Double quantum dot with tunable coupling in an enhancement-mode silicon metal-oxide semiconductor device with lateral geometry

We present transport measurements of a tunable silicon metal-oxide-semiconductor double quantum dot device with lateral geometry. Experimentally extracted gate-to-dot capacitances show that the device is largely symmetric under the gate voltages applied. Intriguingly, these gate voltages themselves are not symmetric. Comparison with numerical simulations indicates that the applied gate voltages serve to offset an intrinsic asymmetry in the physical device. We also show a transition from a large single dot to two well isolated coupled dots, where the central gate of the device is used to controllably tune the interdot coupling.Comment: 4 pages, 3 figures, to be published in Applied Physics Letter

Enhancement mode double top gated MOS nanostructures with tunable lateral geometry

We present measurements of silicon (Si) metal-oxide-semiconductor (MOS) nanostructures that are fabricated using a process that facilitates essentially arbitrary gate geometries. Stable Coulomb blockade behavior free from the effects of parasitic dot formation is exhibited in several MOS quantum dots with an open lateral quantum dot geometry. Decreases in mobility and increases in charge defect densities (i.e. interface traps and fixed oxide charge) are measured for critical process steps, and we correlate low disorder behavior with a quantitative defect density. This work provides quantitative guidance that has not been previously established about defect densities for which Si quantum dots do not exhibit parasitic dot formation. These devices make use of a double-layer gate stack in which many regions, including the critical gate oxide, were fabricated in a fully-qualified CMOS facility.Comment: 11 pages, 6 figures, 3 tables, accepted for publication in Phys. Rev.

Chronic kidney disease of unknown aetiology in Sri Lanka: is cadmium a likely cause?

<p>Abstract</p> <p>Background</p> <p>The rising prevalence of chronic kidney disease (CKD) and subsequent end stage renal failure necessitating renal replacement therapy has profound consequences for affected individuals and health care resources. This community based study was conducted to identify potential predictors of microalbuminuria in a randomly selected sample of adults from the North Central Province (NCP) of Sri Lanka, where the burden of CKD is pronounced and the underlying cause still unknown.</p> <p>Methods</p> <p>Exposures to possible risk factors were determined in randomly recruited subjects (425 females and 461 males) from selected areas of the NCP of Sri Lanka using an interviewer administered questionnaire. Sulphosalicylic acid and the Light Dependent Resister microalbumin gel filtration method was used for initial screening for microalbuminuria and reconfirmed by the <it>Micral </it>strip test.</p> <p>Results</p> <p>Microalbumnuria was detected in 6.1% of the females and 8.5% of the males. Smoking (p < 0.001), alcohol use (p = 0.003), hypertension (p < 0.001), diabetes (p < 0.001), urinary tract infection (UTI) (p = 0.034) and consumption of water from wells in the fields (p = 0.025) were associated with microalbuminuria. In the binary logistic regression analysis, hypertension, diabetes mellitus, UTI, drinking well water in the fields, smoking and pesticide spraying were found to be significant predictors of microalbuminuria.</p> <p>Conclusions</p> <p>Hypertension, diabetes mellitus, UTI, and smoking are known risk factors for microalbuminuria. The association between microalbuminuria and consumption of well water suggests an environmental aetiology to CKD in NCP. The causative agent is yet to be identified. Investigations for cadmium as a potential causative agent needs to be initiated.</p

First Observation of barB0 to D*0 pi+pi+pi-pi- Decays

We report on the observation of B0bar -> D*0 pi+ pi+ pi- pi- decays. The branching ratio is (0.30 +/- 0.07 +/- 0.06)%. Interest in this particular mode was sparked by Ligeti, Luke and Wise who propose it as a way to check the validity of factorization tests in B0bar -> D*+ pi+ pi- pi- pi0 decays.Comment: 11 pages postscript, also available through http://w4.lns.cornell.edu/public/CLNS, Version to appear in Phys. Rev.

Measurement of Inclusive B --> psi Production

Using the combined CLEO II and CLEO II.V data sets of 9.1 fb^{-1} at the Upsilon(4S), we measure properties of Psi mesons produced directly from decays of the B meson, where ``B'' denotes an admixture of B+, B-, B0, and B0bar, and ``Psi'' denotes either J/Psi or Psi(2S). We report first measurements of Psi polarization in B -> Psi(direct) X: alpha(J/Psi) = -0.30 {+0.07 -0.06 stat} {+-0.04 syst} and alpha(Psi(2S)) = -0.45 {+0.22 -0.19 stat} {+-0.04 syst}. We also report improved measurements of the momentum distributions of Psi produced directly from B decays, correcting for measurement smearing. Finally, we report measurements of the inclusive branching fraction for B -> Psi X and B -> Chi_c1 X.Comment: 8 pages postscript, also available through http://w4.lns.cornell.edu/public/CLNS, submitted to PR

Search for Lepton-Flavor-Violating Decays of B Mesons

We have searched a sample of 9.6 million BB-bar events for the lepton-flavor-violating decays B --> h e^{+-} mu^{-+}, B^+ --> h^- e^+ e^+, B^+ --> h^- e^+ mu^+, and B^+ --> h^- mu^+ mu^+, where h is pi, K, rho, and K*(892), a total of sixteen modes. We find no evidence for these decays, and place 90% confidence level upper limits on their branching fractions that range from 1.0 to 8.3 X 10^{-6}.Comment: 8 pages postscript, also available through http://w4.lns.cornell.edu/public/CLNS, PRD R

