467 research outputs found

    Breast cancer recurrence after reoperation for surgical bleeding.

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    BACKGROUND: Bleeding activates platelets that can bind tumour cells, potentially promoting metastatic growth in patients with cancer. This study investigated whether reoperation for postoperative bleeding is associated with breast cancer recurrence. METHODS: Using the Danish Breast Cancer Group database and the Danish National Patient Register (DNPR), a cohort of women with incident stage I-III breast cancer, who underwent breast-conserving surgery or mastectomy during 1996-2008 was identified. Information on reoperation for bleeding within 14 days of the primary surgery was retrieved from the DNPR. Follow-up began 14 days after primary surgery and continued until breast cancer recurrence, death, emigration, 10 years of follow-up, or 1 January 2013. Incidence rates of breast cancer recurrence were calculated and Cox regression models were used to quantify the association between reoperation and recurrence, adjusting for potential confounders. Crude and adjusted hazard ratios according to site of recurrence were calculated. RESULTS: Among 30 711 patients (205 926 person-years of follow-up), 767 patients had at least one reoperation within 14 days of primary surgery, and 4769 patients developed breast cancer recurrence. Median follow-up was 7·0 years. The incidence of recurrence was 24·0 (95 per cent c.i. 20·2 to 28·6) per 1000 person-years for reoperated patients and 23·1 (22·5 to 23·8) per 1000 person-years for non-reoperated patients. The overall adjusted hazard ratio was 1·06 (95 per cent c.i. 0·89 to 1·26). The estimates did not vary by site of breast cancer recurrence. CONCLUSION: In this large cohort study, there was no evidence of an association between reoperation for bleeding and breast cancer recurrence

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

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    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

    Effect of Biodiversity Changes in Disease Risk: Exploring Disease Emergence in a Plant-Virus System

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    The effect of biodiversity on the ability of parasites to infect their host and cause disease (i.e. disease risk) is a major question in pathology, which is central to understand the emergence of infectious diseases, and to develop strategies for their management. Two hypotheses, which can be considered as extremes of a continuum, relate biodiversity to disease risk: One states that biodiversity is positively correlated with disease risk (Amplification Effect), and the second predicts a negative correlation between biodiversity and disease risk (Dilution Effect). Which of them applies better to different host-parasite systems is still a source of debate, due to limited experimental or empirical data. This is especially the case for viral diseases of plants. To address this subject, we have monitored for three years the prevalence of several viruses, and virus-associated symptoms, in populations of wild pepper (chiltepin) under different levels of human management. For each population, we also measured the habitat species diversity, host plant genetic diversity and host plant density. Results indicate that disease and infection risk increased with the level of human management, which was associated with decreased species diversity and host genetic diversity, and with increased host plant density. Importantly, species diversity of the habitat was the primary predictor of disease risk for wild chiltepin populations. This changed in managed populations where host genetic diversity was the primary predictor. Host density was generally a poorer predictor of disease and infection risk. These results support the dilution effect hypothesis, and underline the relevance of different ecological factors in determining disease/infection risk in host plant populations under different levels of anthropic influence. These results are relevant for managing plant diseases and for establishing conservation policies for endangered plant species

    Ocean temperature and salinity components of the Madden-Julian oscillation observed by Argo floats

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    New diagnostics of the Madden-Julian Oscillation (MJO) cycle in ocean temperature and, for the first time, salinity are presented. The MJO composites are based on 4 years of gridded Argo float data from 2003 to 2006, and extend from the surface to 1,400 m depth in the tropical Indian and Pacific Oceans. The MJO surface salinity anomalies are consistent with precipitation minus evaporation fluxes in the Indian Ocean, and with anomalous zonal advection in the Pacific. The Argo sea surface temperature and thermocline depth anomalies are consistent with previous studies using other data sets. The near-surface density changes due to salinity are comparable to, and partially offset, those due to temperature, emphasising the importance of including salinity as well as temperature changes in mixed-layer modelling of tropical intraseasonal processes. The MJO-forced equatorial Kelvin wave that propagates along the thermocline in the Pacific extends down into the deep ocean, to at least 1,400 m. Coherent, statistically significant, MJO temperature and salinity anomalies are also present in the deep Indian Ocean

    Study of the Decays B0 --> D(*)+D(*)-

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    The decays B0 --> D*+D*-, B0 --> D*+D- and B0 --> D+D- are studied in 9.7 million Y(4S) --> BBbar decays accumulated with the CLEO detector. We determine Br(B0 --> D*+D*-) = (9.9+4.2-3.3+-1.2)e-4 and limit Br(B0 --> D*+D-) < 6.3e-4 and Br(B0 --> D+D-) < 9.4e-4 at 90% confidence level (CL). We also perform the first angular analysis of the B0 --> D*+D*- decay and determine that the CP-even fraction of the final state is greater than 0.11 at 90% CL. Future measurements of the time dependence of these decays may be useful for the investigation of CP violation in neutral B meson decays.Comment: 21 pages, 5 figures, submitted to Phys. Rev.

