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        <title>Molecular and Cellular Biochemistry 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 'Molecular and Cellular Biochemistry' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Molecular+and+Cellular+Biochemistry&t=Molecular+and+Cellular+Biochemistry&s=Search&f=source]]></link>
        <lastBuildDate>Thu, 09 Feb 2012 13:38:41 +0100</lastBuildDate>
        <item>
            <title>Phosphorylation of GIT1 tyrosine 321 is required for association with FAK at focal adhesions and for PDGF-activated migration of osteoblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5657994&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22302306%26dopt%3DAbstract</link>
            <description>Authors: Ren Y, Yu L, Fan J, Rui Z, Hua Z, Zhang Z, Zhang N, Yin G
    Abstract
    Osteoblast migration and proliferation are fundamental processes in bone healing. We demonstrated that the G-protein-coupled receptor kinase interacting protein 1(GIT1) is a key regulator of bone mass and osteoblast cell migration, but little is known about GIT1 regulation by upstream signaling systems or the impact of GIT1 on downstream effectors. We found that platelet-derived growth factor (PDGF) stimulated the GIT1 tyrosine phosphorylation in osteoblast cells and increased the association of GIT1 with focal adhesion kinase (FAK) at osteoblast focal adhesions. The Src inhibitor PP2 and FAK siRNA inhibited GIT1 tyrosine phosphorylation and the increased association between GIT1 and FAK following stimulati...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5657994</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5657994</guid>        </item>
        <item>
            <title>Molecular characterization of the porcine MTPAP gene associated with meat quality traits: chromosome localization, expression distribution, and transcriptional regulation.</title>
            <link>http://www.medworm.com/index.php?rid=5658015&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22297614%26dopt%3DAbstract</link>
            <description>In this study, 2,296 bp partial cDNA sequences of the porcine MTPAP gene were obtained, which contained 1,746 bp full-length coding regions flanked by a 500 bp partial 3'-UTR. The porcine MTPAP gene was assigned to SSC10q14-q16 using the radiation hybrid (IMpRH) panel and chromosome electric location methods. Q-PCR analysis showed that MTPAP was expressed in all analyzed tissues, and has higher expression in heart, liver, skeletal muscles, and fat. One single nucleotide polymorphism g.2421T&amp;gt;A in intron5 of MTPAP gene was identified and detected by DdeI PCR-RFLP. Association of the genotypes with economic traits showed that different genotypes were significantly associated with juiciness, individuals with genotype AT displayed a significantly higher juiciness compared to genotype TT. ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658015</comments>
            <pubDate>Thu, 02 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5658015</guid>        </item>
        <item>
            <title>Curcumin causes promoter hypomethylation and increased expression of FANCF gene in SiHa cell line.</title>
            <link>http://www.medworm.com/index.php?rid=5658014&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22297615%26dopt%3DAbstract</link>
            <description>Authors: Parashar G, Parashar NC, Capalash N
    Abstract
    Curcumin and resveratrol were evaluated for their potential to cause reversal of promoter hypermethylation and associated gene expression of FANCF in SiHa cell line. Methylation specific PCR along with bisulphite sequencing revealed the demethylation of 12 CpG sites out of 15 CpG sites spanning +280 to +432 region of FANCF promoter after treatment with curcumin and fivefold up regulation of FANCF gene expression as shown by qRT-PCR. In vitro methylation assay also showed that M.SssI an analogue of DNMT1 was effectively inhibited at 50 μM concentration of curcumin. Resveratrol was not found to be effective in causing reversal of promoter hypermethylation of FANCF gene when used at 20 μM for 4 days in SiHa cell line.
    PMID...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658014</comments>
            <pubDate>Thu, 02 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5658014</guid>        </item>
        <item>
            <title>Human anti-EGFL7 recombinant full-length antibodies selected from a mammalian cell-based antibody display library.</title>
            <link>http://www.medworm.com/index.php?rid=5657999&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22297616%26dopt%3DAbstract</link>
            <description>We describe here the isolation of an EGFL7-specific antibody from a mammalian cell-based full-length antibody display library generated from peripheral blood mononuclear cells of patients with hepatocellular carcinoma. Using a novel vector, contained glycosylphosphatidylinositol anchor and restriction enzyme sites NheI and ClaI, antibody libraries are displayed as whole IgG molecules on the cell surface and screened for specific antigen binding by a combination of magnetic beads and measured by cell ELISA. Anti-EGFL7 antibody was successfully isolated from the library. The mammalian cell-based full-length antibody display library is a great potential application for rapid identification and cloning of human mAbs of targeting hepatocellular carcinoma.
    PMID: 22297616 [PubMed - as supplie...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5657999</comments>
            <pubDate>Thu, 02 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5657999</guid>        </item>
        <item>
            <title>Nocodazole increases the ERK activity to enhance MKP-1 expression which inhibits p38 activation induced by TNF-α</title>
            <link>http://www.medworm.com/index.php?rid=5658016&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22294037%26dopt%3DAbstract</link>
            <description>Authors: Guo X, Zhang X, Li Y, Guo Y, Wang J, Li Y, Shen B, Sun D, Zhang J
    Abstract
    The mitogen-activated protein kinase p38 plays key roles in cell progression, differentiation, inflammation, and apoptosis. p38 is activated by a variety of extracellular stimuli such as UV and proinflammatory cytokine tumor necrosis factor alpha (TNF-α). It has been demonstrated that destruction of microtubules with different reagents led to impaired p38 activation in response to various extracellular stimuli. However, several other groups have reported that microtubule-interfering agents stimulate the activation of MAPK superfamily members including p38 in certain cell context. The discrepancy suggests that destruction of microtubules stimulates the activation of MAPK superfamily members and ther...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658016</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5658016</guid>        </item>
        <item>
            <title>The emerging role of stem cells in ocular neurodegeneration: hype or hope?</title>
            <link>http://www.medworm.com/index.php?rid=5658021&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22290231%26dopt%3DAbstract</link>
            <description>Authors: Jindal N, Mukhopadhyay A, Anand A
    Abstract
    Affecting over a hundred million individuals worldwide, retinal diseases are among the leading causes of irreversible visual impairment and blindness. Thus, an appropriate study models, especially animal models, are essential to furthering our understanding of the etiology, pathology, and progression of these diseases. In this review, we provide an overview of retinal disorders in the context of biotherapeutic approaches in these disorders.
    PMID: 22290231 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658021</comments>
            <pubDate>Tue, 31 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5658021</guid>        </item>
        <item>
            <title>Emerging roles of SIRT6 on telomere maintenance, DNA repair, metabolism and mammalian aging.</title>
            <link>http://www.medworm.com/index.php?rid=5658023&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22286818%26dopt%3DAbstract</link>
            <description>Authors: Jia G, Su L, Singhal S, Liu X
    Abstract
    With the characterization of Sir2 gene in yeast aging, its mammalian homologs Sirtuins 1-7 have been attracting attention from scientists with various research backgrounds. Among Sirtuins, SIRT1 is the most extensively studied. Recent progress on mammalian Sirtuins has shown that SIRT6 as a histone deacetylase may also play a critical role in regulating mammalian aging. This review summarizes recent advances on SIRT6 as a key modulator of telomere structure, DNA repair, metabolism, and NF-kappa B pathway in aging. In addition, we discuss the challenges that remain to be studied in SIRT6 biology.
    PMID: 22286818 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658023</comments>
            <pubDate>Sun, 29 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5658023</guid>        </item>
        <item>
            <title>Cyclophosphamide-induced nephrotoxicity, genotoxicity, and damage in kidney genomic DNA of Swiss albino mice: the protective effect of Ellagic acid.</title>
            <link>http://www.medworm.com/index.php?rid=5658022&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22286819%26dopt%3DAbstract</link>
            <description>In this study, Ellagic acid (EA), a naturally occurring plant polyphenol, was evaluated for its antigenotoxicity and antioxidant efficacy against the CPM-induced renal oxidative stress and genotoxicity in Swiss albino mice. The mice were given a prophylactic treatment of EA orally at a dose of 50 and 100 mg/kg body weight (b wt) for seven consecutive days before the administration of a single intraperitoneal (i.p.) injection of CPM at 50 mg/kg b wt. The modulatory effects of EA on CPM-induced nephrotoxicity and genotoxicity were investigated by assaying oxidative stress biomarkers, serum kidney toxicity markers, DNA fragmentation, alkaline unwinding assay, micronuclei (MN) assay, and by histopathological examination of kidney tissue. A single intraperitoneal administration of CPM in mice...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658022</comments>
            <pubDate>Sun, 29 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5658022</guid>        </item>
        <item>
            <title>Cyclic fluid shear stress promotes osteoblastic cells proliferation through ERK5 signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5658025&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22286747%26dopt%3DAbstract</link>
            <description>This study was designed to investigate the potential involvement of ERK5 in the proliferative response of osteoblastic cells to cyclic fluid shear stress. We reported here that cyclic fluid shear stress promoted ERK5 phosphorylation in MC3T3-E1 cells. Inhibition of ERK5 phosphorylation attenuated the increased expression of AP-1 and cyclin D1 and cell proliferation induced by cyclic fluid flow, but promoted p-16 expression. Further more, we found that cyclic fluid shear stress was a better stimuli for ERK5 activation and cyclin D1 expression compared with continuous fluid shear stress. Moreover, the pharmacological ERK5 inhibitor, BIX02189, which inhibited ERK5 phosphorylation in a time-dependent manner and the suppression lasted for at least 4 h. Taken together, we demonstrate that ERK5/...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658025</comments>
            <pubDate>Sat, 28 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5658025</guid>        </item>
        <item>
            <title>siRNAs target sites selection of ezrin and the influence of RNA interference on ezrin expression and biological characters of osteosarcoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=5658024&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22286748%26dopt%3DAbstract</link>
            <description>Authors: Shang X, Wang Y, Zhao Q, Wu K, Li X, Ji X, He R, Zhang W
    Abstract
    Ezrin, one of the ezrin/radixin/moesin (ERM) protein family which act as membrane organizers and linkers between plasma membrane and cytoskeleton, has attracted much attention as a crucial factor for tumor metastasis. Overexpression of ezrin has been correlated with the metastatic potential of several cancers especially for osteosarcoma. Short interfering RNA (siRNA) downregulate gene expression through an enzyme-mediated process named RNA interference (RNAi). RNAi has rapidly come to be recognized as a powerful tool for the study of gene function and a potential target therapy. In the present study, the human osteosarcoma cell line MG63 was cultured. Three siRNAs targeting ezrin mRNA were designed by the mu...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658024</comments>
            <pubDate>Sat, 28 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5658024</guid>        </item>
        <item>
            <title>Long-term cisplatin exposure impairs autophagy and causes cisplatin resistance in human lung cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5638443&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22278384%26dopt%3DAbstract</link>
            <description>This study thus investigated whether an alteration in autophagy could be responsible for cisplatin resistance in the long-term exposure lung carcinoma cells. The cisplatin resistant clone (H460/cis) of H460 cells was established by exposing the cells with gradually increasing concentrations of cisplatin until chemoresistance acquisition was elucidated by MTT, Hoechst 33342 staining and comet assays. Degree of autophagosome formation and level of LC3 marker were evaluated by acridine orange and western blot analysis, respectively. H460/cis cells exhibited irregular shape with ~3-fold resistant to cisplatin-induced apoptosis compared with H460 cells. Proteins analysis for LC3 indicated that the levels of LC3 in resistant cells were significantly lower than those in H460 cells. Moreover, auto...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5638443</comments>
            <pubDate>Thu, 26 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5638443</guid>        </item>
        <item>
            <title>Astragaloside IV prevents MPP(+)-induced SH-SY5Y cell death via the inhibition of Bax-mediated pathways and ROS production.</title>
            <link>http://www.medworm.com/index.php?rid=5638442&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22278385%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether AS-IV protect against 1-methyl-4-phenylpyridnium ion (MPP(+))-induced dopaminergic neurotoxicity in SH-SY5Y cells and determined the mechanism of AS-IV neuroprotection. We found that pretreatment with AS-IV significantly reversed the loss of cell viability, nuclear condensation, the generation of intracellular reactive oxygen species (ROS), and the increase in Bax/Bcl-2 ratio and the activity of caspase-3 induced by MPP(+). Our study suggests that the neuroprotective effect of AS-IV is related to mechanisms including ROS production and the inhibition of Bax-mediated pathway. The present study supports the notion that AS-IV may be a promising neuroprotective agent for the treatment of neurodegenerative disorders such as PD.
    PMID: 22278385 [PubMed -...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5638442</comments>
            <pubDate>Thu, 26 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5638442</guid>        </item>
        <item>
            <title>Ubiquitin-like protein MNSFβ regulates TLR-2-mediated signal transduction.</title>
            <link>http://www.medworm.com/index.php?rid=5638444&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22273981%26dopt%3DAbstract</link>
            <description>In this study, we further examined the mechanism of action of MNSFβ in TLR-2-mediated signal transduction in macrophage-like cell line Raw264.7 cells. Although MNSFβ siRNA enhanced Pam(3)CDK(4) (TLR-2-specific ligand)-stimulated TNFα production, Bcl-G siRNA did not affect. MNSFβ cDNA inhibited the Pam(3)CDK(4)-stimulated TNFα production. High-molecular weight (130 kDa) MNSFβ-adduct was induced in Pam(3)CDK(4)-stimulated Raw264.7 cells. This MNSFβ-adduct was not induced by LPS, indicative of the specificity of TLR-2-mediated signal transduction. Similar observations were seen in BALB/c peritoneal macrophages. Interestingly, 40-kDa MNSFβ-adduct was tyrosine phosphorylated by Pam(3)CDK(4) stimulation. Collectively, novel MNSFβ-adducts may regulate TLR-2 signaling pathway in macropha...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5638444</comments>
            <pubDate>Wed, 25 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5638444</guid>        </item>
        <item>
            <title>Protein kinase CK2 is implicated in early steps of the differentiation of pre-adipocytes into adipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5638447&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22270543%26dopt%3DAbstract</link>
            <description>Authors: Wilhelm N, Kostelnik K, Götz C, Montenarh M
    Abstract
    Protein kinase CK2 is a ubiquitously expressed serine/threonine kinase which is composed of two catalytic α- or α'-subunits and two non-catalytic β-subunits. CK2 has been shown to be implicated in embryogenesis, spermatogenesis, and the development of certain organs but its role in basal differentiation processes is only sparsely analyzed. 3T3-L1 cells, which are murine pre-adipocytes, can be induced to differentiate into mature adipocytes within 2 weeks using a combination of insulin, dexamethasone, and isobutylmethylxanthine. We found that the activity of CK2 slightly increases until day 6 and subsequently, decreases in fully differentiated adipocytes. The decrease in activity goes along with a lower expression of...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5638447</comments>
            <pubDate>Tue, 24 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5638447</guid>        </item>
        <item>
            <title>Inhibition of immunoglobulin secretion from peripheral blood mononuclear cells by glucose-regulated protein94 (Grp94) in allergic subjects.</title>
            <link>http://www.medworm.com/index.php?rid=5638446&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22270544%26dopt%3DAbstract</link>
            <description>Authors: Tramentozzi E, Zamarchi R, Rossi E, Pagetta A, Frigo G, Finotti P
    Abstract
    Glucose-regulated protein94 (Grp94) is the most represented endoplasmic reticulum-resident HSP with the unique property to modulate the immune response. This has opened the way to the use of Grp94 as effective therapeutic agent in both depressed and exaggerated activity of the immune system. We investigated the effect of native Grp94 on peripheral blood mononuclear cells (PBMCs) isolated from blood of two subjects with a different history of bronchial allergic asthma. Whereas in subject 1 an elevated basal level of Ig and altered morphological aspects of PBMCs suggested an intense antigen-driven stimulation of the immune system, subject 2 had an apparently normal basal humoral response. However, Grp...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5638446</comments>
            <pubDate>Sun, 22 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5638446</guid>        </item>
        <item>
            <title>Mouse Tcf3 represses canonical Wnt signaling by either competing for β-catenin binding or through occupation of DNA-binding sites.</title>
            <link>http://www.medworm.com/index.php?rid=5638445&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22270545%26dopt%3DAbstract</link>
            <description>In this study we show that mouse Tcf3 represses canonical Wnt signaling in mouse neural stem cells and in human HEK 293 cells. We demonstrate that mouse Tcf3 mediates repression of both moderate and high levels of canonical Wnt signaling, by either competing with other members of the Tcf/Lef family for binding to β-catenin, or for binding to DNA. We observed that the repressor activity of mouse Tcf3 was only relieved effectively upon simultaneous disruption of both mechanisms. Immunofluorescence of transfected HEK 293 cells showed co-localization of β-catenin and Tcf3 in the nucleus of cells transfected with full-length Tcf3, but not in cells transfected with N-terminal deleted versions. A direct physical interaction between β-catenin and Tcf3 in the nucleus was confirmed by co-immunopr...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5638445</comments>
            <pubDate>Sun, 22 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5638445</guid>        </item>
        <item>
            <title>β-Adrenergic receptor stimulation induces endoplasmic reticulum stress in adult cardiac myocytes: role in apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5638449&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22270541%26dopt%3DAbstract</link>
            <description>In this study, we tested the hypothesis that β-AR stimulation induces ER stress, and induction of ER stress plays a pro-apoptotic role in cardiac myocytes. Using thapsigargin and brefeldin A, we demonstrate that ER stress induces apoptosis in adult rat ventricular myocytes (ARVMs). β-AR-stimulation (isoproterenol; 3h) significantly increased expression of ER stress proteins, such as GRP-78, Gadd-153, and Gadd-34, while activating caspase-12 in ARVMs. In most parts, these effects were mimicked by thapsigargin. β-AR stimulation for 15 min increased PERK and eIF-2α phosphorylation. PERK phosphorylation remained higher, while eIF-2α phosphorylation declined thereafter, reaching to ~50% below basal levels at 3 h after β-AR stimulation. This decline in eIF-2α phosphorylation was prevent...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5638449</comments>
            <pubDate>Sat, 21 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5638449</guid>        </item>
        <item>
            <title>Urotensin upregulates transforming growth factor-β1 expression of asthma airway through ERK-dependent pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5638448&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22270542%26dopt%3DAbstract</link>
            <description>Authors: Zhang WX, Liang YF, Wang XM, Nie Y, Chong L, Lin L, Chen C, Li CC
    Abstract
    Airway smooth muscle cells (ASMCs) play a key role in the process of asthma airway remodeling. Urotensin II (UII) and transforming growth factor (TGF)-β are potent mitogens for ASMCs proliferation. The study was aimed to determine whether UII-upregulated TGF-β-mediated ASMCs proliferation and extracellular signal-regulated kinase (ERK) was required for such an effect. OVA-sensitized rats were challenged to induce asthma. Lung morphology and airway dynamic parameters were monitored. ASMCs from control and asthma rats were purified for the measurement of UII and TGF-β1 expression. In vitro experiments were conducted to determine the direct effect of UII on TGF-β1 expression by ASMCs. Finally, U012...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5638448</comments>
            <pubDate>Sat, 21 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5638448</guid>        </item>
        <item>
            <title>Excessive dietary calcium in the disruption of structural and functional status of adult male reproductive system in rat with possible mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=5620138&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262485%26dopt%3DAbstract</link>
            <description>Authors: K Chandra A, Sengupta P, Goswami H, Sarkar M
    Abstract
    Calcium is essential for functioning of different systems including male reproduction. However, it has also been reported as chemo-castrative agent. The study has been undertaken to elucidate the effect of excessive dietary calcium on male reproductive system in animals with possible action. Adult male healthy rats fed CaCl(2) at different doses (0.5, 1.0 and 1.5 g%) in diet for 13 and 26 days to investigate reproductive parameters as well as the markers of oxidative stress. Significant alteration was found (P &amp;lt; 0.05) in testicular and accessory sex organs weight, epididymal sperm count, testicular steroidogenic enzyme (Δ(5) 3β-HSD and 17β-HSD) activities, serum testosterone, LH, FSH, LPO, activities of antiox...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620138</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5620138</guid>        </item>
        <item>
            <title>Transcription profile of DNA damage response genes at G(0) lymphocytes exposed to gamma radiation.</title>
            <link>http://www.medworm.com/index.php?rid=5620141&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22258824%26dopt%3DAbstract</link>
            <description>Authors: Saini D, Shelke S, Mani Vannan A, Toprani S, Jain V, Das B, Seshadri M
    Abstract
    Ionizing radiation induces a plethora of DNA damages in human cells which may alter the level of mRNA expression. We have analyzed mRNA expression profile of DNA damage response genes involved in G(0)/G(1) check point pathway in whole blood to assess their radio-adaptive response, if any, to gamma radiation. Blood samples were collected from twenty-five random, normal, and healthy male donors with written informed consent and irradiated at doses between 0.1 and 2.0 Gy (0.7 Gy/min). DNA strand breaks were studied using comet assay, whereas DNA double-strand breaks were visualized using γH2AX as a biomarker. Dose response if any, at transcriptional level was studied for all these dose groups a...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620141</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5620141</guid>        </item>
        <item>
            <title>4G/5G polymorphism modulates PAI-1 circulating levels in obese women.</title>
            <link>http://www.medworm.com/index.php?rid=5620140&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22258825%26dopt%3DAbstract</link>
            <description>Authors: Fernandes KS, Sandrim VC
    Abstract
    The increase in plasminogen activator inhibitor type 1 (PAI-1) has been described as a risk factor to thrombosis-related diseases. In addition, it has been demonstrated that the variant 4G of polymorphism 4G/5G located in promoter region of PAI-1 gene is associated with higher PAI-1 levels. We investigate the role of this polymorphism on circulating PAI-1 concentration in a population of 57 obese women (23%, 4G/4G; 49%, 4G/5G and 28%, 5G/5G genotypes). Our results demonstrate a genotype-specific modulation on PAI-1 levels in obese women, thus 5G/5G genotype presented significantly lower levels of plasma PAI-1 when compared to 4G/4G group (46 ± 19 ng/mL vs. 63  ± 13 ng/mL, respectively). Our findings indicate that obese carriers of ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620140</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5620140</guid>        </item>
        <item>
            <title>The molecular interaction of a copper chelate with human P-glycoprotein.</title>
            <link>http://www.medworm.com/index.php?rid=5620139&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22258826%26dopt%3DAbstract</link>
            <description>This study also demonstrated that CuNG has a drug interaction site different from verapamil-, vinblastine- and progesterone-binding sites on P-gp. Taken together, this is the first report of molecular interaction of any Schiff's base metal chelate CuNG with human P-gp. This information may be useful to design more efficacious nontoxic metal-based drugs as MDR-reversing agents.
