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Background A systematic review of single physical trauma and cancer was carried out, with a meta-analysis where deemed appropriate. Methods A comprehensive search of the literature including databases such as Medline and Embase identified 1529 potentially relevant papers for inclusion. A further 89 potentially relevant studies were identified from bibliographies. After review of titles and abstracts and then full papers, a total of 77 studies were included in the broader review of trauma and cancer, and 31 of these studies considered single physical trauma and cancer. The searches were carried out in June 2016. Results Although physical trauma as a cause of cancer has been an issue of clinical interest for decades, the epidemiological evidence was sparse. Only for traumatic brain injury and brain cancer was there considered a sufficient number of epidemiological studies for a meta-analysis. A random effects meta-relative risk for glioma from cohort studies was 0.96 (95% CI: 0.49 to 1.88) and 1.53 (95% CI: 1.02 to 2.27) for case-control studies. The equivalent results for meningioma were 1.22 (95% CI: 0.85 to 1.76) and 1.88 (95% CI: 0.84 to 1.49) respectively. Conclusions Further work is required to clarify whether physical trauma has a role in cancer development, perhaps by exploiting trauma registries.

(1) Background: There is increasing awareness that the quality of the indoor environment affects our health and well-being. Indoor air quality (IAQ) in particular has an impact on multiple health outcomes, including respiratory and cardiovascular illness, allergic symptoms, cancers, and premature mortality. (2) Methods: We carried out a global systematic literature review on indoor exposure to selected air pollutants associated with adverse health effects, and related household characteristics, seasonal influences and occupancy patterns. We screened records from six bibliographic databases: ABI/INFORM, Environment Abstracts, Pollution Abstracts, PubMed, ProQuest Biological and Health Professional, and Scopus. (3) Results: Information on indoor exposure levels and determinants, emission sources, and associated health effects was extracted from 141 studies from 29 countries. The most-studied pollutants were particulate matter (PM2.5 and PM10); nitrogen dioxide (NO2); volatile organic compounds (VOCs) including benzene, toluene, xylenes and formaldehyde; and polycyclic aromatic hydrocarbons (PAHs) including naphthalene. Identified indoor PM2.5 sources include smoking, cooking, heating, use of incense, candles, and insecticides, while cleaning, housework, presence of pets and movement of people were the main sources of coarse particles. Outdoor air is a major PM2.5 source in rooms with natural ventilation in roadside households. Major sources of NO2 indoors are unvented gas heaters and cookers. Predictors of indoor NO2 are ventilation, season, and outdoor NO2 levels. VOCs are emitted from a wide range of indoor and outdoor sources, including smoking, solvent use, renovations, and household products. Formaldehyde levels are higher in newer houses and in the presence of new furniture, while PAH levels are higher in smoking households. High indoor particulate matter, NO2 and VOC levels were typically associated with respiratory symptoms, particularly asthma symptoms in children. (4) Conclusions: Household characteristics and occupant activities play a large role in indoor exposure, particularly cigarette smoking for PM2.5, gas appliances for NO2, and household products for VOCs and PAHs. Home location near high-traffic-density roads, redecoration, and small house size contribute to high indoor air pollution. In most studies, air exchange rates are negatively associated with indoor air pollution. These findings can inform interventions aiming to improve IAQ in residential properties in a variety of settings.

There are a growing number of studies suggesting a link between night shift work and increased risk of certain types of cancer, including breast cancer. In 2007, the International Agency for Research on Cancer described shift work involving circadian disruption as probably carcinogenic to humans. A systematic review of the epidemiology on shift work and cancer from 2005 to 2015 was carried out. We used standard systematic review methodology to identify, critically appraise and summarize the relevant epidemiological literature. We looked at reviews and meta-analyses from 2005 to 2015 and recent studies published from 2013 to 2015. For breast cancer, the relative risks of working night shifts have been reducing from 1.5 to around 1.2 over the past decade. A recent meta-analysis of prospective cohort studies has suggested that the overall relative risk of breast cancer may not be raised at all. The evidence for a raised risk of cancers other than breast cancer remains somewhat limited. The epidemiolo...

A general lightning data assimilation technique is developed and tested with observations from the World Wide Lightning Location Network (WWLLN). The technique nudges the water vapor mixing ratio toward saturation within 10 km of a lightning observation and is more general than other approaches that require specific model microphysics or flash rates. This approach is applied to both deterministic and ensemble forecasts of the 29 June 2012 derecho event over the eastern United States and a deterministic forecast of the 17 November 2013 convective event over the Midwest using the Weather Research and Forecasting (WRF) Model run at a convection-permitting resolution. Lightning data are assimilated over the first three hours of the forecasts, and the subsequent impact on forecast quality is evaluated. For both events, the deterministic simulations with lightning-based nudging produce more realistic predicted composite reflectivity fields. For the forecasts of the 29 June 2012 event using ensemble data assimilation, forecast improvements from lightning assimilation were more modest than for the deterministic forecasts, suggesting that lightning assimilation may produce greater improvements in convective forecasts where conventional observations (e.g., aircraft, surface, radiosonde, satellite) are less dense or unavailable.

