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        <title>International Journal of Molecular Medicine 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 'International Journal of Molecular Medicine' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=International+Journal+of+Molecular+Medicine&t=International+Journal+of+Molecular+Medicine&s=Search&f=source]]></link>
        <lastBuildDate>Thu, 09 Feb 2012 16:56:42 +0100</lastBuildDate>
        <item>
            <title>Cloning of the surface layer gene sllB from Bacillus sphaericus ATCC             14577 and its heterologous expression and purification.</title>
            <link>http://www.medworm.com/index.php?rid=5637785&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266829%26dopt%3DAbstract</link>
            <description>Cloning of the surface layer gene sllB from Bacillus sphaericus ATCC       14577 and its heterologous expression and purification.
    Int J Mol Med. 2012 Jan 19;
    Authors: Cui YB, Zhou Y, Liu WN, Chen QW, Ma GF, Shi WH, Wang YG, Yang L
    Abstract
    A cDNA fragment encoding the S-layer protein SllB cloned from Bacillus sphaericus       ATCC 14577 was expressed on the surface of E. coli BL21 (DE3) cells and confirmed       by the square lattice structure at the nanoscale level. The amplified gene fragment       designed with PCR primers from a specified reference sequence (GenBank accession       no. AJ849550) showed a high degree of sequence identity with the known sequences       for S-layer protein. The best alignment scores were seen in B. sphaericus strains       JG-A12 and N...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5637785</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>The regulatory role of microRNA-1187 in TNF-α-mediated hepatocyte apoptosis             in acute liver failure.</title>
            <link>http://www.medworm.com/index.php?rid=5637787&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266786%26dopt%3DAbstract</link>
            <description>The regulatory role of microRNA-1187 in TNF-α-mediated hepatocyte apoptosis       in acute liver failure.
    Int J Mol Med. 2012 Jan 17;
    Authors: Yu DS, An FM, Gong BD, Xiang XG, Lin LY, Wang H, Xie Q
    Abstract
    In the current study, we aimed at elucidating the regulatory mechanisms       through which microR-1187 (miR-1187) participates in hepatocyte apoptosis in acute       liver failure (ALF). An ALF model was induced with D-galactosamine (D-GalN) plus       lipopolysaccharide (LPS) in BALB/c mice. The hepatic miRNA expression profile       was detected by microarray analysis and verified by quantitative real-time PCR       (qRT-PCR). The possible underlying mechanism was investigated in vitro using an       embryonic murine hepatocyte cell line (BNLCL2) and miR-1187 mimic....</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5637787</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5637787</guid>        </item>
        <item>
            <title>Epstein-Barr virus oncoprotein LMP1 mediates survivin upregulation by             p53 contributing to G1/S cell cycle progression in nasopharyngeal carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=5637786&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266808%26dopt%3DAbstract</link>
            <description>In this study, we found       that LMP1 simultaneously induced upregulation of both p53 and survivin at the       protein level, as well as their phosphorylation. Knockdown of p53 by siRNA revealed       that LMP1 increased survivin expression by p53 directly. Furthermore, we found       that LMP1 upregulated survivin by p53 at the transcriptional level by increasing       p53-mediated survivin promoter activity and DNA binding activity. Moreover, LMP1       induced the co-localization of p53 and survivin in the nucleus, conferring to       their related functions in NPC tumorigenesis. We further found that p53 promoted       G1/S cell cycle progression, but did not induce apoptosis in LMP1-positive NPC       cells. Collectively, these findings suggest that p53 acting as a transcription   ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5637786</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5637786</guid>        </item>
        <item>
            <title>Niacin protects against UVB radiation-induced apoptosis in cultured             human skin keratinocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5597417&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246168%26dopt%3DAbstract</link>
            <description>In this study, we investigated       the molecular mechanism of the photoprotective effect of niacin in ultraviolet       (UV)-irradiated human skin keratinocytes (HaCaT cells). We found that niacin effectively       suppressed the UV-induced cell death and cell apoptosis of HaCaT cells. Existing       data have shown that AKT activation is involved in the cell survival process.       Yet, the potential mechanism of niacin in protection against UV-induced skin damage       has thus far not fully been eluvidated. We observed that niacin pretreatment enhances       UV induced activation of AKT (Ser473 phosphorylation) as well as that of the downstream       signal mTOR (S6 and 4E-BP1 phosphorylation). The PI3K/AKT inhibitor, LY294002,       and the mTOR inhibitor, rapamycin, largely neutrali...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5597417</comments>
            <pubDate>Thu, 12 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5597417</guid>        </item>
        <item>
            <title>Soybean glyceollins mitigate inducible nitric oxide synthase and cyclooxygenase-2             expression levels via suppression of the NF-κB signaling pathway in RAW 264.7             cells.</title>
            <link>http://www.medworm.com/index.php?rid=5597416&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246209%26dopt%3DAbstract</link>
            <description>Soybean glyceollins mitigate inducible nitric oxide synthase and cyclooxygenase-2       expression levels via suppression of the NF-κB signaling pathway in RAW 264.7       cells.
    Int J Mol Med. 2012 Jan 12;
    Authors: Yoon EK, Kim HK, Cui S, Kim YH, Lee SH
    Abstract
    Glyceollins, produced to induce disease resistance responses against specific       species, such as an incompatible pathogen Phytophthora sojae in soybeans, have       the potential to exhibit anti-inflammatory activity in RAW 264.7 cells. To investigate       the anti-inflammatory effects of elicited glyceollins via a signaling pathway,       we studied the glyceollin signaling pathway using several assays including RNA       and protein expression levels. We found that soybean glyceollins significantly       r...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5597416</comments>
            <pubDate>Thu, 12 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5597416</guid>        </item>
        <item>
            <title>Antiproliferative effect of alpinetin in BxPC-3 pancreatic cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5597419&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246103%26dopt%3DAbstract</link>
            <description>Authors: Du J, Tang B, Wang J, Sui H, Jin X, Wang L, Wang Z
    Abstract
    Alpinetin is a novel plant flavonoid derived from Alpinia katsumadai Hayata,       found to possess strong anticancer effects. However, the antitumor effect of alpinetin       on pancreatic cancer cells and the detailed mechanism remain unclear. The aim       of this study was to investigate alpinetin's beneficial effect on pancreatic cancer       and the possible molecular mechanism involved. Pancreatic cancer cell lines were       treated with alpinetin at various doses and for different times, and the effect       of alpinetin on cell growth inhibition, apoptosis and the cell cycle was determined.       The expression of Bcl-2, Bcl-xL, XIAP and Bax, the activity of caspases and the       levels of cytochrome c...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5597419</comments>
            <pubDate>Wed, 11 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5597419</guid>        </item>
        <item>
            <title>Resveratrol, a polyphenol phytoalexin, protects cardiomyocytes against             anoxia/reoxygenation injury via the TLR4/NF-κB signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5597418&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246136%26dopt%3DAbstract</link>
            <description>In this study, primary       cultures of neonatal rat cardiomyocytes were randomly distributed into three groups:       control group, A/R group (cultured cardiomyocytes were subjected to 3 h anoxia       followed by 2 h reoxygenation), and the resveratrol group (cardiomyocytes were       subjected to 3 h anoxia/2 h reoxygenation, and 5, 10 or 20 µM resveratrol was       applied 5 min after reoxygenation). In order to evaluate cardiomyocyte damage,       cell viability, lactate dehydrogenase (LDH) release, caspase-3 activity, and apoptosis       were analyzed by the cell counting kit (CCK)-8 assay, colorimetric method and       flow cytometry, respectively. The mRNA and protein expression of Toll-like receptor 4       (TLR4) were detected by quantitative real-time PCR and western b...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5597418</comments>
            <pubDate>Wed, 11 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5597418</guid>        </item>
        <item>
            <title>Altered miRNA expression patterns in Tff2 knock-out mice correlate with             cellular pathways of neoplastic development and caloric metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=5597422&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22245972%26dopt%3DAbstract</link>
            <description>Altered miRNA expression patterns in Tff2 knock-out mice correlate with       cellular pathways of neoplastic development and caloric metabolism.
    Int J Mol Med. 2012 Jan 10;
    Authors: Shah AA, Leidinger P, Keller A, Wendschlag A, Meese E, Blin N
    Abstract
    The trefoil peptide family, consisting in mammals of three members namely       TFF1, 2 and 3, plays a cytoprotective role in epithelial cells of various tissues,       mainly in the digestive tract. Tff1, Tff2 or Tff3 knock-out mouse models developed       various kinds of gastrointestinal impairment. microRNAs are known to be novel       gene regulators. We aimed to investigate the physiological role of such miRNAs       in Tff2 knock-out mice. Whole miRNome profiling and in silico analysis were performed       for Tff2-K...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5597422</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5597422</guid>        </item>
        <item>
            <title>Novel RS1 mutations associated with X-linked juvenile retinoschisis.</title>
            <link>http://www.medworm.com/index.php?rid=5597421&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22245991%26dopt%3DAbstract</link>
            <description>Authors: Yi J, Li S, Jia X, Xiao X, Wang P, Guo X, Zhang Q
    Abstract
    To identify mutations in the retinoschisin (RS1) gene in families with X-linked       retinoschisis (XLRS). Twenty families with XLRS were enrolled in this study. All       six coding exons and adjacent intronic regions of RS1 were amplified by polymerase       chain reaction (PCR). The nucleotide sequences of the amplicons were determined       by Sanger sequencing. Ten hemizygous mutations in RS1 were detected in patients       from 14 of the 20 families. Four of the ten mutations were novel, including c:176G&amp;gt;A       (p:Cys59Tyr) in exon 3, c:531T&amp;gt;G (p:Tyr177X), c:607C&amp;gt;G (p:Pro203Ala) and       c:668G&amp;gt;A (p:Cys223Tyr) in exon 6. These four novel mutations were not present       in 176 normal individu...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5597421</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5597421</guid>        </item>
        <item>
            <title>IL-33 regulates TNF-α dependent effects in synovial fibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5597420&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246057%26dopt%3DAbstract</link>
            <description>This study identifies IL-33 as a critical regulator/enhancer       of TNF-α-induced functions in RA-SFs, pointing to a central role of this cytokine       in the perpetuation of pro-inflammatory and pro-destructive processes in rheumatoid       arthritis (RA) and other inflammatory and degenerative diseases.
    PMID: 22246057 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5597420</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5597420</guid>        </item>
        <item>
            <title>Protocadherin-10 is involved in angiogenesis and methylation correlated             with multiple myeloma.</title>
            <link>http://www.medworm.com/index.php?rid=5597423&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22245948%26dopt%3DAbstract</link>
            <description>Protocadherin-10 is involved in angiogenesis and methylation correlated       with multiple myeloma.
    Int J Mol Med. 2012 Jan 9;
    Authors: Li Y, Yang ZS, Song JJ, Liu Q, Chen JB
    Abstract
    Protocadherin-10 (PCDH10) which is located at 4q28.3, is a member of the       cadherin superfamily of cell adhesion molecules. PCDH10 is broadly expressed in       normal adult, but nearly undetectable in multiple myeloma (ΜΜ) tissues and cell       lines. Its promoter methylation was detected in virtually all the silenced or       downregulated cell lines. The silencing of PCDH10 could be reversed by pharmacological       demethylation, indicating a methylation-mediated mechanism. In the current study,       we investigated 44 patients (23 females, 21 males), 77.27% (34/44) of whom presen...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5597423</comments>
            <pubDate>Mon, 09 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5597423</guid>        </item>
        <item>
            <title>Analysis of the coding sequence and expression of the coiled-coil α-helical             rod protein 1 gene in normal and neoplastic epithelial cervical cells.</title>
            <link>http://www.medworm.com/index.php?rid=5577578&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22218424%26dopt%3DAbstract</link>
            <description>Analysis of the coding sequence and expression of the coiled-coil α-helical       rod protein 1 gene in normal and neoplastic epithelial cervical cells.
    Int J Mol Med. 2012 Jan 3;
    Authors: Pacholska-Bogalska J, Myga-Nowak M, Ciepłuch K, Józefiak A, Kwaśniewska A, Goździcka-Józefiak A
    Abstract
    The role of the CCHCR1 (coiled-coil α-helical rod protein 1) protein in       the cell is poorly understood. It is thought to be engaged in processes such as       proliferation and differentiation of epithelial cells, tissue-specific gene transcription       and steroidogenesis. It is supposed to participate in keratinocyte transformation.       It has also been found that this protein interacts with the E2 protein of human       papilloma virus type 16 (HPV16). The oncogenic ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577578</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577578</guid>        </item>
        <item>
            <title>NOD1 and NOD2 stimulation triggers innate immune responses of human             periodontal ligament cells.</title>
            <link>http://www.medworm.com/index.php?rid=5577577&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22218461%26dopt%3DAbstract</link>
            <description>NOD1 and NOD2 stimulation triggers innate immune responses of human       periodontal ligament cells.
    Int J Mol Med. 2012 Jan 3;
    Authors: Jeon DI, Park SR, Ahn MY, Ahn SG, Park JH, Yoon JH
    Abstract
    Nod-like receptors (NLRs) are cytosolic sensors for microbial molecules.       Νucleotide-binding oligomerization domain (NOD)1 and NOD2 recognize the peptidoglycan       derivatives, meso-diaminopimelic acid (meso-DAP) and muramyl dipeptide (MDP),       respectively, and trigger host innate immune responses. In the present study,       we examined the function of NOD1 and NOD2 on innate immune responses in human       periodontal ligament (PDL) cells. The gene expression of NOD1 and NOD2 was examined       by RT-PCR. IL-6 and IL-8 production in culture supernatants was measured...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577577</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577577</guid>        </item>
        <item>
            <title>Hepatitis B virus X protein inhibits extracellular IFN-α-mediated signal             transduction by downregulation of type I IFN receptor.</title>
            <link>http://www.medworm.com/index.php?rid=5577576&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22218495%26dopt%3DAbstract</link>
            <description>Hepatitis B virus X protein inhibits extracellular IFN-α-mediated signal       transduction by downregulation of type I IFN receptor.
    Int J Mol Med. 2012 Jan 3;
    Authors: Cho IR, Oh M, Koh SS, Malilas W, Srisuttee R, Jhun BH, Pallegrini S, Fuchs SY, Chung YH
    Abstract
    We have previously shown that hepatitis B virus (HBV) protein X (HBX), a       regulatory protein of HBV, activates Stat1, leading to type I interferon (IFN)       production. Type I IFN secreted from HBX-expressing hepatic cells enforces antiviral       signals through its binding to the cognate type I IFN receptor. We therefore investigated       how cells handle this detrimental situation. Interestingly, compared to Chang       cells stably expressing an empty vector (Chang-Vec), Chang cells stably expr...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577576</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577576</guid>        </item>
        <item>
            <title>Sensitizing human multiple myeloma cells to the proteasome inhibitor             bortezomib by novel curcumin analogs.</title>
            <link>http://www.medworm.com/index.php?rid=5378814&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22012631%26dopt%3DAbstract</link>
            <description>Sensitizing human multiple myeloma cells to the proteasome inhibitor       bortezomib by novel curcumin analogs.
    Int J Mol Med. 2012 Jan;29(1):102-6
    Authors: Mujtaba T, Kanwar J, Wan SB, Chan TH, Dou QP
    Abstract
    The proteasome plays a vital role in the degradation of proteins involved       in several pathways including the cell cycle, cellular proliferation and apoptosis       and is a validated target in cancer treatment. Bortezomib (Velcade®, PS-341) is       the first US FDA approved proteasome inhibitor anticancer drug used in the treatment       of refractory multiple myeloma. In spite of its improved efficacy compared to       alternative therapies, about 60% of patients do not respond to bortezomib due       to the emergence of resistance. We hypothesized that nove...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378814</comments>
            <pubDate>Sun, 06 Nov 2011 00:00:11 +0100</pubDate>
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        <item>
            <title>KIF21A novel deletion and recurrent mutation in patients with congenital             fibrosis of the extraocular muscles-1.</title>
            <link>http://www.medworm.com/index.php?rid=5275620&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805025%26dopt%3DAbstract</link>
            <description>This study adds to the current       state of knowledge about KIF21A mutations and CFEOM1, which may improve future       clinical practice.
    PMID: 21805025 [PubMed - in process] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275620</comments>
            <pubDate>Mon, 03 Oct 2011 12:33:13 +0100</pubDate>
            <guid isPermaLink="false">5275620</guid>        </item>
        <item>
            <title>Thermosensitization and induction of apoptosis or cell-cycle arrest             via the MAPK cascade by parthenolide, an NF-κB inhibitor, in human prostate cancer             androgen-independent cell lines.</title>
            <link>http://www.medworm.com/index.php?rid=5275619&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805026%26dopt%3DAbstract</link>
            <description>Thermosensitization and induction of apoptosis or cell-cycle arrest       via the MAPK cascade by parthenolide, an NF-κB inhibitor, in human prostate cancer       androgen-independent cell lines.
    Int J Mol Med. 2011 Dec;28(6):1033-42
    Authors: Hayashi S, Koshiba K, Hatashita M, Sato T, Jujo Y, Suzuki R, Tanaka Y, Shioura H
    Abstract
    Parthenolide (PTL), a nuclear factor-κB (NF-κB) inhibitor, has a significant       thermo-enhancement effect. Modification of thermosensitivity by treatment with       PTL prior to hyperthermia was investigated in the human prostate cancer androgen-independent       cell lines PC3 and DU145. In addition, we analyzed the mechanisms related to induction       of apoptosis or G2/M cell-cycle arrest via the effects of ERK1/2, p38 and SAPK/JNK      ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275619</comments>
            <pubDate>Mon, 03 Oct 2011 12:33:03 +0100</pubDate>
            <guid isPermaLink="false">5275619</guid>        </item>
        <item>
            <title>Pen-2 overexpression induces Aβ-42 production, memory defect, motor             activity enhancement and feeding behavior dysfunction in NSE/Pen-2 transgenic             mice.</title>
            <link>http://www.medworm.com/index.php?rid=5275617&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822534%26dopt%3DAbstract</link>
            <description>This study aimed to determine whether Pen-2 overexpression       could regulate the AD-like phenotypes in Tg mice. NSE/hPen-2 Tg mice were produced       by the microinjection of the NSE/hPen-2 gene into the pronucleus of fertilized       eggs. The expression of the hPen-2 gene under the control of the NSE promoter       was successfully detected only in the brain and kidney tissue of NSE/hPen-2 Tg       mice. Also, 12-month-old NSE/hPen-2 Tg mice displayed behavioral dysfunction in       the water maze test, motor activity and feeding behavior dysfunction in food intake/water       intake/motor activity monitoring system. In addition, tissue samples displayed       dense staining with antibody to the Aβ-42 peptide. Furthermore, NSE/hPen-2 Tg       mice exhibiting feeding behavior dysfunc...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275617</comments>
            <pubDate>Mon, 03 Oct 2011 12:32:53 +0100</pubDate>
            <guid isPermaLink="false">5275617</guid>        </item>
        <item>
            <title>Benzyl isothiocyanate sensitizes human pancreatic cancer cells to radiation             by inducing apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5275616&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21833466%26dopt%3DAbstract</link>
            <description>Benzyl isothiocyanate sensitizes human pancreatic cancer cells to radiation       by inducing apoptosis.