    PMID: 22258826 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620139</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5620139</guid>        </item>
        <item>
            <title>Association of CTLA-4 gene polymorphisms with sporadic breast cancer risk and clinical features in Han women of Northeast China.</title>
            <link>http://www.medworm.com/index.php?rid=5620142&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22249287%26dopt%3DAbstract</link>
            <description>Authors: Li D, Zhang Q, Xu F, Fu Z, Yuan W, Li D, Pang D
    Abstract
    Cytotoxic T lymphocyte antigen-4 (CTLA-4) is an inhibitory molecule that plays a pivotal role in downregulating T-cell mediated immune responses. To determine the role of CTLA-4 in tumor immunity, and to validate previous results as well, we investigated four tag single nucleotide polymorphisms (SNPs) of CTLA-4 in a relatively large Chinese Han cohort from northeastern China. Genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 581 patients and 566 age-matched controls. Our data indicated that compared with the common genotype and allele of each SNP, the -1722 CC genotype and C allele showed an increased risk of breast cancer (P = 0.030, odds ratio (OR) = 1...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620142</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5620142</guid>        </item>
        <item>
            <title>Saturated fatty acid induction of endoplasmic reticulum stress and apoptosis in human liver cells via the PERK/ATF4/CHOP signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5620144&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246806%26dopt%3DAbstract</link>
            <description>This study investigated saturated fatty acid induction of endoplasmic reticulum (ER) stress and apoptosis in human liver cells and the underlying causal mechanism. Human liver L02 and HepG2 cell lines were exposed to the saturated fatty acid sodium palmitate. MTT assay was used for cell viability, flow cytometry and Hoechst 33258 staining for apoptosis, RT-PCR for mRNA expression, and Western blot for protein expression. Silence of PRK-like ER kinase (PERK) expression in liver cells was through transient transfection of PERK shRNA. Treatment of L02 and HepG2 cells with sodium palmitate reduced cell viability through induction of apoptosis. Sodium palmitate also induced ER stress in the cells, indicated by upregulation of PERK phosphorylation and expression of BiP, ATF4, and CHOP proteins. ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620144</comments>
            <pubDate>Sun, 15 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5620144</guid>        </item>
        <item>
            <title>Heat shock transcription factor 1 inhibits H(2)O          (2)-induced cardiomyocyte death through suppression of high-mobility group box 1.</title>
            <link>http://www.medworm.com/index.php?rid=5620143&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246807%26dopt%3DAbstract</link>
            <description>In this study, we investigated the effects of HSF1-regulated HMGB1 on cardiomyocyte death. Cultured cardiomyocytes were transfected with empty vector or HSF1 plasmid before the exposure to H(2)O(2). Cell death was assessed by cell staining. Additionally, the levels of intracellular and extracellular HMGB1 as well as its subcellular location were detected, and the expression of heat shock proteins (HSP27 and HSP90) in the cardiomyocytes was also determined. Not only did H(2)O(2) significantly increase cell death, but also elevated the levels of intracellular and extracellular HMGB1 and induced its translocation, whereas, as expected, HSF1 overexpression effectively attenuated cell death. Furthermore, HSF1 inhibited the intracellular expression of HMGB1 at early stage of oxidative stress and...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620143</comments>
            <pubDate>Sun, 15 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5620143</guid>        </item>
        <item>
            <title>Genome-wide analysis of HMGA2 transcription factor binding sites by ChIP on chip in gastric carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=5620145&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246783%26dopt%3DAbstract</link>
            <description>Authors: Zha L, Wang Z, Tang W, Zhang N, Liao G, Huang Z
    Abstract
    High mobility group protein A2 (HMGA2) is an architectural transcription factor that plays an important role in development and progression of malignant neoplasias. Recently, some studies reported that HMGA2 is also implicated in epithelial-mesenchymal transitions (EMT) and cancer stem cells. But the underlying mechanisms of these conditions are poorly understood. Therefore, we established an EMT model of gastric carcinoma cells by overexpressing HMGA2 in vitro, then global mapping of HMGA2 potential transcription factor binding sites was identified by promoter microarray in these cells, and the date obtained from the microarrays were validated via chromatin immunoprecipitation-PCR (ChIP-PCR) and real-time PCR. HMGA2...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620145</comments>
            <pubDate>Sat, 14 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5620145</guid>        </item>
        <item>
            <title>Characterization of antioxidant and anti-inflammatory activities of bioactive fractions recovered from a glucose-lysine Maillard reaction model system.</title>
            <link>http://www.medworm.com/index.php?rid=5620152&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22234502%26dopt%3DAbstract</link>
            <description>Authors: Chen XM, Kitts DD
    Abstract
    A glucose-lysine (Glu-Lys) Maillard reaction mixture heated at 121°C for 60 min was processed by ultrafiltration, ethyl acetate extraction, and semi-preparative HPLC to recover a bioactive fraction, termed F3. F3, characterized by spectral analysis to contain three distinct components, inhibited NO and IL-8 by 70 and 61%, respectively, at a concentration of 50 μg/ml in inflamed Caco-2 cells induced by IFN-γ and phorbol 12-myristate 13-acetate (PMA). F3 significantly (P &amp;lt; 0.05) down-regulated several genes involved in nuclear factor kappa B (NF-κB) signaling pathway. These genes included the cytokine receptors, TNFRSF10A and TNFRSF10B; receptor-associated proteins, IRAK2 and TICAM1; the inhibitor κB kinase, IKBKE; the NF-κB inhibitor, ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620152</comments>
            <pubDate>Wed, 11 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5620152</guid>        </item>
        <item>
            <title>Inducible nitric oxide synthase haplotype associated with migraine and aura.</title>
            <link>http://www.medworm.com/index.php?rid=5620147&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22234503%26dopt%3DAbstract</link>
            <description>Authors: de O S Mansur T, Gonçalves FM, Martins-Oliveira A, Speciali JG, Dach F, Lacchini R, Tanus-Santos JE
    Abstract
    Migraine is a complex neurological disorder with a clear neurogenic inflammatory component apparently including enhanced nitric oxide (NO) formation. Excessive NO amounts possibly contributing to migraine are derived from increased expression and activity of inducible NO synthase (iNOS). We tested the hypothesis that two functional, clinically relevant iNOS genetic polymorphisms (C(-1026)A-rs2779249 and G2087A-rs2297518) are associated with migraine with or without aura. We studied 142 healthy women without migraine (control group) and 200 women with migraine divided into two groups: 148 with migraine without aura (MWA) and 52 with aura (MA). Genotypes were determi...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620147</comments>
            <pubDate>Wed, 11 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5620147</guid>        </item>
        <item>
            <title>Activation of transcriptional activity of HSE by a novel mouse zinc finger protein ZNFD specifically expressed in testis.</title>
            <link>http://www.medworm.com/index.php?rid=5620154&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22231842%26dopt%3DAbstract</link>
            <description>In this study, we identified a novel C(2)H(2) type of zinc finger gene ZNFD from mice which has a 1,002 bp open reading frame and encodes a protein with 333 amino acid residues. The predicted 37.4 kDa protein contains a C(2)H(2) zinc finger domain. ZNFD gene is located on chromosome 18qD1. RT-PCR analysis revealed that the ZNFD gene was specifically expressed in mouse testis but not in other tissues. Subcellular localization analysis demonstrated that ZNFD was localized in the nucleus. Reporter gene assays showed that overexpression of ZNFD in the COS7 cells activates the transcriptional activities of heat shock element (HSE). Overall, these results suggest that ZNFD is a member of the zinc finger transcription factor family and it participates in the transcriptional regulation of HSE. M...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5620154</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5620154</guid>        </item>
        <item>
            <title>Influence of atorvastatin on the pharmacodynamic and pharmacokinetic activity of repaglinide in rats and rabbits.</title>
            <link>http://www.medworm.com/index.php?rid=5577853&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227917%26dopt%3DAbstract</link>
            <description>Authors: Sekhar MC, Reddy PJ
    Abstract
    Dyslipidemia is common in patients with type 2 diabetes. Statins are used as the first choice in treatment of diabetic dyslipidemia. Atorvastatin represents a first-line treatment option, alongside other hydroxyl methylglutaryl coenzyme A reductase inhibitors. Repaglinide is a short-acting, oral, insulin secretagogue that is used in the treatment of type 2 diabetes mellitus. Both the category of drugs undergo extensive metabolism with cytochrome enzyme system. This may lead to drug-drug interaction problems with altered repaglinide activity which is cautious. Repaglinide/atorvastatin/atorvastatin + repaglinide were administered orally to normal, diabetic rats, and to normal rabbits. Blood samples were collected at different time intervals and...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577853</comments>
            <pubDate>Sat, 07 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577853</guid>        </item>
        <item>
            <title>iTRAQ-coupled 2D LC-MS/MS analysis on differentially expressed proteins in denervated tibialis anterior muscle of Rattus norvegicus.</title>
            <link>http://www.medworm.com/index.php?rid=5577852&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227918%26dopt%3DAbstract</link>
            <description>Authors: Sun H, Li M, Gong L, Liu M, Ding F, Gu X
    Abstract
    To understand the molecular aspects of denervation-induced atrophy of skeletal muscles, isobaric tags for relative and absolute quantitation (iTRAQ) coupled with two-dimensional liquid chromatography-tandem mass spectrometry were performed to detect a total of 260 proteins that were differentially expressed in the rat tibialis anterior muscle at different times (1, 4, and 8 weeks) after rat sciatic nerve transection. Western blot, gene ontology, and Kyoto Encyclopedia of Genes and Genomes analyses were further conducted for protein validation, functional annotation, and pathway identification, respectively. Among 260 dysregulated proteins, metabolic enzymes represented the largest class of proteins differentially expressed...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577852</comments>
            <pubDate>Sat, 07 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577852</guid>        </item>
        <item>
            <title>Nuclear-mitochondrial cross-talk in global myocardial ischemia. A time-course analysis.</title>
            <link>http://www.medworm.com/index.php?rid=5577851&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22227919%26dopt%3DAbstract</link>
            <description>Authors: Marín-García J, Damle S, Jugdutt BI, Moe GW
    Abstract
    Myocardial ischemia results in early and progressive damage to mitochondrial structure and function, but the molecular events leading to these changes have not been clearly established. We hypothesized that mitochondrial dysfunction and a coordinated expression of nuclear and mitochondrial genes occur in a time-dependent manner by relating the time courses of changes in parameters of mitochondrial bioenergetics after ischemia-reperfusion. Using a Langendorff rat heart model, mitochondrial bioenergetics and protein levels were assessed at different times of ischemia and ischemia/reperfusion. Mitochondrial and nuclear gene expression (super array analysis) and mitochondrial DNA levels were evaluated after late ischemia. ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577851</comments>
            <pubDate>Sat, 07 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577851</guid>        </item>
        <item>
            <title>Expression and role in glycolysis of human ADP-dependent glucokinase.</title>
            <link>http://www.medworm.com/index.php?rid=5577854&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22219026%26dopt%3DAbstract</link>
            <description>Authors: Richter S, Richter JP, Mehta SY, Gribble AM, Sutherland-Smith AJ, Stowell KM, Print CG, Ronimus RS, Wilson WR
    Abstract
    A novel murine enzyme, ADP-dependent glucokinase (ADPGK), has been shown to catalyse glucose phosphorylation using ADP as phosphoryl donor. The ancestral ADPGK gene appears to have been laterally transferred from Archaea early in metazoan evolution, but its biological role has not been established. Here, we undertake an initial investigation of the functional properties of human ADPGK in human tumour cell lines and specifically test the hypothesis that ADPGK might prime glycolysis using ADP under stress conditions such as hypoxia. Recombinant human ADPGK was confirmed to catalyse ADP-dependent glucose phosphorylation in vitro, with an apparent K           ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577854</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577854</guid>        </item>
        <item>
            <title>Chronic hypobaric hypoxia mediated skeletal muscle atrophy: role of ubiquitin-proteasome pathway and calpains.</title>
            <link>http://www.medworm.com/index.php?rid=5577856&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22215202%26dopt%3DAbstract</link>
            <description>Authors: Chaudhary P, Suryakumar G, Prasad R, Singh SN, Ali S, Ilavazhagan G
    Abstract
    The most frequently reported symptom of exposure to high altitude is loss of body mass and decreased performance which has been attributed to altered protein metabolism affecting skeletal muscles mass. The present study explores the mechanism of chronic hypobaric hypoxia mediated skeletal muscle wasting by evaluating changes in protein turnover and various proteolytic pathways. Male Sprague-Dawley rats weighing about 200 g were exposed to hypobaric hypoxia (7,620 m) for different durations of exposure. Physical performance of rats was measured by treadmill running experiments. Protein synthesis, protein degradation rates were determined by (14)C-Leucine incorporation and tyrosine release, respec...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577856</comments>
            <pubDate>Wed, 04 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577856</guid>        </item>
        <item>
            <title>CYP3A5 and NAT2 gene polymorphisms: role in childhood acute lymphoblastic leukemia risk and treatment outcome.</title>
            <link>http://www.medworm.com/index.php?rid=5577855&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22215203%26dopt%3DAbstract</link>
            <description>This study aimed to evaluate the impact of the CYP3A5 and NAT2 metabolizing enzyme polymorphisms on the risk of childhood acute lymphoblastic leukemia. The analysis was conducted on 204 ALL patients and in 364 controls from a Brazilian population, using PCR-RFLP. The CYP3A5*3 polymorphic homozygous genotype was more frequent among ALL patients and the *3 allele variant was significantly associated with increased risk of childhood ALL (OR = 0.29; 95% CI, 0.14-0.60). The homozygous polymorphic genotype for the *6 allele variant was extremely rare and found in only two individuals. The heterozygous frequencies were similar for the ALL group and the control group. No significant differences were observed between the groups analyzed regarding NAT2 variant polymorphisms. None of the polymorphi...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577855</comments>
            <pubDate>Wed, 04 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577855</guid>        </item>
        <item>
            <title>Overexpression of hepatitis B x-interacting protein in HepG2 cells enhances tumor-induced angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5559478&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22209835%26dopt%3DAbstract</link>
            <description>In this study, the effect of HBXIP on the hepatoma cells-induced angiogenesis was investigated. Proliferation and migration of human umbilical vein endothelial cells (HUVECs) were detected by MTT and transwell assay, respectively. Tube formation and chick chorioallantoic membrane model were used to observe the angiogenesis. Vascular endothelial growth factor activity was assayed using ELISA kits. Western blotting was performed to examine the protein expression. Our results indicated that overexpression of HBXIP increased HepG2 cell-induced endothelial cells migration, proliferation, and angiogenesis, which may be related to increasing phosphorylation of endothelial NO synthase in HUVECs. These results suggest that HBXIP may play an important role in tumorigenesis by enhancing angiogenesis ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5559478</comments>
            <pubDate>Sat, 31 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5559478</guid>        </item>
        <item>
            <title>EPR studies on hydroxyl radical-scavenging activities of pravastatin and fluvastatin.</title>
            <link>http://www.medworm.com/index.php?rid=5559479&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22207075%26dopt%3DAbstract</link>
            <description>In this study, electron paramagnetic resonance spectroscopy in combination with 5,5-dimethyl-1-pyrroline N-oxide (DMPO)-spin-trapping technique was utilized to determine the abilities of pravastatin and fluvastatin in scavenging hydroxyl radical generated from Fe(II) with H(2)O(2) system. In addition, we examined the effects of pravastatin and fluvastatin on oxidative-induced φX-174 RF I plasmid DNA damage. We have demonstrated here for the first time that pravastatin and fluvastatin at physiologically relevant concentrations significantly decreased formation of DMPO-OH adduct indicating that both compounds could directly scavenge hydroxyl radicals. However, pravastatin and fluvastatin were not able to directly protect against oxidative DNA plasmid damage. The hydroxyl radical sequesterin...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5559479</comments>
            <pubDate>Fri, 30 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5559479</guid>        </item>
        <item>
            <title>Hydrogen sulfide protects H9c2 cells against doxorubicin-induced cardiotoxicity through inhibition of endoplasmic reticulum stress.</title>
            <link>http://www.medworm.com/index.php?rid=5559483&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22203419%26dopt%3DAbstract</link>
            <description>In conclusion, we have demonstrated that ROS-mediated inhibition of CSE is involved in DOX-induced cytotoxicity in H9c2 cells, and that exogenous H(2)S can confer protection against DOX-induced cardiotoxicity partly through inhibition of ER stress.
