Supernova Remnants in the Fossil Starburst in M82

We report the discovery of ten compact H-alpha-bright sources in the post-starburst region northeast of the center of M82, ``M82 B.'' These objects have H alpha luminosities and sizes consistent with Type II supernova remnants (SNRs). They fall on the same H alpha surface brightness-diameter (Sigma-D) relation defined by SNRs in other nearby star-forming galaxies, with the M82 candidates lying preferentially at the small diameter end. These are the first candidates for optically-visible SNRs in M82 outside the heavily obscured central starburst within ~250 pc from the galactic center. If these sources are SNRs, they set an upper limit to the end of the starburst in region ``B2,'' about 500 pc from the galaxy's core, of ~50 Myr. Region ``B1,'' about 1000 pc from the core, lacks good SNR candidates and is evidently somewhat older. This suggests star formation in the galaxy has propagated inward toward the present-day intense starburst core.Comment: Re-submitted to AJ, referee's comments taken into account, 15 pages LaTeX preprint style, 4 postscript figures; full-resolution figures available from http://www.astro.virginia.edu/~rd7a/snrs/ Changes: minor textual changes and orientation/axes of Fig.

The National Cancer Institute Cohort Consortium : An International Pooling Collaboration of 58 Cohorts from 20 Countries

Cohort studies have been central to the establishment of the known causes of cancer. To dissect cancer etiology in more detail-for instance, for personalized risk prediction and prevention, assessment of risks of subtypes of cancer, and assessment of small elevations in risk-there is a need for analyses of far larger cohort datasets than available in individual existing studies. To address these challenges, the NCI Cohort Consortium was founded in 2001. It brings together 58 cancer epidemiology cohorts from 20 countries to undertake large-scale pooling research. The cohorts in aggregate include over nine million study participants, with biospecimens available for about two million of these. Research in the Consortium is undertaken by >40 working groups focused on specific cancer sites, exposures, or other research areas. More than 180 publications have resulted from the Consortium, mainly on genetic and other cancer epidemiology, with high citation rates. This article describes the foundation of the Consortium; its structure, governance, and methods of working; the participating cohorts; publications; and opportunities. The Consortium welcomes newmembers with cancer-oriented cohorts of 10,000 or more participants and an interest in collaborative research. (C) 2018 AACR.Peer reviewe

Pulsar Wind Nebulae in Evolved Supernova Remnants

For pulsars similar to the one in the Crab Nebula, most of the energy input to the surrounding wind nebula occurs on a timescale of less than 1000 years; during this time, the nebula expands into freely expanding supernova ejecta. On a timescale 10,000 years, the interaction of the supernova with the surrounding medium drives a reverse shock front toward the center of the remnant, where it crushes the PWN (pulsar wind nebula). One- and two-dimensional, two-fluid simulations of the crushing and re-expansion phases of a PWN show that (1) these phases are subject to Rayleigh-Taylor instabilities that result in the mixing of thermal and nonthermal fluids, and (2) asymmetries in the surrounding interstellar medium give rise to asymmetries in the position of the PWN relative to the pulsar and explosion site. These effects are expected to be observable in the radio emission from evolved PWN because of the long lifetimes of radio emitting electrons. The scenario can explain the chaotic and asymmetric appearance of the Vela X PWN relative to the Vela pulsar without recourse to a directed flow from the vicinity of the pulsar. The displacement of the radio nebulae in G327.1--1.1, MSH15--56 (G326.3--1.8), G0.9+0.1, and W44 relative to the X-ray nebulae may be due to this mechanism. On timescales much greater than the nebular crushing time, the initial PWN may be mixed with thermal gas and become unobservable, so that even the radio emission is dominated by recently injected particles.Comment: 22 pages, 9 figures; submitted to Ap

Linking physical activity to breast cancer:text mining results and a protocol for systematically reviewing three potential mechanistic pathways

Epidemiological research suggests that physical activity is associated with a reduced risk of breast cancer, but the causal nature of this link is not clear. Investigating mechanistic pathways can provide evidence of biological plausibility and improve causal inference. This project will examine three putative pathways (sex steroid hormones, insulin signalling, and inflammation) in a series of two-stage systematic reviews. Stage 1 used Text Mining for Mechanism Prioritisation (TeMMPo) to identify and prioritise relevant biological intermediates. Stage 2 will systematically review the findings from studies of (i) physical activity and intermediates; and (ii) intermediates and breast cancer. Ovid MEDLINE, EMBASE, and SPORTDiscus will be searched using a combination of subject headings and free-text terms. Human intervention and prospective, observational studies will be eligible for inclusion. Meta-analysis will be performed where possible. Risk of bias will be assessed using the Cochrane Collaboration tool, the ROBINS-I or ROBINS-E tool, depending on study type. Strength of evidence will be assessed using the GRADE system. In addition to synthesising the mechanistic evidence that links physical activity with breast cancer risk, this project may also identify priority areas for future research and help inform the design and implementation of physical activity interventions