    Int J Mol Med. 2011 Dec;28(6):1043-1047
    Authors: Ohara M, Kimura S, Tanaka A, Ohnishi K, Okayasu R, Kubota N
    Abstract
    Isothiocyanates are a class of naturally occurring chemopreventive agents       known to suppress proliferation of cancer cells in culture. The present study       was undertaken in order to examine the effects of benzyl isothiocyanate (BITC),       one of the common dietary isothiocyanates, on the radiosensitivity of human pancreatic       cancer cells and to gain insights into the underlying molecular mechanism of BITC-induced       radiosensitization. Two human pancreatic cancer cell lines, PANC-1 and MIAPaCa-2,       were treated with BITC and irradia...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275616</comments>
            <pubDate>Mon, 03 Oct 2011 12:32:43 +0100</pubDate>
            <guid isPermaLink="false">5275616</guid>        </item>
        <item>
            <title>Inhibitory effects of vitamin K3 derivatives on DNA polymerase and inflammatory             activity.</title>
            <link>http://www.medworm.com/index.php?rid=5275615&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21837358%26dopt%3DAbstract</link>
            <description>In conclusion, this study has identified       several vitamin K3 derivatives, such as compound 1, that are promising anti-inflammatory       candidates.
    PMID: 21837358 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275615</comments>
            <pubDate>Mon, 03 Oct 2011 12:32:32 +0100</pubDate>
            <guid isPermaLink="false">5275615</guid>        </item>
        <item>
            <title>ECM-based triple layered scaffolds for vascular tissue engineering.</title>
            <link>http://www.medworm.com/index.php?rid=5275614&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21837361%26dopt%3DAbstract</link>
            <description>Authors: Grandi C, Martorina F, Lora S, Dalzoppo D, Amistà P, Sartore L, Di Liddo R, Conconi MT, Parnigotto PP
    Abstract
    The present study focused on the development of three layered small-diameter       (&amp;lt;6 mm) extracellular matrix (ECM)-based vessels. These were engineered artificially       through the freeze-drying technique. A layer of decellularized bovine aorta (DAM)       was deposited on a mandrel and, after lyophilization, it was dipped into a poly-L-lactide       acid (PLLA)/polyethylene glycol (PEG) 2000 dichloromethane solution then quickly       wrapped with a pre-prepared thin DAM sheet. Mechanical properties of three-layered       scaffolds were evaluated by means of uniaxial tensile measurement. Furthermore,       human endothelial and smooth muscle cells were ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275614</comments>
            <pubDate>Mon, 03 Oct 2011 12:32:21 +0100</pubDate>
            <guid isPermaLink="false">5275614</guid>        </item>
        <item>
            <title>Impact of static magnetic fields on human myoblast cell cultures.</title>
            <link>http://www.medworm.com/index.php?rid=5275613&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21837362%26dopt%3DAbstract</link>
            <description>The objective of this study was to determine the influence of static magnetic       fields (SMF) on human satellite cell cultures as one of the preferred stem cell       sources in skeletal muscle tissue engineering. Experiments were performed using       human satellite cells with and without SMF stimulation after incubation with a       culture medium containing low [differentiation medium (DM)] or high [growth medium       (GM)] concentrations of growth factors. Proliferation analysis using the alamarBlue®       assay revealed no significant influence of SMF on cell division. Real-time RT-PCR       of the following marker genes was investigated: myogenic factor 5 (MYF5), myogenic       differentiation antigen 1 (MYOD1), myogenin (MYOG), skeletal muscle α1 actin (ACTA1),       and emb...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275613</comments>
            <pubDate>Mon, 03 Oct 2011 12:32:11 +0100</pubDate>
            <guid isPermaLink="false">5275613</guid>        </item>
        <item>
            <title>The potential role of human osteoblasts for periprosthetic osteolysis             following exposure to wear particles.</title>
            <link>http://www.medworm.com/index.php?rid=5275612&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21850366%26dopt%3DAbstract</link>
            <description>The potential role of human osteoblasts for periprosthetic osteolysis       following exposure to wear particles.
    Int J Mol Med. 2011 Dec;28(6):1055-1063
    Authors: Lochner K, Fritsche A, Jonitz A, Hansmann D, Mueller P, Mueller-Hilke B, Bader R
    Abstract
    Aseptic loosening in total hip replacement is mainly caused by wear particles       inducing inflammation and osteolysis. Wear can be a consequence of micromotions       at the interface between implant and bone cement. Due to complex cellular interactions,       different mediators (e.g. cytokines, proteinases) are released, which can promote       osteolytic processes in the periprosthetic tissue followed by loosening of the       implant. Furthermore, a reduced matrix synthesis and an induced apoptosis rate       can be ob...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275612</comments>
            <pubDate>Mon, 03 Oct 2011 12:32:00 +0100</pubDate>
            <guid isPermaLink="false">5275612</guid>        </item>
        <item>
            <title>Multidrug resistance-associated protein 3 and Bcl-2 contribute to multidrug             resistance by vinorelbine in lung adenocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=5275611&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21874222%26dopt%3DAbstract</link>
            <description>In conclusion, in the present study, we identified a set of genes responsible       for multidrug resistance in Anip973/NVB cells. Among them, MRP3 and Bcl-2 may       participate in lung adenocarcinoma multidrug resistance induced by NVB.
    PMID: 21874222 [PubMed - in process] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275611</comments>
            <pubDate>Mon, 03 Oct 2011 12:31:49 +0100</pubDate>
            <guid isPermaLink="false">5275611</guid>        </item>
        <item>
            <title>Zanthoxylum avicennae extracts induce cell apoptosis through protein             phosphatase 2A activation in HA22T human hepatocellular carcinoma cells and block             tumor growth in xenografted nude mice.</title>
            <link>http://www.medworm.com/index.php?rid=5275610&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21874223%26dopt%3DAbstract</link>
            <description>In this study,       we investigated the effect of YBB extracts (YBBEs) on HA22T human hepatocellular       carcinoma cells in vitro and in an in vivo mouse xenograft model. HA22T cells       were treated with different concentrations of YBBEs and analyzed with Western       blot analysis, TUNEL, JC-1 staining and siRNA transfection assays. Additionally,       the HA22T-implanted xenograft nude mice model was applied to confirm the cellular       effects. YBBEs-induced apoptosis, up-regulated death receptor apoptotic pathway       markers as well as mitochondrial proteins, and suppressed the survival proteins       in a dose-dependent manner. Pro-survival Bcl-2 family proteins were inhibited       and the pro-apoptotic ones were increased. Protein phosphatase 2A (PP2A) siRNA       or oka...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275610</comments>
            <pubDate>Mon, 03 Oct 2011 12:31:38 +0100</pubDate>
            <guid isPermaLink="false">5275610</guid>        </item>
        <item>
            <title>Novel GATA4 mutations in lone atrial fibrillation.</title>
            <link>http://www.medworm.com/index.php?rid=5275609&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21874226%26dopt%3DAbstract</link>
            <description>In this study, the entire coding sequence and splice junctions       of GATA4, which encodes a zinc-finger transcription factor essential for cardiogenesis,       were sequenced in 160 unrelated patients with lone AF. A total of 200 unrelated       ethnically matched healthy individuals were used as controls. The available relatives       of the patient carrying an identified mutation were genotyped. The functional       characteristics of the mutant GATA4 were analyzed using a luciferase reporter       assay system. As a result, two novel heterozygous GATA4 mutations of p.G16C and       p.H28D, were identified in 2 unrelated families with AF, respectively, which co-segregated       with AF in each family with complete penetrance. Functional analysis demonstrated       that the mutations o...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275609</comments>
            <pubDate>Mon, 03 Oct 2011 12:31:28 +0100</pubDate>
            <guid isPermaLink="false">5275609</guid>        </item>
        <item>
            <title>The potential of mouse skin-derived precursors to differentiate into             mesenchymal and neural lineages and their application to osteogenic induction             in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5275608&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21879252%26dopt%3DAbstract</link>
            <description>The potential of mouse skin-derived precursors to differentiate into       mesenchymal and neural lineages and their application to osteogenic induction       in vivo.
    Int J Mol Med. 2011 Dec;28(6):1001-1011
    Authors: Kang HK, Min SK, Jung SY, Jung K, Jang DH, Kim OB, Chun GS, Lee ZH, Min BM
    Abstract
    Although previous studies indicate that skin-derived precursors (SKPs) are       multipotent dermal precursors that share similarities with neural crest stem cells       (NCSCs), a shared ability for multilineage differentiation toward neural crest       lineages between SKPs and NCSCs has not been fully demonstrated. Here, we report       the derivation of SKPs from adult mouse skin and their directed multilineage differentiation       toward neural crest lineages. Under contro...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275608</comments>
            <pubDate>Mon, 03 Oct 2011 12:31:17 +0100</pubDate>
            <guid isPermaLink="false">5275608</guid>        </item>
        <item>
            <title>Honokiol stimulates osteoblastogenesis by suppressing NF-κB activation.</title>
            <link>http://www.medworm.com/index.php?rid=5275607&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21887456%26dopt%3DAbstract</link>
            <description>In this study, we show that honokiol is a potent       inducer of in vitro osteoblast differentiation by virtue of its capacity to suppress       basal and tumor necrosis factor alpha (TNFα)-induced NF-κB activation and to alleviate       the suppressive action of TNFα on bone morphogenetic protein (BMP)-2-induced Smad       activation. Our data confirm that honokiol may have considerable promise as a       dual anabolic/anti-catabolic agent for the amelioration of multiple osteoporotic       diseases.
    PMID: 21887456 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275607</comments>
            <pubDate>Mon, 03 Oct 2011 12:31:07 +0100</pubDate>
            <guid isPermaLink="false">5275607</guid>        </item>
        <item>
            <title>Suppression of proliferation and oxidative stress by extracts of Ganoderma             lucidum in the ovarian cancer cell line OVCAR-3.</title>
            <link>http://www.medworm.com/index.php?rid=5275606&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21887458%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether Ganoderma lucidum elicits       its anti-tumor effects by suppressing cell growth and inducing antioxidative/detoxification       activity in human ovarian OVCAR-3 cells. The results showed that Ganoderma lucidum       inhibits cell growth and disruption of cell cycle progression via down regulation       of cyclin D1. Chemopreventive activities elicited by Ganoderma lucidum were demonstrated       by the induction of antioxidant SOD and catalase as well as the phase II detoxification       enzyme NAD(P)H:quinone oxidoreductase 1 (NQO1) and glutathione S-transferase P1       (GSTP1) via the Nrf2 mediated signaling pathway known to provide chemoprotection       against carcinogenicity. These findings indicate that Ganoderma lucidum possesses       c...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275606</comments>
            <pubDate>Mon, 03 Oct 2011 12:30:56 +0100</pubDate>
            <guid isPermaLink="false">5275606</guid>        </item>
        <item>
            <title>HDAC inhibitor 4-phenylbutyrate preserves immature phenotype of human             embryonic midbrain stem cells: Implications for the involvement of DNA methyltransferase.</title>
            <link>http://www.medworm.com/index.php?rid=5275605&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21894430%26dopt%3DAbstract</link>
            <description>HDAC inhibitor 4-phenylbutyrate preserves immature phenotype of human       embryonic midbrain stem cells: Implications for the involvement of DNA methyltransferase.
    Int J Mol Med. 2011 Dec;28(6):977-983
    Authors: Khan Z, Akhtar M, Ekström TJ
    Abstract
    Cell replacement and gene therapy using neural stem cells (NSCs) have been       widely touted as a promising treatment for CNS diseases including brain tumors.       Histone deacetylase (HDAC) inhibitors have been used to explore mechanisms behind       the lineage-specific differentiation of NSCs and as modulators of gene therapy.       We have used the human embryonic midbrain stem cell line NGC-407 and the HDAC       inhibitor 4-phenylbutyrate (4-PB) to investigate the differentiation from epigenetic       perspectives. NG...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275605</comments>
            <pubDate>Mon, 03 Oct 2011 12:30:45 +0100</pubDate>
            <guid isPermaLink="false">5275605</guid>        </item>
        <item>
            <title>Mitigation of 2,4-dinitrofluorobenzene-induced atopic dermatitis-related             symptoms by Terminalia chebula Retzius.</title>
            <link>http://www.medworm.com/index.php?rid=5275604&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21901245%26dopt%3DAbstract</link>
            <description>Mitigation of 2,4-dinitrofluorobenzene-induced atopic dermatitis-related       symptoms by Terminalia chebula Retzius.
    Int J Mol Med. 2011 Dec;28(6):1013-1018
    Authors: Nam DY, Lee JM, Heo JC, Lee SH
    Abstract
    To evaluate whether an aqueous seed extract of Terminalia chebula Retzius       inhibited development of atopy in vivo, we used a 2,4-dinitrofluorobenzene (DNFB)-induced       animal model of atopic symptoms to investigate the effects of the extract. We       measured CD4+ cell numbers by hematoxylin and eosin (H&amp;E) staining, and determined       the expression levels of matrix metalloproteinase (MMP)-9, interleukin (IL)-31,       and T-bet genes, in this animal model. The data showed that a Terminalia chebula       extract (100 µg/ml) exhibited strong anti-atopi...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275604</comments>
            <pubDate>Mon, 03 Oct 2011 12:30:35 +0100</pubDate>
            <guid isPermaLink="false">5275604</guid>        </item>
        <item>
            <title>Expression of interleukin-24 and its receptor in human pancreatic myofibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5275603&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21922126%26dopt%3DAbstract</link>
            <description>Authors: Imaeda H, Nishida A, Inatomi O, Fujiyama Y, Andoh A
    Abstract
    Interleukin (IL)-24 is a member of the IL-10 family of cytokines. In this       study, we investigated IL-24 expression in chronic pancreatitis tissue and characterized       the molecular mechanisms responsible for IL-24 expression in human pancreatic       myofibroblasts. IL-24 expression in the tissues was evaluated by immunohistochemical       methods. IL-24 mRNA and protein expression in the pancreatic myofibroblasts was       determined by real-time-PCR and ELISA, respectively. IL-24 was expressed by α-smooth       muscle actin-positive myofibroblasts in the chronic pancreatitis tissues. In isolated       human pancreatic myofibroblasts, IL-1β significantly enhanced IL-24 mRNA and protein       expression...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275603</comments>
            <pubDate>Mon, 03 Oct 2011 12:30:24 +0100</pubDate>
            <guid isPermaLink="false">5275603</guid>        </item>
        <item>
            <title>Beyond neurological disease: New targets for edaravone (Review).</title>
            <link>http://www.medworm.com/index.php?rid=5275602&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21922128%26dopt%3DAbstract</link>
            <description>Authors: Kikuchi K, Uchikado H, Miyagi N, Morimoto Y, Ito T, Tancharoen S, Miura N, Miyata K, Sakamoto R, Kikuchi C, Iida N, Shiomi N, Kuramoto T, Kawahara KI
    Abstract
    Free radicals play major roles in the pathogenesis of tissue damage in many       diseases and clinical conditions, and the removal of free radicals may offer a       treatment option. Several modulators of free radical scavenger pathways have been       developed and some have progressed to clinical trials. One such agent, edaravone,       was approved in 2001 in Japan for the treatment of cerebral infarction. It has       since been shown that edaravone can diffuse into many organs and, in addition       to its effects on hydroxyl radical removal, edaravone modulates inflammatory processes,       matrix metalloprot...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5275602</comments>
            <pubDate>Mon, 03 Oct 2011 12:30:13 +0100</pubDate>
            <guid isPermaLink="false">5275602</guid>        </item>
        <item>
            <title>Inhibition of experimental auto-immune uveitis by the A3 adenosine receptor agonist CF101.</title>
            <link>http://www.medworm.com/index.php?rid=5192367&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21887476%26dopt%3DAbstract</link>
            <description>In this study the effect of CF101 on the development of retinal antigen interphotoreceptor retinoid-binding protein (IRBP)-induced experimental autoimmune uveitis (EAU) was assessed. Oral treatment with CF101 (10 µg/kg, twice daily), initiated upon disease onset, improved uveitis clinical score measured by fundoscopy and ameliorated the pathological manifestations of the disease. Shortly after treatment with CF101 A3AR expression levels were down-regulated in the lymph node and spleen cells pointing towards receptor activation. Downstream events included a decrease in PI3K and STAT-1 and proliferation inhibition of IRPB auto-reactive T cells ex vivo. Inhibition of interleukin-2, tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) production and up-regulation of interleukin-10 w...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192367</comments>
            <pubDate>Sun, 04 Sep 2011 08:44:11 +0100</pubDate>
            <guid isPermaLink="false">5192367</guid>        </item>
        <item>
            <title>Suppression of Th17 response by Streptococcus thermophilus ST28 through induction of IFN-γ.</title>
            <link>http://www.medworm.com/index.php?rid=5192366&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21887477%26dopt%3DAbstract</link>
            <description>In this study, we examined the mechanism for the suppressive effects of S. thermophilus ST28 on the Th17 response in murine splenocytes stimulated with transforming growth factor (TGF)-β plus IL-6. Stimulation with TGF-β plus IL-6 increased mRNA expression of IL-17 and its production in the splenocytes, but ST28 markedly suppressed both. Meanwhile, ST28 increased the mRNA expression of interferon (IFN)-γ as well as its production. Anti-IFN-γ completely cancelled the suppressive effect of ST28 on IL-17 production. From these data, it was concluded that IFN-γ induced by ST28 had an important role on the effect. A genomic DNA (10 µg/ml) from ST28 effectively suppressed IL-17 production, probably via the Toll-like receptor 9. Therefore, modulation of Th1/Th17 balance would be one of th...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5192366</comments>
            <pubDate>Sun, 04 Sep 2011 08:44:07 +0100</pubDate>
            <guid isPermaLink="false">5192366</guid>        </item>
        <item>
            <title>Loss of imprinting and aberrant methylation of IGF2 in placentas from pregnancies complicated with fetal growth restriction.</title>
            <link>http://www.medworm.com/index.php?rid=5095639&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805044%26dopt%3DAbstract</link>
            <description>The objective of this study was to investigate the hypothesis that the altered epigenetic mechanisms that regulate IGF2 imprinting in placentas from fetal growth restricted (FGR) pregnancies affect IGF2 expression leading to impaired fetal growth. We investigated gene transcription, genotyping and the methylation patterns of IGF2 from 31 and 17 placentas from FGR-complicated and normal pregnancies, respectively. A statistically significant decrease in IGF2 mRNA levels was observed in the placentas from the FGR pregnancies. Loss of imprinting (LOI) was only detected in the abnormal placentas. The evaluation of the percentage of the methylated reference (PMR) of two different potentially differentially methylated regions (DMR) demonstrated significant PMR values in both sites for the normal ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5095639</comments>
            <pubDate>Fri, 05 Aug 2011 14:36:26 +0100</pubDate>
            <guid isPermaLink="false">5095639</guid>        </item>
        <item>
            <title>Evaluation of the antioxidant peptide SS31 for treatment of burn-induced insulin resistance.</title>
            <link>http://www.medworm.com/index.php?rid=5095629&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805045%26dopt%3DAbstract</link>
