Achieving very long lifetimes in optical lattices with pulsed cooling

We have realized a one dimensional optical lattice for individual atoms with a lifetime >300 s, which is 5 times longer than previously reported. In order to achieve this long lifetime, it is necessary to laser cool the at-oms briefly every 20 s to overcome heating due to technical fluctuations in the trapping potential. Without cooling, we observe negligible atom loss within the first 20 s followed by an exponential decay with a 62 s time constant. We obtain quantitative agreement with the measured fluctuations of the trapping potential and the corresponding theoretical heating rates.Comment: 4 pages, 5 figure

Holography of Charged Dilaton Black Holes

We study charged dilaton black branes in $AdS_4$. Our system involves a dilaton $\phi$ coupled to a Maxwell field $F_{\mu\nu}$ with dilaton-dependent gauge coupling, ${1\over g^2} = f^2(\phi)$. First, we find the solutions for extremal and near extremal branes through a combination of analytical and numerical techniques. The near horizon geometries in the simplest cases, where $f(\phi) = e^{\alpha\phi}$, are Lifshitz-like, with a dynamical exponent $z$ determined by $\alpha$. The black hole thermodynamics varies in an interesting way with $\alpha$, but in all cases the entropy is vanishing and the specific heat is positive for the near extremal solutions. We then compute conductivity in these backgrounds. We find that somewhat surprisingly, the AC conductivity vanishes like $\omega^2$ at T=0 independent of $\alpha$. We also explore the charged black brane physics of several other classes of gauge-coupling functions $f(\phi)$. In addition to possible applications in AdS/CMT, the extremal black branes are of interest from the point of view of the attractor mechanism. The near horizon geometries for these branes are universal, independent of the asymptotic values of the moduli, and describe generic classes of endpoints for attractor flows which are different from $AdS_2\times R^2$.Comment: 33 pages, 3 figures, LaTex; v2, references added; v3, more refs added; v4, refs added, minor correction

Moduli and (un)attractor black hole thermodynamics

We investigate four-dimensional spherically symmetric black hole solutions in gravity theories with massless, neutral scalars non-minimally coupled to gauge fields. In the non-extremal case, we explicitly show that, under the variation of the moduli, the scalar charges appear in the first law of black hole thermodynamics. In the extremal limit, the near horizon geometry is $AdS_2\times S^2$ and the entropy does not depend on the values of moduli at infinity. We discuss the attractor behaviour by using Sen's entropy function formalism as well as the effective potential approach and their relation with the results previously obtained through special geometry method. We also argue that the attractor mechanism is at the basis of the matching between the microscopic and macroscopic entropies for the extremal non-BPS Kaluza-Klein black hole.Comment: 36 pages, no figures, V2: minor changes, misprints corrected, expanded references; V3: sections 4.3 and 4.5 added; V4: minor changes, matches the published versio

Cytoplasmic dynein nomenclature

A variety of names has been used in the literature for the subunits of cytoplasmic dynein complexes. Thus, there is a strong need for a more definitive consensus statement on nomenclature. This is especially important for mammalian cytoplasmic dyneins, many subunits of which are encoded by multiple genes. We propose names for the mammalian cytoplasmic dynein subunit genes and proteins that reflect the phylogenetic relationships of the genes and the published studies clarifying the functions of the polypeptides. This nomenclature recognizes the two distinct cytoplasmic dynein complexes and has the flexibility to accommodate the discovery of new subunits and isoforms

Genomic surveillance of Escherichia coli and Klebsiella spp. in hospital sink drains and patients

Escherichia coli and Klebsiella spp. are important human pathogens that cause a wide spectrum of clinical disease. In healthcare settings, sinks and other wastewater sites have been shown to be reservoirs of antimicrobial-resistant E. coli and Klebsiella spp., particularly in the context of outbreaks of resistant strains amongst patients. Without focusing exclusively on resistance markers or a clinical outbreak, we demonstrate that many hospital sink drains are abundantly and persistently colonised with diverse populations of E. coli, Klebsiella pneumoniae and Klebsiella oxytoca, including both antimicrobial-resistant and susceptible strains. Using whole genome sequencing (WGS) of 439 isolates, we show that environmental bacterial populations are largely structured by ward and sink, with only a handful of lineages, such as E. coli ST635, being widely distributed, suggesting different prevailing ecologies which may vary as a result of different inputs and selection pressures. WGS of 46 contemporaneous patient isolates identified one (2%; 95% CI 0.05-11%) E. coli urine infection-associated isolate with high similarity to a prior sink isolate, suggesting that sinks may contribute to up to 10% of infections caused by these organisms in patients on the ward over the same timeframe. Using metagenomics from 20 sink-timepoints, we show that sinks also harbour many clinically relevant antimicrobial resistance genes including blaCTX-M, blaSHV and mcr, and may act as niches for the exchange and amplification of these genes. Our study reinforces the potential role of sinks in contributing to Enterobacterales infection and antimicrobial resistance in hospital patients, something that could be amenable to intervention

Measurement of the B-Meson Inclusive Semileptonic Branching Fraction and Electron-Energy Moments

We report a new measurement of the B-meson semileptonic decay momentum spectrum that has been made with a sample of 9.4/fb of electron-positron annihilation data collected with the CLEO II detector at the Y(4S) resonance. Electrons from primary semileptonic decays and secondary charm decays were separated by using charge and angular correlations in Y(4S) events with a high-momentum lepton and an additional electron. We determined the semileptonic branching fraction to be (10.91 +- 0.09 +- 0.24)% from the normalization of the electron-energy spectrum. We also measured the moments of the electron energy spectrum with minimum energies from 0.6 GeV to 1.5 GeV.Comment: 36 pages postscript, als available through http://w4.lns.cornell.edu/public/CLNS/, Submitted to PRD (back-to-back with preceding preprint hep-ex/0403052

