=3422108&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F16</link>
            <description>Conclusion:
In conclusion, the present study points out a slight potential role for PTPH1 in spontaneous pain sensitivity and it indicates that this phosphatase might play a role in the positive regulation of the LPS-induced cytokines release in vivo, in contrast to previous reports indicating PTPH1 as potential negative regulator of immune response. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3422108</comments>
            <pubDate>Mon, 29 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3422108</guid>        </item>
        <item>
            <title>Cytosolic group IVa phospholipase A2 mediates IL-8/CXCL8-induced transmigration of human polymorphonuclear leukocytes in vitro</title>
            <link>http://www.medworm.com/index.php?rid=3380281&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F14</link>
            <description>Conclusion:
We demonstrate that IL-8/CXCL8 causes a) phosphorylation and translocation of cytosolic gIVaPLA2 to the nucleus, b) change in cell shape, c) polymerization of F-actin, and d) migration of PMN in vitro. Inhibition of gIVaPLA2 blocks the deformability and subsequent migration of PMNs caused by IL-8/CXCL8. Our data suggest that activation of gIVaPLA2 is an essential step in PMN migration in vitro. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3380281</comments>
            <pubDate>Thu, 18 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3380281</guid>        </item>
        <item>
            <title>Role of PPAR-delta in the development of zymosan-induced multiple organ failure: an experiment mice study</title>
            <link>http://www.medworm.com/index.php?rid=3285330&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F12</link>
            <description>Conclusions:
In this study, we have shown that GW0742 attenuates the degree of zymosan-induced non-septic shock in mice. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3285330</comments>
            <pubDate>Thu, 18 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3285330</guid>        </item>
        <item>
            <title>Cigarette smoke regulates VEGFR2-mediated survival signaling in rat lungs</title>
            <link>http://www.medworm.com/index.php?rid=3268003&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F11</link>
            <description>Conclusion: The rat lungs exposed to CS in acute, sub-chronic and chronic levels may be representative of smokers where survival signaling is altered but was not associated with lung cell death whereas emphysema is known to be associated with lung cell apoptosis. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3268003</comments>
            <pubDate>Sat, 13 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3268003</guid>        </item>
        <item>
            <title>CD73 represses pro-inflammatory responses in human endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=3245217&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F10</link>
            <description>Conclusions:
These results indicate that CD73 normally suppresses pro-inflammatory responses in human endothelial cells. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3245217</comments>
            <pubDate>Fri, 05 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3245217</guid>        </item>
        <item>
            <title>Histone deacetylase inhibitors induce apoptosis in human eosinophils and neutrophils</title>
            <link>http://www.medworm.com/index.php?rid=3241145&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F9</link>
            <description>Conclusions:
HDAC inhibitors enhance apoptosis in human eosinophils and neutrophils in the absence and presence of survival-prolonging cytokines and glucocorticoids. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3241145</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3241145</guid>        </item>
        <item>
            <title>Suppression of LPS-induced inflammatory responses in macrophages infected with Leishmania</title>
            <link>http://www.medworm.com/index.php?rid=3232983&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F8</link>
            <description>Conclusions:
During uptake by macrophages, Leishmania evades the activation of a broad range of cytokines and chemokines. Further, in the presence of a strong inflammatory stimulus, Leishmania suppresses certain proinflammatory cytokine responses in a parasite-specific manner, however it augments the production of other proinflammatory cytokines. Our findings highlight the complexity of inflammatory cytokine signalling regulation in the context of the macrophage and Leishmania interaction and confirm the utility of the Leishmania/ macrophage infection model as an experimental system for further studies of inflammatory regulation. Such studies may advance the development of therapies against inflammatory disease. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3232983</comments>
            <pubDate>Tue, 02 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3232983</guid>        </item>
        <item>
            <title>Dextran sulfate sodium and 2,4,6-trinitrobenzene sulfonic acid induce lipid peroxidation by the proliferation of intestinal gram-negative bacteria in mice</title>
            <link>http://www.medworm.com/index.php?rid=3225730&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F7</link>
            <description>DiscussionThese findings suggest that DSS and TNBS may cause colitis by inducing lipid peroxidation and enterobacterial proliferation, which may deteriorate the colitis by regulating proinflammatory cytokines via TLR-4-linked NF-kappaB activation pathway. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3225730</comments>
            <pubDate>Mon, 01 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3225730</guid>        </item>
        <item>
            <title>Early lactate clearance is associated with biomarkers of inflammation, coagulation, apoptosis, organ dysfunction and mortality in severe sepsis and septic shock</title>
            <link>http://www.medworm.com/index.php?rid=3218218&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F6</link>
            <description>This study examined the association of early lactate clearance with selected inflammatory, coagulation, apoptosis response biomarkers and organ dysfunction scores in severe sepsis and septic shock.