            <description>In this report the effects of SS31 and SS20 on burn-induced insulin resistance was studied in mice. Oral glucose tolerance tests (OGTT) were performed in 4 groups of 6 mice with thermal injury with or without pre-treatment with SS31 or SS20 and sham controls. In addition, biodistribution of 18FDG was measured in burned mice with and without SS31 treatment and shams (subsets of these animals were also studied by µPET). For comparison purposes, groups of 6 cold-stressed mice with and without SS31 treatment were also studied. The results of these studies demonstrate that SS31 but not SS20 ameliorated burn-induced insulin resistance. In addition, SS31 treatment resulted in marked reduction in the increased 18FDG uptake by brown adipose tissue (BAT) in burned but not cold-stressed animals; sug...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5095629</comments>
            <pubDate>Fri, 05 Aug 2011 14:35:47 +0100</pubDate>
            <guid isPermaLink="false">5095629</guid>        </item>
        <item>
            <title>Role of HSP27 in tumor necrosis factor-α-stimulated interleukin-6 synthesis in osteoblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5095606&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21811758%26dopt%3DAbstract</link>
            <description>Authors: Kato K, Tokuda H, Mizutani J, Adachi S, Matsushima-Nishiwaki R, Natsume H, Kozawa O, Otsuka T
    Heat shock protein 27 (HSP27) is known to act as a molecular chaperone. We have recently reported that HSP27 regulates osteocalcin synthesis in osteoblast-like MC3T3-E1 cells. In the present study, we investigated the role of HSP27 in tumor necrosis factor-α (TNF-α)-stimulated interleukin-6 (IL-6) synthesis in MC3T3-E1 cells. The levels of IL-6 release and IL-6 mRNA stimulated by TNF-α in MC3T3-E1 cells transfected with HSP27 was significantly higher than those in the control cells. In addition, the levels of secreted IL-6 and IL-6 mRNA in the phospho-mimic HSP27-overexpressing cells were significantly higher than those in the non-phosphoryl-atable HSP27-overexpressing cells. Furth...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5095606</comments>
            <pubDate>Mon, 01 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5095606</guid>        </item>
        <item>
            <title>Alleviation of atopic dermatitis-related symptoms by Perilla frutescens Britton.</title>
            <link>http://www.medworm.com/index.php?rid=5095592&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21811759%26dopt%3DAbstract</link>
            <description>Authors: Heo JC, Nam DY, Seo MS, Lee SH
    To ascertain whether an aqueous fraction of Perilla frutescens Britton (PfB/af) has advantageous anti-atopic dermatitis activity, we used a 2,4-dinitrofluorobenzene (DNFB)-induced animal model of atopic dermatitis symptoms to investigate the effects of the extract. We performed an ear swelling assay by comparing thickness of the DNFB-induced ear, and measured the numbers of eosinophils as well as total immune cells. We analyzed the expression levels of matrix metalloproteinase (MMP)-9, interleukin (IL)-31 and of the T-bet transcription factor. The results revealed that PfB/af (100 µg/ml) exhibited strong anti-atopic dermatitis activity, interceding drastic reduction (35%) of the immune response, as measured by the thickness of ear epidermis swe...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5095592</comments>
            <pubDate>Mon, 01 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5095592</guid>        </item>
        <item>
            <title>Different patterns of nigrostriatal degeneration in tremor type versus the akinetic-rigid and mixed types of Parkinson's disease at the early stages: Molecular imaging with 123I-FP-CIT SPECT.</title>
            <link>http://www.medworm.com/index.php?rid=5095531&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21811760%26dopt%3DAbstract</link>
            <description>We examined 47 patients with early idiopathic PD (25 males; 22 females; mean age 58±2 years) and subdivided them in different clinical forms on the basis of dominance of resting tremor (n=20), bradykinesia plus rigidity (n=20) and the presence of both clinical signs [mixed type (MT, n=7)]. We correlated this status with the semi-quantitative analysis of SPECT with 123I-FP-CIT. Tremor type patients showed a lower reduction of 123I-FP-CIT uptake compared to akinetic-rigid type patients in contralateral caudate (P=0.0139) and putamen (P=0.0028) nuclei. 123I-FP-CIT uptake was higher in the ipsilateral caudate (P=0.0050) and putamen (P=0.0012) of tremor type patients compared to akinetic-rigid type patients. Comparisons of the striatal uptake in the tremor type and akinetic-rigid type patients...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5095531</comments>
            <pubDate>Mon, 01 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5095531</guid>        </item>
        <item>
            <title>Identification of biological functions and gene networks regulated by heat stress in U937 human lymphoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=4905446&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21617838%26dopt%3DAbstract</link>
            <description>Authors: Furusawa Y, Tabuchi Y, Wada S, Takasaki I, Ohtsuka K, Kondo T
    Although cancer cells exposed to temperatures &amp;gt;42.5˚C undergo cell death as the temperature rises, exposure of up to 42.5˚C induces slight or no cytotoxicity. The temperature of 42.5˚C is, therefore, well known to be the inflection point of hyperthermia. To better understand the molecular mechanisms underlying cellular responses to heat stress at temperatures higher and lower than the inflection point, we carried out global scale microarray and computational gene expression analyses. Human leukemia U937 cells were incubated at 42˚C or 44˚C for 15 min and cultured at 37˚C for 0-6 h. Apoptosis accompanied by the activation of caspase-3 and DNA fragmentation was only observed in cells treated with heat stres...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4905446</comments>
            <pubDate>Wed, 08 Jun 2011 01:42:57 +0100</pubDate>
            <guid isPermaLink="false">4905446</guid>        </item>
        <item>
            <title>Role of periostin in cancer progression and metastasis: Inhibition of breast cancer progression and metastasis by anti-periostin antibody in a murine model.</title>
            <link>http://www.medworm.com/index.php?rid=4905393&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21617848%26dopt%3DAbstract</link>
            <description>In this study, we focused on the exon 17 region of PN, which is alternatively spliced out. To investigate the function of full-length PN with exon 17, we produced a neutralizing antibody (PN1-Ab) against the peptide encoded by exon 17. In vivo, administration of PN1-Ab significantly inhibited the growth of primary tumors as well as metastatic tumors, associated with prevention of bone destruction, resulting in increased survival of mice. Consistent with in vivo data, the present in vitro study demonstrated that addition of full-length PN significantly inhibited cell adhesion and detached adherent cells, while PN1-Ab inhibited the action of PN in a dose-dependent manner. In addition, PN1-Ab significantly inhibited the proliferation, migration and invasion of 4T1 mouse breast cancer cells...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4905393</comments>
            <pubDate>Tue, 07 Jun 2011 23:33:09 +0100</pubDate>
            <guid isPermaLink="false">4905393</guid>        </item>
        <item>
            <title>ATPase family AAA domain containing 3A is an anti-apoptotic factor and a secretion regulator of PSA in prostate cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4855438&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21584487%26dopt%3DAbstract</link>
            <description>Authors: Huang KH, Chow KC, Chang HW, Lin TY, Lee MC
    In order to investigate the clinical value of ATPase family AAA domain containing 3A (ATAD3A), a potential anti-apoptotic factor in prostate cancer (PCa), immunohistochemistry was used to measure ATAD3A expression in pathological specimens from 86 Chinese patients and in 183 tissue-array samples from American patients. The effect of ATAD3A on the expression of prostate specific antigen (PSA) and drug resistance in PCa cell lines was determined by in vitro experiments. ATAD3A was detected in 74 of 86 (86.0%) Chinese specimens and in 145 of 183 (79.2%) American patient samples. No difference was found in ATAD3A expression between these two patient groups. In vitro, silencing of ATAD3A expression reduced PSA secretion and cisplatin re...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855438</comments>
            <pubDate>Tue, 24 May 2011 20:30:16 +0100</pubDate>
            <guid isPermaLink="false">4855438</guid>        </item>
        <item>
            <title>Transcription factor decoy against NFATc1 in human primary osteoblasts.</title>
            <link>http://www.medworm.com/index.php?rid=4855437&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21584488%26dopt%3DAbstract</link>
            <description>Authors: Penolazzi L, Lisignoli G, Lambertini E, Torreggiani E, Manferdini C, Lolli A, Vecchiatini R, Ciardo F, Gabusi E, Facchini A, Gambari R, Piva R
    The present study describes, for the first time, the removal of the nuclear factor of activated T cells cytoplasmic 1 (NFATc1) by a decoy approach in human primary osteoblasts (hOBs). hOBs with different NFATc1 expression levels were used. The functionality of endogenous NFAT proteins in our experimental model was analyzed by monitoring the transcriptional activity on a luciferase reporter construct driven by three copies of an NFAT response element (pNFAT-TA-luc). Cell treatment with the decoy against NFATc1 resulted in a significant increase in the expression of osteoblastic markers, including ERα and ColXV. On the contrary, the expr...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855437</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855437</guid>        </item>
        <item>
            <title>Effect of fibroblasts on breast cancer cell mammosphere formation and regulation of stem cell-related gene expression.</title>
            <link>http://www.medworm.com/index.php?rid=4855439&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573501%26dopt%3DAbstract</link>
            <description>Authors: Zhang F, Song C, Ma Y, Tang L, Xu Y, Wang H
    The purpose of this study was to investigate the regulatory effects of breast cancer fibroblasts (BCFs) vs. normal mammary fibroblasts (NMFs) on mammosphere formation and stem cell-related gene expression in breast cancer cells. Breast cancer cells (MCF-7) were cultured in suspension to generate primary and secondary mammospheres. The proportion of CD44+/CD24low/- cells was assessed by flow cytometry (FCM), and Wnt1, Notch1, β-catenin, CXCR4, SOX2 and ALDH3A1 gene expression was detected by quantitative real-time PCR. The fibroblasts from either breast cancer tissue or normal mammary tissue were purified from tissue specimens and co-cultured with breast cancer cells. The mammosphere formation efficacy was approximately 180/10,000 MC...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855439</comments>
            <pubDate>Thu, 12 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855439</guid>        </item>
        <item>
            <title>Insulin-dependent diabetes mellitus decreases osteoblastogenesis associated with the inhibition of Wnt signaling through increased expression of Sost and Dkk1 and inhibition of Akt activation.</title>
            <link>http://www.medworm.com/index.php?rid=4855443&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21567076%26dopt%3DAbstract</link>
            <description>Authors: Hie M, Iitsuka N, Otsuka T, Tsukamoto I
    Insulin-dependent diabetes mellitus (IDDM) is known to be associated with an increased risk of osteopenia. However, the cellular and molecular mechanisms for IDDM-induced alterations of the bone are not well understood. The effects of IDDM on bone metabolism were investigated using rats rendered diabetic by an injection of streptozotocin (STZ). After 4 weeks, the diabetic rats exhibited bone loss, low levels of osteocalcin, insulin-like growth factor-I (IGF-I) and bone alkaline phosphatase (ALP) activity with normal levels of bone tartrate-resistant acid phosphatase (TRAP) and cathepsin K activity, and urinary excretion of deoxypyridinoline (Dpd). Histological analysis showed a decrease in the number of osteoblasts with a normal number ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855443</comments>
            <pubDate>Tue, 10 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855443</guid>        </item>
        <item>
            <title>The Rho kinase inhibitor fasudil augments the number of functional endothelial progenitor cells in ex vivo cultures.</title>
            <link>http://www.medworm.com/index.php?rid=4855442&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21567077%26dopt%3DAbstract</link>
            <description>In this study, we investigated the effect of fasudil, another ROCK inhibitor being used in the clinic, on EPC number and examined whether EPCs expanded by fasudil are functional in vitro and in vivo. In ex vivo cultures of EPCs, fasudil effectively increased the number of ac-LDL/UEA-1 positive cells as well as adherent cells, in contrast to H89, a less selective ROCK inhibitor. Fasudil also increased EPC numbers in culture up to 10 µM, in a dose-dependent manner. When EPCs expanded with fasudil were examined for the migratory activity toward stromal cell-derived factor-1 and vascular endothelial growth factor, these cells retained functional properties in migration, albeit with some decrease. Fasudil-cultured EPCs labeled with PKH26 showed an activity similar to non-treated EPCs for c...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855442</comments>
            <pubDate>Tue, 10 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855442</guid>        </item>
        <item>
            <title>Up-regulation of Foxo4 mediated by hepatitis B virus X protein confers resistance to oxidative stress-induced cell death.</title>
            <link>http://www.medworm.com/index.php?rid=4855441&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21567078%26dopt%3DAbstract</link>
            <description>Authors: Srisuttee R, Koh SS, Park EH, Cho IR, Min HJ, Jhun BH, Yu DY, Park S, Park DY, Lee MO, Castrillon DH, Johnston RN, Chung YH
    The hepatitis B virus X (HBX) protein, a regulatory protein of the hepatitis B virus (HBV), has been shown to generate reactive oxygen species (ROS) in human liver cell lines; however, the mechanism by which cells protect themselves under this oxidative stress is poorly understood. Here, we show that HBX induces the up-regulation of Forkhead box class O 4 (Foxo4) not only in Chang cells stably expressing HBX (Chang-HBX) but also in primary hepatic tissues from HBX-transgenic mice. HBX also increased ROS, but reduction of the abundance of ROS using N-acetylcystein (NAC) diminished the levels of Foxo4. Elevated Foxo4 was also detected in nuclei of Chan...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855441</comments>
            <pubDate>Tue, 10 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855441</guid>        </item>
        <item>
            <title>Alteration of the proteome profile of the pancreas in diabetic rats induced by streptozotocin.</title>
            <link>http://www.medworm.com/index.php?rid=4855444&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21567075%26dopt%3DAbstract</link>
            <description>Authors: Jiang YL, Ning Y, Ma XL, Liu YY, Wang Y, Zhang Z, Shan CX, Xu YD, Yin LM, Yang YQ
    Type 1 diabetes mellitus (T1DM) is receiving increased attention. To obtain a better understanding of the mechanism underlying T1DM, we performed a proteomic study on a rat model induced by streptozotocin. Pancreatic proteins were separated by two-dimensional gel electrophoresis. Eighteen protein spots were differentially expressed (P&amp;lt;0.05) with 2-fold or more increased or decreased intensity in the diabetic rats as compared with controls, of which 11 protein spots were up-regulated and 7 protein spots were down-regulated. These protein spots were successfully identified by liquid chromatography-electrospray ionization tandem mass spectrometry. The 60 kDa heat shock protein, the carbonyl redu...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855444</comments>
            <pubDate>Sun, 08 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855444</guid>        </item>
        <item>
            <title>Modulatory activities of Agelanthus dodoneifolius (Loranthaceae) extracts on stimulated equine neutrophils and myeloperoxidase activity.</title>
            <link>http://www.medworm.com/index.php?rid=4855440&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573487%26dopt%3DAbstract</link>
            <description>Authors: Boly R, Dessy S, Kohnen S, Kini F, Lompo M, Mouithys-Mickalad A, Guissou IP, Dubois J, Deby-Dupont G, Serteyn D, Franck T
    Agelanthus dodoneifolius DC Danser (Loranthaceae) is used for the treatment of various diseases including asthma. The aqueous and hydroalcoholic extracts have been reported to have anti-inflammatory, spasmolytic and bronchorelaxant activities. The present study investigates the effects of the aqueous decoction and the diethyl ether, ethyl acetate and butanolic fractions of Agelanthus dodoneifolius DC Danser (Loranthaceae) on reactive oxygen species (ROS) production and myeloperoxidase (MPO) release by phorbol 12-myristate 13-acetate (PMA)-stimulated equine neutrophils and on purified equine MPO activity. ROS production and MPO release by the PMA-stimulated ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855440</comments>
            <pubDate>Sun, 08 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855440</guid>        </item>
        <item>
            <title>Effects of sivelestat on bronchial inflammatory responses after esophagectomy.</title>
            <link>http://www.medworm.com/index.php?rid=4855449&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21567070%26dopt%3DAbstract</link>
            <description>This study aimed to evaluate the effect of prophylactic administration of sivelestat on bronchial inflammatory responses. We randomized 24 patients into two groups. One group received 0.2 mg/kg/h sivelestat from the induction of anesthesia to post-operative day 1 (sivelestat group) and the other group received the same amount of physiological saline (control group). Bronchial alveolar epithelial lining fluid (ELF) samples were obtained from both groups at the induction of anesthesia and at the end of surgery. The serum and ELF levels of interleukin (IL)-6 and IL-8 were measured by enzyme-linked immunosorbent assay, and NE activity was spectrophotometrically determined using the same samples. Although IL-6 levels in the ELF significantly increased at the end of surgery compared with the pr...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855449</comments>
            <pubDate>Thu, 05 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855449</guid>        </item>
        <item>
            <title>Insulin-like growth factor-1 and 17β-estradiol down-regulate prostate apoptosis response-4 expression in MCF-7 breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4855448&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21567071%26dopt%3DAbstract</link>
            <description>In this study, we sought to investigate the mechanisms of regulation of PAR-4 gene expression in MCF-7 cells treated with E2 or IGF-1. E2 (10 nM) and IGF-1 (12.5 nM) each down-regulated PAR-4 expression in MCF-7 cells after 24 h of treatment. The effect of E2 was dependent on ER activation, as demonstrated by an increase in PAR-4 expression when cells were pretreated for 1 h with 1 µM ICI-182,780 (ICI) before receiving E2 plus ICI. The effect of IGF-1 was abolished by pre-treatment for 1 h with 30 µM LY294002 (a specific PI3-K inhibitor), and significantly inhibited by 30 µM SB202190 (a specific p38MAPK inhibitor). We also demonstrated that E2 acts synergistically with IGF-1, resulting in greater down-regulation of PAR-4 mRNA expression compared with E2 or IGF-1 alone. Our resul...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855448</comments>
            <pubDate>Thu, 05 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855448</guid>        </item>
        <item>
            <title>hSav1 interacts with HAX1 and attenuates its anti-apoptotic effects in MCF-7 breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4855447&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21567072%26dopt%3DAbstract</link>
            <description>In this study, we identified hematopoietic cell-specific protein 1 (HS1)-associated protein X-1 (HAX1), a 35-kDa protein localized to cell mitochondria, as a novel binding partner of hSav1 using a yeast two-hybrid screening technique. Our finding was confirmed by immunoprecipitation and glutathione-S-transferase (GST) pull-down assays of both proteins. Using immunofluorescence staining, we showed that HAX1 and hSav1 interact with each other. Analysis of the anti-apoptotic function of HAX1 revealed that the presence of hSav1 attenuated the HAX1 protective effects from hydrogen peroxide (H2O2)-induced cell death in MCF-7 cells, while knockdown of hSav1 by small interfering RNAs (siRNAs) significantly enhanced the anti-apoptotic function of HAX1. Also, using the Oncomine database, we found s...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855447</comments>
            <pubDate>Thu, 05 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855447</guid>        </item>
        <item>
            <title>MMP-2 and MMP-9 are prominent matrix metalloproteinases during atherosclerosis development in the Ldlr-/-Apob100/100 mouse.</title>
            <link>http://www.medworm.com/index.php?rid=4855446&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21567073%26dopt%3DAbstract</link>
            <description>In conclusion, low proteolytic expression at early stages of atherogenesis and a limited repertoire of proteolytic enzymes were associated with the progression of atherosclerosis in Ldlr-/-Apob100/100 mice. The study suggests that MMP-2 and MMP-9 are the main proteases involved in atherogenesis in this mouse model.