    PMID: 22203419 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5559483</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5559483</guid>        </item>
        <item>
            <title>Function of the syndecan-4 cytoplasmic domain in oligomerization and association with α-actinin in turkey muscle satellite cells.</title>
            <link>http://www.medworm.com/index.php?rid=5559482&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22203420%26dopt%3DAbstract</link>
            <description>This study addressed if S4 forms oligomers and interacts with α-actinin in muscle. The S4 cytoplasmic domain was found to interact with α-actinin in a phosphatidylinositol-4,5-bisphosphate dependent manner, but did not associate with vinculin. Through confocal microscopy, both S4 and syndecan-4 without the cytoplasmic domain were localized to the cell membrane. Although the cytoplasmic domain was necessary for the interaction with α-actinin, S4 oligomer formation occurred in the absence of the cytoplasmic domain. These data indicated that S4 function in skeletal muscle is mediated through the formation of oligomers and interaction with the cytoskeletal protein α-actinin.
    PMID: 22203420 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5559482</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5559482</guid>        </item>
        <item>
            <title>Protective effects of arachidonic acid against palmitic acid-mediated lipotoxicity in HIT-T15 cells.</title>
            <link>http://www.medworm.com/index.php?rid=5559481&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22203421%26dopt%3DAbstract</link>
            <description>Authors: Cho YS, Kim CH, Kim KY, Cheon HG
    Abstract
    Saturated fatty acids have been considered major contributing factors in type 2 diabetes, whereas unsaturated fatty acids have beneficial effects for preventing the development of diabetes. However, the effects of polyunsaturated fatty acids in pancreatic β cells have not been reported. Here, we examined the effects of arachidonic acid (AA) on palmitic acid (PA)-mediated lipotoxicity in clonal HIT-T15 pancreatic β cells. AA prevented the PA-induced lipotoxicity as indicated by cell viability, DNA fragmentation and mitochondrial membrane potential, whereas eicosatetraynoic acid (ETYA), a non-metabolizable AA, had little effect on PA-induced lipotoxicity. In parallel with its protective effects against PA-induced lipotoxicity, AA r...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5559481</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5559481</guid>        </item>
        <item>
            <title>TOP2 gene is involved in the pathogenicity of Candida albicans.</title>
            <link>http://www.medworm.com/index.php?rid=5559480&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22203422%26dopt%3DAbstract</link>
            <description>Authors: Zheng H, Yu YS
    Abstract
    Candida albicans is a common cause of morbidity in hospitalized and immunosuppressed patients. There are still many unknown genes involved in the virulence of C. albicans. The present study aims to examine the effect of TOP2 gene in candidal virulence, including hyphal growth, phospholipase and proteinase activity. Targeted gene disruption of both TOP2 alleles in a wild-type strain of C. albicans produced hyphae more efficiently. TOP2 disruption also increased phospholipase and proteinase activities, and enhanced virulence as assessed by host tissue colonization in systemic infection model. The result of reverse transcription PCR displayed that PLB1 and SAP4 expressions of top2 mutants was significantly upregulated when compared with the isogenic pa...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5559480</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5559480</guid>        </item>
        <item>
            <title>Lowered Nudix type 5 (NUDT5) expression leads to cell cycle retardation in HeLa cells.</title>
            <link>http://www.medworm.com/index.php?rid=5548401&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22200976%26dopt%3DAbstract</link>
            <description>Authors: Zhang LQ, Dai DP, Gan W, Takagi Y, Hayakawa H, Sekiguchi M, Cai JP
    Abstract
    The molecule 8-oxo-7,8-dihydroguanine (8-oxoGua), an oxidized form of guanine, can pair with adenine or cytosine during nucleic acid synthesis. Moreover, RNA containing 8-oxoGua causes translational errors, thus leading to the production of abnormal proteins. Human NUDT5, a MutT-related protein, catalyzes the hydrolysis of 8-oxoGDP to 8-oxoGMP, thereby preventing misincorporation of 8-oxoGua into RNA. To investigate the biological roles of NUDT5 in mammalian cells, we established cell lines with decreased level of NUDT5 expression. In NUDT5 inhibited cells, the RNA oxidation was not significantly higher than that of normal cells. However, the cell cycle G1 phase was significantly delayed, and cell ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548401</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548401</guid>        </item>
        <item>
            <title>Upon the tightrope in prostate cancer: two acrobats on the same tightrope to cross the finishline.</title>
            <link>http://www.medworm.com/index.php?rid=5548400&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22200977%26dopt%3DAbstract</link>
            <description>Authors: Farooqi AA, Fayyaz S, Rashid S
    Abstract
    Prostate cancer is a multifactorial, multistep progressive disorder that is undruggable to date because of stumbling blocks in the standardization of therapy. It is triggered by a broad range of proteins, signaling networks and DNA damage response modulators. It is becoming increasingly apparent that DNA repair mediators have split personalities, as they are instrumental in suppressing and promoting carcinogenesis. In this article, we discuss on post-transcriptional processing of regulators of DNA damage response, and how DNA repair proteins trigger shuttling of androgen receptor. Substantial fraction of information has been added into the existing literature of ATM biology; however, the particular area of post-transcriptional proces...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548400</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548400</guid>        </item>
        <item>
            <title>RNA interference against MDM2 suppresses tumor growth and metastasis in pancreatic carcinoma SW1990HM cells.</title>
            <link>http://www.medworm.com/index.php?rid=5548399&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22200978%26dopt%3DAbstract</link>
            <description>In this study, we show that down-regulation of MDM2 through lentivirus-mediated RNA interference could also suppress in vitro proliferation and in vivo tumor growth, and led to an obvious inhibition of both in vitro invasion and in vivo live metastases of SW1990HM cells which had an over-expression of MDM2 and a higher metastatic potential. Moreover, we also show that the down-regulation of MDM2 induced a significant decrease in MMP9, Ki-67 and increase in P53, E-Cadherin expression, and results in an altered expression of genes involved in metastasis, apoptosis, and cell proliferation. Our results suggest that MDM2 plays an important role in metastasis as well as tumor growth of PC. MDM2 could be a hopeful target for the control of PC.
    PMID: 22200978 [PubMed - as supplied by publisher...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548399</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548399</guid>        </item>
        <item>
            <title>Effects of hypoxia on osteogenic differentiation of rat bone marrow mesenchymal stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=5548407&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198287%26dopt%3DAbstract</link>
            <description>In this study, we found that temporary exposure of rBMSCs after osteogenic induction for 7 days to hypoxia (2% oxygen) led to a marked decrease in ALPase activity and the expression of osteocalcin and Runt related transcription factor 2/core binding factor a1 (Runx2/Cbfa1). Meanwhile, we found that exposure to hypoxia led to an early and transient increase in the level of phosphorylated ERK1/2 but had no obvious effects on mitogen-activated protein kinase (p38 MAPK) level. Based on these results, we concluded that hypoxia could inhibit osteogenic differentiation of rBMSCs possibly through MEK-ERK 1/2, while p38 MAPK may not participate in this regulation. Further exploration into the mechanisms of hypoxia on osteogenesis would surely provide reliable evidence for clinical practice.
    P...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548407</comments>
            <pubDate>Sun, 25 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548407</guid>        </item>
        <item>
            <title>Effects of SCR-3 on the immunosuppression accompanied with the systemic inflammatory response syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5548403&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198336%26dopt%3DAbstract</link>
            <description>In this study, SCR-3 gene knockout mice were used to study the effects of SCR-3 on the immunosuppression accompanied with systemic inflammatory response syndrome (SIRS). Bacterial clearance assay was performed by blood culture and frozen sections, and the results showed that the absence of SCR-3 protein serious damaged the innate immune system and the body's ability to inactivate or phagocytosis of bacteria was significantly decreased, and the absence of SCR-3 protein also weakened phagocytes' ability to degrade bacteria and their metabolites. Furthermore, animal model of inflammatory reaction was established and the immune function was determined, and the results revealed that SRC-3 protein may play an important role in maintenance of T-cells' immune function, and severe T-cell immune fun...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548403</comments>
            <pubDate>Sun, 25 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548403</guid>        </item>
        <item>
            <title>De novo characterization of the antler tip of Chinese Sika deer transcriptome and analysis of gene expression related to rapid growth.</title>
            <link>http://www.medworm.com/index.php?rid=5548402&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198337%26dopt%3DAbstract</link>
            <description>Authors: Yao B, Zhao Y, Wang Q, Zhang M, Liu M, Liu H, Li J
    Abstract
    Deer antlers are well known for their regeneration and rapid growth. However, little is known about the genes that are involved in their development, especially the molecular mechanisms responsible for rapid growth. In the present study, we produced more than 41 million sequencing reads using the Illumina sequencing platform. These reads were assembled into 89,001 unique sequences (mean size: 450 bp), representing more than 58 times as many Sika deer sequences previously available in the NCBI database (as of Sep 15, 2011). Based on a similarity search with known proteins, we identified 40,088 sequences with a cut-off E value of 10(-5). Assembled sequences were then annotated using Gene ontology terms, Clusters of...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548402</comments>
            <pubDate>Sun, 25 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548402</guid>        </item>
        <item>
            <title>Protective effects of 7-difluoromethyl-5,4'-dimethoxygenistein against human aorta endothelial injury caused by lysophosphatidyl choline.</title>
            <link>http://www.medworm.com/index.php?rid=5548406&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198288%26dopt%3DAbstract</link>
            <description>Authors: Liu F, Cao JG, Li C, Tan JS, Fu XH
    Abstract
    7-Difluoromethyl-5,4'-dimethoxygenistein (DFMG) is an active new derivative of genistein (GEN). It has shown effective protection in vascular endothelial injury. To further investigate its potential protective effects and its mechanism probably related to atherosclerosis, in present study, human aorta endothelial cells (HAECs) were chosen and treated with various concentrations of lysophosphatidyl choline (LPC) to establish an experimental model. Results showed that 10.0 μmol/l of LPC was optimal for inducing HAEC injury. DFMG pretreatment was able to prevent HAEC injury induced by LPC and restore cell viability in a concentration-dependent manner. The protective efficacy of DFMG (10.0 μmol/l) was significantly greater than t...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548406</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548406</guid>        </item>
        <item>
            <title>Apoptotic signaling in endothelial cells with neutrophil activation.</title>
            <link>http://www.medworm.com/index.php?rid=5548405&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198289%26dopt%3DAbstract</link>
            <description>Authors: Koshio O, Nagao T, Mabuchi A, Ono Y, Suzuki K
    Abstract
    As is the case for tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), degranulated substances (DS) released from polymorphonuclear leukocytes (PMN) and H(2)O(2) cause endothelial cell apoptosis through the phosphorylation of members of the mitogen-activated protein kinase (MAPK) family. Stimulation of human umbilical vein endothelial cells (HUVEC) with IL-1β or TNF-α/cycloheximide (CHX) was found to enhance the phosphorylation of p38 and Jun-N-terminal kinase (JNK) in a time-dependent fashion, but did not affect the time-dependent phosphorylation of extracellular signal-regulated kinase. In addition, IL-1β and TNF-α/CHX induced the phosphorylation of activating transcription factor-2 (ATF-2), but not c...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548405</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548405</guid>        </item>
        <item>
            <title>14-Aminotetradecanoic acid exhibits antioxidant activity and ameliorates xenobiotics-induced cytotoxicity.</title>
            <link>http://www.medworm.com/index.php?rid=5548404&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198290%26dopt%3DAbstract</link>
            <description>In this study, we report the antioxidant and cytoprotective properties of 14-aminotetradecanoic acid (ATDA) isolated from the Decalepis hamiltonii roots. ATDA is a potent scavenger of superoxide (O(2)                  (•-)), hydroxyl ((•)OH), nitric oxide ((•)NO), and lipid peroxide (LOO(•)) physiologically relevant free radicals with IC(50) values in nM (36-323) range. ATDA also exhibits concentration-dependent secondary antioxidant activities like reducing power, metal-chelating activity, and inhibition of protein carbonylation. Further, ATDA at nM concentration prevented CuSO(4)-induced human LDL oxidation. ATDA demonstrated cytoprotective activity in primary hepatocytes and Ehrlich ascites tumor cells against oxidative stress inducing xenobiotics apart from the in vitro free-ra...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548404</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548404</guid>        </item>
        <item>
            <title>MAOA, MTHFR, and TNF-β genes polymorphisms and personality traits in the pathogenesis of migraine.</title>
            <link>http://www.medworm.com/index.php?rid=5548410&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22193458%26dopt%3DAbstract</link>
            <description>Authors: Ishii M, Shimizu S, Sakairi Y, Nagamine A, Naito Y, Hosaka Y, Naito Y, Kurihara T, Onaya T, Oyamada H, Imagawa A, Shida K, Takahashi J, Oguchi K, Masuda Y, Hara H, Usami S, Kiuchi Y
    Abstract
    Migraine is a multifactorial disease with various factors, such as genetic polymorphisms and personality traits, but the contribution of those factors is not clear. To clarify the pathogenesis of migraine, the contributions of genetic polymorphisms and personality traits were simultaneously investigated using multivariate analysis. Ninety-one migraine patients and 119 non-headache healthy volunteers were enrolled. The 12 gene polymorphisms analysis and NEO-FFI personality test were performed. At first, the univariate analysis was performed to extract the contributing factors to pathoge...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548410</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548410</guid>        </item>
        <item>
            <title>Pro-inflammatory cytokines interleukin-1 beta, interleukin 6, and tumor necrosis factor-alpha alter the expression and function of ABCG2 in cervix and gastric cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5548409&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22193459%26dopt%3DAbstract</link>
            <description>In conclusion, pro-inflammatory cytokines were able to modulate the expression of ABCG2 at transcriptional and post-transcriptional levels in human cervix and gastric cancer cells.
    PMID: 22193459 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548409</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548409</guid>        </item>
        <item>
            <title>STAT1 mediates cellular senescence induced by angiotensin II and H(2)O          (2) in human glomerular mesangial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5548408&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22193460%26dopt%3DAbstract</link>
            <description>STAT1 mediates cellular senescence induced by angiotensin II and H(2)O     (2) in human glomerular mesangial cells.