Study of the Composite Supernova Remnant MSH 11-62

We present the analysis of the X-ray data collected during an observation of the supernova remnant (SNR) MSH 11-62 by the Advanced Satellite for Cosmology and Astrophysics (ASCA). We show that MSH 11-62 is a composite remnant whose X-ray emission comes from two distinct contributions. Nonthermal, synchrotron emission, localized to a region of radius (~~)3' (consistent with a point source) dominates the total flux above 2 keV. A second contribution comes from a thermal component, extended up to a radius of (~~)6' and detected only at energies below 2keV. The spatial and spectral analysis imply the presence of a neutron star losing energy at a rate of about (10**36 - 10**37) ergs/s. No pulsed emission is detected and we set a limit on the pulsed fraction of 10%. This is consistent with the lack of a radio pulsar in the remnant, which may indicate that the pulsed emission from the rapidly rotating compact object that should be powering the synchrotron nebula is beamed and our viewing direction is unfavorable. In either event, the central neutron star deposits much of its spin-down energy into the surrounding synchrotron nebula where, through direct imaging with broadband satellites such as ASCA, it is possible to study the energetics and evolution of the compact remnant.Comment: 30 pages, including 5 figures, Latex. To appear in ApJ (May 20, 1998 issue, Vol. 499.

Linking Physical Activity to Breast Cancer via Sex Steroid Hormones, Part 2:The Effect of Sex Steroid Hormones on Breast Cancer Risk

We undertook a systematic review and appraised the evidence for an effect of circulating sex steroid hormones and sex hormone–binding globulin (SHBG) on breast cancer risk in pre- and postmenopausal women. Systematic searches identified prospective studies relevant to this review. Meta-analyses estimated breast cancer risk for women with the highest compared with the lowest level of sex hormones, and the DRMETA Stata package was used to graphically represent the shape of these associations. The ROBINS-E tool assessed risk of bias, and the GRADE system appraised the strength of evidence. In premenopausal women, there was little evidence that estrogens, progesterone, or SHBG were associated with breast cancer risk, whereas androgens showed a positive association. In postmenopausal women, higher estrogens and androgens were associated with an increase in breast cancer risk, whereas higher SHBG was inversely associated with risk. The strength of the evidence quality ranged from low to high for each hormone. Dose–response relationships between sex steroid hormone concentrations and breast cancer risk were most notable for post-menopausal women. These data support the plausibility of a role for sex steroid hormones in mediating the causal relationship between physical activity and the risk of breast cancer. See related reviews by Lynch et al., p. 11 and Swain et al., p. 1

Prospective Evaluation over 15 Years of Six Breast Cancer Risk Models.

Prospective validation of risk models is needed to assess their clinical utility, particularly over the longer term. We evaluated the performance of six commonly used breast cancer risk models (IBIS, BOADICEA, BRCAPRO, BRCAPRO-BCRAT, BCRAT, and iCARE-lit). 15-year risk scores were estimated using lifestyle factors and family history measures from 7608 women in the Melbourne Collaborative Cohort Study who were aged 50-65 years and unaffected at commencement of follow-up two (conducted in 2003-2007), of whom 351 subsequently developed breast cancer. Risk discrimination was assessed using the C-statistic and calibration using the expected/observed number of incident cases across the spectrum of risk by age group (50-54, 55-59, 60-65 years) and family history of breast cancer. C-statistics were higher for BOADICEA (0.59, 95% confidence interval (CI) 0.56-0.62) and IBIS (0.57, 95% CI 0.54-0.61) than the other models (p-difference ≤ 0.04). No model except BOADICEA calibrated well across the spectrum of 15-year risk (p-value < 0.03). The performance of BOADICEA and IBIS was similar across age groups and for women with or without a family history. For middle-aged Australian women, BOADICEA and IBIS had the highest discriminatory accuracy of the six risk models, but apart from BOADICEA, no model was well-calibrated across the risk spectrum.This work was primarily supported by grant 1129136 from the Australian National Health and Medical Research Council (NHMRC) (https://www.nhmrc.gov.au/). MCCS cohort recruitment was funded by Cancer Council Victoria (https://www.cancervic.org.au/) and VicHealth (https://www.vichealth.vic.gov.au/). The MCCS was further supported by Australian NHMRC grants 209057, 396414 and 1074383, and ongoing follow-up and data management has been funded by Cancer Council Victoria since 1995. Cases and their vital status were ascertained through the Victorian Cancer Registry and the Australian Institute of Health and Welfare, including the National Death Index and the Australian Cancer Database.TN-D is a recipient of a Career Development Fellowship from the National Breast Cancer Foundation (Australia). JLH and MCS are Senior Principal and Senior Research Fellows of the National Health and Medical Research Council (Australia), respectively. ACA and AJL are supported by grants from Cancer Research UK (C12292/A20861 and PPRPGM19 Nov20\100002)

