Degradation of adhesion molecules of G361 melanoma cells by a non-thermal atmospheric pressure microplasma

Increased expression of integrins and focal adhesion kinase (FAK) is important for the survival, growth and metastasis of melanoma cells. Based on this well-established observation in oncology, we propose to use degradation of integrin and FAK proteins as a potential strategy for melanoma cancer therapy. A low-temperature radio-frequency atmospheric microplasma jet is used to study their effects on the adhesion molecules of G361 melanoma cells. Microplasma treatment is shown to (1) cause significant cell detachment from the bottom of microtiter plates coated with collagen, (2) induce the death of human melanoma cells, (3) inhibit the expression of integrin 2, integrin 4 and FAK on the cell surface and finally (4) change well-stretched actin filaments to a diffuse pattern. These results suggest that cold atmospheric pressure plasmas can strongly inhibit the adhesion of melanoma cells by reducing the activities of adhesion proteins such as integrins and FAK, key biomolecules that are known to be important in malignant transformation and acquisition of metastatic phenotypes

Proton-proton fusion in pionless effective theory

The proton-proton fusion reaction, $pp\to de^+\nu$, is studied in pionless effective field theory (EFT) with di-baryon fields up to next-to leading order. With the aid of the di-baryon fields, the effective range corrections are naturally resummed up to the infinite order and thus the calculation is greatly simplified. Furthermore, the low-energy constant which appears in the axial-current-di-baryon-di-baryon contact vertex is fixed through the ratio of two- and one-body matrix elements which reproduces the tritium lifetime very precisely. As a result we can perform a parameter free calculation for the process. We compare our numerical result with those from the accurate potential model and previous pionless EFT calculations, and find a good agreement within the accuracy better than 1%.Comment: 14 pages, 5 eps figure

Patients with refractory cytomegalovirus (CMV) infection following allogeneic haematopoietic stem cell transplantation are at high risk for CMV disease and non-relapse mortality

AbstractPre-emptive therapy is an effective approach for cytomegalovirus (CMV) control; however, refractory CMV still occurs in a considerable group of recipients after allogeneic haematopoietic stem cell transplantation (allo-HSCT). Until now, hardly any data have been available about the clinical characteristics and risk factors of refractory CMV, or its potential harmful impact on the clinical outcome following allo-HSCT. We studied transplant factors affecting refractory CMV in the 100 days after allo-HSCT, and the impact of refractory CMV on the risk of CMV disease and non-relapse mortality (NRM). We retrospectively studied 488 consecutive patients with CMV infection after allo-HSCT. Patients with refractory CMV in the 100 days after allo-HSCT had a higher incidence of CMV disease and NRM than those without refractory CMV (11.9% vs. 0.8% and 17.1% vs. 8.3%, respectively). Multivariate analysis showed that refractory CMV infection in the 100 days after allo-HSCT was an independent risk factor for CMV disease (hazard ratio (HR) 10.539, 95% CI 2.467–45.015, p 0.001), and that refractory CMV infection within 60–100 days after allo-HSCT was an independent risk factor for NRM (HR 8.435, 95% CI 1.511–47.099, p 0.015). Clinical factors impacting on the risk of refractory CMV infection included receiving transplants from human leukocyte antigen-mismatched family donors (HR 2.012, 95% CI 1.603–2.546, p <0.001) and acute graft-versus-host disease (HR 1.905, 95% CI 1.352–2.686, p <0.001). We conclude that patients with refractory CMV infection during the early stage after allo-HSCT are at high risk for both CMV disease and NRM

Resultant pressure distribution pattern along the basilar membrane in the spiral shaped cochlea