    Mol Cell Biochem. 2011 Dec 23;
    Authors: Jiao S, Meng F, Zhang J, Yang X, Zheng X, Wang L
    Abstract
    Human glomerular mesangial cells (HMCs) have a finite lifespan and eventually enter irreversible growth arrest known as cellular senescence which is thought to contribute to kidney aging and age-related kidney disorders, such as chronic kidney disease. The signal transducer and activator of transcription 1 (STAT1) is a latent transcription factor involved in a variety of signal transduction pathways, including cell proliferation, apoptosis, and differentiation, but whether it could regulate HMCs senescence still remains to be explored. In our study, induction of A...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548408</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548408</guid>        </item>
        <item>
            <title>Gene/protein expression level, immunolocalization and binding characteristics of fatty acid binding protein from Clonorchis sinensis (CsFABP).</title>
            <link>http://www.medworm.com/index.php?rid=5548412&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22189506%26dopt%3DAbstract</link>
            <description>In this study, binding characteristics of CsFABP have been examined for the first time. The recombinant CsFABP (rCsFABP) was found to bind 11-(dansylamino) undecanoic acid (DAUDA), causing a blue shift in the fluorescence emission from 543 to 531 nm with an excitation wavelength of 345 nm and a substantial increase in fluorescence intensity. Fluorimetric titration of rCsFABP with DAUDA exhibited an apparent dissociation constant (K           (d)) of 1.58 ± 0.14 μM. In the competitive experiment, the rCsFABP efficiently bound saturated C(10)-C(18) fatty acids and unsaturated fatty acids (oleic acid and linoleic acid), and the latter presented the higher affinity. Furthermore, quantitative RT-PCR and western blotting analysis revealed that CsFABP mRNA and protein were differentially e...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548412</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548412</guid>        </item>
        <item>
            <title>Effects of phospholipids on the functional regulation of tBID in membranes.</title>
            <link>http://www.medworm.com/index.php?rid=5548411&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22189507%26dopt%3DAbstract</link>
            <description>Authors: Cho EY, Yun CH, Ahn T
    Abstract
    The functional interplay between tBID and phospholipids was investigated in this study. The binding of tBID to model membranes was increased by an incorporation of phosphatidylserine (PS) into the liposomes. Using limited proteolysis and mass spectrometry, two peptide regions, which correspond to Ser(100)-Arg(114) and His(89)-Arg(114) in BID, revealed the specific PS-binding site. tBID also decreased the light scattering values of PS-containing liposomes and increased the leakage of fluorescent dye encapsulated in vesicles, which suggest that tBID reduces membrane integrity by fragmentation. The membrane fragmentation by tBID was also observed using confocal and transmission electron microscopy. The activity of tBID paralleled results that we...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5548411</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5548411</guid>        </item>
        <item>
            <title>Antiproliferative and antioxidant potential of beta-ionone against benzo(a)pyrene-induced lung carcinogenesis in Swiss albino mice.</title>
            <link>http://www.medworm.com/index.php?rid=5532897&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187222%26dopt%3DAbstract</link>
            <description>This study is aimed to evaluate the therapeutic efficacy of beta-ionone (ION), a precursor for carotenoids against benzo(a)pyrene [B(a)P]-induced lung carcinogenesis. B(a)P (50 mg/kg body weight, orally twice a week for 4 successive weeks)-induced lung cancer in mice was assessed both in tissue and serum in terms of increase LPO and tissue marker enzymes, such as aryl hydrocarbon hydroxylase, γ-glutamyl transpeptidase, 5'-nucleotidase, and lactate dehydrogenase, and serum tumor markers such as carcinoembryonic antigen and neuron-specific enolase with concordant decrease in activities of tissue enzymic and non-enzymic antioxidants were observed on the treatment of ION (60 mg/kg body weight, orally twice a week for 16 weeks) significantly attenuated LPO and restored all cancer marker enz...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532897</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532897</guid>        </item>
        <item>
            <title>Re-expression of miR-21 contributes to migration and invasion by inducing epithelial-mesenchymal transition consistent with cancer stem cell characteristics in MCF-7 cells.</title>
            <link>http://www.medworm.com/index.php?rid=5532896&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187223%26dopt%3DAbstract</link>
            <description>Authors: Han M, Liu M, Wang Y, Mo Z, Bi X, Liu Z, Fan Y, Chen X, Wu C
    Abstract
    MiR-21 is known to play an important role in the development and progression, including migration and invasion, of many malignancies including breast cancer. Accumulating evidence suggest that the induction of epithelial-mesenchymal transition (EMT) phenotype and acquisition of cancer stem cell (CSC) characteristics are highly interrelated, and contribute to tumorigenesis, tumor progression, metastasis, and relapse. The molecular mechanisms underlying EMT and CSC characteristics during miR-21 contributes to cell migration and invasion of breast cancer are poorly understood. Therefore, we established miR-21 re-expressing breast cancer MCF-7 (MCF-7/miR-21) cells, which showed increasing cell growth, migrat...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532896</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532896</guid>        </item>
        <item>
            <title>Ionizing radiation induced signaling of DNA damage response molecules in RAW 264.7 and CD4(+) T cells.</title>
            <link>http://www.medworm.com/index.php?rid=5532898&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22173400%26dopt%3DAbstract</link>
            <description>Authors: Dhariwala FA, Narang H, Krishna M
    Abstract
    Ionizing radiation (IR) treatment results in activation of several DNA damage response molecules, such as ataxia telangiectasia, mutated (ATM), and DNA-dependent protein kinase (DNAPK) in mammals that are increasingly recognized for their potential roles in the sensing of DNA damage and initiating the subsequent protein kinase cascade. In vitro evidence indicates that both ATM and DNA-PK are responsible for efficient repair of DNA double strand breaks in response to IR exposure. To unravel the role of ATM and DNA-PK, we studied the mRNA and protein levels of ATM, DNA-PK and their downstream substrates in two different cell types after irradiation viz. macrophage like RAW264.7 cells and CD4(+) T cells isolated from mice spleen. Our...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532898</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532898</guid>        </item>
        <item>
            <title>Targeting of colorectal cancer growth, metastasis, and anti-apoptosis in BALB/c nude mice via APRIL siRNA.</title>
            <link>http://www.medworm.com/index.php?rid=5532899&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22170570%26dopt%3DAbstract</link>
            <description>In this study, the efficacy of RNAi targeting APRIL was analyzed via relevant experiments on human CRC xenografted in BALB/c nude mice. Both the mRNA and protein levels of APRIL were examined after intratumoral injection of APRIL small interfering RNA (siRNA). Meanwhile, pathological tools were utilized to observe the alterations on the aspects of proliferation, metastasis, apoptosis and cellular necrosis by means of detecting proliferating cell nuclear antigen, Ki-67, MMP-2, MMP-9, TIMP-3, TIMP-4, Bcl-2, Bax and Bcl-xL of CRC. In addition, terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labeling (TUNEL) and hematoxylin and eosin staining were also conducted to examine cell apoptosis and necrosis. It was found that grafted human colorectal tumor growth and meta...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532899</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532899</guid>        </item>
        <item>
            <title>Polymorphic variations in manganese superoxide dismutase (MnSOD), glutathione peroxidase-1 (GPX1), and catalase (CAT) contribute to elevated plasma triglyceride levels in Chinese patients with type 2 diabetes or diabetic cardiovascular disease.</title>
            <link>http://www.medworm.com/index.php?rid=5532901&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22167619%26dopt%3DAbstract</link>
            <description>Authors: Chen H, Yu M, Li M, Zhao R, Zhu Q, Zhou W, Lu M, Lu Y, Zheng T, Jiang J, Zhao W, Xiang K, Jia W, Liu L
    Abstract
    Manganese superoxide dismutase (MnSOD), glutathione peroxidase-1 (GPX1), and catalase (CAT) provide the primary antioxidant defense system. Impaired antioxidant defense increases oxidative stress and contributes to the development of type 2 diabetes and diabetic cardiovascular disease (CVD). We preformed a case-control study in Chinese type 2 diabetes patients, to determine if the MnSOD Val16Ala (T→C), GPX1 Pro198Leu (C→T), and CAT -262C/T (C→T) functional polymorphisms contribute to the development of type 2 diabetes or diabetic CVD. Patients with type 2 diabetes (n = 168) were divided into the non-CVD group (n = 83, &amp;gt;10 year since diagnosis) and C...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532901</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532901</guid>        </item>
        <item>
            <title>Bone morphogenetic protein 4 (BMP4) is required for migration and invasion of breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5532900&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22167620%26dopt%3DAbstract</link>
            <description>Authors: Guo D, Huang J, Gong J
    Abstract
    Bone-morphogenetic proteins (BMPs) play an important role in development and many cellular processes. However, their functional role in the development and progression of breast cancer is not clearly understood. In the present study, we performed a systematic expression analysis of the 14 types of BMPs in 10 human breast cancer cell lines. We found that bone morphogenetic protein 4 (BMP4) was one of the most frequently expressed BMPs. Furthermore, the expression level of BMP4 was maybe correlated with the metastatic potential of the cancer lines. Accordingly, overexpression of BMP4 in the breast cancer cell lines MCF-7 and MBA-MD-231 promoted the migration and invasion phenotypes of the cancer cells, whereas RNAi-mediated knockdown of BMP4 e...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532900</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532900</guid>        </item>
        <item>
            <title>Widdrol activates DNA damage checkpoint through the signaling Chk2-p53-Cdc25A-p21-MCM4 pathway in HT29 cells.</title>
            <link>http://www.medworm.com/index.php?rid=5532909&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160829%26dopt%3DAbstract</link>
            <description>Authors: Yun HJ, Hyun SK, Park JH, Kim BW, Kwon HJ
    Abstract
    Widdrol is an odorant compound isolated from Juniperus chinensis. We previously reported that widdrol induces Gap 1 (G1) phase cell cycle arrest and leads to apoptosis in human colon adenocarcinoma HT29 cells. It was also reported that this cell cycle arrest is associated with the induction of checkpoint kinase 2 (Chk2), p53 phosphorylation and cyclin dependent kinase (Cdk) inhibitor p21 expression. In this paper, we investigated the molecular mechanisms of widdrol on the activation of G1 DNA damage checkpoint at early phase when DNA damages occurred in HT29 cells. First of all, we examined that widdrol breaks DNA directly or not. As the results of DNA electrophoresis and formation of phosphorylated histone H2AX (γH2AX) f...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532909</comments>
            <pubDate>Sun, 11 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532909</guid>        </item>
        <item>
            <title>Functional analysis of pig myostatin gene promoter with some adipogenesis- and myogenesis-related factors.</title>
            <link>http://www.medworm.com/index.php?rid=5532908&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160830%26dopt%3DAbstract</link>
            <description>Authors: Deng B, Wen J, Ding Y, Gao Q, Huang H, Ran Z, Qian Y, Peng J, Jiang S
    Abstract
    Myostatin (MSTN) is primarily expressed in muscle and plays an important role in muscle and fat development in pigs. However, there is little information about the regulation of pig MSTN. In order to elucidate whether pig MSTN could be regulated by muscle- and fat-related factors, the porcine MSTN promoter was amplified and cloned into pGL3-basic vector, and transfected into cells to analyze the transcriptional activity of promoter with muscle- and fat-related factors through Dual-luciferase reporter assays. 5'-deletion expression showed that there was a negative-regulatory region located between nucleotides -1519 and -1236 bp, and there were some positive-regulatory regions located between -12...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532908</comments>
            <pubDate>Sun, 11 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532908</guid>        </item>
        <item>
            <title>External Qi of Yan Xin Qigong induces cell death and gene expression alterations promoting apoptosis and inhibiting proliferation, migration and glucose metabolism in small-cell lung cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5532911&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160803%26dopt%3DAbstract</link>
            <description>Authors: Yan X, Li F, Dozmorov I, Frank MB, Dao M, Centola M, Cao W, Hu D
    Abstract
    Small-cell lung cancer (SCLC) is a highly malignant carcinoma with poor long-term survival. Effective treatment remains highly demanded. In the present study, we demonstrated that External Qi of Yan Xin Qigong (YXQ-EQ) exerted potent cytotoxic effect towards SCLC cell line NCI-H82 via induction of apoptosis. Global gene expression profiling identified 39 genes whose expression was altered by YXQ-EQ in NCI-82 cells. Among them, semi-quantitative RT-PCR and real-time qPCR analyses confirmed that the gene expression levels of apoptotic proteins death-associated protein kinase 2 and cell death-inducing DFFA-like effector b were upregulated, whereas that of oncoproteins DEK and MYCL1, cell migration-promo...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532911</comments>
            <pubDate>Sat, 10 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532911</guid>        </item>
        <item>
            <title>Ouabain increases iNOS-dependent nitric oxide generation which contributes to the hypertrophic effect of the glycoside: possible role of peroxynitrite formation.</title>
            <link>http://www.medworm.com/index.php?rid=5532910&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160804%26dopt%3DAbstract</link>
            <description>In this study, we determined the possible contribution of ouabain-induced iNOS stimulation to the resultant hypertrophic as well as cytotoxic effects of the glycoside on cultured adult rat ventricular myocytes. Myocytes were treated with ouabain (50 μM) for up to 24 h. Ouabain significantly increased gene and protein levels of inducible nitric oxide synthase (iNOS) which was associated with significantly increased release of NO from myocytes as well as increased total release of reactive oxygen species (ROS), superoxide anion (O(2)                (-)), and increased peroxynitrite formation as assessed by protein tyrosine nitration. Administration of ouabain was also associated with increased levels of myocyte toxicity as determined by myocyte morphology, trypan blue staining and lactate...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532910</comments>
            <pubDate>Sat, 10 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532910</guid>        </item>
        <item>
            <title>Comparative epigenetic analysis of Oct4 regulatory region in RA-induced differentiated NT2 cells under adherent and non-adherent culture conditions.</title>
            <link>http://www.medworm.com/index.php?rid=5532907&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160855%26dopt%3DAbstract</link>
            <description>In this study, we induced differentiation of a human embryonic carcinoma cell line, NT2, under two different adherent and non-adherent culture conditions, and compared histone modifications as the epigenetic marks on the regulatory region of Oct4 gene after 3 days of differentiation. Using chromatin immunoprecipitation coupled with real-time PCR technique, it was shown that the after induction of differentiation the repressive epigenetic marks of hypoacetylation and methylation on lysine-9 of histone H3 occurred very effectively on the upstream of Oct4, especially in PP region. Also, comparing the two culturing systems it was shown that methylation of lysine-9 of H3 histone was more drastic in PE region of adherent cells rather than suspension cells. This epigenetic profile was in agreeme...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532907</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532907</guid>        </item>
        <item>
            <title>Isolation and characterization of stem-like cells from a human ovarian cancer cell line.</title>
            <link>http://www.medworm.com/index.php?rid=5532903&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160925%26dopt%3DAbstract</link>
            <description>We report here on the isolation and in vitro propagation of multicellular ovarian cancer spheroids from a well-established ovarian cancer cell line (OVCAR-3). The spheroid-derived cells (SDCs) display self-renewal potential, the ability to produce differentiated progeny, and increased expression of genes previously associated with CICs. SDCs also demonstrate higher invasiveness, migration potential, and enhanced resistance to standard anticancer agents relative to parental OVCAR-3 cells. Furthermore, SDCs display up-regulation of genes associated with epithelial-to-mesenchymal transition (EMT), anticancer drug resistance and/or decreased susceptibility to apoptosis, as well as, down-regulation of genes typically associated with the epithelial cell phenotype and pro-apoptotic genes. Pathway...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532903</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532903</guid>        </item>
        <item>
            <title>Stimulation of mechano-growth factor expression by myofibrillar proteins in murine myoblasts and myotubes.</title>
            <link>http://www.medworm.com/index.php?rid=5532902&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160926%26dopt%3DAbstract</link>
            <description>This study was undertaken to explore the nature of these protein inductors of MGF expression and to investigate the mechanism of their action. We report here that myofibrillar fraction of skeletal muscle homogenate activated MGF expression in murine myoblasts and myotubes in culture. The expression of another splice form of IGF-1 gene, IGF-1Ea, was also stimulated by myofibrils. Three myofibrillar proteins able to stimulate MGF synthesis were isolated. These proteins were identified by MALDI and immunoblotting as myomesin, myosin-binding protein C, and titin. The activation of MGF expression was associated with the increase of cAMP level in the cells. Inhibitor of adenylyl cyclase dideoxyadenosine arrested stimulation of MGF synthesis by all three myofibrillar proteins.
    PMID: 22160926 ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532902</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532902</guid>        </item>
        <item>
            <title>Conditioned medium from hypoxic cells protects cardiomyocytes against ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=5532906&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160856%26dopt%3DAbstract</link>
            <description>Authors: Chanyshev B, Shainberg A, Isak A, Chepurko Y, Porat E, Hochhauser E
    Abstract
    The hypothesis of the present study is that cardiomyocytes subjected to prolonged ischemia, may release survival factors that will protect new cardiac cells from ischemic stress. We exposed neonatal rat cardiomyocyte primary cultures to hypoxia, collected the supernatant, treated intact cardiac cells by this posthypoxic supernatant, and exposed them to hypoxia. The results show cardioprotection of the treated cells compared with the untreated ones. We named the collected posthypoxic supernatant &quot;conditioned medium&quot; (CM), which acts in a dose-dependent manner to protect new cardiac cells from hypoxia: 100 or 75% of CM diluted in phosphate-buffered saline (PBS) protected cells as if they were not ex...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532906</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532906</guid>        </item>
        <item>
            <title>Myocardial infarction in mice alters sarcomeric function via post-translational protein modification.</title>
            <link>http://www.medworm.com/index.php?rid=5532905&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160857%26dopt%3DAbstract</link>
            <description>Authors: Avner BS, Shioura KM, Scruggs SB, Grachoff M, Geenen DL, Helseth DL, Farjah M, Goldspink PH, John Solaro R
    Abstract
    Myocardial physiology in the aftermath of myocardial infarction (MI) before remodeling is an under-explored area of investigation. Here, we describe the effects of MI on the cardiac sarcomere with focus on the possible contributions of reactive oxygen species. We surgically induced MI in 6-7-month-old female CD1 mice by ligation of the left anterior descending coronary artery. Data were collected 3-4 days after MI or sham (SH) surgery. MI hearts demonstrated ventricular dilatation and systolic dysfunction upon echo cardiographic analysis. Sub-maximum Ca-activated tension in detergent-extracted fiber bundles from papillary muscles increased significantly in t...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532905</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532905</guid>        </item>
        <item>
            <title>Endonuclease G interacts with histone H2B and DNA topoisomerase II alpha during apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5532904&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22160858%26dopt%3DAbstract</link>
            <description>Authors: Vařecha M, Potěšilová M, Matula P, Kozubek M
    Abstract
    Apoptosis is a natural form of cell death involved in many physiological changes in the cell. Defects in the process of apoptosis can lead to serious diseases. During some apoptotic pathways, proteins apoptosis-inducing factor (AIF) and endonuclease G (EndoG) are released from the mitochondria and they translocate into the cell nuclei, where they probably participate in chromatin degradation together with other nuclear proteins. Exact mechanism of EndoG activity in cell nucleus is still unknown. Some interacting partners like flap endonuclease 1, DNase I, and exonuclease III were already suggested, but also other interacting partners were proposed. We conducted a living-cell confocal fluorescence microscopy followed...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532904</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532904</guid>        </item>
        <item>
            <title>The hypoxic preconditioning agent deferoxamine induces poly(ADP-ribose) polymerase-1-dependent inhibition of the mitochondrial respiratory chain.</title>
            <link>http://www.medworm.com/index.php?rid=5492772&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22147195%26dopt%3DAbstract</link>
            <description>Authors: Cañuelo A, Martínez-Romero R, Martínez-Lara E, Sánchez-Alcázar JA, Siles E
    Abstract
    We previously reported that treatment with a single dose of deferoxamine (DFO), which acts as a hypoxic-mimetic agent, only induces reactive oxygen species (ROS) production in the presence of poly(ADP-ribose) polymerase (PARP-1). Given that mitochondria are one of the main sources of ROS, the present study was designed to assess the effect of DFO treatment on the activity of mitochondrial respiratory chain complexes, and more importantly, to determine whether this effect is modulated by PARP-1. We found that DFO treatment induced a progressive decline in complex II and IV activity, but that this activity was preserved in PARP-1 knock-out cells, demonstrating that this decrease is media...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492772</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492772</guid>        </item>
        <item>
            <title>β-Hexosaminidase over-expression affects lysosomal glycohydrolases expression and glycosphingolipid metabolism in mammalian cells.</title>
            <link>http://www.medworm.com/index.php?rid=5492771&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22147196%26dopt%3DAbstract</link>
            <description>Authors: Tancini B, Magini A, Bortot B, Polchi A, Urbanelli L, Sonnino S, Severini GM, Emiliani C
    Abstract
    Lysosomes are not only degrading organelles but also involved in other critical cellular processes. In addition, active lysosomal glycohydrolases have been detected in an extra-lysosomal compartment: the presence of glycohydrolases on the plasma membrane (PM) has been widely demonstrated, and a possible role on the modification of the cell surface glycosphingolipids (GSL) participating in the modulation of cell functions such as cell-to-cell interactions and signal transduction pathways has been proposed. On this basis, the coordinated expression of lysosomal glycohydrolases and their translocation to the PM appear to be crucial for many cellular events. In this paper, we repo...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492771</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492771</guid>        </item>
        <item>
            <title>Induction of Fas-mediated extrinsic apoptosis, p21WAF1-related G2/M cell cycle arrest and ROS generation by costunolide in estrogen receptor-negative breast cancer cells, MDA-MB-231.</title>
            <link>http://www.medworm.com/index.php?rid=5492770&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22147197%26dopt%3DAbstract</link>
            <description>In this study, we first observed that costunolide inhibits cell growth in a dose-and time-dependent manner. To examine the mechanism by which costunolide inhibits cell growth, we checked the effect of costunolide on apoptosis and the cell cycle. Costunolide induced apoptosis through the extrinsic pathway, including the activation of Fas, caspase-8, caspase-3, and degradation of PARP. However, did not have the same effect on the intrinsic pathway as revealed by analysis of mitochondrial membrane potential (Δψm) with JC-1 dye and expression of Bcl2 and Bax proteins level. Furthermore, costunolide induced cell cycle arrest in the G2/M phase via decrease in Cdc2, cyclin B1 and increase in p21WAF1 expression, independent of p53 pathway in p53-mutant MDA-MB-231 cells and increases Cdc2-p21WAF1...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492770</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492770</guid>        </item>
        <item>
            <title>Alcohol-associated folate disturbances result in altered methylation of folate-regulating genes.</title>
            <link>http://www.medworm.com/index.php?rid=5492769&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22147198%26dopt%3DAbstract</link>
            <description>In conclusion, the initial deconjugation of polyglutamylated folate by GGH was not impaired in ethanol-fed rats while the conversion of monoglutamylated folate to polyglutamylated form might be impaired. There was tissue-specific altered methylation of folate transporter genes by chronic ethanol feeding.