The Savannah River National Laboratory (SRNL) with the assistance of Georgia Regents University, completed a comparison of the U.S. Environmental Protection Agency's (U.S. EPA) environmental dosimetry code CAP88 PC V3.0 with the recently developed V4.0. CAP88 is a set of computer programs and databases used for estimation of dose and risk from radionuclide emissions to air. At the U.S. Department of Energy's Savannah River Site, CAP88 is used by SRNL for determining compliance with U.S. EPA's National Emission Standards for Hazardous Air Pollutants (40 CFR 61, Subpart H) regulations. Using standardized input parameters, individual runs were conducted for each radionuclide within its corresponding database. Some radioactive decay constants, human usage parameters, and dose coefficients changed between the two versions, directly causing a proportional change in the total effective dose. A detailed summary for select radionuclides of concern at the Savannah River Site (60Co, 137Cs, 3H, 129I, 239Pu, and 90Sr) is provided. In general, the total effective doses will decrease for alpha/beta emitters because of reduced inhalation and ingestion rates in V4.0. However, for gamma emitters, such as 60Co and 137Cs, the total effective doses will increase because of changes U.S. EPA made in the external ground shine calculations.

The aim of this study is to carry out a review of the putative mechanism and health and safety evidence between 2005 and 2015 to inform practice using a systematic review methodology. The International Agency for Research on Cancer highlighted two potentially important mechanisms that may be involved in causing breast cancer following (night) shift work; light at night suppressing melatonin production and epigenetic changes in genes controlling circadian rhythms. Other mechanisms that have been investigated include the effect of chronotype, vitamin D status, psychological stress, fatigue, physiological dysfunction and poor health behaviours including smoking, drinking alcohol, poor diet, the timing of eating food and obesity. Interventions that have been investigated include shift design, pharmacological, chronotype selection, strategic napping and adherence to national cancer screening programmes. Suppression of night time production of melatonin and/or obesity remains the most plausible biological mechanisms for an association between shift work and cancer. Employers should facilitate the overall reduction in cancer risk for shift workers by enabling better health behaviours and facilitate access to national cancer screening programmes.

A systematic review was performed to identify any associations between pesticide exposure and the occurrence (both prevalence and incidence) of airways disease (asthma and chronic obstructive pulmonary disease) and wheezing symptoms. PubMed, MEDLINE, Embase, Scopus, CINAHL, Google Scholar and the Cochrane Database of Systematic Reviews were searched between September 2010 and October 2010 for papers with the inclusion criteria of English language, published after 1990, peer-reviewed and nondietary exposure. From a total of 4390 papers identified, 42 were included after initial assessment of content. After evaluating the included studies for quality, those considered to be at high risk of bias were excluded, leaving a total of 23 relevant papers. Results suggest that exposure to pesticides may be associated with prevalent asthma, but methodological issues, such as cross-sectional/case–control design, measurements of exposure and limited adjustment for confounders, limit the strength of the evidence base in this area. The association between pesticide exposure and asthma appears to be more evident and consistent in children than in adults. Exposure to pesticides may be associated with COPD; however, the strength of evidence for an association with COPD is weaker than for asthma. As the exposure metrics within each health end-point varied across studies, no meta-analyses were carried out.

The International Agency for Research on Cancer has classified shift-work involving circadian disruption as probably carcinogenic in humans, with evidence strongest for long-term female night workers and breast cancer. It regarded the epidemiological data as being limited by possible confounding and inconsistent definitions of shift-work. Epidemiological reviews and studies reporting mechanistic data and health and safety policies and practices since 2005 were identified and selected for review according to specific inclusion/exclusion criteria. Individual cohort and case-control studies studies since 2013 were also included. The relative risk of breast cancer for ever versus never working nights is lower in recent epidemiological studies than when the association first came to our attention 15 years ago, probably due to better control for confounding. There are also increasingly well conducted studies that look at a range of measures associated with chronodisruption and which also account for a large number of known and potential confounding factors. Some of these studies provide evidence of an increasing risk with increased duration of working nights. However, the heterogeneity in exposure-response means that a casual determination remains elusive. We conclude that the most likely causal mechanism for a breast cancer risk amongst night shift workers is suppression of melatonin because of exposure to light at night, although the risk may be modified by other circadian factors such as chronotype. However, it is also plausible that there may be direct or indirect causal pathways because of the tendency for shift workers to be obese, and have other lifestyle risk factors for breast cancer. Aside from the possible indirect benefit of formulating shift patterns that maximise workers’ alertness, we believe the most useful intervention is in health promotion, in which employers actively provide healthy diets, opportunities to exercise, and discourage tobacco smoking and alcohol consumption.

