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Articles by J. Luo
Total Records ( 4 ) for J. Luo
  N Wu , Y Zhao , Y Yin , Y Zhang and J. Luo

Our previous studies have demonstrated that bone morphogenetic protein 9 (BMP-9) is one of the most efficacious BMPs to induce osteoblast differentiation of mesenchymal stem cells (MSCs). However, the molecular mechanism underlying the BMP-9-induced osteogenic differentiation of MSCs remains to be fully elucidated. In this study, dominant negative (DN) type II TGF-β receptors were constructed and introduced into C3H10T1/2 stem cells, then in vitro and in vivo assays were carried out to analyze and identify the type II TGF-β receptors required for BMP-9-induced osteogenesis. We found that three DN type II TGF-β receptors, DN-BMPRII, DN-ActRII, and DN-ActRIIB, diminished BMP-9-induced alkaline phosphatase (ALP) activity, led to a decrease in BMP-9-induced Smad binding element (SBE)-controled reporter activity, reduced BMP-9-induced expressions of Smad6 and Smad7, and decreased BMP-9-induced mineralization in vitro and ectopic bone formation in vivo, finally resulted in decreased bone masses and immature osteogenesis. These findings strongly suggested that three wild-type II TGF-β receptors, BMPRII, ActRII and ActRIIB, may play a functional role in BMP-9-induced osteogenic differentiation of C3H10T1/2 cells. However, C3H10T1/2 stem cells can express BMPRII and ActRII, but not ActRIIB. Using RNA interference (RNAi), we found that luciferase reporter activity and ALP activity induced by BMP-9 were accordingly inhibited along with the knockdown of BMPRII and ActRII. Taken together, our results demonstrated that BMPRII and ActRII are the functional type II TGF-β receptors in BMP-9-induced osteogenic differentiation of C3H10T1/2 cells.

  K He , X Li , J Zhou , X. W Deng , H Zhao and J. Luo

Summary:NTAP is designed to analyze ChIP-chip data generated by the NimbleGen tiling array platform and to accomplish various pattern recognition tasks that are useful especially for epigenetic studies. The modular design of NTAP makes the data processing highly customizable. Users can either use NTAP to perform the full process of NimbleGen tiling array data analysis, or choose post-processing modules in NTAP to analyze pre-processed epigenetic data generated by other platforms. The output of NTAP can be saved in standard GFF format files and visualized in GBrowse.

  J Dong , Y Li , Z Yang and J. Luo

Background and objectives: To explore the correlation between dietary sodium intake and cardiovascular and overall mortality, and then determine whether this correlation can be explained by protein and energy intake paralleled with sodium intake in dialysis patients.

Design, setting, participants, & measurements: This single-center retrospective cohort study enrolled 305 incident patients who started peritoneal dialysis in our unit from July 2002 to February 2007. All patients were followed until death or until being censored in February 2008. Demographic data were collected at baseline. Biochemical, dietary, and nutrition data were examined at baseline and thereafter at regular intervals to calculate the average values throughout the study.

Results: Participants with the highest average sodium intake were more likely to be younger, male, and overweight. Patients in the high tertile of average sodium intake had higher albumin, prealbumin, and lean body mass levels, and more nutrient intakes paralleling with sodium intake. Low average sodium intake independently predicted the increased risk for overall and cardiovascular death after adjusting for recognized confounders. Further adjustment for dietary protein, energy, and other nutrient intakes individually had minimal impact on the association between average sodium intake and overall death, with hazard ratios varying between 0.35 and 0.44, and cardiovascular death, with hazard ratios varying between 0.06 and 0.11.

Conclusions: This study revealed that low dietary sodium intake independently predicts the high overall and cardiovascular mortality in dialysis patients. This correlation could not be entirely explained by deficient protein and energy intake.

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