Amplitude analysis of Ds+→π+π−π+D_s^{+} \rightarrow \pi^{+} \pi^{-} \pi^{+}

Utilizing the data set corresponding to an integrated luminosity of $3.19$ fb$^{-1}$ collected by the BESIII detector at a center-of-mass energy of 4.178 GeV, we perform an amplitude analysis of the $D_s^+\to\pi^+\pi^-\pi^+$ decay. The sample contains 13,797 candidates with a signal purity of $\sim$80%. The amplitude and phase of the contributing $\pi\pi$ ${\cal S}$ wave are measured based on a quasi-model-independent approach, along with the amplitudes and phases of the ${\cal P}$ and ${\cal D}$ waves parametrized by Breit-Wigner models. The fit fractions of different intermediate decay channels are also reported.Comment: 14 pages, 6 figure

Measurement of the absolute branching fractions of J/ψ→γη and η decay modes

Based on a data sample of (1.0087±0.0044)×1010 J/ψ events collected by the BESIII detector at the BEPCII accelerator, the absolute branching fraction (BF) of the decay J/ψ→γη is measured with high precision using events in which the radiative photon converts to e+e-. Using the measured absolute BF of J/ψ→γη, the absolute BFs of four dominant η decay modes are measured for the first time. The results are B(J/ψ→γη)=(1.067±0.005±0.023)×10-3, B(η→γγ)=(39.86±0.04±0.99)%, B(η→π0π0π0)=(31.96±0.07±0.84)%, B(η→π+π-π0)=(23.04±0.03±0.54)%, and B(η→π+π-γ)=(4.38±0.02±0.10)%, where the first and second uncertainties are statistical and systematic, respectively. The results are consistent with the world average values within two standard deviation

Several Polymorphisms of KCNQ1 Gene Are Associated with Plasma Lipid Levels in General Chinese Populations

BACKGROUND: Potassium voltage-gated channel, KQT-like subfamily, member 1 (KCNQ1) is thought to be an important candidate gene of diabetes. Several single nucleotide polymorphisms (SNPs) in a 40-kb linkage disequilibrium (LD) block in its intron 15 have been identified to be associated with diabetes in East Asian populations in recent genome-wide association studies. The aim of this study was to investigate whether KCNQ1 polymorphisms influence the levels of the metabolic phenotypes in general Chinese populations. METHODOLOGY/PRINCIPAL FINDINGS: We investigated the associations of two SNPs (rs2237892 and rs2237895) in the aforementioned 40-kb LD block, a missense variant rs12720449 (P448R) in exon 10, and a synonymous variant rs1057128 (S546S) in exon 13 with metabolic phenotypes in a Uyghur population (n = 478) and replicated these associations in a Han population (n = 2,485). We found that rs2237892-T allele was significantly associated with decreased triglyceride levels (p(combined) = 0.001). The minor G allele of the rs12720449, with sharp difference of the allelic frequency between European and East Asian populations (0.2% versus 14%, respectively), was associated with a lower triglyceride levels than G allele in Uyghur subjects (p = 0.004), in Han subjects (p = 0.052), and in subjects of meta-analysis (p(combined) = 0.001). Moreover, the minor A allele of the rs1057128 was also associated with decreased triglyceride levels in meta-analysis (p(combined) = 0.010). CONCLUSIONS: To the best of our knowledge, this is the first report associating a missense mutation of KCNQ1, rs12720449, with triglyceride levels. Rs2237892, representing the 40-kb LD block, is also associated with triglyceride levels in Han population. Further studies are required to replicate these findings in other East Asian populations

Search for Λˉ\bar{\Lambda}-Λ\Lambda oscillations in the decay J/ψ→pK−Λˉ+c.c.J/\psi \to p K^- \bar{\Lambda}+c.c.