The Complete Genome Sequence of the Emerging Pathogen Mycobacterium haemophilum Explains Its Unique Culture Requirements

Mycobacterium haemophilum is an emerging pathogen associated with a variety of clinical syndromes, most commonly skin infections in immunocompromised individuals. M. haemophilum exhibits a unique requirement for iron supplementation to support its growth in culture, but the basis for this property and how it may shape pathogenesis is unclear. Using a combination of Illumina, PacBio, and Sanger sequencing, the complete genome sequence of M. haemophilum was determined. Guided by this sequence, experiments were performed to define the basis for the unique growth requirements of M. haemophilum. We found that M. haemophilum, unlike many other mycobacteria, is unable to synthesize iron-binding siderophores known as mycobactins or to utilize ferri-mycobactins to support growth. These differences correlate with the absence of genes associated with mycobactin synthesis, secretion, and uptake. In agreement with the ability of heme to promote growth, we identified genes encoding heme uptake machinery. Consistent with its propensity to infect the skin, we show at the whole-genome level the genetic closeness of M. haemophilumwith Mycobacterium leprae, an organism which cannot be cultivated in vitro, and we identify genes uniquely shared by these organisms. Finally, we identify means to express foreign genes in M. haemophilum. These data explain the unique culture requirements for this important pathogen, provide a foundation upon which the genome sequence can be exploited to improve diagnostics and therapeutics, and suggest use of M. haemophilum as a tool to elucidate functions of genes shared with M. leprae. IMPORTANCE Mycobacterium haemophilum is an emerging pathogen with an unknown natural reservoir that exhibits unique requirements for iron supplementation to grow in vitro. Understanding the basis for this iron requirement is important because it is fundamental to isolation of the organism from clinical samples and environmental sources. Defining the molecular basis for M. haemophilium\u27s growth requirements will also shed new light on mycobacterial strategies to acquire iron and can be exploited to define how differences in such strategies influence pathogenesis. Here, through a combination of sequencing and experimental approaches, we explain the basis for the iron requirement. We further demonstrate the genetic closeness of M. haemophilum and Mycobacterium leprae, the causative agent of leprosy which cannot be cultured in vitro, and we demonstrate methods to genetically manipulate M. haemophilum. These findings pave the way for the use of M. haemophilum as a model to elucidate functions of genes shared with M. leprae

First Measurement of Gamma(D*+) and Precision Measurement of m_D*+ - m_D0

We present the first measurement of the D*+ width using 9/fb of e+ e- data collected near the Upsilon(4S) resonance by the CLEO II.V detector. Our method uses advanced tracking techniques and a reconstruction method that takes advantage of the small vertical size of the CESR beam spot to measure the energy release distribution from the D*+ -> D0 pi+ decay. We find Gamma(D*+) = 96 +- 4 (Statistical) +- 22 (Systematic) keV. We also measure the energy release in the decay and compute Delta m = m(D*+) - m(D0) = 145.412 +- 0.002 (Statistical) +- 0.012 (Systematic) MeV/c^2Comment: 24 pages postscript, also available through http://w4.lns.cornell.edu/public/CLNS, submitted to PR

Pittsburgh compound B imaging and cerebrospinal fluid amyloid-β in a multicentre European memory clinic study

The aim of this study was to assess the agreement between data on cerebral amyloidosis, derived using Pittsburgh compound B positron emission tomography and (i) multi-laboratory INNOTEST enzyme linked immunosorbent assay derived cerebrospinal fluid concentrations of amyloid-β 42 ; (ii) centrally measured cerebrospinal fluid amyloid-β 42 using a Meso Scale Discovery enzyme linked immunosorbent assay; and (iii) cerebrospinal fluid amyloid-β 42 centrally measured using an antibody-independent mass spectrometry-based reference method. Moreover, we examined the hypothesis that discordance between amyloid biomarker measurements may be due to interindividual differences in total amyloid-β production, by using the ratio of amyloid-β 42 to amyloid-β 40 . Our study population consisted of 243 subjects from seven centres belonging to the Biomarkers for Alzheimer’s and Parkinson’s Disease Initiative, and included subjects with normal cognition and patients with mild cognitive impairment, Alzheimer’s disease dementia, frontotemporal dementia, and vascular dementia. All had Pittsburgh compound B positron emission tomography data, cerebrospinal fluid INNOTEST amyloid-β 42 values, and cerebrospinal fluid samples available for reanalysis. Cerebrospinal fluid samples were reanalysed (amyloid-β 42 and amyloid-β 40 ) using Meso Scale Discovery electrochemiluminescence enzyme linked immunosorbent assay technology, and a novel, antibody-independent, mass spectrometry reference method. Pittsburgh compound B standardized uptake value ratio results were scaled using the Centiloid method. Concordance between Meso Scale Discovery/mass spectrometry reference measurement procedure findings and Pittsburgh compound B was high in subjects with mild cognitive impairment and Alzheimer’s disease, while more variable results were observed for cognitively normal and non-Alzheimer’s disease groups. Agreement between Pittsburgh compound B classification and Meso Scale Discovery/mass spectrometry reference measurement procedure findings was further improved when using amyloid-β 42/40 . Agreement between Pittsburgh compound B visual ratings and Centiloids was near complete. Despite improved agreement between Pittsburgh compound B and centrally analysed cerebrospinal fluid, a minority of subjects showed discordant findings. While future studies are needed, our results suggest that amyloid biomarker results may not be interchangeable in some individuals