    PMID: 21567073 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855446</comments>
            <pubDate>Thu, 05 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855446</guid>        </item>
        <item>
            <title>Single impact trauma in human early-stage osteoarthritic cartilage: Implication of prostaglandin D2 but no additive effect of IL-1β on cell survival.</title>
            <link>http://www.medworm.com/index.php?rid=4855445&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21567074%26dopt%3DAbstract</link>
            <description>Authors: Joos H, Hogrefe C, Rieger L, Dürselen L, Ignatius A, Brenner RE
    Injury to articular cartilage is often associated with an inflammatory reaction and frequently results in the development of post-traumatic osteoarthritis (post-traumatic OA). Cell death, inflammation and loss of proteoglycans participate in these mechanisms with p38MAPK being one of the pivotal signaling kinases. Therefore, the interaction of trauma and of the pro-inflammatory cytokine IL-1β was investigated in an in vitro tissue model of human osteoarthritic cartilage. Trauma was induced by impacting cartilage explants with a drop-tower system and its effect was measured in terms of cell survival, gene expression and the release of mediators. In addition, the effect of concomitant IL‑1β stimulation and p38...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4855445</comments>
            <pubDate>Thu, 05 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4855445</guid>        </item>
        <item>
            <title>DcR3-TL1A signalling inhibits cytokine-induced proliferation of rheumatoid synovial fibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=4802403&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537832%26dopt%3DAbstract</link>
            <description>Authors: Takahashi M, Miura Y, Hayashi S, Tateishi K, Fukuda K, Kurosaka M
    Decoy receptor 3 (DcR3), a member of the tumour necrosis factor receptor (TNFR) superfamily, lacks the transmembrane domain of conventional TNFRs in order to be a secreted protein. DcR3 competitively binds and inhibits members of the TNF family, including Fas ligand (FasL), LIGHT and TL1A. We previously reported that TNFα-induced DcR3 overexpression in rheumatoid synovial fibroblasts (RA-FLS) protects the cells from Fas-induced apoptosis and that DcR3 induces VLA-4 expression in THP-1 macrophages to inhibit cycloheximide-induced apoptosis. Meanwhile, recent studies have suggested that DcR3 acting as a ligand directly induces the differentiation of macrophages to osteoclasts. Therefore, in the present study, w...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802403</comments>
            <pubDate>Sun, 01 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802403</guid>        </item>
        <item>
            <title>Knockdown of prion protein (PrP) by RNA interference weakens the protective activity of wild-type PrP against copper ion and antagonizes the cytotoxicity of fCJD-associated PrP mutants in cultured cells.</title>
            <link>http://www.medworm.com/index.php?rid=4802402&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537833%26dopt%3DAbstract</link>
            <description>In this report, based on analysis of the known sequences of human PrP, we constructed two small interfering RNA (siRNA) duplexes targeting the segments of amino acids (aa) 108-114 (Ri2) and aa 171-177 (Ri3). Western blot analysis results revealed that these PrP-specific siRNAs could effectively knock down the levels of either endogenous PrP in human neuroblastoma SHSY-5Y cells or recombinant PrP transfected with the plasmid expressing the full-length human PrP in human embryonic kidney (HEK) 293T cells. Meanwhile, the two siRNAs also showed a significant effect on the reduction of the expression of the PrP-PG9 and PrP-PG12 familial Creutzfeldt-Jakob disease (CJD)-associated PrP mutants with four and seven extra octarepeats, in the cells transfected with the respective expression plasmids. ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802402</comments>
            <pubDate>Sun, 01 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802402</guid>        </item>
        <item>
            <title>Endothelin-1 does not impair insulin-induced angiogenesis in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=4802401&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537834%26dopt%3DAbstract</link>
            <description>Authors: Pellegatta F, Brambilla C, Reduzzi A, Bragheri M, Zerbini G, Catapano AL
    Endothelin-1 (ET-1) modulates several vascular functions and plays an important role in the pathogenesis of insulin resistance. However, its role in the pathogenesis of impaired angiogenesis observed under insulin resistance conditions is not known. In the present study, we addressed this issue by analyzing the effect of ET-1 in human umbilical vein endothelial cells (HUVEC) on i) insulin-induced phosphorylation of two protein kinases involved in angiogenesis, Akt and ERK1/2, and on ii) insulin-induced angiogenesis in two in vitro models, those of Matrigel and of fibroblast/endothelial co-culture. Both insulin (100 ng/ml) and ET-1 (10 nmol/l) dose-dependently increased the phosphorylation of Akt and ER...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802401</comments>
            <pubDate>Sun, 01 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802401</guid>        </item>
        <item>
            <title>Effect of glucosamine, a therapeutic agent for osteoarthritis, on osteoblastic cell differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=4802404&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537831%26dopt%3DAbstract</link>
            <description>Authors: Igarashi M, Sakamoto K, Nagaoka I
    Osteoarthritis (OA) is characterized by qualitative and quantitative changes in the architecture and composition of all the joint structures. Glucosamine (GlcN) has been used to treat OA in humans, because GlcN is present in the cartilage tissues as a component of glycosaminoglycans, and exhibits the symptom-modifying effect on OA by normalizing cartilage metabolism. On the other hand, the pathological change of subchondral bone is associated with the initiation and progression of cartilage damage in OA. However, the effect of GlcN on bone metabolism remains unsolved. In the present study, we determined the effect of GlcN on bone metabolism (osteoblastic cell differentiation) using mouse osteoblastic MC3T3-E1 cells by evaluating the expression...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802404</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802404</guid>        </item>
        <item>
            <title>NADPH oxidase-dependent formation of reactive oxygen species contributes to angiotensin II-induced epithelial-mesenchymal transition in rat peritoneal mesothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=4802407&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537828%26dopt%3DAbstract</link>
            <description>In conclusion, NADPH oxidase-dependent formation of ROS mediates Ang II dependent EMT and accumulation of ECM in rat peritoneal mesothelial cells. NADPH oxidase may represent a potential therapeutic target in the management of peritoneal fibrosis.
    PMID: 21537828 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802407</comments>
            <pubDate>Wed, 27 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802407</guid>        </item>
        <item>
            <title>Dynamin-related protein 1 is implicated in endoplasmic reticulum stress-induced pancreatic β-cell apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=4802406&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537829%26dopt%3DAbstract</link>
            <description>In this study, we report that a mitochondrial fission modulator, dynamin-related protein 1 (DRP-1), plays an important role in ER stress-induced β-cell apoptosis. Induction of DRP-1 expression significantly promoted ER stress-induced apoptosis in the DRP-1 WT (DRP-1 wild- type) inducible β-cell line, but not in the DRP-1 K38A (a dominant negative mutant of DRP-1) inducible β-cell line. We further demonstrated that the mitochondrial membrane potential decreased, and that cytochrome c release, caspase-3 activation and generation of reactive oxygen species (ROS) were enhanced by induction of DRP-1 WT, but prevented by DRP-1 K38A in pancreatic β-cells under ER stress conditions. These results indicate that DRP-1 mediates ER stress-induced pancreatic β-cell apoptosis.
    PMID: 215378...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802406</comments>
            <pubDate>Wed, 27 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802406</guid>        </item>
        <item>
            <title>GATA binding protein 3 overexpression and suppression significantly contribute to the regulation of allergic skin inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=4802405&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537830%26dopt%3DAbstract</link>
            <description>Authors: Bae CJ, Lee JW, Shim SB, Jee SW, Lee SH, Woo JM, Lee CK, Hwang DY
    GATA binding protein 3 (GATA3) is a key molecule regulating the balance in the ratio of type 1 helper T (Th1) cells to type 2 helper T (Th2) cells, which is thought to be indicative of the pathogenesis of allergic diseases such as asthma and atopic dermatitis. The aim of this study was to investigate the role of GATA3 in allergic skin inflammation. Transgenic (Tg) mice overexpressing human GATA3 (hGATA3) were produced by the microinjection of pCMV/hGATA3 constructs into fertilized mouse eggs. The hGATA3 gene was successfully expressed at the protein level in the lymph node and thymus of CMV/hGATA3 transfected cells and Tg mice. CMV/hGATA3 Tg mice showed a significant increase in the allergic skin inflammati...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802405</comments>
            <pubDate>Wed, 27 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802405</guid>        </item>
        <item>
            <title>Curcumin stimulates proliferation, stemness acting signals and migration of 3T3-L1 preadipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4802410&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21519785%26dopt%3DAbstract</link>
            <description>Authors: Kim JH, Park SH, Nam SW, Kwon HJ, Kim BW, Kim WJ, Choi YH
    In the present study, the potential of curcumin to stimulate proliferation, stemness acting signals and migration of 3T3-L1 preadipocytes and the associated molecular mechanisms were investigated. Low concentrations of curcumin stimulated cell proliferation, whereas high concentrations were cytotoxic to 3T3-L1 cells. In particular, application of 0.02 µM of curcumin for 24 h resulted in significantly increased cell proliferation and was determined to be the optimal treatment for this study. In a colony-forming cell assay, cells treated with 0.02 µM of curcumin showed an approximately 1.5-fold increase in colony formation. Curcumin treatment up-regulated the proliferation-related marker proteins coupled with increas...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802410</comments>
            <pubDate>Tue, 19 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802410</guid>        </item>
        <item>
            <title>Estrogen induces cardioprotection in male C57BL/6J mice after acute myocardial infarction via decreased activity of matrix metalloproteinase-9 and increased Akt-Bcl-2 anti-apoptotic signaling.</title>
            <link>http://www.medworm.com/index.php?rid=4802409&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21519786%26dopt%3DAbstract</link>
            <description>Authors: Cao J, Zhu T, Lu L, Geng L, Wang L, Zhang Q, Yang K, Wang H, Shen W
    In general, young men have a greater risk than age-matched women for many types of cardiovascular diseases, including ischemic heart diseases, such as acute or chronic myocardial infarction (MI)-induced heart failure. The effects of estrogen-replacement therapy in men have not been extensively studied. We evaluated the cardioprotective effects of supplemental estrogen against left anterior descending coronary ligation-induced MI in male C57BL/6J mice. A significantly lower prevalence of cardiac rupture was observed in estrogen-treated mice regardless of castration status. A reduced prevalence of cardiac rupture was associated with decreased activities of matrix metalloproteinase 9 (MMP-9) and increased expres...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802409</comments>
            <pubDate>Tue, 19 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802409</guid>        </item>
        <item>
            <title>Novel insights into the role of HSP90 in cytoprotection of H2S against chemical hypoxia-induced injury in H9c2 cardiac myocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4802408&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21519787%26dopt%3DAbstract</link>
            <description>In conclusion, these results demonstrate that the increased expression of HSP90 may be one of the endogenous defensive mechanisms for resisting chemical hypoxia-induced injury in H9c2 cells. We also provide novel evidence that HSP90 mediates the cardioprotection of H2S against CoCl2-induced injuries by its antioxidant effect and preservation of mitochondrial function in H9c2 cells.
    PMID: 21519787 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802408</comments>
            <pubDate>Tue, 19 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802408</guid>        </item>
        <item>
            <title>MPZ mutation in an early-onset Charcot-Marie-Tooth disease type 1B family by genome-wide linkage analysis.</title>
            <link>http://www.medworm.com/index.php?rid=4802412&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21503568%26dopt%3DAbstract</link>
            <description>The objective of this study was to find the causative mutation(s) in a demyelinating autosomal dominant CMT family. A high density SNP-based genome-wide linkage scan was performed, and causative mutations were determined by sequencing of candidate genes in the linkage disequilibrium region. Linkage analysis mapped the underlying gene to a region on chromosome 1q22-q23 with a maximum two-point LOD score of 2.036. Sequencing analysis revealed a novel c.243C&amp;gt;G (His81Gln) mutation in the MPZ gene, which encodes the major integral membrane protein of the peripheral nerve system. MPZ is well known as a CMT-causative gene with wide phenotypic spectrum. The clinical symptoms were more similar to those of patients with the His81Arg than patients with the His81Tyr mutation. The novel mutation com...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802412</comments>
            <pubDate>Sun, 17 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802412</guid>        </item>
        <item>
            <title>microRNA-182 inhibits the proliferation and invasion of human lung adenocarcinoma cells through its effect on human cortical actin-associated protein.</title>
            <link>http://www.medworm.com/index.php?rid=4802411&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21503569%26dopt%3DAbstract</link>
            <description>In conclusion, endogenous mature miR-182 expression may have an important role in the pathogenesis of lung cancer through its interference with the target gene CTTN by epigenetic modification.
    PMID: 21503569 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802411</comments>
            <pubDate>Sun, 17 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802411</guid>        </item>
        <item>
            <title>Comparison of the protective effects of truncated bFGF and native bFGF against murine lung carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4802414&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21503566%26dopt%3DAbstract</link>
            <description>Authors: Luo Z, Peng X, Shi H, Gong C, Qian Z, Yang L
    Basic fibroblast growth factor (bFGF), an angiogenic factor, exhibits pro-angiogenic abilities by interacting with tyrosine kinase receptors and heparin-sulfated proteoglycan receptors. Here, we designed an N-, C-terminally truncated basic fibroblast growth factor (tbFGF) for immuno-therapy of murine lung carcinoma with PCEC hydrogel as adjuvant, comparing it with the wild-type bFGF. In vitro, tbFGF did not stimulate NIH-3T3 fibroblast proliferation. In vivo, after immunization, both tbFGF and bFGF were able to induce a robust bFGF-specific immune response. The protective anti-tumor investigation showed a significant inhibition of tumor growth and reduction of tumor vascularization detected by immunohistochemical staining and the a...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802414</comments>
            <pubDate>Wed, 13 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802414</guid>        </item>
        <item>
            <title>Dihydrotestosterone induces p27 degradation via direct binding with SKP2 in ovarian and breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4802413&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21503567%26dopt%3DAbstract</link>
            <description>Authors: Shi P, Zhang Y, Tong X, Yang Y, Shao Z
    The effect of androgens on the prevention or promotion of cell cycle progression in ovarian and breast cancer is controversial. This effect determines the basic rules of how to treat postmenopausal patients properly after surgery. In the present study, we investigated the effects of different androgens, namely dihydrotestosterone (DHT), testosterone and dehydroepiandrosterone (DHEA) in MCF-7 breast cancer and OVCAR-3 ovarian cancer cells. We found that DHT could down-regulate p27, but not p21, within 4 h. Further studies proved that DHT induced p27 degradation through the ubiquitin-proteasome proteolytic pathway. Inhibition of the androgen receptor and of phosphorylation did not hamper the degradation. However, proteolysis inhibitors eff...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802413</comments>
            <pubDate>Wed, 13 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802413</guid>        </item>
        <item>
            <title>Aging reduces susceptibility of vascular smooth muscle cells to H2O2-induced apoptosis through the down-regulation of Jagged1 expression in endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=4802419&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21491077%26dopt%3DAbstract</link>
            <description>Authors: Qian D, Wu X, Jiang H, Gao P, Kuang C, Wang K, Huang L
    In addition to excessive proliferation, reduced apoptosis of vascular smooth muscle cells (VSMCs) plays a key role in aging-exaggerated neointima formation after vascular injury. Our previous studies have shown that impaired expression of Jagged1 in the endothelium may be a key event that leads to enhanced VSMC proliferation in the elderly. Here, we are the first to investigate whether the expression of Jagged1 in endothelial cells (ECs) may regulate apoptosis of VSMCs. We discovered that VSMCs co-cultured with senescent ECs exhibited decreased susceptibility to H2O2-induced apoptosis compared with those co-cultured with young ECs. Senescent ECs also displayed lower Jagged1 expression compared to young ECs, which was more ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802419</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802419</guid>        </item>
        <item>
            <title>Differential expression of ETS family members in prostate cancer tissues and androgen-sensitive and insensitive prostate cancer cell lines.</title>
            <link>http://www.medworm.com/index.php?rid=4802418&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21491078%26dopt%3DAbstract</link>
            <description>Authors: Shaikhibrahim Z, Lindstrot A, Langer B, Buettner R, Wernert N
    The ETS family of transcription factors plays important roles in both normal and neoplastic cells for different biological processes such as proliferation, differentiation, development, transformation, apoptosis, migration, invasion and angiogenesis. The 27 ETS factors are probably a part of complex regulatory networks including interactions among family members. In human prostate cancer, rearrangements have been found in several genes of the ETS family resulting in chimeric oncoproteins. In a previous study we found that the ETS family prototype, Ets-1 affects biological properties of PC3 prostate cancer cells. In a first effort to understand the cooperative interactions between different ETS factors in prostate ca...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802418</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802418</guid>        </item>
        <item>
            <title>Aβ-42 deposition significantly increases the insolubility of synaptophysin in the brains of hAPPsw/hPS2m double transgenic mice.</title>
            <link>http://www.medworm.com/index.php?rid=4802417&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21491079%26dopt%3DAbstract</link>
            <description>Authors: Hwang DY, Jee SW, Lee SH, Bae CJ, Goo JS, Kim JE, Nam SH, Choi SI, Lee HR, Shim SB, Park MH, Hong JT, Kim HS
    Synaptophysin is a synaptic vesicle glycoprotein involved in the regulation process for neurotransmitter release, which is distributed throughout neuroendocrine cells and all neurons in the brain and spinal cord. In an effort to determine whether amyloid β (Aβ)-42 peptides could influence the quantity and biochemical properties of synaptophysin, alterations in the levels of the synaptophysin protein in various soluble fractions were detected in the brains of four genotypes of transgenic mice (Tg) including Non-Tg, neuron-specific enolase (NSE)-hPS2m, NSE-hAPPsw and hAPPsw/hPS2m double Tg mice. Among the four genotypes of Tg mice, the highest levels of Aβ-42 peptides ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802417</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802417</guid>        </item>
        <item>
            <title>AICAR, an activator of AMPK, inhibits adipogenesis via the WNT/β-catenin pathway in 3T3-L1 adipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4802416&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21491080%26dopt%3DAbstract</link>
            <description>Authors: Lee H, Kang R, Bae S, Yoon Y
    AMP-activated protein kinase (AMPK) is known to sense the cellular energy state and regulates various cellular energy metabolism pathways through its activation by AMP, an indicator of a low-energy state. 5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR), an activator of AMPK, efficiently inhibited the adipogenesis of 3T3-L1 cells. To elucidate its possible mechanism of action, the expression levels of β-catenin and other members of the WNT/β-catenin pathway were analyzed during the adipogenesis of 3T3-L1 cells in the presence or absence of AICAR. It was found that AICAR significantly enhanced β-catenin expression and its nuclear accumulation. Transfection of β-catenin small interfering RNA (siRNA) significantly prevented the effects...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802416</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802416</guid>        </item>
        <item>
            <title>Effect of the release from mechanical stress on osteoclastogenesis in RAW264.7 cells.</title>
            <link>http://www.medworm.com/index.php?rid=4802415&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21491081%26dopt%3DAbstract</link>
            <description>In this study, the effects of mechanical stress application and its release on osteoclast differentiation were examined. The number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated osteoclasts derived from RAW264.7 cells were measured and the expression of osteoclast differentiation genes, which was altered in response to the release from mechanical stress according to the Flexercell tension system was evaluated by real-time PCR. Osteoclast differentiation and fusion were suppressed by mechanical stress application and were rapidly induced after mechanical stress release. The mRNA expression of the osteoclast specific genes, TRAP, matrix metalloproteinase-9 (MMP-9), cathepsin-K (cath-k), calcitonin receptor (CTR), ATPase H+ transporting vacuolar proton pump member I (A...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802415</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802415</guid>        </item>
        <item>
            <title>Association analysis of DTD1 gene variations with aspirin-intolerance in asthmatics.</title>
            <link>http://www.medworm.com/index.php?rid=4802420&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21479357%26dopt%3DAbstract</link>
            <description>Authors: Pasaje CF, Bae JS, Park BL, Jang AS, Uh ST, Kim MK, Koh IS, Kim JH, Park TJ, Lee JS, Kim Y, Park CS, Shin HD
    Aspirin ingestion is a common precipitating factor of life-threatening asthma attacks, requiring some patients to undergo mechanical ventilation. The gene, D-tyrosyl-tRNA deacylase 1 (DTD1), may be a risk factor for aspirin-intolerant asthma (AIA) by catalyzing the hydrolysis of D-tryptophan and interacting with the tyrosyl-tRNA synthetase (tyrRS) enzyme, which promotes a pro-inflammatory phenotype. In order to investigate the association of DTD1 variants with the risk of AIA in an asthma cohort, 38 single nucleotide polymorphisms (SNPs) were genotyped and 5 major haplotypes were obtained in 163 AIA cases and 429 aspirin-tolerant asthma (ATA) controls. Differences in D...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802420</comments>
            <pubDate>Tue, 05 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802420</guid>        </item>
        <item>
            <title>Selective leukemia cell death by activation of the double-stranded RNA-dependent protein kinase PKR.</title>
            <link>http://www.medworm.com/index.php?rid=4696356&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21468538%26dopt%3DAbstract</link>
            <description>In this study, we sought to identify targeted PKR activation by Bcr-Abl AS RNA, an anti-sense RNA complementary to the unique mRNA fragments flanking the fusion point of Bcr-Abl, which can be used as an effective anti-leukemia strategy in K562 cells. Moreover, we observed expression of Bcr-Abl AS RNA in K562 cells which resulted in selective apoptosis induction through specific activation of PKR, leading to phosphorylation of eIF2α, global inhibition of protein synthesis, caspase-8 activation and BAX up-regulation. The targeted PKR activation and induced apoptosis were reversed by the PKR inhibitor 2-aminopurine. Taken together, our results indicate that targeted PKR activation led to selective apoptosis induction in K562 cells, which correlated with caspase-8 activity and enhanced ex...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696356</comments>
            <pubDate>Sun, 03 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696356</guid>        </item>
        <item>
            <title>Anti-tumor effect of luteolin is accompanied by AMP-activated protein kinase and nuclear factor-κB modulation in HepG2 hepatocarcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=4696355&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21468539%26dopt%3DAbstract</link>
            <description>In conclusion, we propose that AMPK is a novel regulator of NF-κB in luteolin-induced cancer cell death. Furthermore, our results suggest that AMPK is an attractive target for cancer prevention by flavonoids.
