Role of electromagnetic dipole operator in the electroweak penguin dominated vector meson decays of BB meson

The pure annihilation type decays $B^0_d\to\phi\gamma$ and $B_s\to\rho\gamma$ receive only color suppressed penguin contributions with a very small branching ratio in the standard model. When we include the previously neglected electromagnetic dipole operator, the branching ratios can be enhanced one order magnitude larger than previous study using QCD factorization approach. That is ${\cal BR}(\bar B^0_d\to\phi\gamma)\simeq 1 \times 10^{-11}$ and ${\cal BR}(B_s\to\rho\gamma) \sim (6-16)\times 10^{-10}$. The new effect can also give a large contribution, of order $10^{-9}$, to transverse polarization of $B\to\phi\rho$ and $B\to \omega\phi$ which is comparable to the longitudinal part. These effects can be detected in the LHCb experiment and the Super-B factories.Comment: Revised extensively. 8 pages, 4 figure

Study Pure Annihilation Decays Bs0(Bˉs0)→D±π∓B_s^0(\bar B_s^0)\to D^{\pm}\pi^{\mp} in PQCD Approach

The rare decays $B_s^0\to D^\pm \pi^\mp$ and $\bar B_s^0\to D^\mp \pi^\pm$ can occur only via annihilation type diagrams in the standard model. In this paper, we calculate branching ratios of these decays in perturbative QCD approach ignoring soft final state interaction. From our calculation, we find that their branching ratios are at $\mathcal{O}(10^{-6})$ with large CP asymmetry, which may be measured in LHC-b experiment in future.Comment: 14 pages,4 figures, typos correcte

Ante- and postmortem tau in autosomal dominant and late-onset Alzheimer\u27s disease

Antemortem tau positron emission tomography imaging suggests elevated tau pathology in autosomal dominant versus late-onset Alzheimer\u27s disease at equivalent clinical stages, but does not implicate the specific tau pathologies responsible. Here we made stereological measurements of tau neurofibrillary tangles, neuritic plaques, and neuropil threads and found compared to late-onset Alzheimer\u27s disease, autosomal dominant Alzheimer\u27s disease showed even greater tangle and thread burdens. Regional tau burden resembled that observed in tau imaging of a separate cohort at earlier clinical stages. Finally, our results suggest tau imaging measures total tau burden in Alzheimer\u27s disease, composed predominantly of tangle and thread pathology

The Physics of Heavy Flavours at SuperB

This is a review of the SuperB project, covering the accelerator, detector, and highlights of the broad physics programme. SuperB is a flavour factory capable of performing precision measurements and searches for rare and forbidden decays of $B_{u,d,s}$, $D$, $\tau$ and $\Upsilon({\mathrm{nS}})$ particles. These results can be used to test fundamental symmetries and expectations of the Standard Model, and to constrain many different hypothesised types of new physics. In some cases these measurements can be used to place constraints on the existence of light dark matter and light Higgs particles with masses below $10GeV/c^2$. The potential impact of the measurements that will be made by SuperB on the field of high energy physics is also discussed in the context of data taken at both high energy in the region around the \Upsilon({\mathrm{4S}})$, and near charm threshold.Comment: 49 pages, topical review submitted to J. Phys

Data Resource Profile: Understanding the patterns and determinants of health in South Asians-the South Asia Biobank.

Funder: Singapore Ministry of Health's National Medical Research CouncilFunder: National Institute for Health ResearchFunder: Wellcome Trust or the Department of HealthFunder: NIHR Biomedical Research Centre Cambridge: Nutrition, Diet, and Lifestyle Research Theme; Grant(s): IS-BRC-1215-2001

Select Atrophied Regions in Alzheimer disease (SARA): An improved volumetric model for identifying Alzheimer disease dementia

