Signatures of Emerging Subsurface Structures in Acoustic Power Maps

We show that under certain conditions, subsurface structures in the solar interior can alter the average acoustic power observed at the photosphere above them. By using numerical simulations of wave propagation, we show that this effect is large enough for it to be potentially used for detecting emerging active regions before they appear on the surface. In our simulations, simplified subsurface structures are modeled as regions with enhanced or reduced acoustic wave speed. We investigate the dependence of the acoustic power above a subsurface region on the sign, depth, and strength of the wave speed perturbation. Observations from the Solar and Heliospheric Observatory/Michelson Doppler Imager (SOHO/MDI) prior and during the emergence of NOAA active region 10488 are used to test the use of acoustic power as a potential precursor of magnetic flux emergence.Comment: 7 pages, 5 figures, accepted for publication in Solar Physics on 21 March 201

Growth and properties of ferromagnetic In(1-x)Mn(x)Sb alloys

We discuss a new narrow-gap ferromagnetic (FM) semiconductor alloy, In(1-x)Mn(x)Sb, and its growth by low-temperature molecular-beam epitaxy. The magnetic properties were investigated by direct magnetization measurements, electrical transport, magnetic circular dichroism, and the magneto-optical Kerr effect. These data clearly indicate that In(1-x)Mn(x)Sb possesses all the attributes of a system with carrier-mediated FM interactions, including well-defined hysteresis loops, a cusp in the temperature dependence of the resistivity, strong negative magnetoresistance, and a large anomalous Hall effect. The Curie temperatures in samples investigated thus far range up to 8.5 K, which are consistent with a mean-field-theory simulation of the carrier-induced ferromagnetism based on the 8-band effective band-orbital method.Comment: Invited talk at 11th International Conference on Narrow Gap Semiconductors, Buffalo, New York, U.S.A., June 16 - 20, 200

Elevated plasma TGF-β1 levels in patients with chronic obstructive pulmonary disease

SummaryBackgroundTransforming growth factor-β1 (TGF-β1), a multifunctional cytokine, has been implicated to be responsible for the increased deposition of extracellular matrix in the airways, and increased submucosal collagen expression in chronic obstructive pulmonary disease (COPD). We determined plasma TGF-β1 levels in patients with COPD and explored its association with common functional polymorphisms of TGF-β1 gene at C-509T and T869C in the development of COPD in a case–control study.MethodsStable COPD patients who were ever smokers, and age and pack-years smoked matched healthy controls (n = 205 in each group) were recruited for measurement of plasma TGF-β1 levels using commercially available ELISA kit, and genotyped at C-509T and T869C functional polymorphisms of TGF-β1 gene using polymerase chain reaction and restriction fragment length polymorphism (PCR–RFLP).ResultsCOPD patients had significantly elevated plasma TGF-β1 levels in comparison to healthy controls irrespective of the genotypes. Allele frequencies and genotype distributions at both polymorphic sites were not different among COPD patients or controls. TGF-β1 levels were inversely correlated (Pearson's correlation analysis) with FEV1 (% predicted) (p < 0.001) and FVC (% predicted) (p < 0.001).ConclusionThe findings of elevated plasma TGF-β1 levels in patients with COPD suggest that TGF-β1 may play a role in COPD pathogenesis. The C-509T and T869C functional polymorphisms of TGF-β1 gene do not represent a genetic predisposition to COPD susceptibility in Hong Kong Chinese patients

Observational Constraints on Chaplygin Quartessence: Background Results

We derive the constraints set by several experiments on the quartessence Chaplygin model (QCM). In this scenario, a single fluid component drives the Universe from a nonrelativistic matter-dominated phase to an accelerated expansion phase behaving, first, like dark matter and in a more recent epoch like dark energy. We consider current data from SNIa experiments, statistics of gravitational lensing, FR IIb radio galaxies, and x-ray gas mass fraction in galaxy clusters. We investigate the constraints from this data set on flat Chaplygin quartessence cosmologies. The observables considered here are dependent essentially on the background geometry, and not on the specific form of the QCM fluctuations. We obtain the confidence region on the two parameters of the model from a combined analysis of all the above tests. We find that the best-fit occurs close to the $\Lambda$CDM limit ($\alpha=0$). The standard Chaplygin quartessence ($\alpha=1$) is also allowed by the data, but only at the $\sim2\sigma$ level.Comment: Replaced to match the published version, references update