    PMID: 22147198 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492769</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492769</guid>        </item>
        <item>
            <title>Combination treatment with dihydrotanshinone I and irradiation enhances apoptotic effects in human cervical cancer by HPV E6 down-regulation and caspases activation.</title>
            <link>http://www.medworm.com/index.php?rid=5492768&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22147199%26dopt%3DAbstract</link>
            <description>In this study, MTT, clonogenic assay, flow cytometry, and Western blotting were performed to assess the effect of treatment on cells. After treatment with IR, DI, and DI + IR, the apoptosis was 5.8, 13.3 and 22.5% (P &amp;lt; 0.05 vs. control), respectively. Clonogenic assay revealed that the survival of irradiated HeLa cell was significantly reduced by DI treatment. Combination treatment with IR and DI could down-regulate HPV E6 gene expression. Effect of DI on up-regulation of p21 expression and down-regulation of cyclin B1, p34(cdc2) expression in irradiated HeLa cell was concomitant with cell cycle arrest in G(2) phase. The significant increase in caspase-3 activity was also observed in the combination treatment. When HeLa cells were grown as xenografts in nude mice, combination treatm...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492768</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492768</guid>        </item>
        <item>
            <title>Magnetite induces oxidative stress and apoptosis in lung epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5492767&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22147200%26dopt%3DAbstract</link>
            <description>In this study, we investigated the toxic properties of magnetite stabilized with polyacrylate sodium. The magnetite was characterized by X-ray powder diffraction analysis, and the mean particle diameter was calculated using the Scherrer formula and was found to be 9.3 nm. In this study, we treated lung epithelial cells with different concentrations of magnetite and investigated their effects on oxidative stress and cell proliferation. Our data showed an inhibition of cell proliferation in magnetite-treated cells with a significant dose-dependent activation and induction of reactive oxygen species. Also, we observed a depletion of antioxidants, glutathione, and superoxide dismutase, respectively, as compared with control cells. In addition, apoptotic-related protease/enzyme such as caspase...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492767</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492767</guid>        </item>
        <item>
            <title>Mechanistic insights into the link between visfatin gene C-1535T polymorphism and coronary artery disease: an in vitro study.</title>
            <link>http://www.medworm.com/index.php?rid=5492766&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22147201%26dopt%3DAbstract</link>
            <description>Authors: Wang YS, Gao W, Li HF, Wang ZM, Zhu J, Zhao H, Yan JJ, Jia EZ, Yang ZJ, Wang LS
    Abstract
    Visfatin, a pro-inflammatory cytokine predominantly released from leucocytes, is correlated with coronary artery disease (CAD). We have previously reported that the -1535C&amp;gt;T polymorphism (rs1330082), which located on the promoter region of visfatin, was associated with decreased risk of CAD. Here, we investigated the underlying mechanism by which this polymorphism affects the genetic susceptibility to CAD. The difference of the promoter activities between -1535T variant and -1535C allele was tested by luciferase reporter gene assay. The difference of transcription factor binding activities between T and C allele was evaluated by electrophoretic mobility shift assay. In reporter gene...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492766</comments>
            <pubDate>Wed, 07 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492766</guid>        </item>
        <item>
            <title>Accumulation of the SET protein in HEK293T cells and mild oxidative stress: cell survival or death signaling.</title>
            <link>http://www.medworm.com/index.php?rid=5492776&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22143534%26dopt%3DAbstract</link>
            <description>Authors: Leopoldino AM, Squarize CH, Garcia CB, Almeida LO, Pestana CR, Polizello AC, Uyemura SA, Tajara EH, Gutkind JS, Curti C
    Abstract
    SET protein (I2PP2A) is an inhibitor of PP2A, which regulates the phosphorylated Akt (protein kinase B) levels. We assessed the effects of SET overexpression in HEK293T cells, both in the presence and the absence of mild oxidative stress induced by 50 μM tert-butyl hydroperoxide. Immunoblotting assays demonstrated that SET accumulated in HEK293T cells and increased the levels of phosphorylated Akt and PTEN; in addition, SET decreased glutathione antioxidant defense of cell and increased expression of genes encoding antioxidant defense proteins. Immunofluorescence analysis demonstrated that accumulated SET was equally distributed in cytoplasm an...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492776</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492776</guid>        </item>
        <item>
            <title>Effect of diallyl trisulfide derivatives on the induction of apoptosis in human prostate cancer PC-3 cells.</title>
            <link>http://www.medworm.com/index.php?rid=5492775&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22143535%26dopt%3DAbstract</link>
            <description>Authors: Chen M, Li B, Zhao X, Zuo H, He X, Li Z, Liu X, Chen L
    Abstract
    The effects of five derivatives of diallyl trisulfide (DATS) were investigated on apoptosis in prostate cancer PC-3 cells, including dibutenyl trisulfide (DBTS), bis(2-methylallyl) trisulfide (2-M-DATS), dipentenyl trisulfide (DPTS), bis(3-methylbut-2-enyl) trisulfide (3-M-DBTS), and dihexenyl trisulfide (DHTS). Our present study demonstrated that DATS derivatives can suppress proliferation of PC-3 cells in a dose- and time-dependent manner, and that a change in the DATS structure could have an impact on its biological activity in the following order: 2-M-DATS &amp;gt; DBTS ≈ DPTS ≈ DATS &amp;gt; 3-M-DBTS ≈ DHTS. Typical apoptotic nuclei were shown by Hoechst 33342 staining with 80 μM concentrations ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492775</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492775</guid>        </item>
        <item>
            <title>Expression of FHL1 in gastric cancer tissue and its correlation with the invasion and metastasis of gastric cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5492774&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22143536%26dopt%3DAbstract</link>
            <description>This study was performed to analyze the expression of four and a half LIM domains 1 (FHL1) in gastric carcinoma tissue and its correlation with the clinicopathological characteristics of gastric cancer. In addition, the role of FHL1 in the invasion and metastasis of gastric cancer cells was investigated to provide an experimental basis for future treatments of gastric cancer. FHL1 mRNA and protein expression in gastric carcinoma and the adjacent normal gastric mucosa tissue were determined using RT-PCR and western blots. Correlations of FHL1 expression with the incidence, progression, and clinicopathological characteristics of gastric cancer were analyzed. Changes in the invasion and metastatic potential of MKN45 human gastric cancer cells were observed after the transient transfection wit...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492774</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492774</guid>        </item>
        <item>
            <title>Erratum to: Effect of the modulation of leucine zipper tumor suppressor 2 expression on proliferation of various cancer cells functions as a tumor suppressor.</title>
            <link>http://www.medworm.com/index.php?rid=5492773&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22143537%26dopt%3DAbstract</link>
            <description>Authors: Kim JM, Song JS, Cho HH, Shin KK, Bae YC, Lee BJ, Jung JS
    PMID: 22143537 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492773</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492773</guid>        </item>
        <item>
            <title>Vitamin E ameliorates ox-LDL-induced foam cells formation through modulating the activities of oxidative stress-induced NF-κB pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5492779&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22139346%26dopt%3DAbstract</link>
            <description>Authors: Huang ZG, Liang C, Han SF, Wu ZG
    Abstract
    The role of antioxidant supplementation with vitamin E in the prevention of atherosclerosis has been a topic of considerable recent interest. The relevance of vitamin E for macrophage-derived foam cell formation, a hallmark of atherosclerosis, however, has not been unequivocally resolved. Here, we investigated the effect of Oxidized LDL (ox-LDL) and vitamin E on lipid accumulation and total cholesterol content in U937 macrophages, reactive oxygen species generation and expression of nuclear factor-κB (NF-κB) signaling pathway. The results showed that the mRNA expression and protein levels of P-selectin were evident in U937 macrophages treated with ox-LDL and vitamin E, which indicating that expression of P-selectin is important i...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492779</comments>
            <pubDate>Sun, 04 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492779</guid>        </item>
        <item>
            <title>Human endothelial progenitor cells isolated from COPD patients are dysfunctional.</title>
            <link>http://www.medworm.com/index.php?rid=5492778&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22139347%26dopt%3DAbstract</link>
            <description>Authors: Liu X, Xie C
    Abstract
    Cardiovascular disease is the leading cause of morbidity and mortality in patients with moderate-to-severe chronic obstructive pulmonary disease (COPD). More than 44% of these patients present with generalized atherosclerosis at autopsy. It is accepted that endothelial progenitor cells (EPCs) participate in the repair of dysfunctional endothelium and thus protects against atherosclerosis. However, whether COPD affects the repairing capacity of EPCs is unknown. Therefore, the objective of this study was to determine whether and how EPCs are involved in the vascular repair process in patients with COPD. In our study, EPCs from 25 COPD and 16 control patients were isolated by Ficoll density-gradient centrifugation and identified using fluorescence activa...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492778</comments>
            <pubDate>Sun, 04 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492778</guid>        </item>
        <item>
            <title>Exocytosis of SH-SY5Y single cell with different shapes cultured on ITO micro-pore electrode.</title>
            <link>http://www.medworm.com/index.php?rid=5492777&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22139348%26dopt%3DAbstract</link>
            <description>Authors: Zhao H, Li L, Fan HJ, Wang F, Jiang LM, He PG, Fang YZ
    Abstract
    Communication between cells by release of specific chemical messengers via exocytosis plays crucial roles in biological process. Catecholamines, like dopamine, epinephrine, and norepinephrine, which are types of neurotransmitters released from cells, can be oxidized and detected by the microelectrodes, and amperometric detection of exocytosis is an effective method for studying the communication between cells. The experimental results depend on many factors, among which the property of the microelectrode, cell states, and their positions to each other are particularly important. A type of indium tin oxide (ITO) micro-pore electrodes, which is characterized by its stability, has been developed with photolithogr...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492777</comments>
            <pubDate>Sun, 04 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492777</guid>        </item>
        <item>
            <title>De-regulation of the RBBP6 isoform 3/DWNN in human cancers.</title>
            <link>http://www.medworm.com/index.php?rid=5492782&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22139301%26dopt%3DAbstract</link>
            <description>In conclusion, these findings suggest that RBBP6 isoform 3 is a cell cycle regulator and may be de-regulated in carcinogenesis.
    PMID: 22139301 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492782</comments>
            <pubDate>Sat, 03 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492782</guid>        </item>
        <item>
            <title>An essential role for the Id1/PI3K/Akt/NFkB/survivin signalling pathway in promoting the proliferation of endothelial progenitor cells in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=5492781&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22139302%26dopt%3DAbstract</link>
            <description>This study aimed to investigate the effects of Id1 on the phosphatidylinositol-3-kinase (PI3K)/Akt/nuclear factor kappa B (NFκB)/survivin signalling pathway and its significance in promoting EPC proliferation in vitro. Spleen-derived EPCs were cultured as previously described. Id1 was presented at low levels in EPCs, and was rapidly up-regulated by stimulation with vascular endothelial growth factor. We demonstrated that transient transfection of Id1 into EPCs activated the PI3K/Akt/NFκB/survivin signalling pathway and promoted EPC proliferation. The proliferation of EPCs was extensively inhibited by silencing of endogenous Id1, and knockdown of Id1 expression led to suppression of PI3K/Akt/NFκB/survivin signalling pathway in EPCs. In addition, blockade by the PI3K-specific inhibitor LY...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492781</comments>
            <pubDate>Sat, 03 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492781</guid>        </item>
        <item>
            <title>Senescent endothelial dysfunction is attributed to the up-regulation of sphingosine-1-phosphate receptor-2 in aged rats.</title>
            <link>http://www.medworm.com/index.php?rid=5492780&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22139303%26dopt%3DAbstract</link>
            <description>Authors: Lu H, Yuan H, Chen S, Huang L, Xiang H, Yang G, Deng H, Zhou J
    Abstract
    Sphingosine-1-phosphate (S1P) regulates an array of biological activities in various cell types. Many S1P-regulated functions are mediated by S1P receptor subtypes. Previous studies have shown that the S1P receptor-2 (S1P(2) receptor) is involved in senescence of endothelial cells in vitro. However, the functional outcomes of S1P(2) receptor-mediated signaling pathways in a physiological environment are currently unknown. The main aim of this study was to explore the underlying mechanisms of senescent-associated impairments in pulmonary microvascular endothelial cells (PMECs) isolated from young and aged rats in vivo. The expression of S1P receptor subtypes in PMECs was detected using RT-PCR and Wester...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492780</comments>
            <pubDate>Sat, 03 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492780</guid>        </item>
        <item>
            <title>Inhibition of ROS-activated ERK1/2 pathway contributes to the protection of H(2)S against chemical hypoxia-induced injury in H9c2 cells.</title>
            <link>http://www.medworm.com/index.php?rid=5492784&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22134701%26dopt%3DAbstract</link>
            <description>In conclusion, these results indicate that H(2)S protects H9c2 cells against chemical hypoxia-induced injury partially by inhibiting ROS-mediated activation of ERK1/2.
    PMID: 22134701 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492784</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492784</guid>        </item>
        <item>
            <title>Dose-dependent effects of thyroid hormone on post-ischemic cardiac performance: potential involvement of Akt and ERK signalings.</title>
            <link>http://www.medworm.com/index.php?rid=5492783&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22134702%26dopt%3DAbstract</link>
            <description>In conclusion, TH appears to have a dose-dependent bimodal effect on post-ischemic cardiac performance and this effect may, at least in part, be mediated by a distinct pattern of activation of Akt and ERK signaling.
