A Letter of Intent to Build a MiniBooNE Near Detector: BooNE

There is accumulating evidence for a difference between neutrino and antineutrino oscillations at the $\sim 1$ eV$^2$ scale. The MiniBooNE experiment observes an unexplained excess of electron-like events at low energies in neutrino mode, which may be due, for example, to either a neutral current radiative interaction, sterile neutrino decay, or to neutrino oscillations involving sterile neutrinos and which may be related to the LSND signal. No excess of electron-like events ($-0.5 \pm 7.8 \pm 8.7$), however, is observed so far at low energies in antineutrino mode. Furthermore, global 3+1 and 3+2 sterile neutrino fits to the world neutrino and antineutrino data suggest a difference between neutrinos and antineutrinos with significant ($\sin^22\theta_{\mu \mu} \sim 35$) $\bar \nu_\mu$ disappearance. In order to test whether the low-energy excess is due to neutrino oscillations and whether there is a difference between $\nu_\mu$ and $\bar \nu_\mu$ disappearance, we propose building a second MiniBooNE detector at (or moving the existing MiniBooNE detector to) a distance of $\sim 200$ m from the Booster Neutrino Beam (BNB) production target. With identical detectors at different distances, most of the systematic errors will cancel when taking a ratio of events in the two detectors, as the neutrino flux varies as $1/r^2$ to a calculable approximation. This will allow sensitive tests of oscillations for both $\nu_e$ and $\bar \nu_e$ appearance and $\nu_\mu$ and $\bar \nu_\mu$ disappearance. Furthermore, a comparison between oscillations in neutrino mode and antineutrino mode will allow a sensitive search for CP and CPT violation in the lepton sector at short baseline ($\Delta m^2 > 0.1$ eV$^2$).Comment: 43 pages, 40 figure

Extended spectrum β-lactamase-and AmpC β-lactamase-producing Enterobacterales associated with urinary tract infections in the New Zealand community: A case-control study.

(c) The Author/sOBJECTIVES: To assess whether having a pet in the home is a risk factor for community-acquired urinary tract infections associated with extended spectrum β-lactamase (ESBL)- or AmpC β-lactamase (ACBL)- producing Enterobacterales. METHODS: An unmatched case-control study was conducted between August 2015 and September 2017. Cases (n=141) were people with community-acquired urinary tract infection (UTI) caused by ESBL- or ACBL- producing Enterobacterales. Controls (n=525) were recruited from the community. A telephone questionnaire on pet ownership, and other factors was administered, and associations were assessed using logistic regression. RESULTS: Pet ownership was not associated with ESBL- or ACBL-producing Enterobacterales related human UTIs. A positive association was observed for recent antimicrobial treatment, travel to Asia in the previous year, and a doctor's visit in the previous six months. Among isolates with an ESBL-/ACBL-producing phenotype 126/134 (94%) were Escherichia coli, with sequence type (ST) 131 being the most common (47/126). CONCLUSIONS: Companion animals in the home were not found to be associated with ESBL- or ACBL-producing Enterobacterales related community-acquired UTI in New Zealand. Risk factors included overseas travel, recent antibiotic use, and doctor visits.Published onlin

Whole-genome sequencing of Salmonella Mississippi and Typhimurium Definitive Type 160, Australia and New Zealand

We used phylogenomic and risk factor data on isolates of Salmonella enterica serovars Mississippi and Typhimurium definitive type 160 (DT160) collected from human, animal, and environmental sources to elucidate their epidemiology and disease reservoirs in Australia and New Zealand. Sequence data suggested wild birds as a likely reservoir for DT160; animal and environmental sources varied more for Salmonella Mississippi than for Salmonella Typhimurium. Australia and New Zealand isolates sat in distinct clades for both serovars; the median single-nucleotide polymorphism distance for DT160 was 29 (range 8–66) and for Salmonella Mississippi, 619 (range 565–737). Phylogenomic data identified plausible sources of human infection from wildlife and environmental reservoirs and provided evidence supporting New Zealand–acquired DT160 in a group of travelers returning to Australia. Wider use of real-time whole-genome sequencing in new locations and for other serovars may identify sources and routes of transmission, thereby aiding prevention and control

Overvaluation of shape and weight in adolescents with anorexia nervosa: does shape concern or weight concern matter more for treatment outcome?

BACKGROUND: Overvaluation of shape and weight is a key diagnostic feature of anorexia nervosa (AN); however, limited research has evaluated the clinical utility of differentiating between weight versus shape concerns. Understanding differences in these constructs may have important implications for AN treatment given the focus on weight regain. This study examined differences in treatment outcome between individuals whose primary concern was weight versus those whose primary concern was shape in a randomized controlled trial of treatment for adolescent AN. METHODS: Data were drawn from a two-site randomized controlled trial that compared family-based treatment and adolescent focused therapy for AN. Chi-square tests and logistic regression analyses were conducted. RESULTS: Thirty percent of participants presented with primary weight concern (n = 36; defined as endorsing higher Eating Disorder Examination (EDE) Weight Concern than Shape Concern subscale scores); 60 % presented with primary shape concern (n = 72; defined as endorsing higher EDE Shape Concern than Weight Concern scores). There were no significant differences between the two groups in remission status at the end of treatment. Treatment did not moderate the effect of group status on achieving remission. CONCLUSIONS: Results suggest that treatment outcomes are comparable between adolescents who enter treatment for AN with greater weight concerns and those who enter treatment with greater shape concerns. Therefore, treatment need not be adjusted based on primary weight or primary shape concerns

Measurement of the antineutrino neutral-current elastic differential cross section

arXiv:1309.7257v1 [hep-ex

Measurement of the neutrino component of an anti-neutrino beam observed by a non-magnetized detector

Two independent methods are employed to measure the neutrino flux of the anti-neutrino-mode beam observed by the MiniBooNE detector. The first method compares data to simulated event rates in a high purity \numu induced charged-current single \pip (CC1\pip) sample while the second exploits the difference between the angular distributions of muons created in \numu and \numub charged-current quasi-elastic (CCQE) interactions. The results from both analyses indicate the prediction of the neutrino flux component of the pre-dominately anti-neutrino beam is over-estimated - the CC1\pip analysis indicates the predicted \numu flux should be scaled by $0.76 \pm 0.11$, while the CCQE angular fit yields $0.65 \pm 0.23$. The energy spectrum of the flux prediction is checked by repeating the analyses in bins of reconstructed neutrino energy, and the results show that the spectral shape is well modeled. These analyses are a demonstration of techniques for measuring the neutrino contamination of anti-neutrino beams observed by future non-magnetized detectors.Comment: 15 pages, 7 figures, published in Physical Review D, latest version reflects changes from referee comment

The Paradox of Muscle Hypertrophy in Muscular Dystrophy

Mutations in the dystrophin gene cause Duchenne and Becker muscular dystrophy in humans and syndromes in mice, dogs, and cats. Affected humans and dogs have progressive disease that leads primarily to muscle atrophy. Mdx mice progress through an initial phase of muscle hypertrophy followed by atrophy. Cats have persistent muscle hypertrophy. Hypertrophy in humans has been attributed to deposition of fat and connective tissue (pseudohypertrophy). Increased muscle mass (true hypertrophy) has been documented in animal models. Muscle hypertrophy can exaggerate postural instability and joint contractures. Deleterious consequences of muscle hypertrophy should be considered when developing treatments for muscular dystrophy