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OBJECTIVE--Our objective was to determine the secular trend in prevalence of type 2 diabetes in Shanghai, China. RESEARCH DESIGN AND METHODS--Two consecutive population-based surveys for type 2 diabetes were conducted in randomly selected adults aged 35-74 years in Shanghai in 2002-2003 (n = 12,329) and in 2009 (n = 7,423). Diagnosed type 2 diabetes was determined based on self-report, whereas those undiagnosed were identified by measured fasting and post-load glucose according to 2009 American Diabetes Association criteria. RESULTS--Age-standardized prevalence of diagnosed and undiagnosed type 2 diabetes increased from 5.1 and 4.6% in 2002-2003 to 7.4 and 5.2% in 2009. The prevalence of type 2 diabetes increased with age and was higher among men and in urban residents in both surveys (P < 0.001). Between the two surveys, the increase in the prevalence was more evident in the rural population (P < 0.001) and appeared more rapid in younger birth cohorts (P < 0.05). CONCLUSIONS--Our results suggest that Shanghai has experienced an increasing burden of type 2 diabetes. [ABSTRACT FROM AUTHOR]

We previously reported that bone marrow-derived CD8[sup +]/TCR[sup -] grafting facilitating cells (FC) enhance hematopoietic stem cell (HSC) engraftment in allogeneic and syngeneic recipients and that B220[sup +]/CD11C[sup +]/CD11[sup -] precursor plasmacytoid dendritic cell (p-pre DC) FC subpopulation plays a critical and dominant role in facilitation. NOD mice exhibit a number of defects in innate and adaptive immunity including impaired myeloid differentiation and function in antigen presenting cell, NK cells, NKT cells and regulatory T cells. In the present studies, we evaluated the function of NOD FC. We reported for the first time that FC from NOD mice are functionally impaired in vivo and in vitro. CD8[sup +]/TCR[sup -] FC were sorted from NOD, NOR or B6 bone marrow and evaluated for subpopulations we previously found in B6 FC: NK FC, myeloid cells, CD19 FC, monocytes, and p-preDC. p-pre DC FC represented the major FC subpopulation in all strains examined. The CD 19[sup +] FC subpopulation was selectively significantly decreased in NOD FC compared to those from B6 or NOR mice (12% versus 26%, P <0.05). To test the function of NOD or NOR FC, 500 NOR HSC (c-Kit[sup +]/Sca-l[sup +]/Lin[sup -]) were sorted and transplanted with 30,000 NOR FC (n = 10) or without FC (n=16) into conditioned 950 cGy NOR recipients. The NOR FC significantly enhanced engraftment of NOR HSC compared to the HSC alone (p = 0.029) (Figure 1a). In striking contrast, NOD FC did not facilitate, as evidenced by the similar engraftment of HSC with NOD FC (n=13) compared to the NOD HSC alone (n=17; p = 0.579) (Figure lb). Impaired function of NOD FC was confirmed in vitro using colony forming cell (CFC) assay. NOD FC did not increase colony production when cultured with NOD HSC (Figure 1c), while NOR FC did (Figure ld). These results point without ambiguity to a defect in NOD FC that is not present in the NOR FC. Studies are underway to determine: (1) the mechanism of defective FC in NOD mice; (2) whether function of the FC can be restored in NOD mice with flt3-ligand treatment. [ABSTRACT FROM AUTHOR]