    PMID: 22134702 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492783</comments>
            <pubDate>Fri, 02 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5492783</guid>        </item>
        <item>
            <title>Intracellular trafficking and secretion of mouse mesencephalic astrocyte-derived neurotrophic factor.</title>
            <link>http://www.medworm.com/index.php?rid=5455103&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120531%26dopt%3DAbstract</link>
            <description>Authors: Oh-Hashi K, Tanaka K, Koga H, Hirata Y, Kiuchi K
    Abstract
    Recently, mesencephalic astrocyte-derived neurotrophic factor (MANF) has been reported to prevent cell death under some pathophysiological conditions. MANF, also referred to as arginine rich, mutated in early stage of tumors (Armet), was identified as an endoplasmic reticulum (ER) stress-inducible factor. Using RT-PCR, we found two variants of MANF mRNA: wild type, which contains exon 1 (wt-MANF), and one lacking exon 1, which is presumably not secreted (ΔΝ-MANF) in Neuro2a cells. The latter has a putative translational start site upstream of the second exon in the mouse MANF gene. Comparing the expression of wt-MANF with that of ΔΝ-MANF, we found that the amount of intracellular ΔΝ-MANF was much lower than th...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5455103</comments>
            <pubDate>Sun, 27 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5455103</guid>        </item>
        <item>
            <title>Cyanidin-3-glucoside suppresses TNF-α-induced cell proliferation through the repression of Nox activator 1 in mouse vascular smooth muscle cells: involvement of the STAT3 signaling.</title>
            <link>http://www.medworm.com/index.php?rid=5455105&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120492%26dopt%3DAbstract</link>
            <description>Authors: Luo X, Fang S, Xiao Y, Song F, Zou T, Wang M, Xia M, Ling W
    Abstract
    Cyanidin-3-glucoside (C3G) is a member of the anthocyanin family which belongs to the flavonoid class and possesses antiatherogenic properties. Many studies have demonstrated the protective effects of C3G on vascular endothelial cells and monocytes, however, the precise effects on vascular smooth muscle cells (VSMCs) have been less thoroughly studied. Hence, we investigated the role of C3G in TNF-α-induced VSMCs proliferation and explored the possible mechanisms. TNF-α stimulated VSMCs proliferation, and pretreatment with C3G inhibited the proliferation in dose- and time-dependent manners. Then, we found that C3G attenuated TNF-α-induced ROS over generation by Dihydroethidium staining. The combination ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5455105</comments>
            <pubDate>Sat, 26 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5455105</guid>        </item>
        <item>
            <title>Oct4 was a novel target of Wnt signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5455104&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120493%26dopt%3DAbstract</link>
            <description>Authors: Li J, Li J, Chen B
    Abstract
    The specific expression of Oct4 during early mouse development is required for the correct maintenance of pluripotent cells, and the regulatory control of the Oct4 expression is important. Wnt signaling could have multiple and/or complex effects on embryonic stem (ES) cells characteristics. Elucidation of the molecular mechanisms affecting Wnt signaling in ES cells could provide a better understanding of how these effects occur. The purpose of this study was to determine whether Oct4 was regulated by Wnt signaling in undifferentiated ES cells. Here, we report Oct4 as a novel target of β-catenin-mediated transcription. First, we observe that Wnt signaling pathway is activated in undifferentiated mouse ES cells. In 239T cells, Oct4 promoter was r...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5455104</comments>
            <pubDate>Sat, 26 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5455104</guid>        </item>
        <item>
            <title>Impact of XPD gene polymorphism on risk of prostate cancer on north Indian population.</title>
            <link>http://www.medworm.com/index.php?rid=5455106&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22116596%26dopt%3DAbstract</link>
            <description>Authors: Sobti RC, Berhane N, Melese S, Mahdi SA, Gupta L, Thakur H, Singh N
    Abstract
    Prostate cancer is the second most diagnosed cancer in men next to skin cancer in the developed world. Risk of disease varies most prominently with age, ethnicity, family history, and diet. Genetic polymorphism of some genes has been implicated in increasing the risk. The XPD (Xeroderma pigmentosum group D) gene codes for a DNA helicase involved in transcription and nucleotide excision repair. The aim of this study is to evaluate the effect of XPD 751 Lys/Gln polymorphism on risk of prostate cancer on north Indian patients. Blood sample from 150 prostate cancer patients, 150 from Prostate Hyper Plasia and equal number of samples from healthy control groups was collected from North India. The polym...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5455106</comments>
            <pubDate>Fri, 25 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5455106</guid>        </item>
        <item>
            <title>Regulation of metabolism and transport of sphingosine-1-phosphate in mammalian cells.</title>
            <link>http://www.medworm.com/index.php?rid=5455107&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22113622%26dopt%3DAbstract</link>
            <description>Authors: Liu X, Zhang QH, Yi GH
    Abstract
    Sphingosine-1-phosphate (S1P), which is generated from the sphingosine kinase-catalyzed phosphorylation of sphingosine, is now recognized as a critical regulator of many kinds of physiological and pathological processes, including cancer, cardiovascular function, and diabetes. It can also trigger a wide variety of biological effect, such as cell movement, differentiation, survival, inflammation, immunity, calcium homeostasis, and angiogenesis. As we know, a number of the biological effects of S1P are mediated by its binding to five specific G protein-coupled receptors located on the cell surface or intracellular targets. However, the synthesis and the secretion of S1P are regulated by various endogenetic or ectogenous stimuli and involve man...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5455107</comments>
            <pubDate>Thu, 24 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5455107</guid>        </item>
        <item>
            <title>APOE -491 T allele may reduce the risk of atherosclerotic lesions among middle-aged women.</title>
            <link>http://www.medworm.com/index.php?rid=5455109&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22101914%26dopt%3DAbstract</link>
            <description>Authors: Bañares VG, Bardach A, Peterson G, Tavella MJ, Schreier LE
    Abstract
    Genetic variability of the APOE gene confers susceptibility to coronary artery disease (CAD). Beyond variability on the coding region, polymorphisms in the regulatory region of the APOE gene have been associated with variation on plasma cholesterol levels. It has also been demonstrated a complex and multifactorial association between, APOE gene polymorphisms, gender, plasma lipids levels and risk of CAD. In the present case-control study, we examined polymorphisms -427 T/C and -491 A/T in the promoter region of APOE in relation to lipid profile and the coronary atherosclerosis, in a sample of Argentinean adults with (cases) and without (controls) atherosclerotic injuries regarding gender and age. In femal...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5455109</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5455109</guid>        </item>
        <item>
            <title>Erratum to: Natural vanadium-containing Jeju ground water stimulates glucose uptake through the activation of AMP-activated protein kinase in L6 myotubes.</title>
            <link>http://www.medworm.com/index.php?rid=5455108&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22105776%26dopt%3DAbstract</link>
            <description>Authors: Hwang SL, Chang HW
    PMID: 22105776 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5455108</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5455108</guid>        </item>
        <item>
            <title>Involvement of calcium-sensing receptor in oxLDL-induced MMP-2 production in vascular smooth muscle cells via PI3K/Akt pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5418732&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22083546%26dopt%3DAbstract</link>
            <description>In this study, the expression of MMP-2 was detected by real-time PCR and Western blot analysis, and the gelatinolytic activity of MMP-2 was measured using gelatin zymography. Our results showed that oxLDL enhanced MMP-2 expression and activity in rat aortic VSMCs in a time- and dose-dependent manner. In addition, CaSR expression was up-regulated by oxLDL. Manipulating CaSR function in these cells by NPS2390 (an antagonist of CaSR) or GdCl(3) (an agonist of CaSR) affected the oxLDL-induced MMP-2 production. In VSMCs, oxLDL stimulated the rapid activation of phosphatidylinositol 3-kinase (PI3K)/Akt signal pathway, as determined by Western blot analysis. Phosphorylation of Akt and MMP-2 production stimulated by oxLDL were attenuated by LY294002 (a specific inhibitor of PI3K). Activation of Ak...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5418732</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5418732</guid>        </item>
        <item>
            <title>Progression of apoptic signaling from mesenteric ischemia-reperfusion injury to lungs: correlation in the level of ER chaperones expression.</title>
            <link>http://www.medworm.com/index.php?rid=5418731&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22083547%26dopt%3DAbstract</link>
            <description>Authors: Urban P, Bilecova-Rabajdova M, Marekova M, Vesela J
    Abstract
    Multiple organ dysfunction syndrome (MODS) is characterized by the development of probably reversible, progressive dysfunction of vital systems in two or more organs, directly undamaged by surgery or other trauma. The organs which have the most common potential dysfunction are lungs, liver, kidneys, heart and gastrointestinal tract. The small intestine is the source of production of proinflammatory mediators leading and contributing to multiorgan failure. The endoplasmic reticulum (ER), after ischemia and post-ischemic reperfusion, is significantly involved in the activation of enterocyte apoptosis. The purpose of this study was to determine the stage of apoptosis in the lungs, initiated through inflammatory resp...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5418731</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5418731</guid>        </item>
        <item>
            <title>Genotypes and allele frequencies of angiotensin-converting enzyme (ACE) insertion/deletion polymorphism among Bahraini population with type 2 diabetes mellitus and related diseases.</title>
            <link>http://www.medworm.com/index.php?rid=5418735&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22081332%26dopt%3DAbstract</link>
            <description>Authors: Al-Harbi EM, Farid EM, Gumaa KA, Singh J
    Abstract
    Insertion/deletion (I/D) polymorphism, of a 287-bp Alu repetitive sequence in intron 16 of the angiotensin-converting enzyme (ACE) gene has been shown to be associated with different types of diseases and has been widely investigated in different populations with different ethnic origins. Various reports were published suggesting inter-ethnic variations in the frequency of allelic forms of the ACE gene. The goal of this study was to test the distribution of alleles and the different genotypes of ACE (I/D) polymorphism in Bahraini subjects and compare the results with those obtained from other population studies. The Bahraini population is an Arabic peninsula population with a high prevalence of T2DM and hypertension. A tota...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5418735</comments>
            <pubDate>Sun, 13 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5418735</guid>        </item>
        <item>
            <title>Diverse H. pylori strains, IL-10 promoter polymorphisms with high morbidity of gastric cancer in Hexi area of Gansu Province, China.</title>
            <link>http://www.medworm.com/index.php?rid=5418734&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22081333%26dopt%3DAbstract</link>
            <description>Authors: Zeng X, Li Y, Liu T, Zhang J
    Abstract
    In Hexi area of Gansu Province, people have a higher susceptibility of gastric cancer than people in the rest area of China. There is substantial geographic variation in the incidence of gastric cancer. In this article, the present author explored the roles of H. pylori infection and IL-10 promoter polymorphisms in development of gastric cancer in this area. A total of 304 participants were admitted to our study, and they were divided into two groups: control group and case group. Blood samples from all subjects were collected for gene extraction using DNA extraction kits. IL-10 polymorphisms were determined by SNaPshot Multiplex. To test H. pylori infection and its typing H. pylori antibody Immunoblotting Kits were used. This research...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5418734</comments>
            <pubDate>Sun, 13 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5418734</guid>        </item>
        <item>
            <title>Risk of obesity and type 2 diabetes with tumor necrosis factor-α 308G/A gene polymorphism in metabolic syndrome and coronary artery disease subjects.</title>
            <link>http://www.medworm.com/index.php?rid=5418733&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22081334%26dopt%3DAbstract</link>
            <description>The objective of this work was to determine the role of TNFα-308G/A gene polymorphism in metabolic syndrome (MetS) and coronary artery disease (CAD) with obesity and type 2 diabetes mellitus (T2DM). A total of 250 MetS and 224 CAD patients and 214 controls were studied. TNFα-308G/A polymorphism was detected from the whole blood genomic DNA using PCR-amplification refractory mutation system. The 2 × 2 contingency tables and multiple regression analysis were used for determining the association of genotypes with obesity and type 2 diabetes mellitus (T2DM) in MetS and CAD subjects. In CAD subjects with T2DM, the AG genotypes showed a very strong association (P &amp;lt; 0.0001; OR 0.194, 95%CI 0.103-0.365). In CAD subjects with obesity, the AA (P = 0.049; OR 2.449) and AG genotypes show...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5418733</comments>
            <pubDate>Sun, 13 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5418733</guid>        </item>
        <item>
            <title>Creatine and pyruvate prevent behavioral and oxidative stress alterations caused by hypertryptophanemia in rats.</title>
            <link>http://www.medworm.com/index.php?rid=5418736&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22081291%26dopt%3DAbstract</link>
            <description>In this study, we investigated the effect of tryptophan administration on various parameters of behavior in the open-field task and oxidative stress, and the effects of creatine and pyruvate, on the effect of tryptophan. Forty, 60-day-old male Wistar rats, were randomly divided into four groups: saline, tryptophan, pyruvate + creatine, tryptophan + pyruvate + creatine. Animals received three subcutaneous injections of tryptophan (2 μmol/g body weight each one at 3 h of intervals) and/or pyruvate (200 μg/g body weight 1 h before tryptophan), and/or creatine (400 μg/g body weight twice a day for 5 days before tryptophan twice a day for 5 days before training); controls received saline solution (NaCl 0.85%) at the same volumes (30 μl/g body weight) than the other substances....</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5418736</comments>
            <pubDate>Sat, 12 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5418736</guid>        </item>
        <item>
            <title>mTOR-rictor is the Ser(473) kinase for AKT1 in mouse one-cell stage embryos.</title>
            <link>http://www.medworm.com/index.php?rid=5418737&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22057724%26dopt%3DAbstract</link>
            <description>Authors: Zhang Z, Zhang G, Xu X, Su W, Yu B
    Abstract
    Mammalian target of rapamycin (mTOR) controls cell growth and proliferation via the raptor-mTOR (TORC1) and rictor-mTOR (TORC2) protein complexes. The mTORC2 containing mTOR and rictor is thought to be rapamycin insensitive and it is recently shown that both rictor and mTORC2 are essential for the development of both embryonic and extra embryonic tissues. To explore rictor function in the early development of mouse embryos, we disrupted the expression of rictor, a specific component of mTORC2, in mouse fertilized eggs by using rictor shRNA. Our results showed that one-cell stage eggs that were lack of rictor could not enter into the two-cell stage normally. Recent biochemical studies suggests that TORC2 is the elusive PDK2 (3'-ph...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5418737</comments>
            <pubDate>Sat, 05 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5418737</guid>        </item>
        <item>
            <title>Igf2-derived intronic miR-483 promotes mouse hepatocellular carcinoma cell proliferation.</title>
            <link>http://www.medworm.com/index.php?rid=5379210&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22052201%26dopt%3DAbstract</link>
            <description>Authors: Ma N, Li F, Li D, Hui Y, Wang X, Qiao Y, Zhang Y, Xiang Y, Zhou J, Zhou L, Zheng X, Gao X
    Abstract
    Most intronic micro-RNAs are coexpressed with their host genes, suggesting that they may play similar roles. The function of miR-483 remains unknown, although it is embedded in an intron of Igf2 gene, which is an activator of hepatocellular carcinoma proliferation. In the present study, we provide evidence that Igf2-derived miR-483 can induce proliferation in hepatocellular carcinoma cells. The miR-483 promotion of proliferation was analysed by soft agar colony formation assay and proliferation curve assay. The effect of miR-483 on Socs3 expression was examined by Western blot and a reporter assay. Our results revealed that Igf2-derived intronic miR-483 was identified by the ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379210</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379210</guid>        </item>
        <item>
            <title>Identification of PLSCR1 as a protein that interacts with RELT family members.</title>
            <link>http://www.medworm.com/index.php?rid=5379209&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22052202%26dopt%3DAbstract</link>
            <description>Authors: Cusick JK, Mustian A, Jacobs AT, Reyland ME
    Abstract
    Receptor expressed in lymphoid tissues (RELT) proteins are recently described surface receptors belonging to the larger TNF receptor family. To improve our understanding of RELT-mediated signal transduction, we performed a screen for RELT-interacting proteins. Phospholipid Scramblase 1 (PLSCR1) was identified through a yeast two-hybrid genetic screen utilizing the intracellular portion of the RELT family member, RELL1, as bait. PLSCR1 was observed to physically interact with all known RELT family members as determined by co-immunoprecipitation experiments. The protein kinase, oxidative stress responsive 1 (OSR1) was previously shown to interact and phosphorylate all three RELT family members. In our study, no physical as...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379209</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379209</guid>        </item>
        <item>
            <title>Advanced glycation end products enhance reactive oxygen and nitrogen species generation in neutrophils in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=5379211&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22048812%26dopt%3DAbstract</link>
            <description>This study provides evidence that AGEs may play a key role in the induction of oxidative stress through the augmentation of PMN-mediated ROS and RNI generation and this may be in part responsible for development of AGE-induced diabetic pathology.
    PMID: 22048812 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379211</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379211</guid>        </item>
        <item>
            <title>Cloning and expression analysis of piRNA-like RNAs: adult testis-specific small RNAs in chicken.</title>
            <link>http://www.medworm.com/index.php?rid=5379219&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045059%26dopt%3DAbstract</link>
            <description>In this study, we isolated and cloned 156 small RNAs from adult chicken testes. Since there is a reasonably even distribution from 22 to 33 nt, these small RNAs are slightly longer than miRNAs and endo-siRNAs. Genome mapping indicated that these small RNAs were derived from intergenic regions, exons, introns, and repetitive elements including chicken repeat 1, long terminal repeats, and simple repeats. Since they are similar with piRNAs, we named them piRNA-like RNAs (pil-RNAs). Northern blotting of 16 selected sequences showed that nine are specifically expressed in the adult testis. The vast majority of these pil-RNAs are poorly conserved between species, suggesting that they are unique to the adult chicken testis. Further analysis of the cloned pil-RNAs will improve our understanding of...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379219</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379219</guid>        </item>
        <item>
            <title>Quaternary structural parameters of the congenital cataract causing mutants of αA-crystallin.</title>
            <link>http://www.medworm.com/index.php?rid=5379218&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045060%26dopt%3DAbstract</link>
            <description>Authors: Kore R, Hedges RA, Oonthonpan L, Santhoshkumar P, Sharma KK, Abraham EC
    Abstract
    Pediatric cataract of the congenital type is the most common form of childhood blindness and it is clinically and genetically heterogeneous. Mutations in 22 different genes have been identified to be associated with congenital cataracts, and among them, eight mutants belong to αA-crystallin. To explain how mutations in αA-crystallin lead to the development of cataract, quaternary structural parameters, and chaperone function have been investigated in αA-wt and in the following mutants: R12C, R21L, R21W, R49C, R54C, R116C, and R116H. Average molar mass, mass at the RI peak, mass across the peak, hydrodynamic radius (R           (h)), and polydispersity index (PDI) were determined by dynamic ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379218</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379218</guid>        </item>
        <item>
            <title>MicroRNA- 1 represses Cx43 expression in viral myocarditis.</title>
            <link>http://www.medworm.com/index.php?rid=5379217&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045061%26dopt%3DAbstract</link>
            <description>In this study, we investigated miR-1 expression and its potential role in the mouse model of viral myocarditis (VMC). The expression levels of miR-1 and its target gene Connexin 43 (Cx43) were measured by real-time PCR and western blotting, respectively. The miR-1 expression levels were significantly increased in cardiac myocytes from VMC mice in comparison with control samples (relative expression: 10 ± 2.5 vs. 31 ± 7.6, P &amp;lt; 0.05). Among the target genes of miR-1, the expression Cx43 protein was significantly reduced in such mice while there was no significant difference in the its mRNA levels. Our results revealed an inverse correlation between miR-1 levels and Cx43 protein expression in VMC samples. Using a bioinformatics-based approach, we found two identical potential bindi...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379217</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379217</guid>        </item>
        <item>
            <title>Elevated expression of RGS19 impairs the responsiveness of stress-activated protein kinases to serum.</title>
            <link>http://www.medworm.com/index.php?rid=5379216&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045062%26dopt%3DAbstract</link>
            <description>Authors: Ip AK, Tso PH, Lee MM, Wong YH
    Abstract
    Regulators of G protein signaling (RGS proteins) serve as GTPase activating proteins for the signal transducing Gα subunits. RGS19, also known as Gα-interacting protein (GAIP), has been shown to subserve other functions such as the regulation of macroautophagy and growth factor signaling. We have recently demonstrated that the expression of RGS19 in human embryonic kidney (HEK) 293 cells resulted in the disruption of serum-induced mitogenic response along the classical Ras/Raf/MEK/ERK pathway. Here, we further examined the effect of RGS19 expression on the stress-activated protein kinases (SAPKs). Both c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) became non-responsive to serum in 293/RGS19 cells, ye...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379216</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379216</guid>        </item>
        <item>
            <title>Molecular assessment of c-H-ras p21 expression in Helicobacter pylori-mediated gastric carcinogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5379215&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045063%26dopt%3DAbstract</link>
            <description>This study was carried out in 200 patients, consisting of normal gastric mucosa (n = 20), mucosa with chronic gastritis (n = 63), intestinal metaplasia (n = 20), dysplasia (n = 11), and gastric adenocarcinoma (n = 86), in which the H. pylori status have been analysed. The expression of c-H-ras p21 was studied at mRNA as well as protein level using RT-PCR and western blotting, respectively. The localization of c-H-ras p21 was also studied semiquantitatively by immunohistochemistry. The RT-PCR and western blotting results of c-H-ras p21 mRNA and protein expressions were significantly increased in chronic gastritis, intestinal metaplasia, dysplasia, and gastric adenocarcinoma patients, respectively. Immunohistochemical study also showed the increased expression of c-H-ras p21 in the...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379215</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379215</guid>        </item>
        <item>
            <title>Activity of tumor necrosis factor-α blocked by phytoglycoprotein (38 kDa) at initiation stage in N-nitrosodiethylamine-induced ICR mice.</title>
            <link>http://www.medworm.com/index.php?rid=5379214&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045064%26dopt%3DAbstract</link>
            <description>Authors: Lee J, Lim KT
    Abstract
    Hepatocellular carcinoma is becoming one of the most prominent types of cancer in the world. Recently, from Styrax japonica Siebold et al. Zuccarini (SJSZ), we isolated a glycoprotein which consists of carbohydrate moiety (52.64%) and protein moiety (42.35%). We evaluated whether SJSZ glycoprotein prevents hepatocarcinogenesis induced by N-nitrosodiethylamine (DEN). The purpose of this study was to evaluate the effect of SJSZ glycoprotein in DEN-induced hepatocarcinogenesis in ICR mice. To know chemopreventive effect of SJSZ glycoprotein on hepatocarcinogenesis, ICR mice were intraperitoneally injected with N-nitrosodiethylamine (DEN, 10 mg/kg) for 7 weeks. After sacrifice, we evaluated indicators of liver tissue damage [the activities of lactate d...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379214</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379214</guid>        </item>
        <item>
            <title>Chronic mild hyperhomocysteinemia alters ectonucleotidase activities and gene expression of ecto-5'-nucleotidase/CD73 in rat lymphocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5379213&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045065%26dopt%3DAbstract</link>
            <description>Authors: Scherer EB, Savio LE, Vuaden FC, Ferreira AG, Bogo MR, Bonan CD, Wyse AT
    Abstract
    Since mild hyperhomocysteinemia is a risk factor for cardiovascular and cerebral diseases and extracellular nucleotides/nucleosides, which are controlled by the enzymatic action of ectonucleotidases, can induce an immune response, in the present study, we investigated the effect of chronic mild hyperhomocysteinemia on ectonucleotidase activities and expression in lymphocytes from mesenteric lymph nodes and serum of adult rats. For the chronic chemically induced mild hyperhomocysteinemia, Hcy (0.03 μmol/g of body weight) or saline (control) were administered subcutaneously from the 30th to the 60th day of life. Results showed that homocysteine significantly decreased ATP, ADP, and AMP hydro...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379213</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379213</guid>        </item>
        <item>
            <title>Molecular metabolic fingerprinting approach to investigate the effects of borneol on metabolic alterations in the liver of nitric oxide deficient hypertensive rats.</title>
            <link>http://www.medworm.com/index.php?rid=5379212&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22045066%26dopt%3DAbstract</link>
            <description>In this study, we intended to evaluate the protective role of borneol, a natural terpene on liver metabolism in a nitric oxide deficient model of hypertension through interpretation of FTIR spectral information. Results demonstrate that FTIR can successfully indicate the molecular changes that occur in all groups. The over all findings demonstrate that in nitric oxide deficient animal model of hypertension, the liver metabolic program is altered through increasing the structural modification in proteins and triglycerides, and quantitative alteration in proteins, lipids, and glycogen. All the above mentioned modifications were protected by borneol in liver and showed its ability to exert a novel defensive action on hepatic metabolism.
