High frequency oscillations during magnetar flares

The recent discovery of high frequency oscillations during giant flares from the Soft Gamma Repeaters SGR 1806-20 and SGR 1900+14 may be the first direct detection of vibrations in a neutron star crust. If this interpretation is correct it offers a novel means of testing the neutron star equation of state, crustal breaking strain, and magnetic field configuration. We review the observational data on the magnetar oscillations, including new timing analysis of the SGR 1806-20 giant flare using data from the Ramaty High Energy Solar Spectroscopic Imager (RHESSI) and the Rossi X-ray Timing Explorer (RXTE). We discuss the implications for the study of neutron star structure and crust thickness, and outline areas for future investigation.Comment: 5 pages, 1 figure, to appear in the proceedings of the conference "Isolated Neutron Stars: from the Interior to the Surface" (April 2006, London), eds. D. Page, R. Turolla, & S. Zane, Astrophysics & Space Science in pres

Theory of Neutron Scattering in the Normal and Superconducting State of YBCO

We analyze neutron experiments on \ybco at various stoichiometries in the superconducting state, within the context of a bi-layer theory which yields good agreement with the normal state Cu-NMR and neutron data as a function of \omega, q and T. A d-wave superconducting state exhibits peaks at q = ( \pi , \pi , \pi ) and sharp maxima as a function of \omega, at twice the gap frequency. This behavior may have been observed experimentally. The counterpart behavior for other choices of order parameter symmetry is discussed.Comment: uuencoded postscript file for the entire paper enclose

Vaginal delivery after previous cesarean section in a rural West African hospital

Two hundred twenty women with prior cesarean section were delivered at our institution between January 1987 and February 1990. Vaginal delivery was achieved in 111 (66%) of 169 patients given a trial of labor (TOL). Success of TOL correlated positively with the number of prior vaginal deliveries (P < 0.05) and inversely with the number of prior cesarean sections (P < 0.005). Maternal and fetal outcome were not significantly different between the TOL and non-TOL groups.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/29051/1/0000084.pd

Dual Chamber Laser Ion Source at Lisol

A new type of the gas cell for the resonance ionization laser ion source at the Leuven Isotope Separator On Line (LISOL) has been developed and tested at off-line and on-line conditions. Two-step selective laser ionization is applied to produce purified beams of radioactive isotopes. The selectivity of the ion source has been increased by more than one order of magnitude by separation of the stopping and laser ionization regions. This allows to use electrical fields for further ion purification.Comment: 14 figure

Socioeconomic, Psychosocial, and Clinical Factors Associated with Employment in Women with HIV in the United States: A Correlational Study

Employment is a social determinant of health, and women living with HIV (WLWH) are often underemployed. This correlational study examined the socioeconomic, psychosocial, and clinical factors associated with employment among WLWH (n = 1,357) and women at risk for HIV (n = 560). Descriptive and inferential statistics were used to evaluate factors associated with employment status. Employment was associated (p ≤.05) with better socioeconomic status and quality of life (QOL), less tobacco and substance use, and better physical, psychological, and cognitive health. Among WLWH, employment was associated (p ≤.05) with improved adherence to HIV care visits and HIV RNA viral suppression. Using multivariable regression modeling, differences were found between WLWH and women at risk for HIV. Among WLWH, household income, QOL, education, and time providing childcare remained associated with employment in adjusted multivariable analyses (R2=.272, p <.001). A better understanding of the psychosocial and structural factors affecting employment is needed to reduce occupational disparities among WLWH

Age at symptom onset and death and disease duration in genetic frontotemporal dementia : an international retrospective cohort study

