713 research outputs found

    Secondhand smoke exposure (SHS) and health-related quality of life (HRQoL) in Chinese never smokers in Hong Kong

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    Objective: The evidence on the effect of secondhand smoke (SHS) on Health Related Quality of Life (HRQoL) is limited. We examined the relation between SHS and HRQoL among Chinese in Hong Kong. Methods: Adult never smokers from a probability sample of three cross-sectional waves (2010, 2012, 2013) of The Hong Kong Family and Health Information Trends Survey who completed the Cantonese-version of Short-Form 12 Health Survey Questionnaire (SF12v2) were included in the data analysis conducted in 2014. Models were used to examine associations of SHS with SF12 domains and summary scores of Physical (PCS12) and Mental Component (MCS12) with subgroups analysis by SHS locations. Results: After adjustments, SHS was associated with lower scores on all SF12 domains except physical functioning. PCS12 (regress coefficient=−0.76, 95% CI −1.34 to −0.17) and MCS12 (regress coefficient=−1.35, 95% CI −2.06 to −0.64) were lower in those with SHS exposure than those non-exposed. Those exposed to SHS in outdoor public places had lower scores on most SF12 domains and PSC12 and MCS12. SHS exposure in one's home and workplace was associated with lower scores on role physical, body pain and role emotional while SHS exposure in friends’ homes was additionally associated with lower social functioning and mental health scores. Lower MCS12 was associated with SHS exposure at all locations except one's home. Conclusions: Our study showed that SHS exposure, particularly in outdoor public places, was associated with decreased HRQoL. It can provide new evidence for stronger smoke-free policies on public places and promoting smoke-free homes

    Human Leukocyte Antigen Class I and II Alleles and Overall Survival in Diffuse Large B-Cell Lymphoma and Follicular Lymphoma

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    Genetic variation in the 6p21 chromosomal region, including human leukocyte antigen (HLA) genes and tumor necrosis factor (TNF), has been linked to both etiology and clinical outcomes of lymphomas. We estimated the effects of HLA class I (A, B, and C), class II DRB1 alleles, and the ancestral haplotype (AH) 8.1 (HLAA*01-B*08-DRB1*03-TNF-308A) on overall survival (OS) among patients with diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) in a population-based study of non-Hodgkin lymphoma. During a median followup of 89 months, 31% (52 of 166) DLBCL and 28% (46 of 165) FL patients died. Using multivariate Cox regression models, we observed statistically significant associations between genetic variants and survival: HLA-Cw*07:01 was associated with poorer OS among DLBCL patients (Hazard ratio [HR] = 1.76, 95% confidence interval [CI] = 1.01–3.05); HLA-A*01:01 was associated with poorer OS (HR = 2.23, 95% CI = 1.24–4.01), and HLA-DRB1*13 (HR = 0.12, 95% CI = 0.02–0.90) and HLA-B Bw4 (HR = 0.36, 95% CI = 0.20–0.63) with better OS among FL patients. These results support a role for HLA in the prognosis of DLBCL and FL and represent a promising class of prognostic factors that warrants further evaluation

    Deep-sea coral evidence for lower Southern Ocean surface nitrate concentrations during the last ice age

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    The Southern Ocean regulates the ocean’s biological sequestration of CO_2 and is widely suspected to underpin much of the ice age decline in atmospheric CO_2 concentration, but the specific changes in the region are debated. Although more complete drawdown of surface nutrients by phytoplankton during the ice ages is supported by some sediment core-based measurements, the use of different proxies in different regions has precluded a unified view of Southern Ocean biogeochemical change. Here, we report measurements of the ^(15)N/^(14)N of fossil-bound organic matter in the stony deep-sea coral Desmophyllum dianthus, a tool for reconstructing surface ocean nutrient conditions. The central robust observation is of higher ^(15)N/^(14)N across the Southern Ocean during the Last Glacial Maximum (LGM), 18–25 thousand years ago. These data suggest a reduced summer surface nitrate concentration in both the Antarctic and Subantarctic Zones during the LGM, with little surface nitrate transport between them. After the ice age, the increase in Antarctic surface nitrate occurred through the deglaciation and continued in the Holocene. The rise in Subantarctic surface nitrate appears to have had both early deglacial and late deglacial/Holocene components, preliminarily attributed to the end of Subantarctic iron fertilization and increasing nitrate input from the surface Antarctic Zone, respectively

