A description is provided of the software algorithms developed for the CMS tracker both for reconstructing charged-particle trajectories in proton-proton interactions and for using the resulting tracks to estimate the positions of the LHC luminous region and individual primary-interaction vertices. Despite the very hostile environment at the LHC, the performance obtained with these algorithms is found to be excellent. For tt events under typical 2011 pileup conditions, the average trackreconstruction efficiency for promptly-produced charged particles with transverse momenta of p T > 0.9 GeV is 94% for pseudorapidities of |η| < 0.9 and 85% for 0.9 < |η| < 2.5. The inefficiency is caused mainly by hadrons that undergo nuclear interactions in the tracker material. For isolated muons, the corresponding efficiencies are essentially 100%. For isolated muons of p T = 100 GeV emitted at |η| < 1.4, the resolutions are approximately 2.8% in p T , and respectively, 10 µm and 30 µm in the transverse and longitudinal impact parameters. The position resolution achieved for reconstructed primary vertices that correspond to interesting pp collisions is 10-12 µm in each of the three spatial dimensions. The tracking and vertexing software is fast and flexible, and easily adaptable to other functions, such as fast tracking for the trigger, or dedicated tracking for electrons that takes into account bremsstrahlung.

An experiment to search for light sterile neutrinos is conducted at a reactor with a thermal power of 2.8 GW located at the Hanbit nuclear power complex. The search is done with a detector consisting of a ton of Gd-loaded liquid scintillator in a tendon gallery approximately 24 m from the reactor core. The measured antineutrino event rate is 1976 per day with a signal to background ratio of about 22. The shape of the antineutrino energy spectrum obtained from the eight-month data-taking period is compared with a hypothesis of oscillations due to activesterile antineutrino mixing. No strong evidence of 3+1 neutrino oscillation is found. An excess around the 5 MeV prompt energy range is observed as seen in existing longer-baseline experiments. The mixing parameter sin 2 2θ14 is limited up to less than 0.1 for ∆m The mixing among three neutrinos has been well established by experiments performed in the past two decades since the discovery of neutrino oscillations [1][2][3]. Consistent measurements of the two mass differences and the three mixing angles of the standard, three-neutrino mixing model have been reported by oscillation experiments using atmospheric, solar, reactor, and accelerator neutrinos [4]. Nevertheless, the mass hierarchy, the mass of the lightest neutrino, the Dirac or Majorana nature of the neutrino, and the CP phase are yet to be determined [5].Even though the number of active light neutrinos is limited to three by Z boson decay-width measurements [6], it is still possible to have additional neutrinos if they are sterile. Sterile neutrinos can be identified by the occurrence of activesterile neutrino oscillations. A hint for this is the LSND experiment's report of an observation ofν µ →ν e mixing with a frequency corresponding to a mass-squared difference larger than 0.01 eV 2 [7]. Results from the MiniBooNE's test of the LSND signal are, however, inconclusive [8].In addition to the LSND result, there are two other anomalies that could possibly be signs of active-sterile neutrino oscillations. An apparent ν e disappearance over a baseline of a few meters in the GALLEX and SAGE gallium experiments exposed to radioactive sources was reported [9]; the ratio of the numbers of measured and predicted events is 0.88 ± 0.05. A number of short-baseline reactor antineutrino experiments established limits on the presence of neutrino oscillations with eV mass differences by shape analyses of the measured neutrino energy spectra. Among those experiments, the Bugey experimental limits on sterile neutrinos are the most stringent [10]. Mueller et al. [11] found about a 6% deficit in reactor antineutrino event rates compared with the theoretical expectations for the short-baseline reactor experiments, which is the so-called "reactor antineutrino anomaly" (RAA). It can be interpreted as an active-sterile neutrino oscillation with three active neutrinos plus one or more sterile neutrinos, i.e., a 3 + n ν scenario [12,13], compatible with the LSND result. Recent reactor experiments that measured the θ 13 mixing an...

Presently, co-culture of human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) with BV2 microglia under amyloid-β42 (Aβ42) exposure induced a reduction of Aβ42 in the medium as well as an overexpression of the Aβ-degrading enzyme neprilysin (NEP) in microglia. Cytokine array examinations of co-cultured media revealed elevated release of soluble intracellular adhesion molecule-1 (sICAM-1) from hUCB-MSCs. Administration of human recombinant ICAM-1 in BV2 cells and wild-type mice brains induced NEP expression in time- and dose-dependent manners. In co-culturing with BV2 cells under Aβ42 exposure, knockdown of ICAM-1 expression on hUCB-MSCs by small interfering RNA (siRNA) abolished the induction of NEP in BV2 cells as well as reduction of added Aβ42 in the co-cultured media. By contrast, siRNA-mediated inhibition of the sICAM-1 receptor, lymphocyte function-associated antigen-1 (LFA-1), on BV2 cells reduced NEP expression by ICAM-1 exposure. When hUCB-MSCs were transplanted into the hippocampus of a 10-month-old transgenic mouse model of Alzheimer's disease for 10, 20, or 40 days, NEP expression was increased in the mice brains. Moreover, Aβ42 plaques in the hippocampus and other regions were decreased by active migration of hUCB-MSCs toward Aβ deposits. These data suggest that hUCB-MSC-derived sICAM-1 decreases Aβ plaques by inducing NEP expression in microglia through the sICAM-1/LFA-1 signaling pathway.

SummaryBackground The pathogenesis of melasma has not yet been clearly demonstrated. We tried to determine whether the stem cell factor (SCF) and its receptor c-kit are involved in the mechanism of hyperpigmentation of melasma because this factor is highly implicated in the stimulation of melanocyte function in vitro and in vivo. Objectives The present study was conducted to investigate the expression of SCF and c-kit on the lesions of melasma compared with nonlesional skin. Patients/methods Skin samples were obtained from lesional and nonlesional facial skin of 60 Korean women with melasma. Immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis was performed to determine the expression of SCF and c-kit in melasma. Results The expression of SCF was significantly increased at the lesional dermis compared with nonlesional dermis. However, there was no significant difference in the expression of SCF in lesional and nonlesional epidermis. The expression of c-kit was significantly increased at lesional epidermis compared with nonlesional skin. RT-PCR of SCF and c-kit mRNAs demonstrated increased expression of both types of transcripts in the lesional skin compared with nonlesional skin. Conclusions These results suggest that the increased expression of SCF in the dermis and of c-kit in the epidermis play an important role in the mechanism of hyperpigmentation in melasma.