Extracellular matrix metalloproteinase inducer (EMMPRIN), also known as Hab18G, CD147, Basigin, M6, and neurothelin, is a membrane glycoprotein expressed on the surface of various cell types and many cancer cells. EMMPRIN stimulates adjacent fibroblasts and tumor cells to produce matrix metalloproteinases and plays an important role in tumor invasion and metastasis, angiogenesis, spermatogensis and fertilization, cell-cell adhesion and communication, and other biological processes (reviewed in Ref. 1 and references therein). It was demonstrated that the EMMPRIN extracellular domain (ECD), which structurally belongs to the IgG superfamily, can form homo-oligomers in a cis dependent manner and the N-terminal domain 1 (residues 22-101) was necessary and sufficient to mediate this interaction. The crystal structure of the ECD of recombinant human EMMPRIN (Hab18G/CD147) expressed in E. coli was reported at 2.8 {angstrom} resolution (Yu et al. 2008). The construct consists of residues 22-205 of the mature protein and has both an N-terminal IgC2 domain (ND1, residues 22-101) and a C-terminal IgC2 domain (ND2, residues 107-205). The two domains are joined by a five amino acid residue linker that constitutes a flexible hinge between the two domains. The crystal form has four copies of the molecule in the asymmetric unit, each of which hasmore » a different inter-domain angle that varies from 121{sup o} to 144{sup o}. The two domains each have a conserved disulfide bridge and both are comprised of two {beta}-sheets formed by strands EBA and GFCC, and DEBA and AGFCC for ND1 and ND2, respectively. Based on the crystal packing in this structure, the authors proposed that lateral packing between the two IgG domains of EMMPRIN ECD represents a potential mechanism for cell adhesion. Here we report the 2.0-{angstrom} crystal structure of the N-terminal domain of EMMPRIN ECD (ND1) expressed in mammalian cells. The overall structure of the domain is very similar to that in the full length ECD. Quite unexpectedly, ND1 forms a dimer mediated through the exchange of its last {beta}-strand (strand G). {beta}-strand swapping, which is a subset of 3D domain swapping, has been found to mediate cell-cell adhesion by cadherins. 3D domain swapping has been proposed to be a mechanism of protein oligomerization, aggregation, evolution of oligomeric proteins from single domains and amyloidogenesis. In domain swapped proteins, the same structural elements are involved in the final 3D structure, and so there is little overall energetic difference between the monomer and the swapped oligomers. However, there is often a high energy barrier for the conversion as it often goes through an unfolded state. It is also possible that strand-swapping occurs during folding of nascent polypeptide chains. Frequently, the exchange hinges contain proline-rich motifs which are often in high strain conformations. Domain swapping appears to be a strategy to resolve such local structural strain. The exchange hinge of ND1 contains a Pro-Glu-Pro tripeptide motif. Both of the proline residues adopt extended trans conformations, when compared with cis in the full-length ECD structure. Proline cis-trans isomerization may be the driving force for this exchange. Strand-exchanged dimerization may be a mechanism for the oligomerization of EMMPRIN ECD and its cis-dependent homophilic interactions in cell-cell adhesion.« less

Biologic activities of IL-16 have been well described (e.g., chemotaxis of CD4+ cells, CD25 upregulation, secretion of IL-1b, IL-4 and TNF-a secretion) but very few signaling events have been described. To gain a better understanding of how the biologic activities of IL-16 are regulated following receptor engagement (CD4) we have analyzed the activation state of numerous STAT proteins in primary human peripheral blood mononuclear cells (PBMCs) and the human monocytic cell line THP-1 following IL-16 stimulation. Of the four STAT proteins tested, only STAT6 was activated (phosphorylated) in a dose-dependant manner by IL-16. The activation of STAT6 was completely abolished when IL-16 was pre-incubated with soluble CD4 (the IL-16 cell surface receptor), demonstrating the need for CD4 engagement in STAT6 activation. These results are the first to demonstrate a link between IL-16 and STAT6 activation.

Objectives In 2011 recommendations for the prescription of lung cancer in coke oven workers were made in the UK. In the 1970s, a powered helmet respirator, the Airstream helmet, was introduced to the UK coking industry with the aim of reducing exposure to polycyclic aromatic hydrocarbons (PAH) aerosols and consequent lung cancer risks for workers on the coke oven tops. This review set out to identify the level of protection afforded by the Airstream helmet, when the helmets could be considered to have provided effective protection and whether the levels of protection have been maintained to the current time. Methods Five approaches were taken to identify review material, including searching the peer-reviewed and grey literature; searching material held in the National Archive; using a Freedom of Information to the Health and Safety Executive; interviews with employees involved in the introduction of the Airstream helmet; and acquisition of company reports. Results The two principal companies involved in coke production in the UK took different approaches to the introduction of the Airstream helmets. Because of this, it can only be considered that effective wearing occurred in the industry as a whole from 1982 onwards. Exposure measurements made by British Steel in the late 1970s suggested that the mean protection factor of the Airstream helmet was ~10 (5th percentile~2.5), regardless of whether exposure was assessed as the inhalable aerosol or other measures more specific to aerosol of PAH. More recent data collected using biological monitoring has identified that average urinary levels of 1-hydroxypyrene (1-HP) generally correspond with the inhalation occupational exposure limit for benzene soluble material. Although on occasions, relatively high air concentrations in-mask and urinary 1-HP concentrations have been identified, underlining the necessity to maintain close supervision of workers wearing respirators. Conclusions Overall, we concluded that the wearing of helmet respirators has effectively controlled long-term average exposure to PAH for most workers on coke ovens since 1982.