    PMID: 22045066 [PubMed - as supplied by publisher] (...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379212</comments>
            <pubDate>Wed, 02 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379212</guid>        </item>
        <item>
            <title>A comparative study of recombinant mouse and human apurinic/apyrimidinic endonuclease.</title>
            <link>http://www.medworm.com/index.php?rid=5379220&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22042551%26dopt%3DAbstract</link>
            <description>Authors: Adhikari S, Manthena PV, Kota KK, Karmahapatra SK, Roy G, Saxena R, Uren A, Roy R
    Abstract
    Mammalian apurinic/apyrimidinic endonuclease (APE1) initiates the repair of abasic sites (AP-sites), which are highly toxic, mutagenic, and implicated in carcinogenesis. Also, reducing the activity of APE1 protein in cancer cells and tumors sensitizes mammalian tumor cells to a variety of laboratory and clinical chemotherapeutic agents. In general, mouse models are used in studies of basic mechanisms of carcinogenesis, as well as pre-clinical studies before transitioning into humans. Human APE1 (hAPE1) has previously been cloned, expressed, and extensively characterized. However, the knowledge regarding the characterization of mouse APE1 (mAPE1) is very limited. Here we have expresse...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379220</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379220</guid>        </item>
        <item>
            <title>NOTCH1 regulates migration and invasion of skin cancer cells by E-cadherin repression.</title>
            <link>http://www.medworm.com/index.php?rid=5379224&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22038626%26dopt%3DAbstract</link>
            <description>Authors: Wang Z, Liu L, Wang M, Shen M, Li J, Liu J, Li C, Xin C, Zhu S, Mei Q, Wang Y
    Abstract
    NOTCH1 is a regulator that functions not only in tissue development, but also in cancer pathogenesis. We hypothesized that NOTCH1 is involved in skin cancer cell migration and invasion through regulation of E-cadherin and its transcription factor, Snail. Here, using immunofluorescence and western blots, we show that NOTCH1 is upregulated in skin cancer tissue on skin. Inhibition or activation of NOTCH1 altered expression of E-cadherin and Snail in the skin cancer cell line A431. Our results suggest that this effect is through changing DNA methylation levels of the E-cadherin gene promoter. Activation and inhibition of NOTCH1 also altered the behavior of A431 cells in migration and invasi...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379224</comments>
            <pubDate>Sat, 29 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379224</guid>        </item>
        <item>
            <title>Arginine decreases peroxisome proliferator-activated receptor-γ activity via c-Jun.</title>
            <link>http://www.medworm.com/index.php?rid=5379225&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22038625%26dopt%3DAbstract</link>
            <description>In conclusion, arginine decreased PPARγ transcriptional activity in small bowel intestinal epithelial cells. These changes are due, in part, to phosphorylation of c-Jun and may explain the deleterious effects of enteral arginine in the post ischemic gut.
    PMID: 22038625 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379225</comments>
            <pubDate>Wed, 26 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379225</guid>        </item>
        <item>
            <title>Claudin-5 participates in the regulation of endothelial cell motility.</title>
            <link>http://www.medworm.com/index.php?rid=5379222&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22038628%26dopt%3DAbstract</link>
            <description>In conclusion, this study portrays a new and interesting role for Claudin-5 in cell motility involving the N-WASP and ROCK signalling cascade which is beyond the primarily role of Claudin-5 in keeping the cell barrier tight as it was originally reported.
    PMID: 22038628 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379222</comments>
            <pubDate>Wed, 26 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379222</guid>        </item>
        <item>
            <title>Regional differences in sexually dimorphic protein expression in the spontaneously hypertensive rat (SHR).</title>
            <link>http://www.medworm.com/index.php?rid=5379221&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22038629%26dopt%3DAbstract</link>
            <description>This study tested the hypothesis that endogenous gonadal hormones exert differential effects on protein expression in the kidney and mesentery of SHR. At ~5 weeks of age male and female SHR underwent sham operation, orchidectomy, or ovariectomy (OVX). At 20-23 weeks of age, mean arterial pressure (MAP) was measured in conscious rats. The mesenteric arterial tree and kidneys were collected, processed for Western blots, and probed for Cu Zn superoxide dismutase (SOD1), soluble epoxide hydrolase (sEH), and Alpha 2A adrenergic receptor (A2AR) expression. MAP was unaffected by ovariectomy (Sham 164 ± 4: Ovariecttomy 159 ± 3 mm Hg). MAP was reduced by orchidectomy (Sham 189 ± 5:Orchidectomy 167 ± 2 mm Hg). In mesenteric artery, SOD1 expression was greater in male versus female SH...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379221</comments>
            <pubDate>Wed, 26 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379221</guid>        </item>
        <item>
            <title>The calcium-sensing receptor promotes adipocyte differentiation and adipogenesis through PPARγ pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5379226&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22038624%26dopt%3DAbstract</link>
            <description>In conclusion, our findings suggest that activation of CaSR promotes differentiation and adipogenesis in adipocytes, which might be achieved by upregulating PPARγ and its downstream gene expressions. Therefore, CaSR in adipocytes may be involved in the pathogenesis of obesity by promoting adipocyte differentiation and adipogenesis.
    PMID: 22038624 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379226</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379226</guid>        </item>
        <item>
            <title>The non-receptor tyrosine kinase c-Src mediates the PDGF-induced association between Furin and pro-MT1-MMP in HPAC pancreatic cells.</title>
            <link>http://www.medworm.com/index.php?rid=5379223&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22038627%26dopt%3DAbstract</link>
            <description>Authors: Shi C, Ma Y, Liu H, Zhang Y, Wang Z, Jia H
    Abstract
    Furin is a member of the proprotein convertase family, which is capable of cleaving the precursors of a wide variety of substrates including membrane-type 1 matrix metalloproteinase (MT1-MMP) proenzyme. c-Src is activated by growth factors, and has been linked with a poor prognosis in pancreatic cancer (PCa). Both c-Src and Furin play crucial roles in tumorigenesis, and the mechanism controlling their association is not understood. Modulation of the association between Furin and pro-MT1-MMP by c-Src inhibitor PP2 was evaluated by western blotting, assay of in vitro enzyme, co-immunoprecipitation (co-IP), and confocal immunofluorescence microscopy. Human platelet-derived growth factor BB (PDGF-BB) activated c-Src and induc...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379223</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379223</guid>        </item>
        <item>
            <title>Diverse viscerotropic isolates of Leishmania all express a highly conserved secretory nuclease during human infections.</title>
            <link>http://www.medworm.com/index.php?rid=5379229&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22020747%26dopt%3DAbstract</link>
            <description>Authors: Joshi MB, Hernandez Y, Owings JP, Dwyer DM
    Abstract
    Previously, we characterized a gene encoding the unique nuclease (LdNuc(s)) from a Sudanese isolate of the human pathogen Leishmania donovani. This parasite secretory enzyme is involved in the salvage of host-derived purines and is constitutively expressed by both developmental forms of the parasite. Currently, we assessed whether an LdNuc(s)-like nuclease was conserved among other geographically disparate isolates of L. donovani and whether this enzyme was produced by intracellular amastigotes during human infections. Using RT-PCR and Southern blotting, we showed that LdNuc           (s) gene homologs were present in each of the viscerotropic Leishmania tested (i.e., L. donovani isolates from the Sudan, Ethiopia and Indi...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379229</comments>
            <pubDate>Sat, 22 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379229</guid>        </item>
        <item>
            <title>SNIP1: a new activator of HSE signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5379228&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22020748%26dopt%3DAbstract</link>
            <description>We report here that through quantitative real-time PCR analysis in 18 different human tissues, SNIP1 was found to be expressed ubiquitously. When overexpressed in HeLa cells, SNIP1-EGFP fused protein exhibited a nuclear localization with a characteristic subnuclear distribution in speckles or formed larger discrete nuclear bodies in some cells. Reporter gene assay showed that overexpression of SNIP1 in HEK 293 cells or H1299 cells strongly activated the HSE signaling pathway. Moreover, SNIP1 could selectively regulate the transcription of HSP70A1A and HSP27. Taken together, our findings suggest that SNIP1 might also be a positive regulator of HSE signaling pathway.
    PMID: 22020748 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379228</comments>
            <pubDate>Sat, 22 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379228</guid>        </item>
        <item>
            <title>Antinociceptive effect of VSL#3 on visceral hypersensitivity in a rat model of irritable bowel syndrome: a possible action through nitric oxide pathway and enhance barrier function.</title>
            <link>http://www.medworm.com/index.php?rid=5379227&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22020749%26dopt%3DAbstract</link>
            <description>Authors: Dai C, Guandalini S, Zhao DH, Jiang M
    Abstract
    Irritable bowel syndrome (IBS) is a functional bowel disorder characterized by visceral hypersensitivity and altered bowel function. There are increasing evidences suggested that VSL#3 probiotics therapy has been recognized as an effective method to relieve IBS-induced symptoms. The aim of this study was to examine the effects of VSL#3 probiotics on visceral hypersensitivity (VH), nitric oxide (NO), fecal character, colonic epithelium permeability, and tight junction protein expression. IBS model was induced by intracolonic instillation of 4% acetic acid and restraint stress in rats. After subsidence of inflammation on the seventh experimental day, the rats were subjected to rectal distension, and then the abdominal withdrawal...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379227</comments>
            <pubDate>Sat, 22 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379227</guid>        </item>
        <item>
            <title>Association of angiotensin-converting enzyme I/D polymorphism with heart failure: a meta-analysis.</title>
            <link>http://www.medworm.com/index.php?rid=5379232&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22015653%26dopt%3DAbstract</link>
            <description>The objective was to assess the association between the ACE I/D polymorphism and HF. We performed a meta-analysis of all case-control studies that evaluated the association between ACE I/D polymorphism and HF in humans. Studies were identified in the PUBMED and EMBASE databases, reviews, and reference lists of relevant articles. Two reviewers independently assessed the studies. Seventeen case-control studies with a total of 5576 participants were included in the meta-analysis, including 2453 cases with HF and 3123 controls. The heterogeneity between studies was significant. No association was found under all the four genetic models (D vs. I, DD vs. ID and II, DD and ID vs. II, DD vs. ID). Subgroup analyses for ischemic HF (IHF) and HF because of dilated cardiomyopathy (DHF) also showed no ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379232</comments>
            <pubDate>Fri, 21 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379232</guid>        </item>
        <item>
            <title>Toxicity of octanoate and decanoate in rat peripheral tissues: evidence of bioenergetic dysfunction and oxidative damage induction in liver and skeletal muscle.</title>
            <link>http://www.medworm.com/index.php?rid=5379231&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22015654%26dopt%3DAbstract</link>
            <description>Authors: Scaini G, Simon KR, Tonin AM, Busanello EN, Moura AP, Ferreira GC, Wajner M, Streck EL, Schuck PF
    Abstract
    The accumulation of octanoic (OA) and decanoic (DA) acids in tissue is the common finding in medium-chain acyl-coenzyme A dehydrogenase deficiency (MCADD), the most frequent defect of fatty acid oxidation. Affected patients present hypoketotic hypoglycemia, rhabdomyolysis, hepatomegaly, seizures and lethargy, which may progress to coma and death. At present, the pathophysiological mechanisms underlying hepatic and skeletal muscle alterations in affected patients are poorly known. Therefore, in the present work, we investigated the in vitro effects of OA and DA, the accumulating metabolites in MCADD, on various bioenergetics and oxidative stress parameters. It was veri...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379231</comments>
            <pubDate>Fri, 21 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379231</guid>        </item>
        <item>
            <title>Effect of insulin-like growth factor-1 (IGF-1) on the gluconeogenesis in calf hepatocytes cultured in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=5379230&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22015655%26dopt%3DAbstract</link>
            <description>In this study, to evaluate the role of IGF-1 on gluconeogenesis and nutrient metabolism in dairy cattle, pyruvate carboxylase (PC) and phosphoenolpyruvate carboxykinase (PEPCK) expression and enzyme activity were evaluated in primary cultures of bovine hepatocytes treated with different concentrations of IGF-1 by quantitative polymerase chain reaction and spectrophotometry, respectively. The results showed that expression of PC and PEPCK were significantly lower in bovine hepatocytes by IGF-1 treatment in test group compare to the control group (P &amp;lt; 0.01). As IGF-1 concentration increased, PC and PEPCK enzyme activity in bovine hepatocytes decreased. Evaluating PC and PEPCK mRNA levels and enzyme activity may thus be useful to monitor subclinical ketosis in dairy cows.