Cochlea is an important auditory organ in the inner ear. In most mammals, it is coiled as a spiral. Whether this specific shape influences hearing is still an open problem. By employing a three dimensional fluid model of the cochlea with an idealized geometry, the influence of the spiral geometry of the cochlea is examined. We obtain solutions of the model through a conformal transformation in a long-wave approximation. Our results show that the net pressure acting on the basilar membrane is not uniform along its spanwise direction. Also, it is shown that the location of the maximum of the spanwise pressure difference in the axial direction has a mode dependence. In the simplest pattern, the present result is consistent with the previous theory based on the WKB-like approximation [D. Manoussaki, Phys. Rev. Lett. 96, 088701(2006)]. In this mode, the pressure difference in the spanwise direction is a monotonic function of the distance from the apex and the normal velocity across the channel width is zero. Thus in the lowest order approximation, we can neglect the existance of the Reissner's membrane in the upper channel. However, higher responsive modes show different behavior and, thus, the real maximum is expected to be located not exactly at the apex, but at a position determined by the spiral geometry of the cochlea and the width of the cochlear duct. In these modes, the spanwise normal velocities are not zero. Thus, it indicates that one should take into account of the detailed geometry of the cochlear duct for a more quantitative result. The present result clearly demonstrates that not only the spiral geometry, but also the geometry of the cochlear duct play decisive roles in distributing the wave energy.Comment: 21 pages. (to appear in J. Biol. Phys.

Lepton flavor violation decays τ−→μ−P1P2\tau^-\to \mu^- P_1 P_2 in the topcolor-assisted technicolor model and the littlest Higgs model with TT parity

The new particles predicted by the topcolor-assisted technicolor ($TC2$) model and the littlest Higgs model with T-parity (called $LHT$ model) can induce the lepton flavor violation ($LFV$) couplings at tree level or one loop level, which might generate large contributions to some $LFV$ processes. Taking into account the constraints of the experimental data on the relevant free parameters, we calculate the branching ratios of the $LFV$ decay processes $\tau^-\to\mu^- P_1 P_2$ with $P_1 P_2$ = $\pi^+\pi^-$, $K^+K^-$ and $K^0\bar{K^0}$ in the context of these two kinds of new physics models. We find that the $TC2$ model and the $LHT$ model can indeed produce significant contributions to some of these $LFV$ decay processes.Comment: 24 pages, 7 figure

Disruption of PHF21A causes syndromic intellectual disability with craniofacial anomalies, epilepsy, hypotonia, and neurobehavioral problems including autism

BACKGROUND: PHF21A has been associated with intellectual disability and craniofacial anomalies based on its deletion in the Potocki-Shaffer syndrome region at 11p11.2 and its disruption in three patients with balanced translocations. In addition, three patients with de novo truncating mutations in PHF21A were reported recently. Here, we analyze genomic data from seven unrelated individuals with mutations in PHF21A and provide detailed clinical descriptions, further expanding the phenotype associated with PHF21A haploinsufficiency. METHODS: Diagnostic trio whole exome sequencing, Sanger sequencing, use of GeneMatcher, targeted gene panel sequencing, and MiSeq sequencing techniques were used to identify and confirm variants. RT-qPCR was used to measure the normal expression pattern of PHF21A in multiple human tissues including 13 different brain tissues. Protein-DNA modeling was performed to substantiate the pathogenicity of the missense mutation. RESULTS: We have identified seven heterozygous coding mutations, among which six are de novo (not maternal in one). Mutations include four frameshifts, one nonsense mutation in two patients, and one heterozygous missense mutation in the AT Hook domain, predicted to be deleterious and likely to cause loss of PHF21A function. We also found a new C-terminal domain composed of an intrinsically disordered region. This domain is truncated in six patients and thus likely to play an important role in the function of PHF21A, suggesting that haploinsufficiency is the likely underlying mechanism in the phenotype of seven patients. Our results extend the phenotypic spectrum of PHF21A mutations by adding autism spectrum disorder, epilepsy, hypotonia, and neurobehavioral problems. Furthermore, PHF21A is highly expressed in the human fetal brain, which is consistent with the neurodevelopmental phenotype. CONCLUSION: Deleterious nonsense, frameshift, and missense mutations disrupting the AT Hook domain and/or an intrinsically disordered region in PHF21A were found to be associated with autism spectrum disorder, epilepsy, hypotonia, neurobehavioral problems, tapering fingers, clinodactyly, and syndactyly, in addition to intellectual disability and craniofacial anomalies. This suggests that PHF21A is involved in autism spectrum disorder and intellectual disability, and its haploinsufficiency causes a diverse neurological phenotype