Methods:
Measurements of serum arterial lactate, biomarkers (interleukin-1 receptor antagonist, interleukin-6, interleukin-8, interleukin-10, tumor necrosis factor-alpha, intercellular adhesion molecule-1, high mobility group box-1, D-Dimer and caspase-3), and organ dysfunction scores (Acute Physiology and Chronic Health Evaluation II, Simplified Acute Physiology Score II, Multiple Organ Dysfunction Score, and Sequential Organ Failure Assessment) were obtained in conjunction with a prospective, randomized study examining early goal-directed therapy in severe sepsis and septic shock patients pres...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3218218</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3218218</guid>        </item>
        <item>
            <title>The inflammatory response seen when human omental adipose tissue explants are incubated in primary culture is not dependent upon albumin and is primarily in the nonfat cells</title>
            <link>http://www.medworm.com/index.php?rid=3195202&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F4</link>
            <description>Conclusion:
The marked inflammatory response seen when human omental adipose tissue is incubated in vitro is reduced but not abolished in the presence of albumin with respect to IL-1beta, TNFalpha, IL-8, and is primarily in the nonfat cells of adipose tissue. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3195202</comments>
            <pubDate>Thu, 21 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3195202</guid>        </item>
        <item>
            <title>Neutrophil elastase downmodulates native G-CSFR expression and granulocyte-macrophage colony formation</title>
            <link>http://www.medworm.com/index.php?rid=3195201&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F5</link>
            <description>Conclusions:
These findings indicate that in addition to transcriptional controls and ligand-induced internalization, direct proteolytic cleavage of the G-CSFR by NE also downregulates G-CSFR expression and inhibits G-CSFR-mediated granulopoiesis in vitro. Our results suggest that NE negatively regulates granulopoiesis through a novel negative feedback loop. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3195201</comments>
            <pubDate>Thu, 21 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3195201</guid>        </item>
        <item>
            <title>The anti-inflammatory effects of the tellurium redox modulating compound, AS101, are associated with regulation of NFkappaB signaling pathway and nitric oxide induction in macrophages</title>
            <link>http://www.medworm.com/index.php?rid=3186862&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F3</link>
            <description>Conclusions: Besides AS101, the investigation of therapeutic activities of other tellurium(IV) compounds is scarce in the literature, although tellurium is the fourth most abundant trace element in the human body. Since IKK and NFkB may be regulated by thiol modifications, we may thus envisage, in view of our integrated results, that Te(IV) compounds, may have important roles in thiol redox biological activity in the human body and represent a new class of anti-inflammatory compounds. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186862</comments>
            <pubDate>Wed, 20 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186862</guid>        </item>
        <item>
            <title>Total hip and knee replacement surgery results in changes in leukocyte and endothelial markers</title>
            <link>http://www.medworm.com/index.php?rid=3183099&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F2</link>
            <description>Conclusion:
In general it appeared that most of the leukocyte and endothelial markers measured during these studies peaked between days 1-3 postoperatively. It is proposed that by allowing orthopaedic surgeons access to alternative laboratory markers such as CD11b, H2O2 and elastase, CD62L, vWF and sICAM-1, an accurate assessment of the extent of inflammation due to surgery per se could be made. Ultimately, the leukocyte and endothelial markers assessed during this investigation may have a role in monitoring potential infectious complications that can occur during the postoperative period. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3183099</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3183099</guid>        </item>
        <item>
            <title>Signaling pathways involved in LPS induced TNFalpha production in human adipocytes</title>
            <link>http://www.medworm.com/index.php?rid=3150457&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F7%2F1%2F1</link>
            <description>Conclusion:
This study clearly demonstrates that the LPS induced activation pathway is an integral part of the inflammatory process linked to obesity, and that adipocytes are responsible for most of the secreted TNFalpha in inflamed adipose tissue, through TLR4 activation. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3150457</comments>
            <pubDate>Fri, 08 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3150457</guid>        </item>
        <item>
            <title>Effects of hydrogen sulfide on inflammation in caerulein-induced acute pancreatitis</title>
            <link>http://www.medworm.com/index.php?rid=3127520&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F35</link>
            <description>Conclusion:
In conclusion, these data provide evidence for anti-inflammatory effects of H2S based on its dosage used. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3127520</comments>
            <pubDate>Wed, 30 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3127520</guid>        </item>
        <item>
            <title>Gadolinium decreases inflammation related to myocardial ischemia and reperfusion injury</title>
            <link>http://www.medworm.com/index.php?rid=3072876&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F34</link>
            <description>Conclusions:
GdCl3 treatment prior to ischemia and reperfusion injury decreased circulating monocytes and neutrophils, macrophage secreted cytokines, and leukocyte infiltration into injured myocardium. These results suggest GdCl3 decreased monoctye and neutrophil migration and activation and may be a novel treatment for inflammation during ischemia and reperfusion. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3072876</comments>
            <pubDate>Thu, 10 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3072876</guid>        </item>
        <item>
            <title>Hepcidin is elevated in mice injected with Mycoplasma arthritidis</title>
            <link>http://www.medworm.com/index.php?rid=3024072&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F33</link>
            <description>In conclusion, serum hepcidin regulation in C3H/HeJ mice does not appear to be solely dependent upon TLR4 or IL-6. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3024072</comments>
            <pubDate>Tue, 24 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3024072</guid>        </item>
        <item>
