2-D Equivalent finite element model of quadratic linear electromagnetic actuator

The purpose of this paper is to present a 2-D equivalent finite element model of a quadratic linear electromagnetic actuator that can save space and power as it does not employ an energy conversion system. A 2-D model, while being fairly accurate, is preferable to a 3-D finite element analysis for the design and analysis of a quadratic linear electromagnetic actuator as it requires significantly lower computing resources and results in faster calculations. We calculate the effective coil length for the equivalent 2-D finite element model and validate the accuracy of this model with experimental data

The involvement of Eph–Ephrin signaling in tissue separation and convergence during Xenopus gastrulation movements

AbstractIn Xenopus gastrulation, the involuting mesodermal and non-involuting ectodermal cells remain separated from each other, undergoing convergent extension. Here, we show that Eph–ephrin signaling is crucial for the tissue separation and convergence during gastrulation. The loss of EphA4 function results in aberrant gastrulation movements, which are due to selective inhibition of tissue constriction and separation. At the cellular levels, knockdown of EphA4 impairs polarization and migratory activity of gastrulating cells but not specification of their fates. Importantly, rescue experiments demonstrate that EphA4 controls tissue separation via RhoA GTPase in parallel to Fz7 and PAPC signaling. In addition, we show that EphA4 and its putative ligand, ephrin-A1 are expressed in a complementary manner in the involuting mesodermal and non-involuting ectodermal layers of early gastrulae, respectively. Depletion of ephrin-A1 also abrogates tissue separation behaviors. Therefore, these results suggest that Eph receptor and its ephrin ligand might mediate repulsive interaction for tissue separation and convergence during early Xenopus gastrulation movements

β-Caryophyllene attenuates dextran sulfate sodium-induced colitis in mice via modulation of gene expression associated mainly with colon inflammation

AbstractWe examined the modulatory activity of β-caryophyllene (CA) and gene expression in colitic colon tissues in a dextran sulfate sodium (DSS)-induced colitis model. Experimental colitis was induced by exposing male BALB/c mice to 5% DSS in drinking water for 7 days. CA (30 or 300mg/kg) was administered orally once a day together with DSS. CA administration attenuated the increases in the disease activity index, colon weight/length ratio, inflammation score, and myeloperoxidase activity in DSS-treated mice. Microarray analysis showed that CA administration regulated the expression in colon tissue of inflammation-related genes including those for cytokines and chemokines (Ccl2, Ccl7, Ccl11, Ifitm3, IL-1β, IL-28, Tnfrsf1b, Tnfrsf12a); acute-phase proteins (S100a8, Saa3, Hp); adhesion molecules (Cd14, Cd55, Cd68, Mmp3, Mmp10, Sema6b, Sema7a, Anax13); and signal regulatory proteins induced by DSS. CA significantly suppressed NF-κB activity, which mediates the expression of a different set of genes. These results suggest that CA attenuates DSS-induced colitis, possibly by modulating the expression of genes associated mainly with colon inflammation through inhibition of DSS-induced NF-κB activity

Benefit From Directional Microphone Hearing Aids: Objective and Subjective Evaluations

ObjectivesThe aims of this study were to find and compare the effect of directional (DIR) processing of two different hearing aids via both subjective and objective methods, to determine the association between the results of the subjective and objective evaluations, and to find out individual predictive factors influencing the DIR benefit.MethodsTwenty-six hearing aid users fitted unilaterally with each two different experimental hearing aid performed modified Korean Hearing in Noise Test (K-HINT) in three DIR conditions; omnidirectional (OMNI) mode, OMNI plus noise reduction feature, fixed DIR mode. In order to determine benefits from DIR benefit within a hearing aid and compare performance of the DIR processing between hearing aids, a subjective questionnaire was administrated on speech quality (SQ) and discomfort in noise (DN) domain. Correlation analysis of factors influencing DIR benefit was accomplished.ResultsBenefits from switching OMNI mode to DIR mode within both hearing aids in K-HINT were about 2.8 (standard deviation, 3.5) and 2.1 dB SNR (signal to ratio; SD, 2.5), but significant difference in K-HINT results between OMNI and OMNI plus noise reduction algorithm was not shown. The subjective evaluation resulted in the better SQ and DN scores in DIR mode than those in OMNI mode. However, the difference of scores on both SQ and DN between the two hearing aids with DIR mode was not statistically significant. Any individual factors did not significantly affect subjective and objective DIR benefits.ConclusionDIR benefit was found not only in the objective measurement performed in the laboratory but also in the subjective questionnaires, but the subjective results was failed to have significant correlation with the DIR benefit obtained in the K-HINT. Factors influencing individual variation in perceptual DIR benefit were still hard to explain