INTRODUCTION: Volumetric biomarkers for Alzheimer disease (AD) are attractive due to their wide availability and ease of administration, but have traditionally shown lower diagnostic accuracy than measures of neuropathological contributors to AD. Our purpose was to optimize the diagnostic specificity of structural MRIs for AD using quantitative, data-driven techniques. METHODS: This retrospective study assembled several non-overlapping cohorts (total n = 1287) with publicly available data and clinical patients from Barnes-Jewish Hospital (data gathered 1990-2018). The Normal Aging Cohort (n = 383) contained amyloid biomarker negative, cognitively normal (CN) participants, and provided a basis for determining age-related atrophy in other cohorts. The Training (n = 216) and Test (n = 109) Cohorts contained participants with symptomatic AD and CN controls. Classification models were developed in the Training Cohort and compared in the Test Cohort using the receiver operating characteristics areas under curve (AUCs). Additional model comparisons were done in the Clinical Cohort (n = 579), which contained patients who were diagnosed with dementia due to various etiologies in a tertiary care outpatient memory clinic. RESULTS: While the Normal Aging Cohort showed regional age-related atrophy, classification models were not improved by including age as a predictor or by using volumetrics adjusted for age-related atrophy. The optimal model used multiple regions (hippocampal volume, inferior lateral ventricle volume, amygdala volume, entorhinal thickness, and inferior parietal thickness) and was able to separate AD and CN controls in the Test Cohort with an AUC of 0.961. In the Clinical Cohort, this model separated AD from non-AD diagnoses with an AUC 0.820, an incrementally greater separation of the cohort than by hippocampal volume alone (AUC of 0.801, p = 0.06). Greatest separation was seen for AD vs. frontotemporal dementia and for AD vs. non-neurodegenerative diagnoses. CONCLUSIONS: Volumetric biomarkers distinguished individuals with symptomatic AD from CN controls and other dementia types but were not improved by controlling for normal aging

Endowment Effects in Gorillas (Gorilla gorilla)

Reports of endowment effects in nonhuman primates have received considerable attention in the comparative literature in recent years. However, little is known about the mechanisms underlying these effects. Continuing to explore endowment effects across different species of primate may reveal subtle differences in behavior that can help formulate specific hypotheses about the relevant mechanisms and the social and ecological factors that have shaped them. In this study, we use a paradigm that has previously been used to test chimpanzees (Pan troglodytes) and orangutans (Pongo spp.) to explore whether western lowland gorillas (Gorilla gorilla) exhibit comparable endowment effects. We find that gorillas exhibit endowment effects when in possession of food, but not nonfood, items, and that they show a statistically stronger effect than chimpanzees but not orangutans. These findings are consistent with the hypothesis that mechanisms for endowment effects in primates may be related to inhibitory control or risk aversion

Comparing cortical signatures of atrophy between late-onset and autosomal dominant Alzheimer disease

Defining a signature of cortical regions of interest preferentially affected by Alzheimer disease (AD) pathology may offer improved sensitivity to early AD compared to hippocampal volume or mesial temporal lobe alone. Since late-onset Alzheimer disease (LOAD) participants tend to have age-related comorbidities, the younger-onset age in autosomal dominant AD (ADAD) may provide a more idealized model of cortical thinning in AD. To test this, the goals of this study were to compare the degree of overlap between the ADAD and LOAD cortical thinning maps and to evaluate the ability of the ADAD cortical signature regions to predict early pathological changes in cognitively normal individuals. We defined and analyzed the LOAD cortical maps of cortical thickness in 588 participants from the Knight Alzheimer Disease Research Center (Knight ADRC) and the ADAD cortical maps in 269 participants from the Dominantly Inherited Alzheimer Network (DIAN) observational study. Both cohorts were divided into three groups: cognitively normal controls (nADRC = 381; nDIAN = 145), preclinical (nADRC = 153; nDIAN = 76), and cognitively impaired (nADRC = 54; nDIAN = 48). Both cohorts underwent clinical assessments, 3T MRI, and amyloid PET imaging with either 11C-Pittsburgh compound B or 18F-florbetapir. To generate cortical signature maps of cortical thickness, we performed a vertex-wise analysis between the cognitively normal controls and impaired groups within each cohort using six increasingly conservative statistical thresholds to determine significance. The optimal cortical map among the six statistical thresholds was determined from a receiver operating characteristic analysis testing the performance of each map in discriminating between the cognitively normal controls and preclinical groups. We then performed within-cohort and cross-cohort (e.g. ADAD maps evaluated in the Knight ADRC cohort) analyses to examine the sensitivity of the optimal cortical signature maps to the amyloid levels using only the cognitively normal individuals (cognitively normal controls and preclinical groups) in comparison to hippocampal volume. We found the optimal cortical signature maps were sensitive to early increases in amyloid for the asymptomatic individuals within their respective cohorts and were significant beyond the inclusion of hippocampus volume, but the cortical signature maps performed poorly when analyzing across cohorts. These results suggest the cortical signature maps are a useful MRI biomarker of early AD-related neurodegeneration in preclinical individuals and the pattern of decline differs between LOAD and ADAD