Puzzles in BB physics

I discuss some puzzles observed in exclusive $B$ meson decays, concentrating on the large difference between the direct CP asymmetries in the $B^0\to \pi^\mp K^\pm$ and $B^\pm\to \pi^0 K^\pm$ modes, the large $B^0\to\pi^0\pi^0$ branching ratio, and the large deviation of the mixing-induced CP asymmetries in the $b\to sq\bar q$ penguins from those in the $b\to c\bar c s$ trees.Comment: 6 pages, 1 figure, talk presented at the 9th Workshop on High Energy Physics Phenomenology, Bhubaneswar, Orissa, India, Jan. 3-14, 2006; reference adde

Inflation and nonequilibrium renormalization group

We study de spectrum of primordial fluctuations and the scale dependence of the inflaton spectral index due to self-interactions of the field. We compute the spectrum of fluctuations by applying nonequilibrium renormalization group techniques.Comment: 6 pages, 1 figure, submitted to J. Phys.

Soft end-point and mass corrections to the eta' g*g* vertex function

Power-suppressed corrections arising from end-point integration regions to the space-like vertex function of the massive eta'-meson virtual gluon transition eta' - g*g* are computed. Calculations are performed within the standard hard-scattering approach (HSA) and the running coupling method supplemented by the infrared renormalon calculus. Contributions to the vertex function from the quark and gluon contents of the eta' -meson are taken into account and the Borel resummed expressions for F_{eta' g*g*}(Q2,\omega ,\eta), as well as for F_{eta' g g*}}(Q^{2},\omega =\pm 1,\eta) and F_{eta' g*g*}(Q^{2},\omega =0,\eta) are obtained. It is demonstrated that the power-suppressed corrections \sim (\Lambda ^{2}/Q^{2})^{n}, in the explored range of the total gluon virtuality 1 <Q2 < 25 GeV2, considerably enhance the vertex function relative to the results found in the framework of the standard HSA with a fixed coupling. Modifications generated by the eta ' -meson mass effects are discussed

Performance metrics and auditing framework using application kernels for high‐performance computer systems

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/97468/1/cpe2871.pd

Rationale and protocol for the 7- And 8-year longitudinal assessments of eye health in a cohort of young adults in the Raine Study

Introduction Eye diseases and visual impairment more commonly affect elderly adults, thus, the majority of ophthalmic cohort studies have focused on older adults. Cohort studies on the ocular health of younger adults, on the other hand, have been few. The Raine Study is a longitudinal study that has been following a cohort since their birth in 1989-1991. As part of the 20-year follow-up of the Raine Study, participants underwent a comprehensive eye examination. As part of the 27- and 28-year follow-ups, eye assessments are being conducted and the data collected will be compared with those of the 20-year follow-up. This will provide an estimate of population incidence and updated prevalence of ocular conditions such as myopia and keratoconus, as well as longitudinal change in ocular parameters in young Australian adults. Additionally, the data will allow exploration of the environmental, health and genetic factors underlying inter-subject differential long-term ocular changes. Methods and analysis Participants are being contacted via telephone, email and/or social media and invited to participate in the eye examination. At the 27-year follow-up, participants completed a follow-up eye screening, which assessed visual acuity, autorefraction, ocular biometry and ocular sun exposure. Currently, at the 28-year follow-up, a comprehensive eye examination is being conducted which, in addition to all the eye tests performed at the 27-year follow-up visit, includes tonometry, optical coherence tomography, funduscopy and anterior segment topography, among others. Outcome measures include the incidence of refractive error and pterygium, an updated prevalence of these conditions, and the 8-year change in ocular parameters. Ethics and dissemination The Raine Study is registered in the Australian New Zealand Clinical Trials Registry. The Gen2 20-year, 27-year and 28-year follow-ups are approved by the Human Research Ethics Committee of the University of Western Australia. Findings resulting from the study will be published in health or medical journals and presented at conferences. Trial registration number ACTRN12617001599369; Active, not recruiting

Black Holes from Cosmic Rays: Probes of Extra Dimensions and New Limits on TeV-Scale Gravity

If extra spacetime dimensions and low-scale gravity exist, black holes will be produced in observable collisions of elementary particles. For the next several years, ultra-high energy cosmic rays provide the most promising window on this phenomenon. In particular, cosmic neutrinos can produce black holes deep in the Earth's atmosphere, leading to quasi-horizontal giant air showers. We determine the sensitivity of cosmic ray detectors to black hole production and compare the results to other probes of extra dimensions. With n \ge 4 extra dimensions, current bounds on deeply penetrating showers from AGASA already provide the most stringent bound on low-scale gravity, requiring a fundamental Planck scale M_D > 1.3 - 1.8 TeV. The Auger Observatory will probe M_D as large as 4 TeV and may observe on the order of a hundred black holes in 5 years. We also consider the implications of angular momentum and possible exponentially suppressed parton cross sections; including these effects, large black hole rates are still possible. Finally, we demonstrate that even if only a few black hole events are observed, a standard model interpretation may be excluded by comparison with Earth-skimming neutrino rates.Comment: 30 pages, 18 figures; v2: discussion of gravitational infall, AGASA and Fly's Eye comparison added; v3: Earth-skimming results modified and strengthened, published versio