Background: Frontotemporal dementia is a heterogenous neurodegenerative disorder, with about a third of cases being genetic. Most of this genetic component is accounted for by mutations in GRN, MAPT, and C9orf72. In this study, we aimed to complement previous phenotypic studies by doing an international study of age at symptom onset, age at death, and disease duration in individuals with mutations in GRN, MAPT, and C9orf72. Methods: In this international, retrospective cohort study, we collected data on age at symptom onset, age at death, and disease duration for patients with pathogenic mutations in the GRN and MAPT genes and pathological expansions in the C9orf72 gene through the Frontotemporal Dementia Prevention Initiative and from published papers. We used mixed effects models to explore differences in age at onset, age at death, and disease duration between genetic groups and individual mutations. We also assessed correlations between the age at onset and at death of each individual and the age at onset and at death of their parents and the mean age at onset and at death of their family members. Lastly, we used mixed effects models to investigate the extent to which variability in age at onset and at death could be accounted for by family membership and the specific mutation carried. Findings: Data were available from 3403 individuals from 1492 families: 1433 with C9orf72 expansions (755 families), 1179 with GRN mutations (483 families, 130 different mutations), and 791 with MAPT mutations (254 families, 67 different mutations). Mean age at symptom onset and at death was 49\ub75 years (SD 10\ub70; onset) and 58\ub75 years (11\ub73; death) in the MAPT group, 58\ub72 years (9\ub78; onset) and 65\ub73 years (10\ub79; death) in the C9orf72 group, and 61\ub73 years (8\ub78; onset) and 68\ub78 years (9\ub77; death) in the GRN group. Mean disease duration was 6\ub74 years (SD 4\ub79) in the C9orf72 group, 7\ub71 years (3\ub79) in the GRN group, and 9\ub73 years (6\ub74) in the MAPT group. Individual age at onset and at death was significantly correlated with both parental age at onset and at death and with mean family age at onset and at death in all three groups, with a stronger correlation observed in the MAPT group (r=0\ub745 between individual and parental age at onset, r=0\ub763 between individual and mean family age at onset, r=0\ub758 between individual and parental age at death, and r=0\ub769 between individual and mean family age at death) than in either the C9orf72 group (r=0\ub732 individual and parental age at onset, r=0\ub736 individual and mean family age at onset, r=0\ub738 individual and parental age at death, and r=0\ub740 individual and mean family age at death) or the GRN group (r=0\ub722 individual and parental age at onset, r=0\ub718 individual and mean family age at onset, r=0\ub722 individual and parental age at death, and r=0\ub732 individual and mean family age at death). Modelling showed that the variability in age at onset and at death in the MAPT group was explained partly by the specific mutation (48%, 95% CI 35\u201362, for age at onset; 61%, 47\u201373, for age at death), and even more by family membership (66%, 56\u201375, for age at onset; 74%, 65\u201382, for age at death). In the GRN group, only 2% (0\u201310) of the variability of age at onset and 9% (3\u201321) of that of age of death was explained by the specific mutation, whereas 14% (9\u201322) of the variability of age at onset and 20% (12\u201330) of that of age at death was explained by family membership. In the C9orf72 group, family membership explained 17% (11\u201326) of the variability of age at onset and 19% (12\u201329) of that of age at death. Interpretation: Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership. Although estimation of age at onset will be an important factor in future pre-symptomatic therapeutic trials for all three genetic groups, our study suggests that data from other members of the family will be particularly helpful only for individuals with MAPT mutations. Further work in identifying both genetic and environmental factors that modify phenotype in all groups will be important to improve such estimates. Funding: UK Medical Research Council, National Institute for Health Research, and Alzheimer's Society

Identification of regulatory variants associated with genetic susceptibility to meningococcal disease

Non-coding genetic variants play an important role in driving susceptibility to complex diseases but their characterization remains challenging. Here, we employed a novel approach to interrogate the genetic risk of such polymorphisms in a more systematic way by targeting specific regulatory regions relevant for the phenotype studied. We applied this method to meningococcal disease susceptibility, using the DNA binding pattern of RELA - a NF-kB subunit, master regulator of the response to infection - under bacterial stimuli in nasopharyngeal epithelial cells. We designed a custom panel to cover these RELA binding sites and used it for targeted sequencing in cases and controls. Variant calling and association analysis were performed followed by validation of candidate polymorphisms by genotyping in three independent cohorts. We identified two new polymorphisms, rs4823231 and rs11913168, showing signs of association with meningococcal disease susceptibility. In addition, using our genomic data as well as publicly available resources, we found evidences for these SNPs to have potential regulatory effects on ATXN10 and LIF genes respectively. The variants and related candidate genes are relevant for infectious diseases and may have important contribution for meningococcal disease pathology. Finally, we described a novel genetic association approach that could be applied to other phenotypes

Untangling the effects of overexploration and overexploitation on organizational performance: The moderating role of environmental dynamism

Because a firm's optimal knowledge search behavior is determined by unique firm and industry conditions, organizational performance should be contingent oil the degree to which a firm's actual level of knowledge search deviates from the optimal level. It is thus hypothesized that deviation from the optimal search, in the form of either overexploitation or overexploration, is detrimental to organizational performance. Furthermore, the negative effect of search deviation oil organizational performance varies with environmental dynamism: that is, overexploitation is expected to become more harmful. whereas overexploration becomes less so with all increase in environmental dynamism. The empirical analyses yield results consistent with these arguments. Implications for research and practice are correspondingly discussed

Genetic determinants of telomere length from 109,122 ancestrally diverse whole-genome sequences in TOPMed

Genetic studies on telomere length are important for understanding age-related diseases. Prior GWASs for leukocyte TL have been limited to European and Asian populations. Here, we report the first sequencing-based association study for TL across ancestrally diverse individuals (European, African, Asian, and Hispanic/Latino) from the NHLBI Trans-Omics for Precision Medicine (TOPMed) program. We used whole-genome sequencing (WGS) of whole blood for variant genotype calling and the bioinformatic estimation of telomere length in n = 109,122 individuals. We identified 59 sentinel variants (p < 5 × 10−9) in 36 loci associated with telomere length, including 20 newly associated loci (13 were replicated in external datasets). There was little evidence of effect size heterogeneity across populations. Fine-mapping at OBFC1 indicated that the independent signals colocalized with cell-type-specific eQTLs for OBFC1 (STN1). Using a multi-variant gene-based approach, we identified two genes newly implicated in telomere length, DCLRE1B (SNM1B) and PARN. In PheWAS, we demonstrated that our TL polygenic trait scores (PTSs) were associated with an increased risk of cancer-related phenotypes