    PMID: 21468539 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696355</comments>
            <pubDate>Sun, 03 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696355</guid>        </item>
        <item>
            <title>Effects of electrolytes on virus inactivation by acidic solutions.</title>
            <link>http://www.medworm.com/index.php?rid=4696354&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21468540%26dopt%3DAbstract</link>
            <description>Authors: Nishide M, Tsujimoto K, Uozaki M, Ikeda K, Yamasaki H, Koyama AH, Arakawa T
    Acidic pH is frequently used to inactivate viruses. We have previously shown that arginine synergizes with low pH in enhancing virus inactivation. Considering a potential application of the acid inactivation of viruses for the prevention and treatment of superficial virus infection at body surfaces and fixtures, herein we have examined the effects of various electrolytes on the acid-induced inactivation of the herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2), the influenza A virus (IAV) and the poliovirus upon their incubation at 30˚C for 5 min. Eight electrolytes, i.e., phosphate, NaCl, glutamate, aspartate, pyrrolidone carboxylate, citrate, malate and acetate were tested. No detectable inactiv...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696354</comments>
            <pubDate>Sun, 03 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696354</guid>        </item>
        <item>
            <title>Characteristics of occult hepatitis B virus infection in the Solomon Islands.</title>
            <link>http://www.medworm.com/index.php?rid=4696362&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455562%26dopt%3DAbstract</link>
            <description>In conclusion, occult HBV infection was documented in 12.5% of individuals that demonstrated serologic evidence of resolved HBV infection in this study. The prevalence of occult infection was also influenced by ethnicity; it was more prevalent in Melanesians than Micronesians. In addition, occult HBV infection demonstrated a weak association with the S-variants.
    PMID: 21455562 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696362</comments>
            <pubDate>Wed, 30 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696362</guid>        </item>
        <item>
            <title>Analysis of matrix metalloproteinase-9 gene polymorphism -1562 C/T in patients suffering from systemic sclerosis with and without ulcers.</title>
            <link>http://www.medworm.com/index.php?rid=4696361&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455563%26dopt%3DAbstract</link>
            <description>The objective of this study was to determine whether the matrix metalloproteinase-9 (MMP-9) rs3918242 single nucleotide polymorphism may confer susceptibility to systemic sclerosis (SSc) with and without ulcers in an Italian Caucasian population. The MMP-9 rs3918242 functional polymorphism was genotyped in 461 subjects of Italian Caucasian origin: 228 patients with SSc (92 with and 136 without ulcers) and 233 unrelated healthy individuals. The SNP under study was in Hardy-Weinberg equilibrium in the control population. Genotype and allele distributions between SSc patients, with or without ulcers, were not statistically significant (p&amp;gt;0.05). A significant increase of the genotype C/T was observed in male SSc patients without ulcers when compared to patients with ulcers (P=0.04). The MMP...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696361</comments>
            <pubDate>Wed, 30 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696361</guid>        </item>
        <item>
            <title>Effects of glucosamine derivatives and uronic acids on the production of glycosaminoglycans by human synovial cells and chondrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4696360&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455564%26dopt%3DAbstract</link>
            <description>In this study, to elucidate the chondroprotective action of GlcN, we examined the effects of GlcN-derivatives (GlcN and N-acetyl-D-glucosamine) and uronic acids (D-glucuronic acid and D-galacturonic acid) (0.1-1 mM) on the production of glycosaminoglycans (GAG), such as hyaluronic acid (HA), keratan sulfate and sulfated GAG by human synovial cells and chondrocytes. The results indicate that among GlcN-derivatives and uronic acids, GlcN but not N-acetyl-D-glucosamine, D-glucuronic acid and D-galacturonic acid induce the production of HA by synovial cells and chondrocytes at &amp;gt;0.25 and &amp;gt;0.1 mM (p&amp;lt;0.05), respectively, and the production levels are much higher (&amp;gt;10-fold) in synovial cells compared to chondrocytes. In contrast, neither N-acetyl-D-glucosamine, D-glucuronic acid nor ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696360</comments>
            <pubDate>Wed, 30 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696360</guid>        </item>
        <item>
            <title>Silencing of the icb-1 gene inhibits the induction of differentiation-associated genes by vitamin D3 and all-trans retinoic acid in gynecological cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4696359&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455565%26dopt%3DAbstract</link>
            <description>Authors: Haselberger M, Springwald A, Konwisorz A, Lattrich C, Goerse R, Ortmann O, Treeck O
    Icb-1 (C1orf38) is a human gene initially described by our group to be involved in differentiation processes of cancer cells. To further elucidate the function of the icb-1 gene in differentiation of breast and endometrial cancer cells, we knocked down its expression by means of shRNA transfection. Knockdown of icb-1 inhibited the vitamin D3-induced up-regulation of E-cadherin expression in both MCF-7 and HEC-1B cells. Induction of E-cadherin expression by all-trans retinoic acid (ATRA) was also blocked in both cell lines expressing icb-1 siRNA. Examination of icb-1 and E-cadherin expression in 66 breast cancer tissue samples revealed a significant positive correlation between the two genes. I...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696359</comments>
            <pubDate>Wed, 30 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696359</guid>        </item>
        <item>
            <title>Differential expression of microRNAs in cardiac myocytes compared to undifferentiated P19 cells.</title>
            <link>http://www.medworm.com/index.php?rid=4696358&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455566%26dopt%3DAbstract</link>
            <description>Authors: Hu DL, Liu YQ, Chen FK, Sheng YH, Yang R, Kong XQ, Cao KJ, Zhang JS, Qian LM
    microRNA (miRNA) expression is tightly controlled in a tissue-specific and developmental stage-specific manner; some are highly and specifically expressed in cardiovascular tissues. miRNA expression profiling, using miRNA microarrays facilitates studying the biological function of miRNAs. We investigated changes in miRNA expression profiles during differentiation of P19 cells into cardiac myocytes in order to elucidate the mechanisms of heart development. The morphology of P19 cells during differentiation was observed using an inverted microscope. Western blot analysis was performed to detect cardiac troponin I (cTnI) expression. Total RNA was extracted from P19 cells for microarray and real-time quan...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696358</comments>
            <pubDate>Wed, 30 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696358</guid>        </item>
        <item>
            <title>Ultraviolet A exposure induces reversible disruption of gap junction intercellular communication in lens epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=4696357&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455567%26dopt%3DAbstract</link>
            <description>Authors: Wu D, Zhao J, Wu D, Zhang J
    Gap junction intercellular communication (GJIC) is essential for the proper function of many organs including the lens. Disruption of GJIC can cause lens metabolic disorder and can induce cataracts. The purpose of this study was to investigate the signal transduction pathways involved in GJIC disruption following ultraviolet A (UVA) exposure in lens epithelial cells. Following exposure of human lens epithelial cells to UVA, connexin 43 (Cx43), the main component of gap junctions, was down-regulated at both the mRNA and protein levels. Furthermore, we observed that UVA exposure can increase protein kinase C activity and stimulate reactive oxygen species generation and lipid peroxidation. Using scrape load dye transfer technique, we found that the ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696357</comments>
            <pubDate>Wed, 30 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696357</guid>        </item>
        <item>
            <title>Fasudil, a Rho-associated protein kinase inhibitor, attenuates retinal ischemia and reperfusion injury in rats.</title>
            <link>http://www.medworm.com/index.php?rid=4696363&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455561%26dopt%3DAbstract</link>
            <description>In conclusion, fasudil can protect the rat retina from I/R injury by inhibiting apoptosis and iNOS expression, suggesting that fasudil may have a therapeutic potential for the prevention of retinal diseases associated with I/R.
    PMID: 21455561 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696363</comments>
            <pubDate>Tue, 29 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696363</guid>        </item>
        <item>
            <title>Analysis and optimization of interactions between peptides mimicking the GD2 ganglioside and the monoclonal antibody 14G2a.</title>
            <link>http://www.medworm.com/index.php?rid=4696367&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455557%26dopt%3DAbstract</link>
            <description>Authors: Horwacik I, Kurciński M, Bzowska M, Kowalczyk AK, Czaplicki D, Koliński A, Rokita H
    Overexpression of the GD2 ganglioside (GD2) is a hallmark of neuroblastoma. The antigen is used in neuroblastoma diagnosis and to target newly developed therapies to cancer cells. Peptide mimetics are novel approaches in the design of antigens for vaccine development. We previously reported the isolation of five GD2-mimicking peptides from the LX-8 phage display library with the monoclonal antibody (mAb) 14G2a. The goal of our current study was to analyze and optimize the binding of the peptide mimetics to the mAb 14G2a. Therefore, we performed further experiments and supported them with molecular modeling to investigate structure-activity relationships that are the basis for the observed mim...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696367</comments>
            <pubDate>Wed, 23 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696367</guid>        </item>
        <item>
            <title>Flagellin promotes the proliferation of gastric cancer cells via the Toll-like receptor 5.</title>
            <link>http://www.medworm.com/index.php?rid=4696366&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455558%26dopt%3DAbstract</link>
            <description>In this study, we examined the expression of TLR5 in gastric cancer cells and its function in cell proliferation. RT-PCR revealed that the TLR5 gene was expressed in all gastric cancer cell lines examined, SNU638, SNU601, SNU216, and AGS. The TLR5 agonist, flagellin, induced IL-8 production and NF-κB activation in the gastric cancer cell lines. In addition, flagellin enhanced the proliferation of all gastric cancer cells examined, whereas LPS did not affect that of SNU638 cells. Blockade of TLR5 using an antibody, restored the proliferation of SNU638 cells enhanced by flagellin, indicating that TLR5 is essential for cell proliferation by flagellin. Flagellin also led to phosphorylation of ERK in SNU638 cells. The ERK inhibitor, PD98059, restored the proliferation ability of SNU638 cells e...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696366</comments>
            <pubDate>Wed, 23 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696366</guid>        </item>
        <item>
            <title>Expression of membrane and nuclear progesterone receptors in two human placental choriocarcinoma cell lines (JEG-3 and BeWo): Effects of syncytialization.</title>
            <link>http://www.medworm.com/index.php?rid=4696365&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455559%26dopt%3DAbstract</link>
            <description>Authors: Zachariades E, Foster H, Goumenou A, Thomas P, Rand-Weaver M, Karteris E
    A vital function of the human placenta is to produce steroid hormones such as progesterone, which are essential for the maintenance of pregnancy and the onset of parturition. Although choriocarcinoma cell lines are valuable placental models for investigations of steroid hormone actions, little is known about the expression of progesterone receptors (PRs) in these cell lines. Therefore, in this study, the expression of membrane and nuclear PRs was investigated in cultures of fusigenic (BeWo) and non-fusigenic (JEG-3) human choriocarcinoma cell lines. In addition, the effects of an inducer of syncytialization (forskolin) on the PR expression in BeWo cells were assessed. Quantitative RT-PCR revealed that in ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696365</comments>
            <pubDate>Wed, 23 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696365</guid>        </item>
        <item>
            <title>Cocktail therapy with a combination of interferon, ribavirin and angiotensin-II type 1 receptor blocker attenuates murine liver fibrosis development.</title>
            <link>http://www.medworm.com/index.php?rid=4696364&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455560%26dopt%3DAbstract</link>
            <description>Authors: Yoshiji H, Noguchi R, Ikenaka Y, Kaji K, Aihara Y, Shirai Y, Yoshii J, Yanase K, Fukui H
    An effective therapeutic strategy for suppressing liver fibrosis development should improve the overall prognosis of patients with chronic liver diseases. Despite efforts to develop anti-fibrotic agents, no drugs have yet been approved as anti-fibrotic treatments for humans. An alternative strategy may be to employ a clinically available agent that also exhibits anti-fibrotic activities, for which the safety of long-term administration has been proven. The aim of the current study was to elucidate the combined effect of clinically used interferon (IFN), ribavirin (Rib) and angiotensin-II receptor blocker (ARB) on liver fibrosis development in mice. A model of CCl4-induced hepatic fibrosis ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4696364</comments>
            <pubDate>Wed, 23 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4696364</guid>        </item>
        <item>
            <title>Genome-wide expression profiling of urinary bladder implicates desmosomal and cytoskeletal dysregulation in the bladder exstrophy-epispadias complex.</title>
            <link>http://www.medworm.com/index.php?rid=4637716&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21431277%26dopt%3DAbstract</link>
            <description>This study provides the first expression profile of urogenital genes during bladder development and points to the high-probability candidate genes for BEEC.