            <title>CCR2 and CXCR4 regulate peripheral blood monocyte pharmacodynamics and link to efficacy in experimental autoimmune encephalomyelitis</title>
            <link>http://www.medworm.com/index.php?rid=2982621&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F32</link>
            <description>Conclusions:
CCR2 antagonism in vivo has tractable pharmacodynamic effects that can be used to align target engagement with biologic effects on disease activity. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982621</comments>
            <pubDate>Wed, 11 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2982621</guid>        </item>
        <item>
            <title>Cleavage of functional IL-2 receptor alpha chain (CD25) from murine corneal and conjunctival epithelia by MMP-9</title>
            <link>http://www.medworm.com/index.php?rid=2945061&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F31</link>
            <description>Conclusions:
Our results indicate that functional IL-2R is produced by the ocular surface epithelia and that CD25 is proteolytic cleaved to its soluble form by MMP-9, which increases in desiccating stress. These findings provide new insight into IL-2 signaling in mucosal epithelia. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2945061</comments>
            <pubDate>Sat, 31 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2945061</guid>        </item>
        <item>
            <title>Activity of the cyclooxygenase 2-prostaglandin-E prostanoid receptor pathway in mice exposed to house dust mite aeroallergens, and impact of exogenous prostaglandin E2</title>
            <link>http://www.medworm.com/index.php?rid=2968685&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com</link>
            <description>Conclusions:
The lung COX-2/PGE2/EP2 receptor pathway is upregulated in HDM-exposed mice, possibly as an effort to attenuate allergen-induced airway inflammation. Exogenous PGE2 downregulates its endogenous counterpart but maintains EP2 overexpression, a phenomenon that might be required for administered PGE2 to exert its protective effect. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2968685</comments>
            <pubDate>Fri, 30 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2968685</guid>        </item>
        <item>
            <title>Protein kinase C promotes restoration of calcium homeostasis to platelet activating factor-stimulated human neutrophils by inhibition of phospholipase C</title>
            <link>http://www.medworm.com/index.php?rid=2940973&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F29</link>
            <description>Conclusion:
Although generally considered to initiate and/or amplify intracellular signalling cascades which activate and sustain the pro-inflammatory activities of neutrophils and other cell types, the findings of the current study have identified a potentially important physiological, anti-inflammatory function for PKC, at least in neutrophils. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2940973</comments>
            <pubDate>Fri, 30 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2940973</guid>        </item>
        <item>
            <title>Lactobacillus casei modulates the inflammation-coagulation interaction in a pneumococcal pneumonia experimental model</title>
            <link>http://www.medworm.com/index.php?rid=2896249&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F28</link>
            <description>Conclusions:
L. casei proved effective to regulate coagulation activation and fibrinolysis inhibition during infection, leading to a decrease in fibrin deposits in lung. This protective effect of L. casei would be mediated by the induction of higher levels of IL-4 and IL-10 which could regulate the anti-inflammatory, procoagulant and antifibrinolytic effects of TNF-alpha, IL-1beta and IL-6. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2896249</comments>
            <pubDate>Thu, 15 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2896249</guid>        </item>
        <item>
            <title>Homocysteine-induced macrophage inflammatory protein-2 production by glomerular mesangial cells is mediated by PI3 Kinase and p38 MAPK.</title>
            <link>http://www.medworm.com/index.php?rid=2833198&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F27</link>
            <description>Conclusions:
The data suggest that Hcy participates in inflammatory cytokines production by glomerular MC and that Hcy-induced MIP-2 mediates leukocyte adhesion to MC. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2833198</comments>
            <pubDate>Fri, 25 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2833198</guid>        </item>
        <item>
            <title>Rho iso-alpha acids from hops inhibit the GSK-3/NF-kappaB pathway and reduce inflammatory markers associated with bone and cartilage degradation</title>
            <link>http://www.medworm.com/index.php?rid=2739069&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F26</link>
            <description>Conclusions:
RIAA may have potential as an anti-inflammatory therapeutic. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2739069</comments>
            <pubDate>Wed, 26 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2739069</guid>        </item>
        <item>
            <title>Inhibitory effect of IL-8 on insulin action in human adipocytes via MAP kinase pathway</title>
            <link>http://www.medworm.com/index.php?rid=2735737&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F25</link>
            <description>Conclusion:
These data suggest that IL-8 is a main adipocytokine producing insulin resistance via the inhibition of insulin-induced Akt phosphorylation in adipocytes. The attenuation of IL-8 action might be a target for prevention of diabetes and its complications. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2735737</comments>
            <pubDate>Wed, 26 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2735737</guid>        </item>
        <item>
            <title>Modulation of expression and cellular distribution of p21 by macrophage migration inhibitory factor</title>
            <link>http://www.medworm.com/index.php?rid=2728168&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F24</link>
            <description>Conclusion:
The results demonstrate that in the absence of MIF p21 expression and nuclear distribution is reduced which is associated with a reduction in cell growth and increased apoptosis. MIF may therefore play a role in maintaining homeostatic control of p21. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2728168</comments>
            <pubDate>Sun, 23 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2728168</guid>        </item>
        <item>
            <title>Gender-Based Reciprocal Expression of Transforming Growth Factor-Beta1 and the Inducible Nitric Oxide Synthase in a Rat Model of Cyclophosphamide-Induced Cystitis</title>
            <link>http://www.medworm.com/index.php?rid=2713937&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F23</link>
            <description>Conclusions:
