Parity Mixing of 0+ and 0- Levels in 18F

The circular polarization of the γ rays emitted in the transition from the 1.081-MeV state to the ground state in 18F has been measured to be (1.6±5.6)×10^-4, corresponding to a parity-nonconserving (PNC) matrix element |〈0+, I=1|VPNC|0-, I=0〉|=0.03±0.10 eV. The weak pion-nucleon coupling constant deduced from the weighted average of all recent 18F measurements is (0.28-0.28+0.89)×10^-7. This result, together with PNC matrix elements in other experiments, suggests that the isovector weak NN interaction may be strongly suppressed compared with the isoscalar weak NN interaction

The Millennium Galaxy Catalogue: Bulge/Disc Decomposition of 10095 Nearby Galaxies

We have modelled the light distribution in 10095 galaxies from the Millennium Galaxy Catalogue (MGC), providing publically available structural catalogues for a large, representative sample of galaxies in the local Universe. Three different models were used: (1) a single Sersic function for the whole galaxy, (2) a bulge-disc decomposition model using a de Vaucouleurs (R^{1/4}) bulge plus exponential disc, (3) a bulge-disc decomposition model using a Sersic (R^{1/n}) bulge plus exponential disc. Repeat observations for 700 galaxies demonstrate that stable measurements can be obtained for object components with a half-light radius comparable to, or larger than, the seeing half-width at half maximum. We show that with careful quality control, robust measurements can be obtained for large samples such as the MGC. We use the catalogues to show that the galaxy colour bimodality is due to the two-component nature of galaxies (i.e. bulges and discs) and not to two distinct galaxy populations. We conclude that understanding galaxy evolution demands the routine bulge-disc decomposition of the giant galaxy population at all redshifts.Comment: Accepted for publication in MNRAS. 23 pages, 20 figure

The Sudbury Neutrino Observatory

The Sudbury Neutrino Observatory is a second generation water Cherenkov detector designed to determine whether the currently observed solar neutrino deficit is a result of neutrino oscillations. The detector is unique in its use of D2O as a detection medium, permitting it to make a solar model-independent test of the neutrino oscillation hypothesis by comparison of the charged- and neutral-current interaction rates. In this paper the physical properties, construction, and preliminary operation of the Sudbury Neutrino Observatory are described. Data and predicted operating parameters are provided whenever possible.Comment: 58 pages, 12 figures, submitted to Nucl. Inst. Meth. Uses elsart and epsf style files. For additional information about SNO see http://www.sno.phy.queensu.ca . This version has some new reference

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

The Sudbury Neutrino Observatory

Two experiments now in progress have reported measurements of the flux of high energy neutrinos from the Sun. Since about 1970, Davis and his co-workers have been using a [sup 37]Cl-based detector to measure the [sup 7]Be and [sup 8]B solar neutrino flux and have found it to be at least a factor of three lower than that predicted by the Standard Solar Model (SSM). The Kamiokande collaborations has been taking data since 1986 using a large light-water Cerenkov detector and have confirmed that the flux is about two times lower than predicted. Recent results from the SAGE and GALLEX gallium-based detectors show that there is also a deficit of the low energy pp solar neutrinos. These discrepancies between experiment and theory could arise because of inadequacies in the theoretical models of solar energy generation or because of previously unobserved properties of neutrinos. The Sudbury Neutrino Observatory (SNO) will provide the information necessary to decide which of these solutions to the solar neutrino problem'' is correct