Rota tecnológica para a gestão sustentável de resíduos sólidos domiciliares

Orientador : Prof. Dr. Vitor Afonso HoeflichMonografia (especialização) - Universidade Federal do Paraná, Setor de Ciências Agrárias, Curso de Especialização em Direito AmbientalInclui referência

Lifetime alcohol intake is associated with an increased risk of KRAS+ and BRAF-/KRAS- but not BRAF+ colorectal cancer.

Ethanol in alcoholic beverages is a causative agent for colorectal cancer. Colorectal cancer is a biologically heterogeneous disease, and molecular subtypes defined by the presence of somatic mutations in BRAF and KRAS are known to exist. We examined associations between lifetime alcohol intake and molecular and anatomic subtypes of colorectal cancer. We calculated usual alcohol intake for 10-year periods from age 20 using recalled frequency and quantity of beverage-specific consumption for 38,149 participants aged 40-69 years from the Melbourne Collaborative Cohort Study. Cox regression was performed to derive hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between lifetime alcohol intake and colorectal cancer risk. Heterogeneity in the HRs across subtypes of colorectal cancer was assessed. A positive dose-dependent association between lifetime alcohol intake and overall colorectal cancer risk (mean follow-up = 14.6 years; n = 596 colon and n = 326 rectal cancer) was observed (HR = 1.08, 95% CI: 1.04-1.12 per 10 g/day increment). The risk was greater for rectal than colon cancer (phomogeneity  = 0.02). Alcohol intake was associated with increased risks of KRAS+ (HR = 1.07, 95% CI: 1.00-1.15) and BRAF-/KRAS- (HR = 1.05, 95% CI: 1.00-1.11) but not BRAF+ tumors (HR = 0.89, 95% CI: 0.78-1.01; phomogeneity  = 0.01). Alcohol intake is associated with an increased risk of KRAS+ and BRAF-/KRAS- tumors originating via specific molecular pathways including the traditional adenoma-carcinoma pathway but not with BRAF+ tumors originating via the serrated pathway. Therefore, limiting alcohol intake from a young age might reduce colorectal cancer originating via the traditional adenoma-carcinoma pathway

Association of Markers of Inflammation, the Kynurenine Pathway and B Vitamins with Age and Mortality, and a Signature of Inflammaging

Under embargo until: 2022-06-12Background Inflammation is a key feature of aging. We aimed to (i) investigate the association of 34 blood markers potentially involved in inflammatory processes with age and mortality and (ii) develop a signature of “inflammaging.” Methods Thirty-four blood markers relating to inflammation, B vitamin status, and the kynurenine pathway were measured in 976 participants in the Melbourne Collaborative Cohort Study at baseline (median age = 59 years) and follow-up (median age = 70 years). Associations with age and mortality were assessed using linear and Cox regression, respectively. A parsimonious signature of inflammaging was developed and its association with mortality was compared with 2 marker scores calculated across all markers associated with age and mortality, respectively. Results The majority of markers (30/34) were associated with age, with stronger associations observed for neopterin, cystatin C, interleukin (IL)-6, tumor necrosis factor alpha (TNF-α), several markers of the kynurenine pathway and derived indices KTR (kynurenine/tryptophan ratio), PAr index (ratio of 4-pyridoxic acid and the sum of pyridoxal 5′-phosphate and pyridoxal), and HK:XA (3-hydroxykynurenine/xanthurenic acid ratio). Many markers (17/34) showed an association with mortality, in particular IL-6, neopterin, C-reactive protein, quinolinic acid, PAr index, and KTR. The inflammaging signature included 10 markers and was strongly associated with mortality (hazard ratio [HR] per SD = 1.40, 95% CI: 1.24–1.57, p = 2 × 10−8), similar to scores based on all age-associated (HR = 1.38, 95% CI: 1.23–1.55, p = 4 × 10−8) and mortality-associated markers (HR = 1.43, 95% CI: 1.28–1.60, p = 1 × 10−10), respectively. Strong evidence of replication of the inflammaging signature association with mortality was found in the Hordaland Health Study. Conclusion Our study highlights the key role of the kynurenine pathway and vitamin B6 catabolism in aging, along with other well-established inflammation-related markers. A signature of inflammaging based on 10 markers was strongly associated with mortality.acceptedVersio