The results of this study suggest that there exists an inverse relationship between the expression of TGF-beta1 and iNOS/NO2-/NO3- in CYP-inflamed bladder. The gender of the animal appears to magnify the differences in urine levels of TGF-beta1 and NO2-/NO3- in this inflammatory setting. These results support the hypothesis that TGF-beta1 can suppress iNOS expression associated with bladder inflammation and reduce systemic levels of NO2-/NO3-, and further suggest that this feature of TGF-beta1 can be harnessed for therapy and diagnosis of interstitial cystitis. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2713937</comments>
            <pubDate>Tue, 18 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2713937</guid>        </item>
        <item>
            <title>CCR5 signalling, but not DARC or D6 regulatory, chemokine receptors are targeted by herpesvirus U83A chemokine which delays receptor internalisation via diversion to a caveolin-linked pathway</title>
            <link>http://www.medworm.com/index.php?rid=2655185&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F22</link>
            <description>Conclusions:
U83A diverts human chemokines from signalling, but not regulatory or scavenger, receptors facilitating their clearance, while occupying signalling receptors at the cell surface. This can enhance virus specific inflammation, facilitating dissemination to replication sensitive leukocytes while evading clearance; this has implications for linked neuro-inflammatory pathologies. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2655185</comments>
            <pubDate>Wed, 29 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2655185</guid>        </item>
        <item>
            <title>Is inflammation a consequence of extracellular hyperosmolarity?</title>
            <link>http://www.medworm.com/index.php?rid=2489075&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F21</link>
            <description>Conclusion:
The present study further suggests inflammation and hyperosmolarity are closely related phenomena if not synonymous. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2489075</comments>
            <pubDate>Mon, 22 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2489075</guid>        </item>
        <item>
            <title>Protein Never in Mitosis Gene A Interacting-1 regulates calpain activity and the degradation of cyclooxygenase-2 in endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=2489076&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F20</link>
            <description>Conclusions:
PIN1 reduced calpain activity and slowed the degradation of COX-2 in MAEC, an effect recapitulated by an inhibitor of calpain. Given the sensitivity of COX-2 and iNOS to calpain, PIN1 may normally limit induction of these and other calpain substrates by maintaining calpain activity in endothelial cells. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2489076</comments>
            <pubDate>Sun, 21 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2489076</guid>        </item>
        <item>
            <title>Cadmium induces lung inflammation independent of lung cell proliferation: a molecular approach</title>
            <link>http://www.medworm.com/index.php?rid=2477044&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F19</link>
            <description>Conclusion:
Our results prove that cadmium causes both inflammation and cell proliferation when applied in a low dose but proliferative changes occur independent of inflammation. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2477044</comments>
            <pubDate>Fri, 12 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2477044</guid>        </item>
        <item>
            <title>TNF-alpha and IL-10 downregulation and marked oxidative stress in Neuromyelitis Optica</title>
            <link>http://www.medworm.com/index.php?rid=2449329&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F18</link>
            <description>Conclusions:
These results suggest that there is a breakdown in immunoregulatory mechanisms and noteworthy pro-oxidant environment contributing to NMO pathogenesis. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2449329</comments>
            <pubDate>Tue, 02 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2449329</guid>        </item>
        <item>
            <title>Role of TRPV3 in immune response to development of dermatitis</title>
            <link>http://www.medworm.com/index.php?rid=2432804&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F17</link>
            <description>Conclusions:
Our results confirm the contribution of the TRPV3Gly573Ser gene to the development of repeated hapten dermatitis, but not spontaneous dermatitis in NC/Nga mice. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2432804</comments>
            <pubDate>Mon, 25 May 2009 03:40:52 +0100</pubDate>
            <guid isPermaLink="false">2432804</guid>        </item>
        <item>
            <title>Alterations in transcriptional responses associated with vascular aging</title>
            <link>http://www.medworm.com/index.php?rid=2429443&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F16</link>
            <description>Vascular aging is an independent risk factor for cardiovascular disease that can occur in the absence of other traditional risk factors. A hallmark of vascular aging is inflammation that ultimately leads to structural changes in the vessel wall including an increase in medial thickness and perivascular fibrosis. Several classes of transcription factors have been identified that participate in the regulation of cellular responses associated with vascular aging. Nuclear factor (NF)-kappaB is the prototypic example of a transcriptional activator in the setting of inflammation, being activated in response to multiple inflammatory mediators including pro-inflammatory cytokines and bacterial endotoxin. In contrast, the activation of the nuclear hormone receptor and transcription factor peroxisom...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2429443</comments>
            <pubDate>Thu, 21 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2429443</guid>        </item>
        <item>
            <title>Inhibition of NFkappaB by the natural product Withaferin A in cellular models of Cystic Fibrosis inflammation</title>
            <link>http://www.medworm.com/index.php?rid=2407571&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F15</link>
            <description>Cystic Fibrosis (CF) is one of the most common autosomal genetic disorders in humans. This disease is caused by mutations within a single gene, coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The phenotypic hallmark of CF is chronic lung infection and associated inflammation from opportunistic microbes such as Pseudomonas aeruginosa (PA), Haemophilus influenzae, and Staphylococcus aureus. This eventually leads to deterioration of lung function and death in most CF patients. Unfortunately, there is no approved therapy for correcting the genetic defect causal to the disease. Hence, controlling inflammation and infection in CF patients is critical to disease management. Accordingly, anti-inflammatory agents and antibiotics are used to manage chronic inflamma...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2407571</comments>
