In our risk score, 39% of individuals with previously undiagnosed diabetes will be missed. We found that false-negative individuals had lower PBG and LDL levels; however, there was no different in FPG and TC levels as compared with true-positive individuals. Furthermore, the resting HR and BP parameters were significantly difference between the two groups. This is partly because BMI, HT and HR score can not completely reflect these differences. In the risk score system, BMI was the strongest predictor of dyslipidemia; however, the risk factors can not completely represent contribution of lipid profile on CAN. Screening is an ongoing process, presumably, some of the false-negative individuals will become true positive over time and will be picked up in a subsequent screening. Several limitations of the study deserve comment. First, the design of the present study was cross-sectional study and thus the temporal sequence between risk factors and outcome was questionable. Second, participants recruited from Shanghai and external validation has not been performed. So generalizability of our prediction model should be needed to determine. Finally, it is important to mention that our study was performed on Chinese individuals, and our findings may not be relevant to people of other ethnicities. In conclusion, the simple CAN risk score Vorinostat developed here can be applied in a stepwise screening strategy. People with a high-risk score should be referred for further standard CA function tests and changes to a healthier lifestyle for primary prevention. Antigen presentation by B lymphocytes is required to mount high affinity humoral immune responses, for coordinating antigen specific cytotoxicity, and for propagating some T cell responses. B lymphocytes differ from other antigen presenting cells in several fundamental ways. The most important difference is that B cells are clonotypic, and they usually only efficiently capture and process antigens recognized by the B cell antigen receptor. The primacy of the BCR as the portal for entry of antigen ensures coordination of B and T cell responses. In B cells, most antigens are processed in specialized MHC class II containing late endosomes which are Lamp-1+, acidic and contain cathepsins, thiol reductases, and other molecules required for efficient antigen processing. MIIC vesicles consist of a limiting membrane studded with Lamp-1 and a lumen containing multivesicular bodies. These intraluminal vesicles are derived from BCR-laden transport vesicles that have gained access to the MIIC compartment. BCR trafficking to late endosomes is also required for coupling antigen recognition to the activation of the toll-like receptors 7 and 9. This is because these receptors only productively bind ligands in late endosomes. The mechanisms underlying this requirement have been best defined for TLR9. In resting B cells, TLR9 resides outside the MIIC.