    PMID: 21431277 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637716</comments>
            <pubDate>Tue, 22 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637716</guid>        </item>
        <item>
            <title>Postprandial activation of protein kinase Cµ regulates the expression of adipocytokines via the transcription factor AP-2β</title>
            <link>http://www.medworm.com/index.php?rid=4637719&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424113%26dopt%3DAbstract</link>
            <description>Authors: Kondo M, Ugi S, Morino K, Fuke T, Obata T, Yoshizaki T, Nishio Y, Maeda S, Kashiwagi A, Maegawa H
    Abnormal secretion of adipocytokines promotes atherosclerosis, diabetes and insulin resistance, and is mainly induced by adipocyte hypertrophy. Recently, the circulating adipocytokine concentrations were reported to change in the postprandial period, as the levels of TNFα, IL-6 IL-8 and MCP-1 increased after a meal, whereas that of adiponectin decreased. These data suggest that prandial modulation of cytokines may be involved in the pathogenesis of atherosclerosis in type 2 diabetes. However, the regulatory mechanism of such change is still unclear. In the present study, we identified this mechanism with a special focus on the functions of protein kinase C (PKC) and of the transc...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637719</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637719</guid>        </item>
        <item>
            <title>Comprehensive gene expression microarray analysis of Ets-1 blockade in PC3 prostate cancer cells and correlations with prostate cancer tissues: Insights into genes involved in the metastatic cascade.</title>
            <link>http://www.medworm.com/index.php?rid=4637718&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424114%26dopt%3DAbstract</link>
            <description>Authors: Shaikhibrahim Z, Lindstrot A, Langer B, Buettner R, Wernert N
    Ets-1 is the prototype of the ETS family of transcription factors and is suggested to play an important role in the malignant progression of prostatic carcinomas. Therefore, in this study we investigated the effect of blocking Ets-1 in PC3 prostate cancer cells on genes involved in the metastatic cascade, and correlated these findings with prostate cancer tissues. Two stable PC3 cell cultures were established by transfection with either an Ets-1 inverse antisense expression vector or a mock control vector. The effect of blocking Ets-1 on genes involved in the metastatic cascade was assessed by a comprehensive gene expression microarray analysis of Ets-1 inverse and mock control cells. Correlating the sets of genes f...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637718</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637718</guid>        </item>
        <item>
            <title>Genotypic and phenotypic features of citrin deficiency: Five-year experience in a Chinese pediatric center.</title>
            <link>http://www.medworm.com/index.php?rid=4637717&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424115%26dopt%3DAbstract</link>
            <description>Authors: Song YZ, Deng M, Chen FP, Wen F, Guo L, Cao SL, Gong J, Xu H, Jiang GY, Zhong L, Kobayashi K, Saheki T, Wang ZN
    Citrin is a liver-type aspartate/glutamate carrier (AGC) encoded by the gene SLC25A13. Two phenotypes for human citrin deficiency have been described, namely the adult-onset citrullinemia type II (CTLN2) and the neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD). However, citrin deficiency currently remains a perplexing and poorly recognized disorder. In particular, description of post-NICCD clinical presentations before CTLN2 onset is rather limited. Analysis of SLC25A13 mutations, identification of dysmorphic erythrocytes, hepatobiliary scintigraphic imaging and investigation of post-NICCD clinical presentations were performed in a citrin-deficie...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637717</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637717</guid>        </item>
        <item>
            <title>Activated protein C inhibits bisphosphonate-induced endothelial cell death via the endothelial protein C receptor and nuclear factor-κB pathways.</title>
            <link>http://www.medworm.com/index.php?rid=4637721&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424111%26dopt%3DAbstract</link>
            <description>In conclusion, the present study demonstrates that APC inhibits bisphosphonate-induced endothelial cell death via EPCR-induced inactivation of caspase-3 and NF-κB, and also suggests that APC has the potential to be a therapeutic drug in various vascular diseases induced by endothelial cell damage.
    PMID: 21424111 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637721</comments>
            <pubDate>Thu, 17 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637721</guid>        </item>
        <item>
            <title>Blood levels of dual-specificity phosphatase-1 independently predict risk for post-operative morbidities causing prolonged hospitalization after coronary artery bypass grafting.</title>
            <link>http://www.medworm.com/index.php?rid=4637720&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424112%26dopt%3DAbstract</link>
            <description>Authors: Hägg S, Alserius T, Noori P, Ruusalepp A, Ivert T, Tegnér J, Björkegren J, Skogsberg J
    New technologies to generate high-dimensional data provide unprecedented opportunities for unbiased identification of biomarkers that can be used to optimize pre-operative planning, with the goal of avoiding costly post-operative complications and prolonged hospitalization. To identify such markers, we studied the global gene expression profiles of three organs central to the metabolic and inflammatory homeostasis isolated from coronary artery disease (CAD) patients during coronary artery bypass grafting (CABG) surgery. A total of 198 whole-genome expression profiles of liver, skeletal muscle and visceral fat from 66 CAD patients of the Stockholm Atherosclerosis Gene Expression (STAGE) co...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637720</comments>
            <pubDate>Thu, 17 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637720</guid>        </item>
        <item>
            <title>Oncostatin M promotes proliferation of ovarian cancer cells through signal transducer and activator of transcription 3.</title>
            <link>http://www.medworm.com/index.php?rid=4637723&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399864%26dopt%3DAbstract</link>
            <description>Authors: Li Q, Zhu J, Sun F, Liu L, Liu X, Yue Y
    Oncostatin M (OSM), a pleiotropic cytokine, has been shown to have distinctive effects in different tissues. In ovarian carcinoma, it is commonly co-expressed together with its receptors but its precise role and the underlying molecular mechanism governing its activity remains unclear. The aim of the present study was to investigate the function of the recombinant human OSM (rH-OSM) in human ovarian cancer. The study demonstrated that rH-OSM promotes the proliferation of SKOV3 ovarian cancer cells. Western blot analysis showed that phosphorylated-signal transducer and activator of transcription 3 (p-STAT3), phosphorylated-extracellular signal-regulated protein kinase 1/2 (p-ERK1/2) and p-p38 protein levels increased in the cell lines tre...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637723</comments>
            <pubDate>Fri, 11 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637723</guid>        </item>
        <item>
            <title>Quick detection of overexpressed genes caused by myeloma-specific chromosomal translocations using multiplex RT-PCR.</title>
            <link>http://www.medworm.com/index.php?rid=4637722&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399865%26dopt%3DAbstract</link>
            <description>Authors: Htwe SS, Maeda M, Matsumoto R, Sakamoto N, Murakami S, Yamamoto S, Katoh M, Kumagai N, Hayashi H, Nishimura Y, Ohkura M, Wada H, Taniwaki M, Sugihara T, Otsuki T
    Multiple myeloma (MM) is a malignancy of the plasmocyte and is associated with various symptoms such as anemia, immunodeficiency, bone lesions and kidney insufficiency. Although prognosis was poor until some years ago, recent advances that introduced newer molecular targeting agents such as bortezomib and thalidomide have resulted in a better prognosis for MM. However, clinical manifestations and the relationship between cellular and molecular findings, including chromosomal translocation and the related overexpression of oncogenes such as CCND1 (cyclin D1) and FGFR3 (fibroblast growth factor receptor 3), remain uncle...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637722</comments>
            <pubDate>Fri, 11 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637722</guid>        </item>
        <item>
            <title>Female patients with atrial fibrillation have increased oxidized and glycated lipoprotein properties and lower apolipoprotein A-I expression in HDL.</title>
            <link>http://www.medworm.com/index.php?rid=4637724&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399863%26dopt%3DAbstract</link>
            <description>Authors: Kim SM, Lee JH, Kim JR, Shin DG, Lee SH, Cho KH
    It is well-known that oxidative stress and inflammatory processes are linked to the incidence of atrial fibrillation (AF). In order to provide prognostic biomarkers for AF based on lipoprotein levels, we compared the lipid and protein parameters of oxidation and inflammation in individual lipoproteins from middle-aged females with AF. We analyzed plasma and lipoproteins (VLDL, LDL, HDL2, HDL3) from 11 female patients (mean age, 56±15 years) with paroxysmal lone AF and from a reference group of 10 female patients of similar age (mean age, 54±15 years). The AF group had normal levels of serum lipids and an inflammatory profile, except for a 7.5- and 6-fold elevation in hsCRP and tropoinin I levels, respectively. No significant d...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637724</comments>
            <pubDate>Wed, 09 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637724</guid>        </item>
        <item>
            <title>Intracoronary adiponectin at reperfusion reduces infarct size in a porcine myocardial infarction model.</title>
            <link>http://www.medworm.com/index.php?rid=4637727&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399860%26dopt%3DAbstract</link>
            <description>Authors: Dębiński M, Buszman PP, Milewski K, Wojakowski W, Jackiewicz W, Pająk J, Szurlej D, Fryc-Stanek J, Wiernek S, Jelonek M, Spurlock ME, Martin J, Bochenek A, Buszman PE
    Reperfusion injury (RI) remains an important limitation of myocardial revascularization. The aim of the present study was to evaluate the influence of the intracoronary injection of adiponectin on RI and cardiomyocyte death in a porcine myocardial infarction model. Acute infarction in 14 Polish domestic pigs was induced by inflation of an over the wire balloon (OTW) catheter in the medial left anterior descending artery for 60 min. The study group consisted of 7 pigs in which intracoronary adiponectin (50 µg) was infused through the OTW catheter immediately before reperfusion. The control group (n=7) was ad...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637727</comments>
            <pubDate>Tue, 08 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637727</guid>        </item>
        <item>
            <title>Enhancement of basic fibroblast growth factor-stimulated VEGF synthesis by Wnt3a in osteoblasts.</title>
            <link>http://www.medworm.com/index.php?rid=4637726&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399861%26dopt%3DAbstract</link>
            <description>Authors: Tokuda H, Adachi S, Matsushima-Nishiwaki R, Kato K, Natsume H, Otsuka T, Kozawa O
    It is currently recognized that the Wnt signaling pathway regulates bone mass. We have previously reported that the basic fibroblast growth factor (FGF-2) stimulates the synthesis of the vascular endothelial growth factor (VEGF) at least in part via the p44/p42 mitogen-activated protein (MAP) kinase and the stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK) in osteoblast-like MC3T3-E1 cells. In the present study, we investigated the effect of Wnt3a on FGF-2-stimulated VEGF synthesis in MC3T3-E1 cells. Wnt3a significantly augmented the FGF-2-stimulated VEGF release in a dose-dependent manner in the range between 1 and 30 ng/ml. Lithium chloride and SB216763, inhibitors of glycog...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637726</comments>
            <pubDate>Tue, 08 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637726</guid>        </item>
        <item>
            <title>Genetic variations in MyD88 adaptor-like are associated with atopic dermatitis.</title>
            <link>http://www.medworm.com/index.php?rid=4637725&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399862%26dopt%3DAbstract</link>
            <description>The objective of this study was to detect polymorphisms in the Mal gene and to investigate their association with allergic diseases. Mal gene polymorphisms were genotyped in 310 subjects. The functional effects of Mal variants were analyzed in vitro. One Mal polymorphism, c.303 G&amp;gt;A (Q101Q), was found at a significantly lower frequency in atopic dermatitis patients (p=0.016). Q101Q is in linkage disequilibrium with -103 A&amp;gt;G (rs1893352) and c.539 C&amp;gt;T (S180L) (rs8177374) in the HapMap database. The A allele of -103 A&amp;gt;G showed significantly reduced transcription of Mal compared with the G allele. In addition, three rare variants were identified in this study, c.394 G&amp;gt;A (E132K), c.428 G&amp;gt;A (R143Q) and c.570 G&amp;gt;C (E190D), and were shown to lead to loss-of-function of Mal. It i...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4637725</comments>
            <pubDate>Tue, 08 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4637725</guid>        </item>
        <item>
            <title>Novel compound heterozygous mutations T2C and 1149insT in the KCNQ1 gene cause Jervell and Lange-Nielsen syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=4577834&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21380488%26dopt%3DAbstract</link>
            <description>In this study, we identified and characterized two novel KCNQ1 mutations that caused JLNS. A 6-year-old deaf girl suffering from recurrent syncope had a documented electrocardiogram with polymorphic ventricular fibrillation since the age of 4 years. The baseline electrocardiogram showed a significantly prolonged corrected QT interval (524 msec). Genetic analysis revealed that the proband carried two heterozygous mutations of T2C and 1149insT in the KCNQ1 gene on separate alleles. Patch-clamp analysis demonstrated that the T2C mutation resulted in significant reduction in the slowly activated delayed rectifier current (IKs). Furthermore, western blot analysis and confocal imaging revealed that the T2C mutation produced a truncated protein with trafficking defects. In contrast, the 1149insT...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577834</comments>
            <pubDate>Fri, 04 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577834</guid>        </item>
        <item>
            <title>Pectenotoxin-2 induces G1 arrest of the cell cycle in synovial fibroblasts of patients with rheumatoid arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=4577840&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373746%26dopt%3DAbstract</link>
            <description>This study investigated the mechanisms underlying the anti-proliferative action of pectenotoxin-2 (PTX-2), isolated from marine sponges, in synovial fibroblasts obtained from RA patients. PTX-2 concentration-dependently inhibited the growth of synovial fibroblasts, arresting them in the G1 phase of their cell cycle. The G1 arrest was correlated with down-regulation of cyclin D1 and cyclin-dependent kinase (Cdk) 6, with a concomitant up-regulation of the tumor suppressor, p53, and the Cdk inhibitor, p21 (WAF1/CIP1). Following PTX-2 treatment of synovial fibroblasts, an increased binding of p21 with Cdk2 and Cdk6 was paralleled by a significant decrease in retinoblastoma protein (pRB) phosphorylation and in the protein levels of E2F transcription factors. Thus, PTX-2 might help identify new ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577840</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577840</guid>        </item>
        <item>
            <title>cAMP regulates ADP-induced HSP27 phosphorylation in human platelets.</title>
            <link>http://www.medworm.com/index.php?rid=4577839&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373747%26dopt%3DAbstract</link>
            <description>Authors: Enomoto Y, Adachi S, Doi T, Natsume H, Kato K, Matsushima-Nishiwaki R, Akamatsu S, Tokuda H, Yoshimura S, Otsuka T, Ogura S, Kozawa O, Iwama T
    Elevation of cAMP in platelets is recognized to play a suppressive role in platelet functions. We have previously shown that adenosine diphosphate (ADP)-induced phosphorylation of heat shock protein 27 (HSP27) via p38 mitogen-activated protein (MAP) kinase is correlated with platelet-derived growth factor (PDGF)-AB secretion and soluble CD40 ligand (sCD40L) release. In the present study, we investigated the relationship between cAMP and HSP27 phosphorylation in platelet function. 8-Bromoadenosine-3',5'-cyclic monophosphate (8-bromo-cAMP), a plasma membrane-permeable cAMP analogue, or cilostazol, an inhibitor of cAMP phosphodiesterase, ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577839</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577839</guid>        </item>
        <item>
            <title>Involvement of a novel GATA4 mutation in atrial septal defects.</title>
            <link>http://www.medworm.com/index.php?rid=4577838&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373748%26dopt%3DAbstract</link>
            <description>In this study, the entire coding region of GATA4, a gene encoding a zinc-finger transcription factor crucial to embryogenesis, was initially sequenced in 120 unrelated patients with ASD. The available relatives of patients carrying the identified mutation and 200 ethnicity-matched unrelated control individuals were genotyped. The functional characteristics of the GATA4 mutant were compared to its wild-type counterpart using a luciferase reporter assay system. A novel heterozygous missense GATA4 mutation, p.G21V, was identified in 2 unrelated families with ASD, which was not detected in the control population nor reported in the human gene mutation database. Alignment of multiple GATA4 proteins displayed that the affected amino acid residue was highly conserved across species. Functional an...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577838</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577838</guid>        </item>
        <item>
            <title>Preliminary identification of potential PDZ-domain proteins downstream of ephrin B2 during osteoclast differentiation of RAW264.7 cells.</title>
            <link>http://www.medworm.com/index.php?rid=4577837&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373749%26dopt%3DAbstract</link>
            <description>This study focuses on the preliminary identification of downstream PDZ-domain proteins involved in EphB4/ephrin B2 reverse signaling in osteoclasts. Similarly to primary osteoclast precursors isolated from the bone, we observed that the RAW264.7 cell line, a mouse monocyte/macrophage cell line that is used in conventional assays for osteoclast function, expressed ephrin B2 during RANKL-induced osteoclast differentiation, and that preclustered EphB4 inhibited this osteoclast differentiation. The results demonstrate that RAW264.7 cells provide a good model for further research of EphB4/ephrin B2 signaling in osteoclasts. Immunofluorescence staining and Western blot analysis revealed that all of the eight PDZ-domain proteins previously reported to interact with ephrin B ligands were expre...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577837</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577837</guid>        </item>
        <item>
            <title>Hypermethylation-modulated down-regulation of CDH1 expression contributes to the progression of esophageal cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4577836&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373750%26dopt%3DAbstract</link>
            <description>Authors: Ling ZQ, Li P, Ge MH, Zhao X, Hu FJ, Fang XH, Dong ZM, Mao WM
    CDH1, a cell adhesion molecule, which plays a key role in maintaining the epithelial phenotype, is regarded as an invasion-suppressor gene in light of accumulating evidence from in vitro experiments and clinical observations. In an attempt to clarify the mechanism responsible for inactivation of this gene in carcinomas, we investigated the methylation status of the CDH1 gene 5'-CpG islands and its regulatory mechanism in the progression of esophageal squamous cell carcinoma. Real-time methylation-specific polymerase chain reaction (qMSP) and treatment with the demethylating agent 5-aza-2'-deoxycytidine (5-Aza-CdR) were conducted to analyze the methylation status at the CDH1 promoter region in the human esophageal ca...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577836</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577836</guid>        </item>
        <item>
            <title>Priming with a combination of proangiogenic growth factors improves wound healing in normoglycemic mice.</title>
            <link>http://www.medworm.com/index.php?rid=4577835&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373751%26dopt%3DAbstract</link>
            <description>Authors: Ackermann M, Wolloscheck T, Wellmann A, Li VW, Li WW, Konerding MA
    Growth factors and/or angiogenic factors are supposed to improve wound healing. The aim of our study was to evaluate the effects of subcutaneous pretreatment with combinatory proangiogenic factors on wound closure, mechanical properties, vessel density and morphology. Twenty-eight Balb/c mice were divided equally into two groups. A mixture of VEGF (35.0 µg), bFGF (2.5 µg) and PDGF (3.5 µg) was administered subcutaneously 3, 5 and 7 days to 14 mice before full thickness skin punch biopsy wounding, whereas 14 control animals received three injections of 0.2 ml saline solution. Wound sizes were assessed daily and the repaired tissues were harvested 7 days after complete wound closure. Complete closure (...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577835</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577835</guid>        </item>
        <item>
            <title>BubR1 is required for the mitotic block induced by combretastatin-A4 and a novel cis-restricted ß-lactam analogue in human cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4577843&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21369694%26dopt%3DAbstract</link>
            <description>In this study, we describe the effects of combretastatin A-4 (CA-4) and a synthetic cis-restricted 3,4-diaryl-2-azetidinone (ß-lactam) analogue (CA-432) on the modulation and phosphorylation of BubR1 in human cervical cancer-derived cells. We demonstrate that CA-4 and CA-432 depolymerise the microtubular network of human cervical carcinoma-derived cells. Both compounds induced the disassembly of the microtubules and the loss of microtubule tension led to the early phosphorylation of BubR1 and the late cleavage of BubR1. The phosphorylation of BubR1 correlated with the onset of G2M cell cycle arrest whilst the cleavage of BubR1 coincided with apoptosis induced by the combretastatins. The combretastatin-induced apoptosis and the BubR1 cleavage were caspase-dependent. In vitro enzyme digests...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577843</comments>
            <pubDate>Wed, 02 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577843</guid>        </item>
        <item>
            <title>Superior mineralization and neovascularization capacity of adult human metaphyseal periosteum-derived cells for skeletal tissue engineering applications.</title>
            <link>http://www.medworm.com/index.php?rid=4577842&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21369695%26dopt%3DAbstract</link>
            <description>In conclusion, hMPCs represent a promising cellular candidate for bone tissue engineering.
    PMID: 21369695 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577842</comments>
            <pubDate>Wed, 02 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577842</guid>        </item>
        <item>
            <title>Group B Streptococcus serotypes III and V induce apoptosis and necrosis of human epithelial A549 cells.</title>
            <link>http://www.medworm.com/index.php?rid=4577841&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21369696%26dopt%3DAbstract</link>
            <description>In conclusion, GBS serotypes III and V induce apoptosis of epithelial cells in the early stages of GBS infection, resulting in tissue destruction, bacterial spreading and, in consequence, invasive disease or systemic infection.
