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Articles by T. Chen
Total Records ( 2 ) for T. Chen
  C. C. Hsu , S. J. Hwang , T. Y. Tai , T. Chen , M. C. Huang , S. J. Shin , C. P. Wen , Y. T. Shih , H. J. Yang , C. T. Chang , C. J. Chang , C. H. Loh , M. T. Fuh , Y. S. Li and H.-Y. Chang
  Aims  Cigarette smoking is a well-known risk factor associated with diabetic nephropathy. The objective of this study was to further investigate the dose-response effect of tobacco exposure on proteinuria in males with Type 2 diabetes.

Methods  Five hundred and nine males with Type 2 diabetes were selected from a cohort participating in a glucose control study in Taiwan. Pack-years of cigarette smoking were calculated to define tobacco exposure. Proteinuria was identified if albumin-to-creatinine ratio was ≥ 30 mg/g in at least two of three consecutive urine tests. Logistic regression and trend tests were used to delineate the association between smoking status and proteinuria.

Results  Compared with non-smokers, those who had smoked 15-30 or more than 30 pack-years were respectively 2.78 (95% CI 1.34-5.76, < 0.01) and 3.20 (95% CI 1.74-5.86, < 0.001) times more likely to develop proteinuria. The dose-response effect of tobacco exposure on the development of proteinuria is highly significant in all subjects (P = 0.001) and in subgroups with relatively short duration of diabetes mellitus (P < 0.001), good blood pressure control (P = 0.001) and those of young age (P = 0.007).

Conclusions  The current study shows a clear dose-response effect of cigarette smoking on development of proteinuria in male Type 2 diabetic patients. These findings reinforce the urgent need to encourage diabetic patients to stop smoking regardless of age, duration of diabetes mellitus or status of blood pressure control.

  T. Chen , H. Xu , H.Q. Wang , Y. Zhao , C.F. Zhu , Y.H. Zhang , M.J. Ji , Y.B. Hua and W.X. Wu
  Severe graft rejection remains an important obstacle in intestinal transplantation. In this study, dendritic cells (DCs) isolated from rat bone marrow were cultured for 5 days, and triptolide applied for 3 more days. The recipient rats were pretreated with donor triptolide-modified or not modified DC. Small bowel transplantation was performed to observed survival times. We demonstrated that triptolide markedly inhibited both the expression of CD80 and MHCII expression on DCs. Triptolide-modified DCs stimulated lower proliferative responses among allogeneic T cells, prolonging the survival of intestinal allografts in rats. These results suggested that pretreatment with triptolide-modified DC prolonged the survival of rat small bowel allografts after transplantation.
 
 
 
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