We report the first search for $\bar\Lambda$--$\Lambda$ oscillations in the decay $J/\psi \to p K^- \bar{\Lambda} + c.c.$ by analyzing $1.31\times10^9$ $J/\psi$ events accumulated with the BESIII detector at the BEPCII collider. The $J/\psi$ events are produced using $e^+e^-$ collisions at a center of mass energy $\sqrt{s}= 3.097$~GeV. No evidence for hyperon oscillations is observed. The upper limit for the oscillation rate of $\bar\Lambda$ to $\Lambda$ hyperons is determined to be $\mathcal{P}(\Lambda)=\frac{\mathcal{B}(J/\psi\to pK^-\Lambda+c.c.)}{\mathcal{B}(J/\psi\to pK^-\bar\Lambda+c.c.)}<4.4\times10^{-6}$ corresponding to an oscillation parameter $\delta m_{\Lambda\bar\Lambda}$ of less than $3.8\times10^{-18}$~GeV at the 90\% confidence level.Comment: 7 pages, 1 figur

Double Beta Decay

We review recent developments in double-beta decay, focusing on what can be learned about the three light neutrinos in future experiments. We examine the effects of uncertainties in already measured neutrino parameters and in calculated nuclear matrix elements on the interpretation of upcoming double-beta decay measurements. We then review a number of proposed experiments.Comment: Some typos corrected, references corrected and added. A less blurry version of figure 3 is available from authors. 41 pages, 5 figures, submitted to J. Phys.

Mutations disrupting neuritogenesis genes confer risk for cerebral palsy

In addition to commonly associated environmental factors, genomic factors may cause cerebral palsy. We performed whole-exome sequencing of 250 parent-offspring trios, and observed enrichment of damaging de novo mutations in cerebral palsy cases. Eight genes had multiple damaging de novo mutations; of these, two (TUBA1A and CTNNB1) met genome-wide significance. We identified two novel monogenic etiologies, FBXO31 and RHOB, and showed that the RHOB mutation enhances active-state Rho effector binding while the FBXO31 mutation diminishes cyclin D levels. Candidate cerebral palsy risk genes overlapped with neurodevelopmental disorder genes. Network analyses identified enrichment of Rho GTPase, extracellular matrix, focal adhesion and cytoskeleton pathways. Cerebral palsy risk genes in enriched pathways were shown to regulate neuromotor function in a Drosophila reverse genetics screen. We estimate that 14% of cases could be attributed to an excess of damaging de novo or recessive variants. These findings provide evidence for genetically mediated dysregulation of early neuronal connectivity in cerebral palsy

Improved Measurement of Electron Antineutrino Disappearance at Daya Bay

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Gene Expression Profiling in Gastric Mucosa from Helicobacter pylori-Infected and Uninfected Patients Undergoing Chronic Superficial Gastritis

Helicobacter pylori infection reprograms host gene expression and influences various cellular processes, which have been investigated by cDNA microarray using in vitro culture cells and in vivo gastric biopsies from patients of the Chronic Abdominal Complaint. To further explore the effects of H. pylori infection on host gene expression, we have collected the gastric antral mucosa samples from 6 untreated patients with gastroscopic and pathologic confirmation of chronic superficial gastritis. Among them three patients were infected by H. pylori and the other three patients were not. These samples were analyzed by a microarray chip which contains 14,112 cloned cDNAs, and microarray data were analyzed via BRB ArrayTools software and Ingenuity Pathways Analysis (IPA) website. The results showed 34 genes of 38 differentially expressed genes regulated by H. pylori infection had been annotated. The annotated genes were involved in protein metabolism, inflammatory and immunological reaction, signal transduction, gene transcription, trace element metabolism, and so on. The 82% of these genes (28/34) were categorized in three molecular interaction networks involved in gene expression, cancer progress, antigen presentation and inflammatory response. The expression data of the array hybridization was confirmed by quantitative real-time PCR assays. Taken together, these data indicated that H. pylori infection could alter cellular gene expression processes, escape host defense mechanism, increase inflammatory and immune responses, activate NF-κB and Wnt/β-catenin signaling pathway, disturb metal ion homeostasis, and induce carcinogenesis. All of these might help to explain H. pylori pathogenic mechanism and the gastroduodenal pathogenesis induced by H. pylori infection