Supermassive Binaries and Extragalactic Jets

Some quasars show Doppler shifted broad emission line peaks. I give new statistics of the occurrence of these peaks and show that, while the most spectacular cases are in quasars with strong radio jets inclined to the line of sight, they are also almost as common in radio-quiet quasars. Theories of the origin of the peaks are reviewed and it is argued that the displaced peaks are most likely produced by the supermassive binary model. The separations of the peaks in the 3C 390.3-type objects are consistent with orientation-dependent "unified models" of quasar activity. If the supermassive binary model is correct, all members of "the jet set" (astrophysical objects showing jets) could be binaries.Comment: 31 pages, PostScript, missing figure is in ApJ 464, L105 (see http://www.aas.org/ApJ/v464n2/5736/5736.html

The phenotype of Floating-Harbor syndrome: Clinical characterization of 52 individuals with mutations in exon 34 of SRCAP

Background: Floating-Harbor syndrome (FHS) is a rare condition characterized by short stature, delays in expressive language, and a distinctive facial appearance. Recently, heterozygous truncating mutations in SRCAP were determined to be disease-causing. With the availability of a DNA based confirmatory test, we set forth to define the clinical features of this syndrome. Methods and results. Clinical information on fifty-two individuals with SRCAP mutations was collected using standardized questionnaires. Twenty-four males and twenty-eight females were studied with ages ranging from

No evidence that protein truncating variants in BRIP1 are associated with breast cancer risk: implications for gene panel testing.

BACKGROUND: BRCA1 interacting protein C-terminal helicase 1 (BRIP1) is one of the Fanconi Anaemia Complementation (FANC) group family of DNA repair proteins. Biallelic mutations in BRIP1 are responsible for FANC group J, and previous studies have also suggested that rare protein truncating variants in BRIP1 are associated with an increased risk of breast cancer. These studies have led to inclusion of BRIP1 on targeted sequencing panels for breast cancer risk prediction. METHODS: We evaluated a truncating variant, p.Arg798Ter (rs137852986), and 10 missense variants of BRIP1, in 48 144 cases and 43 607 controls of European origin, drawn from 41 studies participating in the Breast Cancer Association Consortium (BCAC). Additionally, we sequenced the coding regions of BRIP1 in 13 213 cases and 5242 controls from the UK, 1313 cases and 1123 controls from three population-based studies as part of the Breast Cancer Family Registry, and 1853 familial cases and 2001 controls from Australia. RESULTS: The rare truncating allele of rs137852986 was observed in 23 cases and 18 controls in Europeans in BCAC (OR 1.09, 95% CI 0.58 to 2.03, p=0.79). Truncating variants were found in the sequencing studies in 34 cases (0.21%) and 19 controls (0.23%) (combined OR 0.90, 95% CI 0.48 to 1.70, p=0.75). CONCLUSIONS: These results suggest that truncating variants in BRIP1, and in particular p.Arg798Ter, are not associated with a substantial increase in breast cancer risk. Such observations have important implications for the reporting of results from breast cancer screening panels.The COGS project is funded through a European Commission's Seventh Framework Programme grant (agreement number 223175 - HEALTH-F2-2009-223175). BCAC is funded by Cancer Research UK [C1287/A10118, C1287/A12014] and by the European Community´s Seventh Framework Programme under grant agreement number 223175 (grant number HEALTH-F2-2009-223175) (COGS). Funding for the iCOGS infrastructure came from: the European Community's Seventh Framework Programme under grant agreement n° 223175 (HEALTH-F2-2009-223175) (COGS), Cancer Research UK (C1287/A10118, C1287/A 10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007, C5047/A10692, C8197/A16565), the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 16 CA148065 and 1U19 CA148112 - the GAME-ON initiative), the Department of Defense (W81XWH-10-1- 0341), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund. This study made use of data generated by the Wellcome Trust Case Control consortium. Funding for the project was provided by the Wellcome Trust under award 076113. The results published here are in part based upon data generated by The Cancer Genome Atlas Project established by the National Cancer Institute and National Human Genome Research Institute.This is the author accepted manuscript. The final version is available from BMJ Group at http://dx.doi.org/10.1136/jmedgenet-2015-103529