TCF/β-catenin plays an important role in HCCR-1 oncogene expression

<p>Abstract</p> <p>Background</p> <p>Oncogene <it>HCCR-1 </it>functions as a negative regulator of the p53 and contributes to tumorigenesis of various human tissues. However, it is unknown how <it>HCCR-1 </it>contributes to the cellular and biochemical mechanisms of human tumorigenesis.</p> <p>Results</p> <p>In this study, we showed how the expression of <it>HCCR-1 </it>is modulated. The luciferase activity assay indicated that the <it>HCCR-1 </it>5'-flanking region at positions -166 to +30 plays an important role in <it>HCCR-1 </it>promoter activity. Computational analysis of this region identified two consensus sequences for the T-cell factor (TCF) located at -26 to -4 (Tcf1) and -136 to -114 (Tcf2). Mutation at the Tcf1 site led to a dramatic decrease in promoter activity. Mobility shift assays (EMSA) revealed that nuclear proteins bind to the Tcf1 site, but not to the Tcf2 site. LiCl, Wnt signal activator by GSK-3β inhibition, significantly increased reporter activities in wild-type Tcf1-containing constructs, but were without effect in mutant Tcf1-containing constructs in HEK/293 cells. In addition, endogenous <it>HCCR-1 </it>expression was also increased by treatment with GSK-3β inhibitor, LiCl or AR-A014418 in HEK/293 and K562 cells. Finally, we also observed that the transcription factor, TCF, and its cofactor, β-catenin, bound to the Tcf1 site.</p> <p>Conclusion</p> <p>These findings suggest that the Tcf1 site on the <it>HCCR-1 </it>promoter is a major element regulating <it>HCCR-1 </it>expression and abnormal stimulation of this site may induce various human cancers.</p

Human AP endonuclease suppresses DNA mismatch repair activity leading to microsatellite instability

The multifunctional mammalian apurinic/apyrimidinic (AP) endonuclease (APE) participates in the repair of AP sites in the cellular DNA as well as participating in the redox regulation of the transcription factor function. The function of APE is considered as the rate-limiting step in DNA base excision repair. Paradoxically, an unbalanced increase in APE protein leads to genetic instability. Therefore, we investigated the mechanisms of genetic instability that are induced by APE. Here, we report that the overexpression of APE protein disrupts the repair of DNA mismatches, which results in microsatellite instability (MSI). We found that expression of APE protein led to the suppression of the repair of DNA mismatches in the normal human fibroblast cells. Western blot analysis revealed that hMSH6 protein was markedly reduced in the APE-expressing cells. Moreover, the addition of purified Mutα (MSH2 and MSH6 complex) to the extracts from the APE-expressing cells led to the restoration of mismatch repair (MMR) activity. By performing MMR activity assay and MSI analysis, we found that the co-expression of hMSH6 and APE exhibited the microsatellite stability, whereas the expression of APE alone generated the MSI-high phenotype. The APE-mediated decrease in MMR activity described here demonstrates the presence of a new and highly effective APE-mediated mechanism for MSI

High mobility solution-processed hybrid light emitting transistors

We report the design, fabrication, and characterization of high-performance, solution-processed hybrid (inorganic-organic) light emitting transistors (HLETs). The devices employ a high-mobility, solution-processed cadmium sulfide layer as the switching and transport layer, with a conjugated polymer Super Yellow as an emissive material in non-planar source/drain transistor geometry. We demonstrate HLETs with electron mobilities of up to 19.5 cm2/V s, current on/off ratios of &gt;107, and external quantum efficiency of 10-2% at 2100 cd/m2. These combined optical and electrical performance exceed those reported to date for HLETs. Furthermore, we provide full analysis of charge injection, charge transport, and recombination mechanism of the HLETs. The high brightness coupled with a high on/off ratio and low-cost solution processing makes this type of hybrid device attractive from a manufacturing perspective.open0