    Measurement of B(/\c->pKpi)

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    The /\c->pKpi yield has been measured in a sample of two-jet continuum events containing a both an anticharm tag (Dbar) as well as an antiproton (e+e- -> Dbar pbar X), with the antiproton in the hemisphere opposite the Dbar. Under the hypothesis that such selection criteria tag e+e- -> Dbar pbar (/\c) X events, the /\c->pkpi branching fraction can be determined by measuring the pkpi yield in the same hemisphere as the antiprotons in our Dbar pbar X sample. Combining our results from three independent types of anticharm tags, we obtain B(/\c->pKpi)=(5.0+/-0.5+/-1.2)

    Observation of the Ωc0\Omega_{c}^{0} Charmed Baryon at CLEO

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    The CLEO experiment at the CESR collider has used 13.7 fb1^{-1} of data to search for the production of the Ωc0\Omega_c^0 (css-ground state) in e+ee^{+}e^{-} collisions at s10.6\sqrt{s} \simeq 10.6 {\rm GeV}. The modes used to study the Ωc0\Omega_c^0 are Ωπ+\Omega^- \pi^+, Ωπ+π0\Omega^- \pi^+ \pi^0, ΞKpi+π+\Xi^- K^- pi^+ \pi^+, Ξ0Kpi+\Xi^0 K^- pi^+, and Ωπ+ππ+\Omega^- \pi^+ \pi^- \pi^+. We observe a signal of 40.4±\pm9.0(stat) events at a mass of 2694.6±\pm2.6(stat)±\pm1.9(syst) {\rm MeV/c2c^2}, for all modes combined.Comment: 10 pages postscript, also available through http://w4.lns.cornell.edu/public/CLN

    Measurement of the Relative Branching Fraction of Υ(4S)\Upsilon(4S) to Charged and Neutral B-Meson Pairs

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    We analyze 9.7 x 10^6 B\bar{B}$ pairs recorded with the CLEO detector to determine the production ratio of charged to neutral B-meson pairs produced at the Y(4S) resonance. We measure the rates for B^0 -> J/psi K^{(*)0} and B^+ -> J/psi K^{(*)+} decays and use the world-average B-meson lifetime ratio to extract the relative widths f+-/f00 = Gamma(Y(4S) -> B+B-)/Gamma(Y(4S) -> B0\bar{B0}) = = 1.04 +/- 0.07(stat) +/- 0.04(syst). With the assumption that f+- + f00 = 1, we obtain f00 = 0.49 +/- 0.02(stat) +/- 0.01(syst) and f+- = 0.51 +/- 0.02(stat) +/- 0.01(syst). This production ratio and its uncertainty apply to all exclusive B-meson branching fractions measured at the Y(4S) resonance.Comment: 11 pages postscript, also available through http://w4.lns.cornell.edu/public/CLN

    Measurements of B --> D_s^{(*)+} D^{*(*)} Branching Fractions

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    This article describes improved measurements by CLEO of the B0Ds+DB^0 \to D_s^+ D^{*-} and B0Ds+DB^0 \to D_s^{*+} D^{*-} branching fractions, and first evidence for the decay B+Ds()+Dˉ0B^+ \to D_s^{(*)+} \bar{D}^{**0}, where Dˉ0\bar{D}^{**0} represents the sum of the Dˉ1(2420)0\bar{D}_1(2420)^0, Dˉ2(2460)0\bar{D}_2^*(2460)^0, and Dˉ1(j=1/2)0\bar{D}_1(j=1/2)^0 L=1 charm meson states. Also reported is the first measurement of the Ds+D_s^{*+} polarization in the decay B0Ds+DB^0 \to D_s^{*+} D^{*-}. A partial reconstruction technique, employing only the fully reconstructed Ds+D_s^+ and slow pion πs\pi_s^- from the DDˉ0πsD^{*-} \to \bar{D}^0 \pi^-_s decay, enhances sensitivity. The observed branching fractions are B(B0Ds+D)=(1.10±0.18±0.10±0.28){\mathcal B} (B^0 \to D_s^+ D^{*-}) = (1.10 \pm 0.18 \pm 0.10 \pm 0.28)%, B(B0Ds+D)=(1.82±0.37±0.24±0.46){\mathcal B} (B^0 \to D_s^{*+} D^{*-}) = (1.82 \pm 0.37 \pm 0.24 \pm 0.46)%, and B(B+Ds()+Dˉ0)=(2.73±0.78±0.48±0.68){\mathcal B} (B^+ \to D_s^{(*)+} \bar{D}^{**0}) = (2.73 \pm 0.78 \pm 0.48 \pm 0.68)%, where the first error is statistical, the second systematic, and the third is due to the uncertainty in the Ds+ϕπ+D_s^+ \to \phi \pi^+ branching fraction. The measured Ds+D_s^{*+} longitudinal polarization, ΓL/Γ=(50.6±13.9±3.6)\Gamma_L/\Gamma = (50.6 \pm 13.9 \pm 3.6)%, is consistent with the factorization prediction of 54%.Comment: 26 pages (LaTeX), 15 figures. To be submitted to PR
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