B→KB\to K Transition Form Factor up to O(1/mb2){\cal O}(1/m^2_b) within the kTk_T Factorization Approach

In the paper, we apply the $k_T$ factorization approach to deal with the $B\to K$ transition form factor $F^{B\to K}_{+,0}(q^2)$ in the large recoil regions. The B-meson wave functions $\Psi_B$ and $\bar\Psi_B$ that include the three-particle Fock states' contributions are adopted to give a consistent PQCD analysis of the form factor up to ${\cal O} (1/m^2_b)$. It has been found that both the wave functions $\Psi_B$ and $\bar\Psi_B$ can give sizable contributions to the form factor and should be kept for a better understanding of the $B$ meson decays. Then the contributions from different twist structures of the kaon wavefunction are discussed, including the $SU_f(3)$-breaking effects. A sizable contribution from the twist-3 wave function $\Psi_p$ is found, whose model dependence is discussed by taking two group of parameters that are determined by different distribution amplitude moments obtained in the literature. It is also shown that $F^{B\to K}_{+,0}(0)=0.30\pm0.04$ and $[F^{B\to K}_{+,0}(0)/F^{B\to \pi}_{+,0}(0)]=1.13\pm0.02$, which are more reasonable and consistent with the light-cone sum rule results in the large recoil regions.Comment: 22 pages and 6 figure

Identification of a RAI1-associated disease network through integration of exome sequencing, transcriptomics, and 3D genomics.

Smith-Magenis syndrome (SMS) is a developmental disability/multiple congenital anomaly disorder resulting from haploinsufficiency of RAI1. It is characterized by distinctive facial features, brachydactyly, sleep disturbances, and stereotypic behaviors. We investigated a cohort of 15 individuals with a clinical suspicion of SMS who showed neither deletion in the SMS critical region nor damaging variants in RAI1 using whole exome sequencing. A combination of network analysis (co-expression and biomedical text mining), transcriptomics, and circularized chromatin conformation capture (4C-seq) was applied to verify whether modified genes are part of the same disease network as known SMS-causing genes. Potentially deleterious variants were identified in nine of these individuals using whole-exome sequencing. Eight of these changes affect KMT2D, ZEB2, MAP2K2, GLDC, CASK, MECP2, KDM5C, and POGZ, known to be associated with Kabuki syndrome 1, Mowat-Wilson syndrome, cardiofaciocutaneous syndrome, glycine encephalopathy, mental retardation and microcephaly with pontine and cerebellar hypoplasia, X-linked mental retardation 13, X-linked mental retardation Claes-Jensen type, and White-Sutton syndrome, respectively. The ninth individual carries a de novo variant in JAKMIP1, a regulator of neuronal translation that was recently found deleted in a patient with autism spectrum disorder. Analyses of co-expression and biomedical text mining suggest that these pathologies and SMS are part of the same disease network. Further support for this hypothesis was obtained from transcriptome profiling that showed that the expression levels of both Zeb2 and Map2k2 are perturbed in Rai1 (-/-) mice. As an orthogonal approach to potentially contributory disease gene variants, we used chromatin conformation capture to reveal chromatin contacts between RAI1 and the loci flanking ZEB2 and GLDC, as well as between RAI1 and human orthologs of the genes that show perturbed expression in our Rai1 (-/-) mouse model. These holistic studies of RAI1 and its interactions allow insights into SMS and other disorders associated with intellectual disability and behavioral abnormalities. Our findings support a pan-genomic approach to the molecular diagnosis of a distinctive disorder

Reconstructing large running-index inflaton potentials

Recent fits of cosmological parameters by the first year Wilkinson Microwave Anisotropy Probe (WMAP) measurement seem to favor a primordial scalar spectrum with a large varying index from blue to red. We use the inflationary flow equations to reconstruct large running-index inflaton potentials and comment on current status on the inflationary flow. We find previous negligence of higher order slow rolling contributions when using the flow equations would lead to unprecise results.Comment: Final version to appear in Class. Quant. Grav. References adde

Genetic variation affects morphological retinal phenotypes extracted from UK Biobank optical coherence tomography images

Optical Coherence Tomography (OCT) enables non-invasive imaging of the retina and is used to diagnose and manage ophthalmic diseases including glaucoma. We present the first large-scale genome-wide association study of inner retinal morphology using phenotypes derived from OCT images of 31,434 UK Biobank participants. We identify 46 loci associated with thickness of the retinal nerve fibre layer or ganglion cell inner plexiform layer. Only one of these loci has been associated with glaucoma, and despite its clear role as a biomarker for the disease, Mendelian randomisation does not support inner retinal thickness being on the same genetic causal pathway as glaucoma. We extracted overall retinal thickness at the fovea, representative of foveal hypoplasia, with which three of the 46 SNPs were associated. We additionally associate these three loci with visual acuity. In contrast to the Mendelian causes of severe foveal hypoplasia, our results suggest a spectrum of foveal hypoplasia, in part genetically determined, with consequences on visual function