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Articles by L Tian
Total Records ( 4 ) for L Tian
  C Bian , F Zhang , F Wang , Z Ling , M Luo , H Wu , Y Sun , J Li , B Li , J Zhu , L Tang , Y Zhou , Q Shi , Y Ji , L Tian , G Lin , Y Fan , N Wang and B. Sun

DNA immunization is an efficient method for high-affinity monoclonal antibody generation. Here, we describe the generation of several high-quality monoclonal antibodies (mAbs) against retinol-binding protein 4 (RBP4), an important marker for kidney abnormality and dysfunction, with a combination method of DNA priming and protein boost. The mAbs generated could bind to RBP4 with high sensitivity and using these mAbs, an immunocolloidal gold fast test strip was constructed. The strip can give a result in <5 min and is very sensitive with a detection limit of about 1 ng/ml. A small-scale clinical test revealed that the result of this strip was well in accordance with that of an enzyme-labeled immunosorbent assay kit currently available on the market. Consequently, it could be useful for more convenient and faster RBP4 determination in the clinic.

  T Cai , L Tian , H Uno , S. D Solomon and L. J. Wei

For modern evidence-based medicine, decisions on disease prevention or management strategies are often guided by a risk index system. For each individual, the system uses his/her baseline information to estimate the risk of experiencing a future disease-related clinical event. Such a risk scoring scheme is usually derived from an overly simplified parametric model. To validate a model-based procedure, one may perform a standard global evaluation via, for instance, a receiver operating characteristic analysis. In this article, we propose a method to calibrate the risk index system at a subject level. Specifically, we developed point and interval estimation procedures for t-year mortality rates conditional on the estimated parametric risk score. The proposals are illustrated with a dataset from a large clinical trial with post-myocardial infarction patients.

  M. M McDermott , L Ferrucci , J Guralnik , L Tian , K Liu , F Hoff , Y Liao and M. H. Criqui

Background— Associations of pathophysiological calf muscle characteristics with functional decline in people with lower extremity peripheral arterial disease are unknown.

Methods and Results— Three hundred seventy participants with peripheral arterial disease underwent baseline measurement of calf muscle area, density, and percent fat with the use of computed tomography. Participants were followed up annually for 2 years. The outcome of mobility loss was defined as becoming unable to walk 1/4 mile or walk up and down 1 flight of stairs without assistance among those without baseline mobility limitations. Additional outcomes were ≥20% decline in 6-minute walk distance and becoming unable to walk for 6 minutes continuously among participants who walked continuously for 6 minutes at baseline. With adjustment for age, sex, race, body mass index, the ankle-brachial index, smoking, physical activity, relevant medications, and comorbidities, lower calf muscle density (P for trend <0.001) and lower calf muscle area (P for trend=0.039) were each associated with increased mobility loss rates. Compared with participants in the highest baseline tertiles, participants in the lowest tertile of calf muscle percent fat had a hazard ratio of 0.18 for incident mobility loss (95% confidence interval, 0.06 to 0.55; P=0.003), and participants in the lowest tertile of muscle density had a 3.50 hazard ratio for incident mobility loss (95% confidence interval, 1.28 to 9.57; P=0.015). No significant associations of calf muscle characteristics with 6-minute walk outcomes were observed.

Conclusions— Our findings suggest that interventions to prevent mobility loss in peripheral arterial disease should focus on reversing pathophysiological findings in calf muscle.

  M Zamisch , L Tian , R Grenningloh , Y Xiong , K. F Wildt , M Ehlers , I C Ho and R. Bosselut

The transcription factor Ets1 contributes to the differentiation of CD8 lineage cells in the thymus, but how it does so is not understood. In this study, we demonstrate that Ets1 is required for the proper termination of CD4 expression during the differentiation of major histocompatability class 1 (MHC I)–restricted thymocytes, but not for other events associated with their positive selection, including the initiation of cytotoxic gene expression, corticomedullary migration, or thymus exit. We further show that Ets1 promotes expression of Runx3, a transcription factor important for CD8 T cell differentiation and the cessation of Cd4 gene expression. Enforced Runx3 expression in Ets1-deficient MHC I–restricted thymocytes largely rescued their impaired Cd4 silencing, indicating that Ets1 is not required for Runx3 function. Finally, we document that Ets1 binds at least two evolutionarily conserved regions within the Runx3 gene in vivo, supporting the possibility that Ets1 directly contributes to Runx3 transcription. These findings identify Ets1 as a key player during CD8 lineage differentiation and indicate that it acts, at least in part, by promoting Runx3 expression.

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