            <pubDate>Wed, 13 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2407571</guid>        </item>
        <item>
            <title>Inhibition of zymosan-induced kidney dysfunction by tyrphostin AG-490</title>
            <link>http://www.medworm.com/index.php?rid=2391766&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F13</link>
            <description>Conclusions:
Tyrphostin AG-490 reduced the magnitude of the initial inflammatory response in zymosan-induced shock and prevented the development of severe kidney dysfunction. Our data suggest that the drug might be used as a therapeutic approach in cases where shock is combined with acute renal injury. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2391766</comments>
            <pubDate>Tue, 05 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2391766</guid>        </item>
        <item>
            <title>Cigarette smoke regulates the expression of TLR4 and IL-8 production by human macrophages</title>
            <link>http://www.medworm.com/index.php?rid=2383888&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F12</link>
            <description>Conclusion:
TLR4 may be involved in the pathogenesis of lung emphysema and oxidative stress and seems to be a crucial contributor in lung inflammation (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2383888</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2383888</guid>        </item>
        <item>
            <title>Enhanced release of IgE-dependent early phase mediators from nasal polyp tissue</title>
            <link>http://www.medworm.com/index.php?rid=2343278&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F11</link>
            <description>Conclusions:
This human nasal challenge model mimics the allergic early phase reaction. The release of histamine, cys-leukotrienes and PGD2 was significantly higher in nasal polyps versus inferior turbinates, however, this observation could not be explained by differences in mast cell or FcepsilonRI+ cell numbers. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2343278</comments>
            <pubDate>Mon, 20 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2343278</guid>        </item>
        <item>
            <title>Evaluation of anti-IL-6 monoclonal antibody therapy using murine type II collagen-induced arthritis</title>
            <link>http://www.medworm.com/index.php?rid=2333094&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F10</link>
            <description>Interleukin-6 is a multifunctional cytokine that is critical for T/B-cell differentiation and maturation, immunoglobulin secretion, acute-phase protein production, and macrophage/monocyte functions. Extensive research into the biology of IL-6 has implicated IL-6 in the pathophysiology and pathogenesis of RA. An anti-murine IL-6 mAb that neutralizes mouse IL-6 activities was tested in animal model of collagen-induced arthritis. Prophylactic treatment with anti-IL-6 mAb significantly reduced the incidence and severity of arthritis compared to control mAb treated mice. The mitogenic response of B and T cells isolated from the lymph nodes of anti-IL-6 treated mice was significantly reduced compared to cells isolated from control mAb treated mice. The overall histopathology score for paws from ...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2333094</comments>
            <pubDate>Wed, 15 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2333094</guid>        </item>
        <item>
            <title>Inflammatory markers in a 2-year soy intervention among premenopausal women</title>
            <link>http://www.medworm.com/index.php?rid=2307967&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F9</link>
            <description>Conclusions:
During this 2-year intervention, soy foods did not modify serum levels of CRP, IL-6, leptin, and adiponectin in premenopausal women although leptin levels remained stable among women in the intervention group who were obese or of Asian ancestry. Further studies with diverse markers of inflammation are necessary to clarify the specific effect of soy on immune responses. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2307967</comments>
            <pubDate>Tue, 07 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2307967</guid>        </item>
        <item>
            <title>Stimulation with Peptidoglycan Induces Interleukin 6 and TLR2 Expression and a Concomitant Downregulation of Expression of Adiponectin Receptors 1 and 2 in 3T3-L1 Adipocytes</title>
            <link>http://www.medworm.com/index.php?rid=2307968&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F8</link>
            <description>Inflammation is a major component of obesity and diabetes. Toll-like receptors (TLRs) play critical roles in the regulation of inflammation in adipocytes in response to pathogen associated molecular patterns (PAMPs), fatty acids, and extracellular matrix proteins. Although immune cells are primarily responsible for recognition and clearance of pathogens, current evidence indicates that adipocytes are also closely involved in the regulation of innate immunity and inflammation. Whereas it has been demonstrated that adipocytes respond to TLR4 stimulation with lipopolysacccharide, very little is known about their response to the TLR2 agonist, peptidoglycan. We investigated herein adipocyte response to peptidoglycan from Staphylococcus aureus, a gram positive bacteria. Adipocyte stimulation pep...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2307968</comments>
            <pubDate>Mon, 06 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2307968</guid>        </item>
        <item>
            <title>Post heat shock tolerance: a neuroimmunological anti-inflammatory phenomenon</title>
            <link>http://www.medworm.com/index.php?rid=2307969&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F7</link>
            <description>We previously showed that the progression of burn-induced injury was inhibited by exposing the peripheral area of injured skin to sublethal hyperthermia following the burn. We called this phenomenon post-heat shock tolerance. Here we suggest a mechanism for this phenomenon. Exposure of the peripheral primary hyperalgesic/allodynic area of burned skin to local hyperthermia (45°C, 30 seconds), which is a non-painful stimulus for normal skin, results in a painful sensation transmitted by nociceptors. This hyperthermia is too mild to induce any tissue injury, but it does result in pain due to burn-induced hyperalgesia/allodynia. This mild painful stimulus can result in the induction of descending anti-nociceptive mechanisms, especially in the adjacent burned area. Some of these inhibitory mec...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2307969</comments>
            <pubDate>Fri, 27 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2307969</guid>        </item>
        <item>
            <title>Young adult obese subjects with and without insulin resistance: what is the role of chronic inflammation and how to weigh it non-invasively?</title>