    PMID: 21369696 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577841</comments>
            <pubDate>Wed, 02 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577841</guid>        </item>
        <item>
            <title>MOVAS-1 cell line: A new in vitro model of vascular calcification.</title>
            <link>http://www.medworm.com/index.php?rid=4577845&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21369692%26dopt%3DAbstract</link>
            <description>In conclusion, we demonstrated that the MOVAS-1 line is a reliable, convenient and economical system in which to investigate vascular calcification in vitro, and will make a useful contribution to increasing our understanding of this pathological process.
    PMID: 21369692 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577845</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577845</guid>        </item>
        <item>
            <title>The antagonist of the JAK-1/STAT-1 signaling pathway improves the severity of cerulein-stimulated pancreatic injury via inhibition of NF-κB activity.</title>
            <link>http://www.medworm.com/index.php?rid=4577844&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21369693%26dopt%3DAbstract</link>
            <description>This study indicates that the JAK-1/STAT-1 signaling pathway activity is an early event in pancreatic inflammatory injury. Therefore, early treatment with its inhibitors might be beneficial for attenuation of pancreatic injury in SAP.
    PMID: 21369693 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577844</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577844</guid>        </item>
        <item>
            <title>Immunodetection of the MCHR1 antibody in vitiligo patient sera.</title>
            <link>http://www.medworm.com/index.php?rid=4577847&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21369690%26dopt%3DAbstract</link>
            <description>Authors: Zhou M, Guan C, Lin F, Xu W, Fu L, Hong W, Wan Y, Xu A
    Human vitiligo is an acquired depigmenting skin disorder characterized by milk-white skin macules resulting from a chronic and progressive loss of melanocytes. It has been suggested that autoimmune mechanisms are involved in this disorder. We undertook this project to obtain an MCHR1-C linear peptide containing four main MCHR1 B-cell epitopes in an attempt to detect the IgG antibody against MCHR1 in vitiligo. The target gene encoding the MCHR1-C peptide was cloned into a pGEX-4T-2 expression vector, expressed in Escherichia coli BL21, and purified using a GST column. The molecular weight was analyzed by SDS-PAGE and western blotting. The IgG antibody response to MCHR1 was detected by ELISA with MCHR1-C as a coated antigen,...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577847</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577847</guid>        </item>
        <item>
            <title>Induction of β-catenin by the suppression of signal regulatory protein α1 in K562 cells.</title>
            <link>http://www.medworm.com/index.php?rid=4577846&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21369691%26dopt%3DAbstract</link>
            <description>Authors: Maekawa T, Imoto A, Satoh T, Okazaki T, Takahashi S
    The signal regulatory protein (SIRP) α1 is a cell surface receptor expressed predominantly in monocytes, granulocytes, dendritic cells, as well as hematopoietic stem cells. In contrast, SIRPα1 expression is significantly reduced in the majority of myeloid malignancies. SIRPα1 is a negative regulator of signaling and its reduced expression is considered to play a role in the pathogenesis of these diseases through aberrant signaling. To identify SIRPα1 downstream target genes, we established SIRP α1-knockdown chronic myeloid leukemia K562 (K562SIRPα1KD) cells expressing reduced levels of SIRPα1 by stably transfecting SIRPα1 siRNAs. Microarray analysis demonstrated that several genes, including β-catenin, were significa...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4577846</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4577846</guid>        </item>
        <item>
            <title>Association of polymorphisms of BTN2A1 and ILF3 with myocardial infarction in Japanese individuals with or without hypertension, diabetes mellitus or chronic kidney disease.</title>
            <link>http://www.medworm.com/index.php?rid=4524601&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21347509%26dopt%3DAbstract</link>
            <description>Authors: Yoshida T, Kato K, Oguri M, Horibe H, Kawamiya T, Yokoi K, Fujimaki T, Watanabe S, Satoh K, Aoyagi Y, Tanaka M, Yoshida H, Shinkai S, Nozawa Y, Yamada Y
    Recent evidence suggests that genetic variants that confer susceptibility to myocardial infarction (MI) may differ between men and women or between individuals with or without conventional risk factors for MI. We previously showed that rs6929846 of BTN2A1 and rs2569512 of ILF3 were significantly associated with MI in Japanese individuals. In the present study, we examined the associations of rs6929846 of BTN2A1 or rs2569512 of ILF3 to MI among individuals stratified by the absence or presence of hypertension, diabetes mellitus (DM) and chronic kidney disease (CKD). The study population was comprised of 5689 unrelated Japanese ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524601</comments>
            <pubDate>Wed, 23 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524601</guid>        </item>
        <item>
            <title>Reduction of serum free fatty acids and triglycerides by liver-targeted expression of long chain acyl-CoA synthetase 3.</title>
            <link>http://www.medworm.com/index.php?rid=4524600&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21347510%26dopt%3DAbstract</link>
            <description>Authors: Wu M, Cao A, Dong B, Liu J
    ACSL3 is a member of the long chain acyl-CoA synthetase (ACSL) family that consists of 5 isozymes responsible for cellular fatty acid metabolism in various tissues in an isozyme-specific manner. Our previous studies have demonstrated that expression of ACSL3 mRNA and protein in liver was specifically increased after feeding hamsters with a fat- and cholesterol-enriched diet, providing the first in vivo evidence for the regulated expression of ACSL3 in liver tissue. The aim of the current study was to further investigate the role of ACSL3 in regulating hepatic lipid metabolism in vitro and in vivo. We utilized an adenoviral-mediated gene delivery approach to exogenously express hamster ACSL3 in hamster liver as well as in HepG2 cells. Transduction of ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524600</comments>
            <pubDate>Wed, 23 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524600</guid>        </item>
        <item>
            <title>Purification and biochemical characterization of a novel glutamyl endopeptidase secreted by a clinical isolate of Staphylococcus aureus.</title>
            <link>http://www.medworm.com/index.php?rid=4524599&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21347511%26dopt%3DAbstract</link>
            <description>In this study, a 34‑kDa glutamate-specific serine protease (named VSPase) secreted by a clinical isolate of S. aureus sp. strain C-66 was purified and characterized, and VSPase-encoding gene was also cloned by PCR. VSPase enzyme purified from culture supernatant and its recombinant enzyme expressed in E. coli exhibited a proteolytic activity over a broad range of pH (6.0-8.5) and showed an optimal activity at 45˚C. The enzyme activity was completely inhibited by DFP. The N-terminal sequence of native VSPase showed that the enzyme was produced as a form of zymogen and activated to a functional enzyme by losing its N-terminal 68 amino acid residues. VSPase specifically cleaved peptide bonds at the carboxyl sides of glutamate residues in a protein substrate such as prothrombin and exhibi...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524599</comments>
            <pubDate>Wed, 23 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524599</guid>        </item>
        <item>
            <title>Prion peptide-mediated cellular prion protein overexpression and neuronal cell death can be blocked by aspirin treatment.</title>
            <link>http://www.medworm.com/index.php?rid=4524598&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21347512%26dopt%3DAbstract</link>
            <description>Authors: Jeong JK, Moon MH, Seol JW, Seo JS, Lee YJ, Park SY
    Prion diseases are infectious neurodegenerative disorders characterized by the conversion of the cellular prion protein (PrPc) to the misfolded isoform (PrPsc). Prion peptide PrP 106‑126 [PrP (106‑126)] shares many physiological properties with PrPsc; it is neurotoxic in vitro and in vivo. PrP (106‑126) induces neurotoxicity by the overexpression of PrPc and activation of the mitogen-activated protein (ERK1/2). Aspirin, an anti-inflammatory drug, is a known ERK inhibitor and prevents neurodegenerative disorders including prion diseases. The influence of aspirin treatment on prion protein-mediated neurotoxicity and expression of PrPc were the focus of this study. Cell viability and apoptosis were assessed by crystal vi...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524598</comments>
            <pubDate>Wed, 23 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524598</guid>        </item>
        <item>
            <title>In vivo hepatic differentiation potential of human cord blood-derived mesenchymal stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=4524597&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21347513%26dopt%3DAbstract</link>
            <description>Authors: Kim S, Kim HS, Lee E, Kim HO
    Although recent studies have demonstrated the in vitro hepatic differentiation potential of mesenchymal stem cells (MSCs), the evidence supporting the in vivo engraftment of MSCs, hepatic differentiation and improvement of hepatic function is still lacking. We investigated in vivo hepatic differentiation potential and therapeutic effect of cord blood derived-MSCs (CBMSCs) transplantation in a cirrhotic rat model. CBMSCs (2x106) were infused in Wistar rats with thioacetamide-induced chronic liver injury. Biochemical markers, liver fibrosis and engraftment of CBMSCs were assessed. Infused CBMSCs were detected in the perivascular or fibrous region of the liver and did not acquire mature hepatic phenotypes. There was no difference in biochemical mar...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524597</comments>
            <pubDate>Wed, 23 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524597</guid>        </item>
        <item>
            <title>Chemokine receptor 7 promotes cell migration and adhesion in metastatic squamous cell carcinoma of the head and neck by activating integrin αvβ3.</title>
            <link>http://www.medworm.com/index.php?rid=4524596&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21347514%26dopt%3DAbstract</link>
            <description>Authors: Li P, Liu F, Sun L, Zhao Z, Ding X, Shang D, Xu Z, Sun C
    The mechanisms leading to squamous cell carcinoma of the head and neck (SCCHN) metastasis are incompletely understood. Although evidence shows that the chemokine receptor 7 (CCR7) and its ligand CCL19 may regulate tumor dissemination, their role in SCCHN is not clearly defined. CCR7 has been shown to regulate integrins, which facilitate adhesion of cancer cells to and/or migration through the extracellular matrix (ECM). To investigate the relationship between CCR7 and integrin αvβ3 in metastatic SCCHN, we used adhesion and migration assays, immunofluorescence staining and western blotting to determine whether integrin αvβ3 can be activated by CCL19 in the metastatic SCCHN cell line PCI-37B, which was pre-incubated wi...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524596</comments>
            <pubDate>Wed, 23 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524596</guid>        </item>
        <item>
            <title>Association between lipid accumulation and the cannabinoid system in Huh7 cells expressing HCV genes.</title>
            <link>http://www.medworm.com/index.php?rid=4524602&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21331443%26dopt%3DAbstract</link>
            <description>In this study, we examined the expression of a cannabinoid receptor (CB1) and the lipid accumulation in the hepatic Huh7 cell line, expressing HCV genes. We utilized Huh7/Rep-Feo-1b cells stably expressing HCV non-structural proteins (NS) 3, NS4, NS5A, and NS5B, as well as Tet-On Core-2 cells, in which the HCV core protein expression is inducible. Significantly higher levels of stored triglycerides were found in Huh7/Rep-Feo-1b cells compared to Huh7 cells. Also, triglyceride accumulation and CB1 receptor expression were down-regulated in Huh7/Rep-Feo-1b cells after HCV reduction by IFNα. Moreover, lipid accumulation appeared to increase after CB1 agonist treatment, while it decreased after CB1 antagonist treatment, although significant differences were not found compared to untreated cel...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524602</comments>
            <pubDate>Thu, 17 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524602</guid>        </item>
        <item>
            <title>An active part of Artemisia sacrorum Ledeb. inhibits adipogenesis via the AMPK signaling pathway in 3T3-L1 adipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4524604&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21327327%26dopt%3DAbstract</link>
            <description>In this study, we investigated the effect of ASL on adipocyte differentiation in 3T3-L1 cells. ASL significantly suppressed 3T3-L1 differentiation in a concentration-dependent manner. A significant increase of AMP-activated protein kinase (AMPK) was observed when the cells were treated with ASL. Activation of AMPK was also demonstrated by measuring the phosphorylation of acetyl-CoA carboxylase, a substrate of AMPK. These effects were abolished by pre-treatment with the AMPK inhibitor, compound C. In addition, ASL down-regulated the adipogenesis-related gene expression of the sterol regulatory element-binding protein 1c (SREBP1c) and its target genes, such as fatty acid synthase (FAS), stearoyl-CoA desaturase 1 (SCD1) and glycerol-3-phosphate acyltransferase (GPAT) in a concentration-depend...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524604</comments>
            <pubDate>Tue, 15 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524604</guid>        </item>
        <item>
            <title>Visfatin/PBEF/Nampt induces EMMPRIN and MMP-9 production in macrophages via the NAMPT-MAPK (p38, ERK1/2)-NF-κB signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=4524603&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21327328%26dopt%3DAbstract</link>
            <description>In conclusion, we have demonstrated that visfatin enhances atheroma inflammation through the NAMPT-MAPK (p38, ERK1/2)-NF-κB-EMMPRIN/MMP-9 pathway, a key feature of atherosclerotic diseases linked to metabolic disorders.
    PMID: 21327328 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524603</comments>
            <pubDate>Tue, 15 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524603</guid>        </item>
        <item>
            <title>Basic helix-loop-helix transcription factors DEC1 and DEC2 regulate the paclitaxel-induced apoptotic pathway of MCF-7 human breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4524607&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21327324%26dopt%3DAbstract</link>
            <description>In this study, we sought to examine the roles of DEC1 and DEC2 in MCF-7 human breast cancer cells that had been treated with paclitaxel. The expression of DEC1 and DEC2 was up-regulated in paclitaxel-treated MCF-7 cells. Knockdown of DEC1 by siRNA decreased the amount of cleaved poly (ADP-ribose) polymerase (PARP), after treatment with paclitaxel, whereas DEC2 knockdown increased the amount of cleaved PARP in both the presence and absence of paclitaxel. Immunofluorescent staining revealed that paclitaxel treatment increased the amount of DEC1 in the nucleus, and increased the amount of DEC2 in both the nucleus and cytoplasm. These results indicate that DEC1 has pro-apoptotic effects, whereas DEC2 has anti-apoptotic effects on the paclitaxel-induced apoptosis in human breast cancer MCF-7 ce...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524607</comments>
            <pubDate>Mon, 14 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524607</guid>        </item>
        <item>
            <title>Cimetidine inhibits the adhesion of gastric cancer cells expressing high levels of sialyl Lewis x in human vascular endothelial cells by blocking E-selectin expression.</title>
            <link>http://www.medworm.com/index.php?rid=4524606&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21327325%26dopt%3DAbstract</link>
            <description>Authors: Liu FR, Jiang CG, Li YS, Li JB, Li F
    Cimetidine has been shown to have anti-metastatic activity and improves the survival of patients with colorectal cancer. One hypothesis is its modulation of the expression of the cell adhesion molecule by target organ endothelial cells. Because of the inconclusive results in clinical trials of gastric cancer, we investigated the effects of cimetidine on the adhesion of gastric cancer cells to activated endothelial cells and on the expression of some cell adhesion molecules. Human endothelial cells were pre-incubated with cimetidine for 6 h, incubated with the cytokine tumor necrosis factor for 4 h, and the endothelial surface expression of E-selectin was evaluated by flow cytometry, immunostaining and ELISA. Further, we investigated E-sele...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524606</comments>
            <pubDate>Mon, 14 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524606</guid>        </item>
        <item>
            <title>Roles of exogenously regulated bFGF expression in angiogenesis and bone regeneration in rat calvarial defects.</title>
            <link>http://www.medworm.com/index.php?rid=4524605&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21327326%26dopt%3DAbstract</link>
            <description>Authors: Chen M, Song K, Rao N, Huang M, Huang Z, Cao Y
    Regulation of transgene expression and function is important for gene therapy because it allows complex biological processes to be controlled and monitored. Basic fibroblast growth factor (bFGF) is an effective angiogenic factor and bone regeneration factor; it can induce differentiation of mesenchymal stem cells (MSCs) in vitro and bone regeneration in vivo. Further, exogenous regulation of controllable bFGF expression in the bone regeneration area safely allows bone formation and regeneration. In our study, we constructed a recombinant adeno-associated virus type 2 (rAAV2)-based bFGF gene delivery system, which is regulated by tetracycline or doxycycline (Dox, an analogue of tetracycline). We evaluated the regulatory effects o...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524605</comments>
            <pubDate>Mon, 14 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524605</guid>        </item>
        <item>
            <title>Hepatocyte growth factor improves the survival of rats with pulmonary arterial hypertension via the amelioration of pulmonary hemodynamics.</title>
            <link>http://www.medworm.com/index.php?rid=4524608&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21318217%26dopt%3DAbstract</link>
            <description>In this study, we investigated the effect of administration of recombinant human HGF on pulmonary arterial hypertension. Pulmonary arterial hypertension was induced in rats by a single injection of monocrotaline (MCT) and recombinant human HGF (0.12 mg/day) was administered into the right ventricle cavity using osmotic pumps, which were implanted subcutaneously 21 days after MCT injection. Continuous intravenous delivery of recombinant human HGF for 14 days led to prolonged survival of animals suffering from severe MCT-induced pulmonary arterial hypertension. Although a bolus injection of recombinant human HGF did not affect pulmonary arterial pressure, a 14-day administration of recombinant human HGF attenuated the inflammatory cell infiltrate, matrix accumulation and vascular medial thic...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4524608</comments>
            <pubDate>Thu, 10 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4524608</guid>        </item>
        <item>
            <title>Elevation and characteristics of Rab30 and S100a8/S100a9 expression in an early phase of liver regeneration in the mouse.</title>
            <link>http://www.medworm.com/index.php?rid=4466949&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21308349%26dopt%3DAbstract</link>
            <description>In conclusion, Rab30 and S100a8/S100a9 were indicated to play roles in the initiation of liver regeneration as well as possibly in the functional switch of the liver in the newborn stage.
    PMID: 21308349 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4466949</comments>
            <pubDate>Wed, 09 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4466949</guid>        </item>
        <item>
            <title>Diverse inhibition of plasminogen activator inhibitor type 1 by theaflavins of black tea.</title>
            <link>http://www.medworm.com/index.php?rid=4466948&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21308350%26dopt%3DAbstract</link>
            <description>In this study we report results for four pure (&amp;gt;98%) theaflavins. Inactivation of PAI-1 was tested by clot formation and by its lysis using thromboelastometry and measurements of human plasma turbidity. Among four tested theaflavins, theaflavin-3'-gallate was the most potent in PAI-1 inhibition trailed by theaflavin-3,3'-digallate, while the other two i.e., theaflavin and theaflavin-3-gallate did not show inhibitory activity.