The impact of atrial fibrillation on prognosis in aortic stenosis

Background Atrial fibrillation (AF) and aortic stenosis (AS) are both highly prevalent and often coexist. Various studies have focused on the prognostic value of AF in patients with AS, but rarely considered left ventricular (LV) diastolic function as a prognostic factor. Objective To evaluate the prognostic impact of AF in patients with AS while correcting for LV diastolic function. Methods Patients with first diagnosis of significant AS were selected and stratified according to history of AF. The endpoint was all-cause mortality. Results In total, 2849 patients with significant AS (mean age 72 +/- 12 years, 54.8% men) were evaluated, and 686 (24.1%) had a history of AF. During a median follow-up of 60 (30-97) months, 1182 (41.5%) patients died. Ten-year mortality rate in patients with AF was 46.8% compared to 36.8% in patients with sinus rhythm (SR) (log-rank P < 0.001). On univariable (HR: 1.42; 95% CI: 1.25-1.62; P < 0.001) and multivariable Cox regression analysis (HR: 1.19; 95% CI: 1.02-1.38; P = 0.026), AF was independently associated with mortality. However, when correcting for indexed left atrial volume, E/e' or both, AF was no longer independently associated with all-cause mortality. Conclusion Patients with significant AS and AF have a reduced survival as compared to patients with SR. Nonetheless, when correcting for markers of LV diastolic function, AF was not independently associated with outcomes in patients with significant AS.Cardiolog

Measurements of the Mass and Full-Width of the ηc\eta_c Meson

In a sample of 58 million $J/\psi$ events collected with the BES II detector, the process J/$\psi\to\gamma\eta_c$ is observed in five different decay channels: $\gamma K^+K^-\pi^+\pi^-$, $\gamma\pi^+\pi^-\pi^+\pi^-$, $\gamma K^\pm K^0_S \pi^\mp$ (with $K^0_S\to\pi^+\pi^-$), $\gamma \phi\phi$ (with $\phi\to K^+K^-$) and $\gamma p\bar{p}$. From a combined fit of all five channels, we determine the mass and full-width of $\eta_c$ to be $m_{\eta_c}=2977.5\pm1.0 ({stat.})\pm1.2 ({syst.})$ MeV/$c^2$ and $\Gamma_{\eta_c} = 17.0\pm3.7 ({stat.})\pm7.4 ({syst.})$ MeV/$c^2$.Comment: 9 pages, 2 figures and 4 table. Submitted to Phys. Lett.

A Measurement of Psi(2S) Resonance Parameters

Cross sections for e+e- to hadons, pi+pi- J/Psi, and mu+mu- have been measured in the vicinity of the Psi(2S) resonance using the BESII detector operated at the BEPC. The Psi(2S) total width; partial widths to hadrons, pi+pi- J/Psi, muons; and corresponding branching fractions have been determined to be Gamma(total)= (264+-27) keV; Gamma(hadron)= (258+-26) keV, Gamma(mu)= (2.44+-0.21) keV, and Gamma(pi+pi- J/Psi)= (85+-8.7) keV; and Br(hadron)= (97.79+-0.15)%, Br(pi+pi- J/Psi)= (32+-1.4)%, Br(mu)= (0.93+-0.08)%, respectively.Comment: 8 pages, 6 figure

Search for a W' boson decaying to a bottom quark and a top quark in pp collisions at sqrt(s) = 7 TeV

Results are presented from a search for a W' boson using a dataset corresponding to 5.0 inverse femtobarns of integrated luminosity collected during 2011 by the CMS experiment at the LHC in pp collisions at sqrt(s)=7 TeV. The W' boson is modeled as a heavy W boson, but different scenarios for the couplings to fermions are considered, involving both left-handed and right-handed chiral projections of the fermions, as well as an arbitrary mixture of the two. The search is performed in the decay channel W' to t b, leading to a final state signature with a single lepton (e, mu), missing transverse energy, and jets, at least one of which is tagged as a b-jet. A W' boson that couples to fermions with the same coupling constant as the W, but to the right-handed rather than left-handed chiral projections, is excluded for masses below 1.85 TeV at the 95% confidence level. For the first time using LHC data, constraints on the W' gauge coupling for a set of left- and right-handed coupling combinations have been placed. These results represent a significant improvement over previously published limits.Comment: Submitted to Physics Letters B. Replaced with version publishe