QPO in RE J1034+396: model constraints from observed trends

We analyze the time variability of the X-ray emission of RE J1034+396, an active galactic nucleus with the first firm detection of a quasi-periodic oscillations (QPO). Based on the results of a wavelet analysis, we find a drift in the QPO central frequency. The change inthe QPO frequency correlates with the change in the X-ray flux with a short time delay. Linear structures such as shocks, spiral waves, orvery distant flares seem to be a favored explanation for this particular QPO event.Comment: to appear in the proceedings to "The Central Kiloparsec in Galactic Nuclei (AHAR2011)", Journal of Physics: Conference Series (JPCS), IOP Publishin

Trap-Assisted Tunneling in the Schottky Barrier

The paper presents a new way how to calculate the currents in a Schottky barrier. The novel phenomeno-logical model extends the Shockley-Read-Hall recombi-nation-generation theory of trap-assisted tunneling. The proposed approach explains the occurrence of large leakage currents in Schottky structures on wide band semi-conductors with a high Schottky barrier (above 1 eV) and with a high density of traps. Under certain conditions, trap-assisted tunneling (TAT) plays a more important role than direct tunneling

Reductions in cardiovascular, cerebrovascular, and respiratory mortality following the national Irish smoking ban: Interrupted time-series analysis

Copyright @ 2013 Stallings-Smith et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.This article has been made available through the Brunel Open Access Publishing Fund.Background: Previous studies have shown decreases in cardiovascular mortality following the implementation of comprehensive smoking bans. It is not known whether cerebrovascular or respiratory mortality decreases post-ban. On March 29, 2004, the Republic of Ireland became the first country in the world to implement a national workplace smoking ban. The aim of this study was to assess the effect of this policy on all-cause and cause-specific, non-trauma mortality. Methods: A time-series epidemiologic assessment was conducted, utilizing Poisson regression to examine weekly age and gender-standardized rates for 215,878 non-trauma deaths in the Irish population, ages ≥35 years. The study period was from January 1, 2000, to December 31, 2007, with a post-ban follow-up of 3.75 years. All models were adjusted for time trend, season, influenza, and smoking prevalence. Results: Following ban implementation, an immediate 13% decrease in all-cause mortality (RR: 0.87; 95% CI: 0.76-0.99), a 26% reduction in ischemic heart disease (IHD) (RR: 0.74; 95% CI: 0.63-0.88), a 32% reduction in stroke (RR: 0.68; 95% CI: 0.54-0.85), and a 38% reduction in chronic obstructive pulmonary disease (COPD) (RR: 0.62; 95% CI: 0.46-0.83) mortality was observed. Post-ban reductions in IHD, stroke, and COPD mortalities were seen in ages ≥65 years, but not in ages 35-64 years. COPD mortality reductions were found only in females (RR: 0.47; 95% CI: 0.32-0.70). Post-ban annual trend reductions were not detected for any smoking-related causes of death. Unadjusted estimates indicate that 3,726 (95% CI: 2,305-4,629) smoking-related deaths were likely prevented post-ban. Mortality decreases were primarily due to reductions in passive smoking. Conclusions: The national Irish smoking ban was associated with immediate reductions in early mortality. Importantly, post-ban risk differences did not change with a longer follow-up period. This study corroborates previous evidence for cardiovascular causes, and is the first to demonstrate reductions in cerebrovascular and respiratory causes

Coordinated multi-wavelength observations of Sgr A*

We report on recent near-infrared (NIR) and X-ray observations of Sagittarius A* (Sgr A*), the electromagnetic manifestation of the ~4x10^6 solar masses super-massive black hole (SMBH) at the Galactic Center. The goal of these coordinated multi-wavelength observations is to investigate the variable emission from Sgr A* in order to obtain a better understanding of the underlying physical processes in the accretion flow/outflow. The observations have been carried out using the NACO adaptive optics (AO) instrument at the European Southern Observatory's Very Large Telescope (July 2005, May 2007) and the ACIS-I instrument aboard the Chandra X-ray Observatory (July 2005). We report on a polarized NIR flare synchronous to a 8x1033 erg/s X-ray flare in July 2005, and a further flare in May 2007 that shows the highest sub-flare to flare contrast observed until now. The observations can be interpreted in the framework of a model involving a temporary disk with a short jet. In the disk component flux density variations can be explained due to hot spots on relativistic orbits around the central SMBH. The variations of the sub-structures of the May 2007 flare are interpreted as a variation of the hot spot structure due to differential rotation within the disk.Comment: 15 pages, 7 figures, contribution for the conference "The Universe under the Microscope" (AHAR 2008), to be published in Journal of Physics: Conference Series by Institute of Physics Publishin

