6,133 research outputs found
Measurement of CP Violation at the without Time Ordering or
I derive the expressions for the CP-violating asymmetry arising from
interference between mixed and direct decays in the Upsilon(4S) system, for the
case in which only one of the B decay times is observed, integrating over the
decay time of the other B. I observe that neither the difference of the decay
times Delta t, nor even their time-ordering, need be detected. A technique for
measurement of the CP-violating weak decay parameter sin(2beta) is described
which exploits this observation.Comment: 9 pages postscript, also available through
http://w4.lns.cornell.edu/public/CLN
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Prospects of measuring CP violation in B decays at CDF
We summarize the prospects of measuring the CP asymmetry in B{sup 0} {r_arrow} J/{psi}K{sup 0}{sub s} and B{sup 0} {r_arrow} {pi}{sup +}{pi}{sub -} with the CDF detector in Run II in 1999. We also explore the feasibility to determine sin 2{gamma} and discuss Run I results relevant to measurement of CP violation at CDF
Cytoskeleton structure, pattern of mitochondrial activity and ultrastructure of frozen or vitrified sheep embryos.
Even though sheep embryo cryopreservation is a commonly used procedure the survival and pregnancy outcomes can vary greatly. This study investigated whether cryopreservation was causing subtle changes in ultrastructure, mitochondrial activity or cytoskeletal integrity. Sheep embryos were either slow cooled in 1.5 M EG (n = 22), or vitrified in 20% EG + 20% DMSO with 0.5 M sucrose in Open Pulled Straws (OPS) (n = 24). One hour after warming the cryopreserved embryos differed from control embryos in that they had no mitochondrial activity combined with cytoskeletal disorganization and large vesicles. Vitrified embryos also showed many points of cytoskeleton disruption. Ultrastructural alterations resulting from actin filaments disorganization were observed in both cryopreserved groups. This includes areas presenting no cytoplasmic organelles, Golgi complex located far from the nucleus and a decrease of specialized intercellular junctions. Additionally, large vesicles were observed in vitrified morulae and early blastocysts. The alterations after cryopreservation were proportional to embryo quality as assessed using the stereomicroscope. Even in the absence of mitochondrial activity, grade I and II cryopreserved embryos contained mitochondria with normal ultrastructure. Embryos classified as grade I or II in the stereomicroscope revealed mild ultrastructural alterations, meaning that this tool is efficient to evaluate embryos after cryopreservation
Mesenchymal stem cells as therapeutic candidates for halting the progression of diabetic nephropathy
Mesenchymal stem cells (MSCs) possess pleiotropic properties that include immunomodulation, inhibition of apoptosis, fibrosis and oxidative stress, secretion of trophic factors, and enhancement of angiogenesis. These properties provide a broad spectrum for their potential in a wide range of injuries and diseases, including diabetic nephropathy (DN). MSCs are characterized by adherence to plastic, expression of the surface molecules CD73, CD90, and CD105 in the absence of CD34, CD45, HLA-DR, and CD14 or CD11b and CD79a or CD19 surface molecules, and multidifferentiation capacity in vitro. MSCs can be derived from many tissue sources, consistent with their broad, possibly ubiquitous distribution. This article reviews the existing literature and knowledge of MSC therapy in DN, as well as the most appropriate rodent models to verify the therapeutic potential of MSCs in DN setting. Some preclinical relevant studies are highlighted and new perspectives of combined therapies for decreasing DN progression are discussed. Hence, improved comprehension and interpretation of experimental data will accelerate the progress towards clinical trials that should assess the feasibility and safety of this therapeutic approach in humans. Therefore, MSC-based therapies may bring substantial benefit for patients suffering from DN.FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo/Sao Paulo Research Foundation) [2013/19560-6]CNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico/National Counsel of Technological and Scientific Development) [456959/2013-0]EFSD (European Foundation for the Study of Diabetes)Sociedade Beneficente Albert Einstein, Albert Einstein Hospital, 05652 São Paulo, SP, Brazil[University of São Paulo, 01246 São Paulo, SP, BrazilFederal University of São Paulo, 04023 São Paulo, SP, BrazilFederal University of São Paulo, 04023 São Paulo, SP, BrazilFAPESP: 2013/19560-6CNPq: 456959/2013-0Web of Scienc
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