            <link>http://www.medworm.com/index.php?rid=2269857&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F6</link>
            <description>Conclusions:
Increases in spleen size and CRP levels represent a reliable tool in diagnosing insulin resistance. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2269857</comments>
            <pubDate>Mon, 16 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2269857</guid>        </item>
        <item>
            <title>Antiinflammatory effects of the gorgonian Pseudopterogorgia elisabethae collected at the islands of Providencia and San Andres (SW Caribbean)</title>
            <link>http://www.medworm.com/index.php?rid=2251770&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F5</link>
            <description>Conclusions:
All results presented contribute to demonstrate that the compounds isolated in this work from P. elisabethae are promising molecules with an interesting anti-inflammatory activity profile. Additionally, the results obtained could provide preliminary insights towards their structure-activity relationship. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2251770</comments>
            <pubDate>Tue, 10 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2251770</guid>        </item>
        <item>
            <title>Polyphenol-rich pomegranate fruit extract (POMx) suppresses PMACI-induced expression of pro-inflammatory cytokines by inhibiting the activation of MAP Kinases and NF-κB in human KU812 cells</title>
            <link>http://www.medworm.com/index.php?rid=2100400&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F1</link>
            <description>Conclusion:
These novel pharmacological actions of POMx provide new suggestion that POMx or POMx-derived compounds may be of therapeutic use for the treatment of inflammatory diseases by suppressing mast cells/basophils activation. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2100400</comments>
            <pubDate>Thu, 08 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2100400</guid>        </item>
        <item>
            <title>Polyphenol-rich pomegranate fruit extract (POMx) suppresses PMACI- induced expression of pro-inflammatory cytokines by inhibiting the activation of MAP Kinases and NF-kappaB in human KU812 cells</title>
            <link>http://www.medworm.com/index.php?rid=2089285&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F1</link>
            <description>Conclusion:
These novel pharmacological actions of POMx provide new suggestion that POMx or POMx-derived compounds may be of therapeutic value for the treatment of inflammatory diseases by suppressing mast cells/basophils activation. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2089285</comments>
            <pubDate>Thu, 08 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2089285</guid>        </item>
        <item>
            <title>Terameprocol, a methylated derivative of nordihydroguaiaretic acid, inhibits production of prostaglandins and several key inflammatory cytokines and chemokines</title>
            <link>http://www.medworm.com/index.php?rid=2089284&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F6%2F1%2F2</link>
            <description>Conclusions:
TMP inhibited the LPS-induced production of lipid mediators and several key inflammatory cytokines and chemokines, both in vitro and in vivo, raising the possibility that TMP might be useful as a treatment for a variety of inflammatory disorders. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2089284</comments>
            <pubDate>Thu, 08 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2089284</guid>        </item>
        <item>
            <title>Possible contribution of endogenous carbon monoxide to the development of allergic rhinitis in guinea pigs</title>
            <link>http://www.medworm.com/index.php?rid=2016042&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F23</link>
            <description>Background:
The mechanisms responsible for the development of allergic rhinitis(AR) are not fully understood. The present study was designed to explore the possible roles of carbon monoxide(CO) on the pathogenesis of AR. Methods: AR guinea pig model was established by nasal ovalbumin sensitization. Twenty-four AR guinea pigs were divided into four groups, 6 in each: Saline control group, AR sensitized group, Hemin treated group, and Zinc protoporphyrin (ZnPP) treated group. The frequency of sneezing and nose rubbing was recorded. Leukocyte infiltration in nasal lavage fluid, serum IgE level and plasma CO were measured. Expression of heme oxygenase-1 (HO-1) mRNA in nasal mucosa was determined by real time RT-PCR, and expression of HO-1 protein was detected by immunohistochemistry. Results: ...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2016042</comments>
            <pubDate>Fri, 05 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2016042</guid>        </item>
        <item>
            <title>Cellular and molecular mechanisms of cigarette smoke-induced lung damage and prevention by vitamin C</title>
            <link>http://www.medworm.com/index.php?rid=1951076&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F21</link>
            <description>Conclusion:
p-Benzosemiquinone appears to be a major causative factor of cigarette smoke-induced oxidative protein damage that leads to apoptosis and lung injury. The pathophysiological events are prevented by a moderately large dose of vitamin C. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1951076</comments>
            <pubDate>Tue, 11 Nov 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1951076</guid>        </item>
        <item>
            <title>Product inhibition of secreted phospholipase A2 may explain lysophosphatidylcholines' unexpected therapeutic properties</title>
            <link>http://www.medworm.com/index.php?rid=1900176&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F17</link>
            <description>Conclusions:
The results may explain the efficacy of lysoPC therapy during periods of elevated inflammatory activity and further highlight the utility uncompetitive enzyme inhibitors. In this case, the inhibitor is a product of the enzyme reaction, and therefore represents an example of activity-driven feedback inhibition. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1900176</comments>
            <pubDate>Wed, 22 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1900176</guid>        </item>
        <item>
            <title>Augmentation of Pulmonary Epithelial Cell IL-8 Expression and Permeability by Pre-B-cell Colony Enhancing Factor</title>
            <link>http://www.medworm.com/index.php?rid=1814777&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F15</link>
            <description>Conclusions:
These results suggest that PBEF may play a vital role in basal and TNFalpha-mediated pulmonary inflammation and pulmonary epithelial barrier dysfunction via its regulation of other inflammatory cytokines such as IL-8, which could in part explain the role of PBEF in the susceptibility and pathogenesis of ALI. These results lend further support to the potential of PBEF to serve as a diagnostic and therapeutic target to ALI. 