Smoking Cessation and Cardiovascular Disease Risk Factors: Results from the Third National Health and Nutrition Examination Survey

BACKGROUND: Cigarette smoking is a major risk factor for the development and progression of cardiovascular disease. While smoking is associated with increased levels of inflammatory markers and accelerated atherosclerosis, few studies have examined the impact of smoking cessation on levels of inflammatory markers. The degree and rate at which inflammation subsides after smoking cessation are uncertain. It also remains unclear as to whether traditional risk factors can adequately explain the observed decline in cardiovascular risk following smoking cessation. METHODS AND FINDINGS: Using data from 15,489 individuals who participated in the Third National Health and Nutrition Examination Survey (NHANES III), we analyzed the association between smoking and smoking cessation on levels of inflammatory markers and traditional cardiovascular risk factors. In particular, we examined changes in C-reactive protein, white blood cell count, albumin, and fibrinogen. Inflammatory markers demonstrated a dose-dependent and temporal relationship to smoking and smoking cessation. Both inflammatory and traditional risk factors improved with decreased intensity of smoking. With increased time since smoking cessation, inflammatory markers resolved more slowly than traditional cardiovascular risk factors. CONCLUSION: Inflammatory markers may be more accurate indicators of atherosclerotic disease. Inflammatory markers returned to baseline levels 5 y after smoking cessation, consistent with the time frame associated with cardiovascular risk reduction observed in both the MONICA and Northwick Park Heart studies. Our results suggest that the inflammatory component of cardiovascular disease resulting from smoking is reversible with reduced tobacco exposure and smoking cessation

Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis

Background: Impaired signaling in the IFN-g/IL-12 pathway causes susceptibility to severe disseminated infections with mycobacteria and dimorphic yeasts. Dominant gain-of-function mutations in signal transducer and activator of transcription 1 (STAT1) have been associated with chronic mucocutaneous candidiasis. Objective: We sought to identify the molecular defect in patients with disseminated dimorphic yeast infections. Methods: PBMCs, EBV-transformed B cells, and transfected U3A cell lines were studied for IFN-g/IL-12 pathway function. STAT1 was sequenced in probands and available relatives. Interferon-induced STAT1 phosphorylation, transcriptional responses, protein-protein interactions, target gene activation, and function were investigated. Results: We identified 5 patients with disseminated Coccidioides immitis or Histoplasma capsulatum with heterozygous missense mutations in the STAT1 coiled-coil or DNA-binding domains. These are dominant gain-of-function mutations causing enhanced STAT1 phosphorylation, delayed dephosphorylation, enhanced DNA binding and transactivation, and enhanced interaction with protein inhibitor of activated STAT1. The mutations caused enhanced IFN-g–induced gene expression, but we found impaired responses to IFN-g restimulation. Conclusion: Gain-of-function mutations in STAT1 predispose to invasive, severe, disseminated dimorphic yeast infections, likely through aberrant regulation of IFN-g–mediated inflammationFil: Sampaio, Elizabeth P.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unidos. Instituto Oswaldo Cruz. Laboratorio de Leprologia; BrasilFil: Hsu, Amy P.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Pechacek, Joseph. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Hannelore I.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unidos. Erasmus Medical Center. Department of Medical Microbiology and Infectious Disease; Países BajosFil: Dias, Dalton L.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Paulson, Michelle L.. Clinical Research Directorate/CMRP; Estados UnidosFil: Chandrasekaran, Prabha. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Rosen, Lindsey B.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Carvalho, Daniel S.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unidos. Instituto Oswaldo Cruz, Laboratorio de Leprologia; BrasilFil: Ding, Li. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Vinh, Donald C.. McGill University Health Centre. Division of Infectious Diseases; CanadáFil: Browne, Sarah K.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Datta, Shrimati. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Allergic Diseases. Allergic Inflammation Unit; Estados UnidosFil: Milner, Joshua D.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Allergic Diseases. Allergic Inflammation Unit; Estados UnidosFil: Kuhns, Douglas B.. Clinical Services Program; Estados UnidosFil: Long Priel, Debra A.. Clinical Services Program; Estados UnidosFil: Sadat, Mohammed A.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Host Defenses. Infectious Diseases Susceptibility Unit; Estados UnidosFil: Shiloh, Michael. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: De Marco, Brendan. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: Alvares, Michael. University of Texas. Southwestern Medical Center. Division of Allergy and Immunology; Estados UnidosFil: Gillman, Jason W.. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: Ramarathnam, Vivek. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: de la Morena, Maite. University of Texas. Southwestern Medical Center. Division of Allergy and Immunology; Estados UnidosFil: Bezrodnik, Liliana. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutierrez"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Moreira, Ileana. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutierrez"; ArgentinaFil: Uzel, Gulbu. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Johnson, Daniel. University of Chicago. Comer Children; Estados UnidosFil: Spalding, Christine. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Zerbe, Christa S.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados UnidosFil: Wiley, Henry. National Eye Institute. Clinical Trials Branch; Estados UnidosFil: Greenberg, David E.. University of Texas. Southwestern Medical Center. Division of Infectious Diseases; Estados UnidosFil: Hoover, Susan E.. University of Arizona. College of Medicine. Valley Fever Center for Excellence; Estados UnidosFil: Rosenzweig, Sergio D.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Host Defenses Infectious Diseases Susceptibility Unit; Estados Unidos. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Primary Immunodeficiency Clinic; Estados UnidosFil: Galgiani, John N.. University of Arizona. College of Medicine. Valley Fever Center for Excellence; Estados UnidosFil: Holland, Steven M.. National Institutes of Health. National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Immunopathogenesis Section; Estados Unido

The Role of Self-Efficacy in Achieving Health Behavior Change

The concept of self-efficacy is receiving increasing recognition as a predictor of health behavior change and maintenance. The purpose of this article is to facilitate a clearer understanding of both the concept and its relevance for health education research and practice. Self-efficacy is first defined and distinguished from other related concepts. Next, studies of the self-efficacy concept as it relates to health practices are examined. This review focuses on cigarette smoking, weight control, contraception, alcohol abuse and exercise behaviors. The studies reviewed suggest strong relationships between self-efficacy and health behavior change and maintenance. Experimental manipulations of self-efficacy suggest that efficacy can be enhanced and that this enhancement is related to subsequent health behavior change. The findings from these studies also suggest methods for modifying health practices. These methods diverge from many of the current, traditional methods for changing health practices. Recommendations for incorporating the enhancement of self-efficacy into health behavior change programs are made in light of the reviewed findings.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/68171/2/10.1177_109019818601300108.pd

The effects of acute exercise on subsequent cigarette smoking

The present study was conducted to examine the effects of acute aerobic exercise on smoking behavior. On alternate days, 10 healthy young smokers were subjected to half an hour of sustained high exercise (about 56% of maximum work capacity) or of low exercise (about 28% of maximum, simulating normal daytime activity). During the high-exercise condition, there were pronounced increases in physiological markers of physical activity such as mean work, heart rate, and lactic acid as well as elevations in circulating hormones (norepinephrine, epinephrine, and immunoreactive beta-endorphin and cortisol) known to be affected by vigorous exercise. Despite a trend toward decreased desire for cigarettes after the high exercise condition, there were no differences in plasma nicotine levels following the smoking of a usual-brand cigarette 35 min later. The sustained effects of the two exercise conditions were also similar: plasma cotinine levels 24 hr later (reflecting nicotine intake over the entire exercise day) revealed no significant differences between hight and low exercise.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44810/1/10865_2004_Article_BF00846420.pd