    PMID: 21308350 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4466948</comments>
            <pubDate>Wed, 09 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4466948</guid>        </item>
        <item>
            <title>Suicide gene therapy in head and neck carcinoma cells: An in vitro study.</title>
            <link>http://www.medworm.com/index.php?rid=4466953&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21305248%26dopt%3DAbstract</link>
            <description>Authors: Schmidt M, Gruensfelder P, Roller J, Hagen R
    The aim of gene therapy includes the tight spatial and temporal control of transgenic expression. There are several approaches concerning the externally inducible gene promoters used for the control of suicide genes. We have tested the mifepristone-dependent system GeneSwitch to regulate the expression of a deletion mutant of Pseudomonas exotoxin A in the hypopharyngeal carcinoma cell line, FADU. The GeneSwitch system consists of two plasmids, the regulatory plasmid, pSwitch, and the pGene/V5-His plasmid, in which we cloned the toxin mutant (pGene/V5-His-ETA). We stably transfected FADU cells with pSwitch and subsequently transiently separated pSwitch clones with pGene/V5-His-ETA. We tested the inductive capacities of single pSwitc...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4466953</comments>
            <pubDate>Thu, 03 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4466953</guid>        </item>
        <item>
            <title>Effects and relationship of ERK1 and ERK2 in interleukin-1β-induced alterations in MMP3, MMP13, type II collagen and aggrecan expression in human chondrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4466952&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21305249%26dopt%3DAbstract</link>
            <description>Authors: Wang X, Li F, Fan C, Wang C, Ruan H
    Interleukin (IL)-1β plays an important role in the pathogenesis of osteoarthritis and catabolic processes in articular cartilage. Growing evidence suggests that ERK1/2 activation is involved in IL-1β-mediated matrix metalloproteinase (MMP) 3, MMP13, type II collagen and aggrecan expression in chondrocytes. To investigate the respective effects and the relationship of ERK1 and ERK2, knockdown of ERK1 and/or ERK2 was performed in human chondrocytes using specific small interfering RNAs (siRNAs), and the cells were treated with IL-1β (10 ng/ml) for 24 h. Uninfected chondrocytes treated with IL-1β (10 ng/ml) were used as a positive control. Other cells cultured without IL-1β or siRNA treatment were used as a negative control. The mRNA l...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4466952</comments>
            <pubDate>Thu, 03 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4466952</guid>        </item>
        <item>
            <title>Involvement of endoplasmic reticulum stress-associated apoptosis in a heart failure model induced by chronic myocardial ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=4466951&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21305250%26dopt%3DAbstract</link>
            <description>This study aimed to demonstrate whether ERS-associated apoptosis is involved in the pathogenesis of CMI-induced HF. We established a HF model induced by CMI in mini pigs via placement of an ameroid constrictor around the proximal anterior descending branch of the left coronary artery (LAD). Furthermore, we used myocardial perfusion imaging, echocardiographic and hemodynamic measurements, hematoxylin-eosin staining, and terminal deoxynucleotidyl transferase-mediated DNA nick-end labeling staining to identify the existence of myocardial ischemia and cardiac dysfunction and of enhanced apoptosis in the ischemic heart. We performed immunohistochemistry, Western blot, and real-time PCR to analyze the hallmark of ERS glucose-regulated protein 78 (GRP78). The ERS-associated apoptotic pathways, CC...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4466951</comments>
            <pubDate>Thu, 03 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4466951</guid>        </item>
        <item>
            <title>Increased expression of neutrophil gelatinase-associated lipocalin receptor by interleukin-1β in human mesangial cells via MAPK/ERK activation.</title>
            <link>http://www.medworm.com/index.php?rid=4466950&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21305251%26dopt%3DAbstract</link>
            <description>In conclusion, the data show that NGALR is differentially expressed in human glomerular disease and is significantly up-regulated by Il-1β in HMC via MAPK/ERK activation. Furthermore, exogenous NGAL can be uptaken into HMC.
    PMID: 21305251 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4466950</comments>
            <pubDate>Thu, 03 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4466950</guid>        </item>
        <item>
            <title>RAP-PCR fingerprinting reveals time-dependent expression of matrix-related molecules following stem-cell based TGFβ1-induced chondrocyte development.</title>
            <link>http://www.medworm.com/index.php?rid=4466955&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21286661%26dopt%3DAbstract</link>
            <description>Authors: Schedel J, Lowin T, Kujat R, Judex M, Schölmerich J, Nerlich M, Müller-Ladner U, Angele P
    Different approaches of engineering cartilage to treat defects in the articulating surfaces of the joints have been designed, which mainly use mesenchymal stem cells or autologous chondrocytes for in situ transplantation. However, these cells are poorly characterized with respect to viability, degree of differentiation and morphology or production of extracellular matrix. At present, one of the key approaches to generate chondrocytes is the stimulation of stem cells with transforming growth factor (TGF) β1. To characterize the molecular alterations occuring during the cellular transformation induced by TGF-β1 exposure, the differentiation process of bone marrow-derived stem cells into...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4466955</comments>
            <pubDate>Tue, 01 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4466955</guid>        </item>
        <item>
            <title>Polymer fraction of Aloe vera exhibits a protective activity on ethanol-induced gastric lesions.</title>
            <link>http://www.medworm.com/index.php?rid=4466954&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21286662%26dopt%3DAbstract</link>
            <description>Authors: Park CH, Nam DY, Son HU, Lee SR, Lee HJ, Heo JC, Cha TY, Baek JH, Lee SH
    For centuries, Aloe has been used as a herbal plant remedy against skin disorders, diabetes, and for its cardiac stimulatory activity. Here, we examined the gastroprotective effects of an Aloe vera polymer fraction (Avpf; molecular weight cut-off ≥50 kDa; 150 mg/kg body weight, p.o.) on an ethanol-induced gastric lesion mouse model. Mice pre-treated with Avpf had significantly fewer gastric lesions than their respective controls. To further examine the potential mechanism underlying this effect, we used reverse transcription-polymerase chain reaction to examine nitric oxide synthase and matrix metalloproteinase (MMP)mRNA expression on tissues from gastric lesions. Our results revealed that the mRNA expr...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4466954</comments>
            <pubDate>Tue, 01 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4466954</guid>        </item>
        <item>
            <title>Autophagy inhibition enhances etoposide-induced cell death in human hepatoma G2 cells.</title>
            <link>http://www.medworm.com/index.php?rid=4466957&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21274505%26dopt%3DAbstract</link>
            <description>Authors: Xie BS, Zhao HC, Yao SK, Zhuo DX, Jin B, Lv DC, Wu CL, Ma DL, Gao C, Shu XM, Ai ZL
    Induction of autophagy usually acts as a survival mechanism of cancer cells in response to chemotherapy. However, the function and molecular mechanism of autophagy in human hepatoma cells under drug treatment is still not clear. To address this issue, we established an experimental model in which HepG2 cells were treated with etoposide, a widely used anticancer agent. We demonstrate the etoposide-induced accumulation of GFP-LC3 dots by fluorescent microscopy, the up-regulation of LC3-II protein expression by Western blotting and the increased number of autophagic vacuoles by electron microscopy, confirming the activation of autophagy by etoposide in HepG2 cells. Inhibition of autophagy by either...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4466957</comments>
            <pubDate>Thu, 27 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4466957</guid>        </item>
        <item>
            <title>Protective role of parnaparin in reducing systemic inflammation and atherosclerotic plaque formation in ApoE-/- mice.</title>
            <link>http://www.medworm.com/index.php?rid=4466956&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21279309%26dopt%3DAbstract</link>
            <description>Authors: Artico M, Riganò R, Buttari B, Profumo E, Ionta B, Bosco S, Rasile M, Bianchi E, Bruno M, Fumagalli L
    Atherosclerosis is a degenerative disease whose role in the onset and development of cardiovascular pathologies and complications is of importance. Due to its silent but progressive development, and considering the endothelial, immunological and inflammatory processes that are involved in its clinical course, this still relatively unknown pathological condition has been and continues to be a matter of investigation worldwide. Our experience with previous studies on atherosclerosis led us to investigate the possible influence of a low molecular weight heparin (LMWH) - Parnaparin® on the development and clinical course of atherosclerosis in double knock-out laboratory animals ...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4466956</comments>
            <pubDate>Thu, 27 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4466956</guid>        </item>
        <item>
            <title>Fundamentals of prions and their inactivation (Review).</title>
            <link>http://www.medworm.com/index.php?rid=4466958&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21271212%26dopt%3DAbstract</link>
            <description>Authors: Sakudo A, Ano Y, Onodera T, Nitta K, Shintani H, Ikuta K, Tanaka Y
    Prion is an infectious particle composed of an abnormal isoform of the prion protein (PrPSc) and causes prion diseases such as bovine spongiform encephalopathy (BSE), Creutzfeldt-Jakob disease (CJD) and scrapie. Host cells express cellular prion protein (PrPC), which plays roles in normal functions such as anti-oxidative stress. PrPSc is derived from PrPC and produced by conformational conversion. Prion is notorious as a resistant pathogen, being difficult to inactivate with conventional sterilization procedures. Therefore, to prevent prion-caused iatrogenic diseases, the use of appropriate procedures to inactivate prions is important. For examples, alcohol treatment, autoclave (121˚C, 20 min) and γ-ray irrad...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4466958</comments>
            <pubDate>Tue, 25 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4466958</guid>        </item>
        <item>
            <title>Intracellular glutathione levels are involved in carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone-induced apoptosis in As4.1 juxtaglomerular cells.</title>
            <link>http://www.medworm.com/index.php?rid=4399929&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21258765%26dopt%3DAbstract</link>
            <description>In conclusion, these results suggest that compared to ROS levels, intracellular GSH levels are more closely linked to FCCP-induced apoptosis in As4.1 juxtaglomerular cells.
    PMID: 21258765 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4399929</comments>
            <pubDate>Fri, 21 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4399929</guid>        </item>
        <item>
            <title>Inhibitory action of Celastrol on hypoxia-mediated angiogenesis and metastasis via the HIF-1α pathway.</title>
            <link>http://www.medworm.com/index.php?rid=4399933&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21249310%26dopt%3DAbstract</link>
            <description>In this study, we have demonstrated that Celastrol is a potent inhibitor of hypoxia-induced angiogenic and metastatic activity as shown by a decrease in the proliferation of both endothelial and cancer cells, blocking of migration as well as of tube formation of endothelial cells, and by inhibition of cancer cell invasion under hypoxic conditions. Moreover, Celastrol decreased hypoxia-inducible factor-1α (HIF-1α) mRNA levels under both normoxia and hypoxia and inhibited hypoxia-induced accumulation of nuclear HIF-1α protein. Meanwhile, inhibition of nuclear HIF-1α protein levels were accompanied by a reduction in the transcriptional activity of HIF-1α target genes, including VEGF. In addition, the inhibitory effect of Celastrol on HIF-1α protein was partly due to its suppression of H...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4399933</comments>
            <pubDate>Tue, 18 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4399933</guid>        </item>
        <item>
            <title>Enhancement of radiation sensitivity in lung cancer cells by celastrol is mediated by inhibition of Hsp90.</title>
            <link>http://www.medworm.com/index.php?rid=4399932&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21249311%26dopt%3DAbstract</link>
            <description>Authors: Lee JH, Choi KJ, Seo WD, Jang SY, Kim M, Lee BW, Kim JY, Kang S, Park KH, Lee YS, Bae S
    The radiosensitizing activity of celastrol, a quinone methide triterpene was examined. We found that celastrol treatment of the NCI-H460 lung cancer cell line increased radiation-induced cell killing. The increased radiosensitivity was correlated with decreased levels of Hsp90 clients, such as EGFR, ErbB2 and survivin as well as with increased p53 expression. Celastrol inhibited the ATP-binding activity of Hsp90. Furthermore, celastrol treatment dissociated an Hsp90 client protein, EGFR, and this in turn resulted in degradation of the client protein. These results were not observed with another structurally similar triterpenoid, 6β-acetonyl-22β-hydroxytingenol (TG), suggesting that a spec...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4399932</comments>
            <pubDate>Tue, 18 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4399932</guid>        </item>
        <item>
            <title>Role of tumor necrosis factor-α in the pathogenesis of indomethacin-induced small intestinal injury in mice.</title>
            <link>http://www.medworm.com/index.php?rid=4399931&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21249312%26dopt%3DAbstract</link>
            <description>Authors: Fukumoto K, Naito Y, Takagi T, Yamada S, Horie R, Inoue K, Harusato A, Hirata I, Omatsu T, Mizushima K, Hirai Y, Yoshida N, Uchiyama K, Ishikawa T, Handa O, Konishi H, Wakabayashi N, Yagi N, Kokura S, Ichikawa H, Kita M, Yoshikawa T
    The pathogenesis of small intestinal damage caused by non-steroidal anti-inflammatory drugs (NSAIDs) such as indomethacin is still unclear. For this reason, there is currently no therapeutic strategy for ameliorating such damage. On the other hand, molecular treatment strategies targeting tumor necrosis factor (TNF)-α exert beneficial effects on intestinal lesions in patients with inflammatory bowel disease (IBD). To clarify the participation of TNF-α in NSAID-induced small intestinal damage, we investigated the effects of indomethacin administra...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
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            <pubDate>Tue, 18 Jan 2011 00:00:00 +0100</pubDate>
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            <title>Involvement of Cyr61 in the growth, invasiveness and adhesion of esophageal squamous cell carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=4399930&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21249313%26dopt%3DAbstract</link>
            <description>In this study, we have shown that there are high levels of Cyr61 in ESCC cell lines. Furthermore, using RNA interference (RNAi), we stably silenced the expression of Cyr61 in EC109 cells, an ESCC cell line. The colony formation, MTT, cell migration, cell invasiveness and cell adhesion assays were employed to address the roles of Cyr61 in the growth, migration and adhesion of ESCC cells. The results have shown that Cyr61 knockdown by RNAi leads to a significant reduction of colony formation and cell growth. The migration and invasiveness ability of EC109 cells were also suppressed with the Cyr61 down-regulation. Furthermore, the adhesion of the EC109 cells was decreased in the Cyr61 knockdown cells compared to the control cells. Taken together, our data suggest that Cyr61 may play crucial r...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
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            <pubDate>Tue, 18 Jan 2011 00:00:00 +0100</pubDate>
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            <title>An ethanol extract of Iris nertschinskia induces p53-dependent apoptosis in the MCF7 human breast cancer cell line.</title>
            <link>http://www.medworm.com/index.php?rid=4399934&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21240456%26dopt%3DAbstract</link>
            <description>In this study, we investigated the anti-tumor effect of the plant extract on MCF7 human breast cancer cells. An ethanol extract of Iris nertschinskia triggered cell death in a dose-dependent manner. Moreover, treatment with the extract promoted p53 phosphorylation in MCF7 cells. Increased phosphorylation of p53, in turn, led to induction of Bax protein, a key regulator of p53-dependent apoptotic cell death, as well as of caspase-7 cleavage in MCF7 cells. Consistently, cells treated with p53-specific siRNA or the caspase inhibitor, Z-VAD, resisted apoptotic cell death induced by the Iris nertschinskia extract. Our results suggest that p53 sensitizes tumor cells to the ethanol extract of Iris nertschinskia by Bax protein induction and caspase-dependent apoptosis.
    PMID: 21240456 [PubMed -...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4399934</comments>
            <pubDate>Fri, 14 Jan 2011 00:00:00 +0100</pubDate>
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            <title>microRNA-155 regulates angiotensin II type 1 receptor expression in umbilical vein endothelial cells from severely pre-eclamptic pregnant women.</title>
            <link>http://www.medworm.com/index.php?rid=4399935&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21234519%26dopt%3DAbstract</link>
            <description>In conclusion, endogenous mature miR-155 expression may be an important contributor to the pathogenesis of severe pre-eclampsia.
    PMID: 21234519 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4399935</comments>
            <pubDate>Thu, 13 Jan 2011 00:00:00 +0100</pubDate>
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            <title>Autophagy is required for toll-like receptor-mediated interleukin-8 production in intestinal epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=4399937&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21225224%26dopt%3DAbstract</link>
            <description>In conclusion, autophagy may be an important intracellular machinery for inducing the innate immune system in IECs.
    PMID: 21225224 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4399937</comments>
            <pubDate>Tue, 11 Jan 2011 00:00:00 +0100</pubDate>
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            <title>Evaluation of PMI-5011, an ethanolic extract of Artemisia dracunculus L., on peripheral neuropathy in streptozotocin-diabetic mice.</title>
            <link>http://www.medworm.com/index.php?rid=4399936&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21225225%26dopt%3DAbstract</link>
            <description>In conclusion, PMI-5011, a safe and non-toxic botanical extract, may find use in the treatment of diabetic peripheral neuropathy.
    PMID: 21225225 [PubMed - as supplied by publisher] (Source: International Journal of Molecular Medicine)</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4399936</comments>
            <pubDate>Tue, 11 Jan 2011 00:00:00 +0100</pubDate>
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            <title>IL-17 expression is correlated with hepatitis B‑related liver diseases and fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=4399939&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21225222%26dopt%3DAbstract</link>
            <description>In this study, we examined the expression of IL‑17 in patients with different chronic HBV-related diseases, and assessed the association between IL-17 expression and the degree of fibrosis. The method of immunohistochemistry was used to evaluate the localization of intrahepatic IL-17. We demonstrated significantly increased expression of IL‑17 in HBV-related chronic liver diseases, especially in liver fibrosis, and that the level of IL-17 is strongly correlated with the degree of fibrosis. Furthermore, we found that intrahepatic IL‑17 was mainly localized in the fibrosis region. Our data reveal important roles of IL-17 and IL-17-producing cells in the progression of HBV related chronic liver diseases, especially in the formation of liver fibrosis.
    PMID: 21225222 [PubMed - as supp...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
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            <pubDate>Mon, 10 Jan 2011 00:00:00 +0100</pubDate>
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            <title>Role of heat shock protein 27 in transforming growth factor-β-stimulated vascular endothelial growth factor release in osteoblasts.</title>
            <link>http://www.medworm.com/index.php?rid=4399938&amp;cid=s_36720_67_f&amp;fid=36720&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21225223%26dopt%3DAbstract</link>
            <description>Authors: Kato K, Tokuda H, Adachi S, Matsushima-Nishiwaki R, Yamauchi J, Natsume H, Minamitani C, Mizutani J, Otsuka T, Kozawa O
    We have previously reported that transforming growth factor-β (TGF-β) stimulates heat shock protein 27 (HSP27) induction via p44/p42 mitogen-activated protein (MAP) kinase, p38 MAP kinase and stress-activated protein kinase/c-Jun N-terminal kinase in osteoblast-like MC3T3-E1 cells, and that the release of vascular endothelial growth factor (VEGF) is induced by TGF-β in these cells. In the present study, we investigated the effect of HSP27 knockdown on the TGF-β-stimulated VEGF release in these cells. Gene silencing using short interfering RNA against HSP27 (HSP27-siRNA) significantly suppressed the TGF-β-induced VEGF release. Immunofluorescence microsco...</description>
            <author>International Journal of Molecular Medicine</author>
            <type>journals</type>
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            <pubDate>Mon, 10 Jan 2011 00:00:00 +0100</pubDate>
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