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Tatum, Rodney,Zhang, Yuguo,Lu, Qun,Kim, Kwonseop,Jeansonne, Beverly G.,Chen, Yan-Hua North-Holland Pub 2007 FEBS letters Vol.581 No.20
<P><B>Abstract</B></P><P>Mutations in WNK4 have been linked to hypertension in PHAII. Paracellular ion transport has been reported to be involved in this disease process; however, the specific molecular target has not been identified. In this study, we found that TJ protein claudin-7 and WNK4 were partially co-localized in renal tubules of rat kidney and co-immunoprecipitated in kidney epithelial cells. The wild-type and PHAII-causing mutant, but not the kinase-dead mutant, phosphorylated claudin-7. We have identified ser<SUP>206</SUP> in the COOH-terminus of claudin-7 as a putative phosphorylation site for WNK4. More importantly, disease-causing mutant enhanced claudin-7 phosphorylation and significantly increased paracellular permeability to Cl<SUP>−</SUP>.</P>
Chwan-Li Shen,Jodie Peterson,Owatha L. Tatum,Dale M. Dunn 한국식품영양과학회 2008 Journal of medicinal food Vol.11 No.1
This study examined the effects of eicosapentaenoic acid (EPA) and arachidonic acid (AA) on inflammation mediators during osteoblastogenesis, in terms of modulation of the cyclooxygenase (COX)-2 and the inducible nitric oxide (NO) synthase (iNOS) pathways. We hypothesized that n-3 polyunsaturated fatty acid (PUFA) would reduce the production of inflammation mediators, including prostaglandin E2 (PGE2) and NO, and related mRNA gene expression during osteoblastogenesis. Mouse bone marrow stromal cells (ST-2) were treated with 40 M ethanol (as a control), 40 M AA, or 40 M EPA in osteogenic medium for 7, 14, 21, or 28 days. Prior to harvest, cells were treated with respective treatments along with cytokine mixtures for an additional 24 hours, and then cells were harvested for mRNA expression. In addition, cells were also treated with respective treatments along with the same cytokine mixtures for an additional 48 hours for experiment measuring PGE2 and NO production using conditioned culture medium and protein expression using cells. Except for 7 days of culture, AA treatment resulted in the highest value for PGE2 production throughout 28 days of culture. AA treatment also enhanced COX-2 mRNA expression up to 21 days. AA treatment resulted in a higher value for NO production after 7 days, while EPA treatment yielded a higher value for NO production relative to those receiving AA treatment after 14 and 21 days. Our investigation has corroborated that the protective action of EPA on osteoblastogensis was mediated by the modulation of PGE2 and the NO pathway.
( Robert Martin ),( Javier Irurzun ),( Jordi Munchart ),( Igor Trofimov ),( Alexander Scupchenko ),( Cliff Tatum ),( Govindarajan Narayanan ) 대한간학회 2011 Clinical and Molecular Hepatology(대한간학회지) Vol.17 No.1
Background/Aims: It has been shown that the drug-eluting beads loaded with doxorubicin (DEBDOX) are effective for the treatment of hepatocellular carcinoma (HCC). However, the optimal safety and efficacy still remain to be established by using various bead sizes, doxorubicin doses, and the degree of stasis.The aim of this study was to determine the optimal safety and efficacy of DEBDOX in the treatment of HCC. Methods: Analysis of a 503-patient prospective, multicenter, multinational Bead Registry Database from 2007 to 2010 identified 206 patients who had been treated for HCC with DEBDOX. Primary endpoints were to compare safety, tolerance, response rates, and overall survival based on bead size (100-300, 300-500, 500-700, and 700-900 μm), number of vials, doxorubicin dose, and degree of stasis. Results: In total, 206 patients underwent 343 treatments. The use of all four bead sizes was similar based on Child-Pugh class and Okuda stage, with a significantly higher use (50%) of beads of size 100-300 μm in patients with portal vein thrombosis (P=0.05). Significant differences were seen for the number of median treatments, median doxorubicin dose, lobar infusion), and degree of complete stasis. The rate of adverse events was higher for larger beads than for smaller beads (28% vs. 16%; P=0.02). Conclusions: Bead size and dose may vary according to disease distribution. Smaller beads offer the opportunity for repeated treatments, a larger cumulative dose delivery, a lesser degree of complete stasis, and fewer adverse events.