Methods:
Human pulmonary alveolar epithelial cells (cell line and primary cells) were transfected with human PBEF cDNA or PBEF siRNA and then cultured in the presence or absence of TNF. PBEF and IL-8 expression were analyzed by RT-PCR and Western blotting. In addition, changes in pulmonary epithelial cell barrier regulation with altered PBEF expression was e...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1814777</comments>
            <pubDate>Mon, 22 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1814777</guid>        </item>
        <item>
            <title>15-deoxy-delta12,14-prostaglandin J2 attenuates endothelial-monocyte interaction: implication for inflammatory diseases</title>
            <link>http://www.medworm.com/index.php?rid=1767995&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F14</link>
            <description>Conclusion:
These findings suggest that 15d-PGJ2 inhibits inflammation at multiple steps and thus is a potential therapeutic target for various inflammatory diseases. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1767995</comments>
            <pubDate>Fri, 08 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1767995</guid>        </item>
        <item>
            <title>A novel hybrid aspirin-NO-releasing compound inhibits TNFalpha release from LPS-activated human monocytes and macrophages</title>
            <link>http://www.medworm.com/index.php?rid=1733123&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F12</link>
            <description>Conclusion:
Here we show that furoxan-aspirin, B8, significantly reduces TNFα release from both monocytes and macrophages and suggest that inhibition of NF-κB activation is a likely mechanism for the effect. This anti-inflammatory action highlights a further therapeutic potential of drugs of this class. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1733123</comments>
            <pubDate>Thu, 31 Jul 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1733123</guid>        </item>
        <item>
            <title>Anti-inflammatory effects of ciprofloxacin in S. aureus Newman induced nasal inflammation in vitro</title>
            <link>http://www.medworm.com/index.php?rid=1663399&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F11</link>
            <description>Conclusion: Ciprofloxacin exerts anti-inflammatory effects in S. aureus Newman driven nasal inflammation. Inhibitory effects were comparable to those of prednisolone and clarithromycin. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1663399</comments>
            <pubDate>Tue, 29 Jul 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1663399</guid>        </item>
        <item>
            <title>Serum tumor necrosis factor-alpha concentrations are negatively correlated with serum 25(OH)D concentrations in healthy women</title>
            <link>http://www.medworm.com/index.php?rid=1651822&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F10</link>
            <description>Background:
Circulating 25 hydroxyvitamin D (25 (OH)D), an accurate measure of vitamin D status, is markedly greater in individuals with increased exposure to ultraviolet B (UVB) light via sunlight or the use of artificial UV light. Aside from the known relationship between vitamin D and bone, vitamin D has also been implicated in immune function and inflammation. Furthermore, a mass of evidence is accumulating that vitamin D deficiency could lead to immune malfunction. Our overall objective was to study the relationship between vitamin D status (as determined by serum 25(OH) D concentrations) and inflammatory markers in healthy women.