Moments of the B Meson Inclusive Semileptonic Decay Rate using Neutrino Reconstruction

We present a measurement of the composition of B meson inclusive semileptonic decays using 9.4 fb^-1 of e^+e^- data taken with the CLEO detector at the Upsilon(4S) resonance. In addition to measuring the charged lepton kinematics, the neutrino four-vector is inferred using the hermiticity of the detector. We perform a maximum likelihood fit over the full three-dimensional differential decay distribution for the fractional contributions from the B -> X_c l nu processes with X_c = D, D*, D**, and nonresonant X_c, and the process B -> X_u l nu. From the fit results we extract the first and second moments of the M_X^2 and q^2 distributions with minimum lepton-energy requirements of 1.0 GeV and 1.5 GeV. We find = 0.456 +- 0.014 +- 0.045 +- 0.109 (GeV/c^2)^2 with a minimum lepton energy of 1.0 GeV and = 0.293 +- 0.012 +- 0.033 +- 0.048 (GeV/c^2)^2 with minimum lepton energy of 1.5 GeV. The uncertainties are from statistics, detector systematic effects, and model dependence, respectively. As a test of the HQET and OPE calculations, the results for the M^X_c moment as a function of the minimum lepton energy requirement are compared to the predictions.Comment: 26 pages postscript, als available through http://w4.lns.cornell.edu/public/CLNS/, Submitted to PRD (back-to-back with following preprint hep-ex/0403053

Associations between Potentially Modifiable Risk Factors and Alzheimer Disease: A Mendelian Randomization Study.

BACKGROUND: Potentially modifiable risk factors including obesity, diabetes, hypertension, and smoking are associated with Alzheimer disease (AD) and represent promising targets for intervention. However, the causality of these associations is unclear. We sought to assess the causal nature of these associations using Mendelian randomization (MR). METHODS AND FINDINGS: We used SNPs associated with each risk factor as instrumental variables in MR analyses. We considered type 2 diabetes (T2D, NSNPs = 49), fasting glucose (NSNPs = 36), insulin resistance (NSNPs = 10), body mass index (BMI, NSNPs = 32), total cholesterol (NSNPs = 73), HDL-cholesterol (NSNPs = 71), LDL-cholesterol (NSNPs = 57), triglycerides (NSNPs = 39), systolic blood pressure (SBP, NSNPs = 24), smoking initiation (NSNPs = 1), smoking quantity (NSNPs = 3), university completion (NSNPs = 2), and years of education (NSNPs = 1). We calculated MR estimates of associations between each exposure and AD risk using an inverse-variance weighted approach, with summary statistics of SNP-AD associations from the International Genomics of Alzheimer's Project, comprising a total of 17,008 individuals with AD and 37,154 cognitively normal elderly controls. We found that genetically predicted higher SBP was associated with lower AD risk (odds ratio [OR] per standard deviation [15.4 mm Hg] of SBP [95% CI]: 0.75 [0.62-0.91]; p = 3.4 × 10(-3)). Genetically predicted higher SBP was also associated with a higher probability of taking antihypertensive medication (p = 6.7 × 10(-8)). Genetically predicted smoking quantity was associated with lower AD risk (OR per ten cigarettes per day [95% CI]: 0.67 [0.51-0.89]; p = 6.5 × 10(-3)), although we were unable to stratify by smoking history; genetically predicted smoking initiation was not associated with AD risk (OR = 0.70 [0.37, 1.33]; p = 0.28). We saw no evidence of causal associations between glycemic traits, T2D, BMI, or educational attainment and risk of AD (all p > 0.1). Potential limitations of this study include the small proportion of intermediate trait variance explained by genetic variants and other implicit limitations of MR analyses. CONCLUSIONS: Inherited lifetime exposure to higher SBP is associated with lower AD risk. These findings suggest that higher blood pressure--or some environmental exposure associated with higher blood pressure, such as use of antihypertensive medications--may reduce AD risk.We thank the International Genomics of Alzheimer's Project (IGAP) for providing summary results data for these analyses. The investigators within IGAP contributed to the design and implementation of IGAP and/or provided data but did not participate in analysis or writing of this report. IGAP was made possible by the generous participation of the control subjects, the patients, and their families. The i–Select chips were funded by the French National Foundation on Alzheimer's disease and related disorders. EADI was supported by the LABEX (laboratory of excellence program investment for the future) DISTALZ grant, Inserm, Institut Pasteur de Lille, Université de Lille 2 and the Lille University Hospital. GERAD was supported by the Medical Research Council (Grant n° 503480), Alzheimer's Research UK (Grant n° 503176), the Wellcome Trust (Grant n° 082604/2/07/Z) and German Federal Ministry of Education and Research (BMBF): Competence Network Dementia (CND) grant n° 01GI0102, 01GI0711, 01GI0420. CHARGE was partly supported by the NIH/NIA grant R01 AG033193 and the NIA AG081220 and AGES contract N01–AG–12100, the NHLBI grant R01 HL105756, the Icelandic Heart Association, and the Erasmus Medical Center and Erasmus University. ADGC was supported by the NIH/NIA grants: U01 AG032984, U24 AG021886, U01 AG016976, and the Alzheimer's Association grant ADGC–10–196728.This is the final version of the article. It first appeared from PLOS via http://dx.doi.org/10.1371/journal.pmed.100184