    Defining the genetic susceptibility to cervical neoplasia - a genome-wide association study

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    Funding: MAB was funded by a National Health and Medical Research Council (Australia) Senior Principal Research Fellowship. Support was also received from the Australian Cancer Research Foundation. JL holds a Tier 1 Canada Research Chair in Human Genome Epidemiology. The Seattle study was supported by the following grants: NIH, National Cancer Institute grants P01CA042792 and R01CA112512. Cervical Health Study (from which the NSW component was obtained) was funded by NHMRC Grant 387701, and CCNSW core grant. The Montreal study was funded by the Canadian Institutes of Health Research (grant MOP-42532) and sample processing was funded by the Reseau FRQS SIDA-MI. The Swedish Research Council, the Swedish Foundation for Strategic Research, the ALF/LUA research grant in Gothenburg and Umeå, the Lundberg Foundation, the Torsten and Ragnar Soderberg’s Foundation, the Novo Nordisk Foundation, and the European Commission grant HEALTH-F2-2008-201865-GEFOS, BBMRI.se, the Swedish Society of Medicine, the KempeFoundation (JCK-1021), the Medical Faculty of Umeå University, the County Council of Vasterbotten (Spjutspetsanslag VLL:159:33-2007). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscriptPeer reviewedPublisher PDFPublisher PD

    The specificity and patterns of staining in human cells and tissues of p16INK4a antibodies demonstrate variant antigen binding

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    The validity of the identification and classification of human cancer using antibodies to detect biomarker proteins depends upon antibody specificity. Antibodies that bind to the tumour-suppressor protein p16INK4a are widely used for cancer diagnosis and research. In this study we examined the specificity of four commercially available anti-p16INK4a antibodies in four immunological applications. The antibodies H-156 and JC8 detected the same 16 kDa protein in western blot and immunoprecipitation tests, whereas the antibody F-12 did not detect any protein in western blot analysis or capture a protein that could be recognised by the H-156 antibody. In immunocytochemistry tests, the antibodies JC8 and H-156 detected a predominately cytoplasmic localised antigen, whose signal was depleted in p16INK4a siRNA experiments. F-12, in contrast, detected a predominately nuclear located antigen and there was no noticeable reduction in this signal after siRNA knockdown. Furthermore in immunohistochemistry tests, F-12 generated a different pattern of staining compared to the JC8 and E6H4 antibodies. These results demonstrate that three out of four commercially available p16INK4a antibodies are specific to, and indicate a mainly cytoplasmic localisation for, the p16INK4a protein. The F-12 antibody, which has been widely used in previous studies, gave different results to the other antibodies and did not demonstrate specificity to human p16INK4a. This work emphasizes the importance of the validation of commercial antibodies, aside to the previously reported use, for the full verification of immunoreaction specificity

    The role of TG2 in regulating S100A4-mediated mammary tumour cell migration

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    The importance of S100A4, a Ca2+-binding protein, in mediating tumour cell migration, both intracellularly and extracellularly, is well documented. Tissue transglutaminase (TG2) a Ca2+-dependent protein crosslinking enzyme, has also been shown to enhance cell migration. Here by using the well characterised non-metastatic rat mammary R37 cells (transfected with empty vector) and highly metastatic KP1 cells (R37 cells transfected with S100A4), we demonstrate that inhibition of TG2 either by TG2 inhibitors or transfection of cells with TG2 shRNA block S100A4-accelerated cell migration in the KP1cells and in R37 cells treated with exogenous S100A4. Cell migration was also blocked by the treatment with the non-cell permeabilizing TG2 inhibitor R294, in the human breast cancer cell line MDA-MB-231 (Clone 16, which has a high level of TG2 expression). Inhibition was paralleled by a decrease in S100A4 polymer formation. co-immunoprecipitation and Far Western blotting assays and cross-linking assays showed not only the direct interaction between TG2 and S100A4, but also confirmed S100A4 as a substrate for TG2. Using specific functional blocking antibodies, a targeting peptide and a recombinant protein as a competitive treatment, we revealed the involvement of syndecan-4 and a5ß1 integrin co-signalling pathways linked by activation of PKCa in this TG2 and S100A4-mediated cell migration. We propose a mechanism for TG2-regulated S100A4-related mediated cell migration, which is dependent on TG2 crosslinking
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