Biometrics

Biometrics uses methods for unique recognition of humans based upon one or more intrinsic physical or behavioral traits. In computer science, particularly, biometrics is used as a form of identity access management and access control. It is also used to identify individuals in groups that are under surveillance. The book consists of 13 chapters, each focusing on a certain aspect of the problem. The book chapters are divided into three sections: physical biometrics, behavioral biometrics and medical biometrics. The key objective of the book is to provide comprehensive reference and text on human authentication and people identity verification from both physiological, behavioural and other points of view. It aims to publish new insights into current innovations in computer systems and technology for biometrics development and its applications. The book was reviewed by the editor Dr. Jucheng Yang, and many of the guest editors, such as Dr. Girija Chetty, Dr. Norman Poh, Dr. Loris Nanni, Dr. Jianjiang Feng, Dr. Dongsun Park, Dr. Sook Yoon and so on, who also made a significant contribution to the book

Dichotomic role of NAADP/two-pore channel 2/Ca2+ signaling in regulating neural differentiation of mouse embryonic stem cells

Poster Presentation - Stem Cells and Pluripotency: abstract no. 1866The mobilization of intracellular Ca2+stores is involved in diverse cellular functions, including cell proliferation and differentiation. At least three endogenous Ca2+mobilizing messengers have been identified, including inositol trisphosphate (IP3), cyclic adenosine diphosphoribose (cADPR), and nicotinic adenine acid dinucleotide phosphate (NAADP). Similar to IP3, NAADP can mobilize calcium release in a wide variety of cell types and species, from plants to animals. Moreover, it has been previously shown that NAADP but not IP3-mediated Ca2+increases can potently induce neuronal differentiation in PC12 cells. Recently, two pore channels (TPCs) have been identified as a novel family of NAADP-gated calcium release channels in endolysosome. Therefore, it is of great interest to examine the role of TPC2 in the neural differentiation of mouse ES cells. We found that the expression of TPC2 is markedly decreased during the initial ES cell entry into neural progenitors, and the levels of TPC2 gradually rebound during the late stages of neurogenesis. Correspondingly, perturbing the NAADP signaling by TPC2 knockdown accelerates mouse ES cell differentiation into neural progenitors but inhibits these neural progenitors from committing to the final neural lineage. Interestingly, TPC2 knockdown has no effect on the differentiation of astrocytes and oligodendrocytes of mouse ES cells. Overexpression of TPC2, on the other hand, inhibits mouse ES cell from entering the neural lineage. Taken together, our data indicate that the NAADP/TPC2-mediated Ca2+signaling pathway plays a temporal and dichotomic role in modulating the neural lineage entry of ES cells; in that NAADP signaling antagonizes ES cell entry to early neural progenitors, but promotes late neural differentiation.postprin