    PMID: 22015...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379230</comments>
            <pubDate>Fri, 21 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379230</guid>        </item>
        <item>
            <title>Interleukin-23 as a potential therapeutic target for rheumatoid arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=5379236&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22012611%26dopt%3DAbstract</link>
            <description>Authors: Rong C, Hu W, Wu FR, Cao XJ, Chen FH
    Abstract
    Cytokine-mediated immunity plays a crucial role in the pathogenesis of various autoimmune diseases, including rheumatoid arthritis (RA). Increasing evidence has revealed the importance of IL-23, which closely resembles IL-12 structurally and immunologically, in linking innate and adaptive immunity. IL-23, a newly identified heterodimeric pro-inflammatory cytokine, is composed of a p40 subunit in common with IL-12 and a unique p19 subunit. Recent evidence suggests that IL-23, rather than IL-12, is the crucial factor in the pathogenesis of various immune-mediated disorders. In addition, recent studies have explored the role of IL-23 in patients with RA. An elevated expression of IL-23 has been demonstrated in the synovial fibrobl...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379236</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379236</guid>        </item>
        <item>
            <title>Chronic methylphenidate administration alters antioxidant defenses and butyrylcholinesterase activity in blood of juvenile rats.</title>
            <link>http://www.medworm.com/index.php?rid=5379235&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22012612%26dopt%3DAbstract</link>
            <description>Authors: Schmitz F, Scherer EB, da Cunha MJ, da Cunha AA, Lima DD, Delwing D, Netto CA, Wyse AT
    Abstract
    Methylphenidate (MPH), a psychostimulant that affects both dopaminergic and noradrenergic systems, is one of the most frequently prescribed treatments for attention-deficit hyperactivity disorder. The present study investigated the effects of chronic administration of MPH on some parameters of oxidative stress, as well as on butyrylcholinesterase (BuChE) activity in blood of young rats. Rats received intraperitoneal injections of MPH (2.0 mg/kg) once a day, from the 15th to the 45th day of age or an equivalent volume of 0.9% saline solution (controls). Two hours after the last injection, animals were euthanized, and blood was collected. Results demonstrated that MPH did not alt...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379235</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379235</guid>        </item>
        <item>
            <title>Upregulation of TRB2 induced by miR-98 in the early lesions of large artery of type-2 diabetic rat.</title>
            <link>http://www.medworm.com/index.php?rid=5379234&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22012613%26dopt%3DAbstract</link>
            <description>Authors: Xie S, Xie N, Li Y, Wang P, Zhang C, Li Q, Liu X, Deng J, Zhang C, Lv C
    Abstract
    To characterize the roles of tribble 2 (TRB2) and its targeted microRNAs (miRNAs) in the pathogenesis of the early vascular injury involved in diabetic-2 rat. Goto-Kakizaki (GK) rat and Wistar rat were used as the animal models. Each eligible rat was killed and the rat aorta tissues were analyzed by immunohistochemistry, ELISA, reverse transcription-polymerase chain reaction (RT-PCR), and real-time PCR detection. GFP expression in RAOEC cells (rat vascular aortic endothelial cell)were detected by flow cytometry and fluorescent microscope. TRB2 gene expression was increased in endothelia cell and the adventitia of Goto-Kakizaki (GK) rat compared with Wistar rat. Next, studies using RAOEC cells ...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379234</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379234</guid>        </item>
        <item>
            <title>Resveratrol mobilizes Ca(2+) from intracellular stores and induces c-Jun N-terminal kinase activation in tumoral AR42J cells.</title>
            <link>http://www.medworm.com/index.php?rid=5379233&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22012614%26dopt%3DAbstract</link>
            <description>In this study, the effects of resveratrol on intracellular free Ca(2+) concentration ([Ca(2+)](c)) and on cell viability in tumoral AR42J pancreatic cells are examined. The results show that resveratrol (100 μM and 1 mM) induced changes in [Ca(2+)](c), that consisted of single or short lasting spikes followed by a slow reduction toward a value close to the resting level. Lower concentrations of resveratrol (1 and 10 μM) did not show detectable effects on [Ca(2+)](c). Depletion of intracellular Ca(2+) stores by stimulation of cells with 1 nM CCK-8, 20 pM CCK-8 or 1 μM thapsigargin, blocked Ca(2+) responses evoked by resveratrol. Conversely, prior stimulation of cells with resveratrol inhibited Ca(2+) mobilization in response to a secondary application of CCK-8 or thapsigargin. In a...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379233</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379233</guid>        </item>
        <item>
            <title>Knockdown of zinc finger protein, X-linked (ZFX) inhibits cell proliferation and induces apoptosis in human laryngeal squamous cell carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=5379240&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22009483%26dopt%3DAbstract</link>
            <description>Authors: Fang J, Yu Z, Lian M, Ma H, Tai J, Zhang L, Han D
    Abstract
    ZFX (zinc finger protein, X-linked) gene locus on the human X chromosome is structurally similar to the zinc finger protein, Y-linked gene, which may constitute the primary sex-determining signal. However, the pathological roles of the dysfunction of ZFX gene in human disease such as cancer have not been addressed. Here, we analyzed the expression of ZFX in human laryngeal squamous cell carcinoma (LSCC) tissue specimens and found a significant up-regulation compared to corresponding non-tumorous LSCC tissue. Recombinant lentivirus expressing ZFX short hairpin RNA (shZFX) was constructed and infected Hep-2 human LSCC cells. We found that knockdown of ZFX gene resulted in suppression of proliferation and colony-formi...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379240</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379240</guid>        </item>
        <item>
            <title>Activation of erythropoietin-producing hepatocellular receptor A2 attenuates cell adhesion of human fallopian tube epithelial cells via focal adhesion kinase dephosphorylation.</title>
            <link>http://www.medworm.com/index.php?rid=5379239&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22009484%26dopt%3DAbstract</link>
            <description>In this study, primary cultured fallopian tube epithelial cells were used as a model treated with EphrinA1-Fc or IgG-Fc (control), to explore the role of EphA2 signal and its network involved in the regulation of cell adhesion of tubal epithelia cells. The activation of EphA2 and focal adhesion kinase (FAK) was evaluated by western blotting assay in the cultured fallopian tube epithelia cells, of which the cell adhesion activity was determined by MTT assay. A significantly negative correlation was found between phosphorylated-EphA2 (Pho-EphA2) and phosphorylated-FAK (Pho-FAK) after exposure to EphrinA1-Fc (P = 0.000; r = -0.848). EphrinA1-Fc increased Pho-EphA2 and reduced Pho-FAK in seconds, with the apex level of Pho-EphA2 and the nadir level of Pho-FAK detected at the same time (10...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379239</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379239</guid>        </item>
        <item>
            <title>Contractility of ventricular myocytes is well preserved despite altered mechanisms of Ca(2+) transport and a changing pattern of mRNA in aged type 2 Zucker diabetic fatty rat heart.</title>
            <link>http://www.medworm.com/index.php?rid=5379238&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22009485%26dopt%3DAbstract</link>
            <description>The objective of the study was to investigate ventricular myocyte shortening, intracellular Ca(2+) signalling and expression of genes encoding cardiac muscle proteins in the aged Zucker diabetic fatty (ZDF) rat. There was a fourfold elevation in non-fasting blood glucose in ZDF rats (478.43 ± 29.22 mg/dl) compared to controls (108.22 ± 2.52 mg/dl). Amplitude of shortening, time to peak (TPK) and time to half (THALF) relaxation of shortening were unaltered in ZDF myocytes compared to age-matched controls. Amplitude and THALF decay of the Ca(2+) transient were unaltered; however, TPK Ca(2+) transient was prolonged in ZDF myocytes (70.0 ± 3.2 ms) compared to controls (58.4 ± 2.3 ms). Amplitude of the L-type Ca(2+) current was reduced across a wide range of test potentials (-30...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379238</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379238</guid>        </item>
        <item>
            <title>In vitro study of the differentiation of bone marrow stromal cells into cardiomyocyte-like cells.</title>
            <link>http://www.medworm.com/index.php?rid=5379237&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22009486%26dopt%3DAbstract</link>
            <description>This study aimed to differentiate the BMSCs into cardiomyocyte. BMSCs were exposed to 5-azacytidine for 24 h. Seven days after the induction of cell differentiation by 5-azacytidine, the cardiomyogenic cells were stained by fushin and binucleated cells were counted and compared with the neonate cardiomyocyte as positive control. In addition, immunofluorescence analysis and western blot were performed using the antibodies against α-actinin, desmin, troponin T, and β-myosin heavy chain. Our results showed that there was no significant difference between the number of binucleated cells within the cardiomyogenic cell group and positive control group; however, a statistically significant difference was observed between both of these groups and undifferentiated cell group (P &amp;lt; 0.005). In...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5379237</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5379237</guid>        </item>
        <item>
            <title>A novel nitro-oxy substituted analogue of rofecoxib reduces human colon cancer cell growth.</title>
            <link>http://www.medworm.com/index.php?rid=5325590&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22002318%26dopt%3DAbstract</link>
            <description>In this study, the antiproliferative activity of a novel dinitro-oxy-substituted analogue of rofecoxib (NO-rofe), potentially less cardiotoxic, has been investigated in vitro on human colon cancer cells and compared with the action of the parent drug. Due to the fact that COX-2 inhibition is the main characteristic of coxibs, we performed all experiments in COX-2-overexpressing (HT-29) and COX-2-negative (SW-480) human colon cancer cells, to elucidate whether the observed effects were dependent on COX-2 inhibition. Moreover, experiments were performed in order to evaluate whether COX-2 pharmacological inhibition may affect beta-catenin/E-cadherin signaling pathway. NO-rofe exerted a significant antiproliferative activity on COX-2 positive HT-29 human colon cancer cells, being less effectiv...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325590</comments>
            <pubDate>Sat, 15 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325590</guid>        </item>
        <item>
            <title>Insulin-like growth factor binding protein-6 interacts with the thyroid hormone receptor α1 and modulates the thyroid hormone-response in osteoblastic differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5325593&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21997736%26dopt%3DAbstract</link>
            <description>In conclusion, these studies provide evidence that overexpression of IGFBP-6 suppresses osteoblastic differentiation regulated by TR in the present of T3.
    PMID: 21997736 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325593</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325593</guid>        </item>
        <item>
            <title>Cell apoptosis induced by zinc deficiency in osteoblastic MC3T3-E1 cells via a mitochondrial-mediated pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5325592&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21997737%26dopt%3DAbstract</link>
            <description>Authors: Guo B, Yang M, Liang D, Yang L, Cao J, Zhang L
    Abstract
    Deficiency of zinc plays an important role in the pathogenesis of osteoporosis; however, the underlying mechanism is not well understood. Apoptosis of osteoblast causing the loss of bone mass is an important event in the osteoporosis. In this article, we investigated whether zinc deficiency would induce cell apoptosis in MC3T3-E1 cells and ask if it is involved in mitochondrial-mediated pathway. Significant increased apoptosis were observed in zinc deficiency group (ZnD: 5 μM TPEN and 1 μM zinc) compared with untreated control or zinc adequacy group (ZnA: 5 μM TPEN and 15 μM zinc). The mitochondrial membrane potential was strikingly reduced in ZnD group. Furthermore, we observed that the levels of Bax in mitoc...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325592</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325592</guid>        </item>
        <item>
            <title>The effect of sevoflurane on the expression of M(1) acetylcholine receptor in the hippocampus and cognitive function of aged rats.</title>
            <link>http://www.medworm.com/index.php?rid=5325591&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21997738%26dopt%3DAbstract</link>
            <description>Authors: Peng S, Zhang Y, Li GJ, Zhang DX, Sun DP, Fang Q
    Abstract
    Our aim is to investigate the effect of 1.5 and 3.0% sevoflurane on the expression of M(1) acetylcholine receptor (mAChR M(1)) in the hippocampus and the cognitive function of aged rats. Forty Sprague-Dawley (SD) rats of 12-month old were randomly divided into five groups. All SD rats received 1.5 or 3.0% sevoflurane in a special glass anesthesia box for 2 h, respectively, except for the normal control group. Y-maze was used to test the ability of learning and memory after being received sevoflurane for 1 or 7 days at the same moment portion. The expression of mAChR M(1) in the hippocampus of rats was tested by RT-PCR. The results showed that 3% sevoflurane induced the decline of cognitive function and significant...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325591</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325591</guid>        </item>
        <item>
            <title>Thrombin-dependent modulation of β(1)-integrin-mediated signaling up-regulates prolidase and HIF-1α through p-FAK in colorectal cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5325594&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21993963%26dopt%3DAbstract</link>
            <description>Authors: Karna E, Szoka L, Palka J
    Abstract
    Products of prolidase [E.C. 3.4.13.9] activity, proline or hydroxyproline, contribute to up-regulation of hypoxia-inducible factor-1α (HIF-1α). Prolidase activity is regulated by β(1)-integrin signaling. We studied the effects of echistatin (a well-known disintegrin) and thrombin (a serine protease capable of activation of integrin α(2)β(1) receptor) on prolidase activity and expressions of prolidase, α(2)β(1)-integrin receptor, focal adhesion kinase (FAK), MAP-kinases (ERK(1) and ERK(2)), and nuclear HIF-1α in human colon adenocarcinoma (DLD-1) cells. It has been found that treatment of the cells with thrombin contributes to decrease in the expression of prolidase and simultaneously increase in its phosphorylation, resulting in m...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325594</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325594</guid>        </item>
        <item>
            <title>Genetic association of Glutathione peroxidase-1 (GPx-1) and NAD(P)H:Quinone Oxidoreductase                   1(NQO1) variants and their association of CAD in patients with type-2 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5325598&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21989715%26dopt%3DAbstract</link>
            <description>Genetic association of Glutathione peroxidase-1 (GPx-1) and NAD(P)H:Quinone Oxidoreductase          1(NQO1) variants and their association of CAD in patients with type-2 diabetes.
    Mol Cell Biochem. 2011 Oct 12;
    Authors: Ramprasath T, Murugan PS, Kalaiarasan E, Gomathi P, Rathinavel A, Selvam GS
    Abstract
    Coronary artery disease (CAD) is a major health concern and the leading cause of death in individuals with type-2 diabetes mellitus (T2DM). Glutathione peroxidase-1 (GPx-1) and NAD(P)H: quinone oxidoreductase (NQO1) are known for its broad range of detoxification. The role of functional variants of these genes in the development of various disorders is proven. Hereby, we investigated the possible role of these variants in the development of CAD in T2DM patients of South Indi...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325598</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325598</guid>        </item>
        <item>
            <title>Ω3-Polyunsaturated fatty acids prevent lipoperoxidation, modulate antioxidant enzymes, and reduce lipid content but do not alter glycogen metabolism in the livers of diabetic rats fed on a high fat thermolyzed diet.</title>
            <link>http://www.medworm.com/index.php?rid=5325597&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21989716%26dopt%3DAbstract</link>
            <description>In this study, our aim was to investigate the effects of Ω3-PUFAs on oxidative stress, including antioxidant enzyme activity and hepatic lipid and glycogen metabolism in the livers of diabetic and non-diabetic rats fed on a high fat thermolyzed diet. Rats were divided into six groups: (1) the control group (C), (2) the control diabetic group (D), (3) the high fat thermolyzed diet group (HFTD), which were fed a diet that was enriched in fat that was heated for 60 min at 180°C, (4) the high fat thermolyzed diet diabetic group (D + HFTD), (5) the high fat thermolyzed diet + Ω3 polyunsaturated fatty acid group (HFTD + Ω3), and (6) the high fat thermolyzed diet + Ω3 polyunsaturated fatty acid diabetic group (D + HFTD + Ω3). The most important finding of this study was that Ω...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325597</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325597</guid>        </item>
        <item>
            <title>PTEN inhibits proliferation and functions of hypertrophic scar fibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5325596&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21989717%26dopt%3DAbstract</link>
            <description>Authors: Guo L, Chen L, Bi S, Chai L, Wang Z, Cao C, Tao L, Li S
    Abstract
    Hypertrophic scar (HS) remains a major problem in plastic surgery. In order to explore the regulative effect of phosphatase and tensin homolog (PTEN) on HS, PTEN and AKT expression was detected by reverse transcription PCR, immunohistochemistry and western blot. Adenovirus-mediated PTEN overexpression in cultured hypertrophic scar fibroblasts (HSFBs) and normal skin fibroblasts was also introduced to evaluate its biological function. Our results showed that PTEN expression was significantly decreased in HS whereas p-Akt level was significantly higher in HS compared with normal skin (P &amp;lt; 0.01). Furthermore, we found that adenovirus-mediated PTEN overexpression led to decreased AKT activation, and signific...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325596</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325596</guid>        </item>
        <item>
            <title>Chemoprevention of DMH-induced rat colon carcinoma initiation by combination administration of piroxicam and C-phycocyanin.</title>
            <link>http://www.medworm.com/index.php?rid=5325595&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21989718%26dopt%3DAbstract</link>
            <description>Authors: Saini MK, Vaiphei K, Sanyal SN
    Abstract
    Cancer research illustrated that combinatorial studies can provide significant improvement in safety and effectiveness over the monotherapy regimens. A combination of two drugs may restrain precancerous colon polyps, opening a new possible opportunity for chemoprevention of colon cancer. In this context, chemopreventive efficacy of a combination regimen of C-phycocyanin, a biliprotein present in Spirulina platensis, a cyanobacterium, which is a selective cycloxygenase-2 (COX-2) inhibitor and piroxicam, a traditional non-steroidal anti-inflammatory drug was considered in 1,2 dimethylhyadrazine (DMH)-induced colon carcinogenesis in rats. Western blotting, immunohistochemistry, DNA fragmentation, fluorescent staining, PGE(2) enzyme immu...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325595</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325595</guid>        </item>
        <item>
            <title>shRNA targeting β1-integrin suppressed proliferative aspects and migratory properties of airway smooth muscle cells.</title>
            <link>http://www.medworm.com/index.php?rid=5325604&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21987234%26dopt%3DAbstract</link>
            <description>In conclusion, the overexpression of β1-integrin in ASM cells is essential for airway dysfunction development because it promotes proliferative aspects and migratory properties of ASM cells. Importantly, shRNA targeting β1-integrin may provide a new approach to preventing airway remodeling in chronic asthma.
    PMID: 21987234 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325604</comments>
            <pubDate>Tue, 11 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325604</guid>        </item>
        <item>
            <title>Does lycopene offer human LDL any protection against myeloperoxidase activity?</title>
            <link>http://www.medworm.com/index.php?rid=5325600&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21987235%26dopt%3DAbstract</link>
            <description>In this study, isolated human LDL was challenged with myeloperoxidase or copper, and the LDL was screened for lipoperoxidation and oxidation of apolipoprotein B100, depletion of lycopene and oxidation of cholesterol. Myeloperoxidase induced oxidation of LDL through direct interaction with apolipoprotein B100. No lipoperoxidation was observed following myeloperoxidase treatment; however, 7-ketocholesterol was detected indicating the products of myeloperoxidase interact with the surface of the LDL particles. Lycopene does react with the products of myeloperoxidase in solvent, but played no role in protecting against enzyme derived oxidation of human LDL.
    PMID: 21987235 [PubMed - as supplied by publisher] (Source: Molecular and Cellular Biochemistry)</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325600</comments>
            <pubDate>Tue, 11 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325600</guid>        </item>
        <item>
            <title>Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (BNIP3) expression is epigenetically regulated by one-carbon metabolism in invasive duct cell carcinoma of breast.</title>
            <link>http://www.medworm.com/index.php?rid=5325599&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21987236%26dopt%3DAbstract</link>
            <description>Authors: Naushad SM, Prayaga A, Digumarti RR, Gottumukkala SR, Kutala VK
    Abstract
    In view of recent studies highlighting the prognostic relevance of expression and CpG island methylator phenotype (CIMP) of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (BNIP3) in invasive duct cell carcinoma (IDC), we hypothesized in this article that impaired one-carbon metabolism might influence CIMP phenotype of BNIP3. In order to substantiate the prognostic relevance of BNIP3, we explored its association with 8-oxo-2'deoxyguanosine (8-oxodG), a marker of oxidative stress with prognostic relevance. BNIP3 expression and CIMP phenotype were studied using semi-quantitative RT-PCR and combined bisulfite restriction analysis (COBRA), respectively, in 56 IDC tumors. Eight polymorphisms in one-carb...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325599</comments>
            <pubDate>Tue, 11 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325599</guid>        </item>
        <item>
            <title>Regulation of PMA-induced MUC5AC expression by heparin in human bronchial epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5325608&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21984036%26dopt%3DAbstract</link>
            <description>Authors: Li Q, Lei RX, Zhou XD, Kolosov VP, Perelman JM
    Abstract
    Mucus hypersecretion is a major pathophysiologic feature in chronic inflammatory airway diseases. Oxidative stress plays a pivotal role in this process. Recent studies have found that heparin has antioxidant effects which can reduce free radical damage. Here, we hypothesized that heparin has some influence on the expression of mucin 5AC (MUC5AC) induced by phorbol myristate acetate (PMA) in a bronchial epithelial cell line (HBE16), also we have investigated the potential mechanism involved in the process. We found that ROS, the mRNA of Duox1, EGFR and MUC5AC, as well as the protein levels of Duox1, p-EGFR, EGFR, and MUC5AC in the PMA group were significantly increased when compared with the control group (all P &amp;lt;...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325608</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325608</guid>        </item>
        <item>
            <title>Post-conditioning protecting rat cardiomyocytes from apoptosis via attenuating calcium-sensing receptor-induced endo(sarco)plasmic reticulum stress.</title>
            <link>http://www.medworm.com/index.php?rid=5325607&amp;cid=s_37698_60_f&amp;fid=37698&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21984037%26dopt%3DAbstract</link>
            <description>Authors: Gan R, Hu G, Zhao Y, Li H, Jin Z, Ren H, Dong S, Zhong X, Li H, Yang B, Xu C, Lu F, Zhang W
    Abstract
    Our previous studies demonstrated that caclium-sensing receptor (CaR) stimulation elicited phospholipase C (PLC)-mediated inositol triphosphate (IP(3)) formation, leading to an elevation in [Ca(2+)](             i           ) released from the endo(sarco)plasmic reticulum (ER) to induce ER stress and perturbations of ER function, which cause cardiomyocyte apoptosis during ischemia/reperfusion (I/R). The aim of this study was to determine whether the protection of post-conditioning (PC) from I/R heart injury involved relieving calcium-sensing receptor (CaR)-induced ER stress. Male Wistar rats were subjected to 30 min of ischemia followed by 2 h of reperfusion. The rats wer...</description>
            <author>Molecular and Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5325607</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5325607</guid>        </item>
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