Methods:
This observational study included 69 healthy women, age 25-82 years. Women with high UVB exposure and women with minimal UVB exposure were specific...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1651822</comments>
            <pubDate>Thu, 24 Jul 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1651822</guid>        </item>
        <item>
            <title>Bioavailable constituents/metabolites of pomegranate (Punica granatum L) preferentially inhibit COX2 activity ex vivo and IL-1beta-induced PGE2 production in human chondrocytes in vitro</title>
            <link>http://www.medworm.com/index.php?rid=1541565&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F9</link>
            <description>Several recent studies have documented that supplementation with pomegranate fruit extract inhibits inflammatory symptoms in vivo. However, the molecular basis of the observed effects has not been fully revealed. Although previous studies have documented the inhibition of nitric oxide and cyclooxygenase (COX) activity in vitro by plant and fruit extracts added directly into the culture medium but whether concentrations of bioactive compounds sufficient enough to exert such inhibitory effects in vivo can be achieved through oral consumption has not been reported. In the present study we determined the effect of rabbit plasma obtained after ingestion of a polyphenol rich extract of pomegranate fruit (PFE) on COX enzyme activity ex vivo and the IL-1β-induced production of NO and PGE2 in chon...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1541565</comments>
            <pubDate>Fri, 13 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1541565</guid>        </item>
        <item>
            <title>IFN-gamma regulation of ICAM-1 receptors in bronchial epithelial cells: soluble ICAM--1 release inhibits human rhinovirus infection</title>
            <link>http://www.medworm.com/index.php?rid=1493883&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F8</link>
            <description>Conclusions:
These findings support the hypothesis that in epithelial cells conditioned to IFN- and subsequently exposed to HRV-14 infection, differential modulation in the ratio of ICAM-1 receptors prevails in favour of an anti-viral milieu, appearing to limit further target cell viral attachment and propagation. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1493883</comments>
            <pubDate>Thu, 05 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1493883</guid>        </item>
        <item>
            <title>Treatment of experimental colitis in mice 
with LMP-420, an inhibitor of TNF transcription</title>
            <link>http://www.medworm.com/index.php?rid=1290763&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F4</link>
            <description>Conclusions:
These studies demonstrate that short-term treatment with a transcriptional inhibitor of TNF production can decrease systemic and local colonic levels of TNF but may not decrease the histologic severity of colitis. Longer term studies using colitis models that are more dependent on TNF elevation should be performed to more accurately assess the potential of LMP-420 for therapy of inflammatory bowel disease. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1290763</comments>
            <pubDate>Mon, 10 Mar 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1290763</guid>        </item>
        <item>
            <title>Inhibition of oncogene-induced inflammatory chemokines using a farnesyltransferase inhibitor</title>
            <link>http://www.medworm.com/index.php?rid=1261212&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F3</link>
            <description>Conclusions:
These data suggest that FTI may be applied as an effective inhibitor for RET/PTC3-oncogene induced pro-inflammatory mediators. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1261212</comments>
            <pubDate>Wed, 27 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1261212</guid>        </item>
        <item>
            <title>Does CD4+CD25+FoxP3+ cell (Treg) and IL-10 profile determine susceptibility to immune reconstitution inflammatory syndrome (IRIS) in HIV disease?</title>
            <link>http://www.medworm.com/index.php?rid=1239110&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F2</link>
            <description>HIV-specific T-lymphocyte responses that underlie IRIS are incomplete and largely remain hypothetical. Of the several mechanisms presented by the host to control host immunological damage, Treg cells are believed to play a critical role. Using the available experimental evidence, it is proposed that enormous synthesis of conventional FoxP3A Th cells (responsive) often renders subjects inherently vulnerable to IRIS, whereas that of natural FoxP3+ Treg cell synthesis predominate among subjects that may not progress to IRIS. We also propose that IRIS non-developers generate precursor T-cells with a high avidity to generate CD4+CD25+FoxP3+ Tregs whereas IRIS developers generate T-cells of intermediate avidity yielding Th0 cells and effector T-cells to mediate the generation of proinflammatory ...</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1239110</comments>
            <pubDate>Mon, 18 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1239110</guid>        </item>
        <item>
            <title>Topical anti-inflammatory activity of Polygonum cuspidatum extract in the TPA model of mouse ear inflammation</title>
            <link>http://www.medworm.com/index.php?rid=1217556&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F5%2F1%2F1</link>
            <description>Conclusion:
PCE inhibits development of edema and neutrophil infiltration in the TPA-treated mouse ear model of topical inflammation. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1217556</comments>
            <pubDate>Fri, 08 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1217556</guid>        </item>
        <item>
            <title>Detection of inflammatory bowel disease by proton magnetic resonance spectroscopy (1H MRS) using an animal model</title>
            <link>http://www.medworm.com/index.php?rid=1051010&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F4%2F1%2F24</link>
            <description>Conclusion:
1H MRS is a sensitive tool to detect early colonic inflammation in an animal model of IBD. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1051010</comments>
            <pubDate>Mon, 26 Nov 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1051010</guid>        </item>
        <item>
            <title>Sensitivity of mice to lipopolysaccharide is increased by a high saturated fat and cholesterol diet</title>
            <link>http://www.medworm.com/index.php?rid=1020897&amp;cid=s_32553_13_f&amp;fid=32553&amp;url=http%3A%2F%2Fwww.journal-inflammation.com%2Fcontent%2F4%2F1%2F22</link>
            <description>Conclusions:
HCD increased the sensitivity of mice to LPS without affecting its plasma level. Although increased serum amyloid A and CD14 in the circulation may inhibit LPS actions, their overexpression, along with hepatic toll-like receptor-4 or other factors, may contribute to the heightened sensitivity to LPS. (Source: Journal of Inflammation)</description>
            <author>Journal of Inflammation</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1020897</comments>
            <pubDate>Mon, 12 Nov 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1020897</guid>        </item>
    </channel>
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