Particulate matter air pollution and national and county life expectancy loss in the USA: a spatiotemporal analysis

Background Exposure to fine particulate matter pollution (PM2.5) is hazardous to health. Our aim was to directly estimate the health and longevity impacts of current PM2.5 concentrations, and the benefits of reductions from 1999 to 2015, nationally and at county level, for the entire contemporary population of the contiguous United States. Methods and findings We used vital registration and population data with information on sex, age, cause of death and county of residence. We used four Bayesian spatio-temporal models, with different adjustments for other determinants of mortality, to directly estimate mortality and life expectancy loss due to current PM2.5 pollution, and the benefits of reductions since 1999, nationally and by county. The covariates included in the adjusted models were per capita income; percentage of population whose family income is below the poverty threshold, who are of Black or African American race, who have graduated from high-school, who live in urban areas, and who are unemployed; cumulative smoking; and mean temperature and relative humidity. In the main model, which adjusted for these covariates and for unobserved county characteristics through the use of county random intercepts, PM2.5 pollution in excess of the lowest observed concentration (2.8 µg/m3) was responsible for an estimated 15,612 deaths (95% credible interval 13,248-17,945) in females and in 14,757 deaths (12,617-16,919) for males. These deaths would lower national life expectancy by an estimated 0.15 years (0.13-0.17) for women and 0.13 years (0.11-0.15) for men. The life expectancy loss due to PM2.5 was largest around Los Angeles and in some southern states, such as Arkansas, Oklahoma or Alabama. At any PM2.5 concentration, life expectancy loss was, on average, larger in counties with lower income than in wealthier counties. Reductions in PM2.5 since 1999 have lowered mortality in all but 14 counties where PM2.5 increased slightly. The main limitation of our study, similar to other observational studies, is that it is not guaranteed for the observed associations to be causal. We did not have annual county-level data on other important determinants of mortality, such as healthcare access and quality and diet, but these factors were adjusted for with use of county random intercepts. Conclusions According to our estimates, recent reductions in particulate matter pollution in the USA have resulted in public health benefits. Nonetheless, we estimate that current concentrations are associated with mortality impacts and loss of life expectancy, with larger impacts in counties with lower income and higher poverty rate

Pseudoascites: Unusual presentation of omental cyst

An unusual case of omental cyst is described. The child initially presented with a unilocular intraperitoneal fluid collection on CT. After paracentesis, CT showed freely layering peritoneal fluid, with eventual complete resolution of fluid. CT eight months later demonstrated re-appearance of a multiseptated cystic mass. At surgery, an omental cyst was found.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46693/1/247_2005_Article_BF02011393.pd

The resilience of postglacial hunter-gatherers to abrupt climate change

Understanding the resilience of early societies to climate change is an essential part of exploring the environmental sensitivity of human populations. There is significant interest in the role of abrupt climate events as a driver of early Holocene human activity, but there are very few well-dated records directly compared with local climate archives. Here, we present evidence from the internationally important Mesolithic site of Star Carr showing occupation during the early Holocene, which is directly compared with a high-resolution palaeoclimate record from neighbouring lake beds. We show that-once established-there was intensive human activity at the site for several hundred years when the community was subject to multiple, severe, abrupt climate events that impacted air temperatures, the landscape and the ecosystem of the region. However, these results show that occupation and activity at the site persisted regardless of the environmental stresses experienced by this society. The Star Carr population displayed a high level of resilience to climate change, suggesting that postglacial populations were not necessarily held hostage to the flickering switch of climate change. Instead, we show that local, intrinsic changes in the wetland environment were more significant in determining human activity than the large-scale abrupt early Holocene climate events

Employing the Gini coefficient to measure participation inequality in treatment-focused Digital Health Social Networks

Digital Health Social Networks (DHSNs) are common; however, there are few metrics that can be used to identify participation inequality. The objective of this study was to investigate whether the Gini coefficient, an economic measure of statistical dispersion traditionally used to measure income inequality, could be employed to measure DHSN inequality. Quarterly Gini coefficients were derived from four long-standing DHSNs. The combined data set included 625,736 posts that were generated from 15,181 actors over 18,671 days. The range of actors (8–2323), posts (29–28,684), and Gini coefficients (0.15–0.37) varied. Pearson correlations indicated statistically significant associations between number of actors and number of posts (0.527–0.835, p < .001), and Gini coefficients and number of posts (0.342–0.725, p < .001). However, the association between Gini coefficient and number of actors was only statistically significant for the addiction networks (0.619 and 0.276, p < .036). Linear regression models had positive but mixed R2 results (0.333–0.527). In all four regression models, the association between Gini coefficient and posts was statistically significant (t = 3.346–7.381, p < .002). However, unlike the Pearson correlations, the association between Gini coefficient and number of actors was only statistically significant in the two mental health networks (t = −4.305 and −5.934, p < .000). The Gini coefficient is helpful in measuring shifts in DHSN inequality. However, as a standalone metric, the Gini coefficient does not indicate optimal numbers or ratios of actors to posts, or effective network engagement. Further, mixed-methods research investigating quantitative performance metrics is required

Comparative Developmental Expression Profiling of Two C. elegans Isolates

Gene expression is known to change during development and to vary among genetically diverse strains. Previous studies of temporal patterns of gene expression during C. elegans development were incomplete, and little is known about how these patterns change as a function of genetic background. We used microarrays that comprehensively cover known and predicted worm genes to compare the landscape of genetic variation over developmental time between two isolates of C. elegans. We show that most genes vary in expression during development from egg to young adult, many genes vary in expression between the two isolates, and a subset of these genes exhibit isolate-specific changes during some developmental stages. This subset is strongly enriched for genes with roles in innate immunity. We identify several novel motifs that appear to play a role in regulating gene expression during development, and we propose functional annotations for many previously unannotated genes. These results improve our understanding of gene expression and function during worm development and lay the foundation for linkage studies of the genetic basis of developmental variation in gene expression in this important model organism

The pragmatic-semiotic construction of male identities in contemporary advertising of male grooming products

[EN] This article aims to unveil how male identities are constructed in a corpus of male toiletry TV ads through a pragmatic and multimodal analysis of a set of implicit assumptions conveyed about the male participants in the ads. The validity of these assumptions is first empirically tested with a group of 10 male informants and then those implied meanings are bundled into thematic cores for their qualitative and quantitative description. Findings reveal that these ads still rely on stereotypical constructs and traditional discourses of what it takes to be a man. For example, men are invited to consume grooming products but reminded to do it the men's way. Men are also reminded of their sexual power to seduce and attract women with the aid of the product. Likewise, by portraying male ad personae in traditional manly activities while emphasizing their toughness and body strength, or their resourcefulness when faced with challenging situations, the ads portray a rather skewed view of contemporary men, which fails to take into account the myriad roles a modern man can play in contemporary societies.I am really grateful to the reviewers for their insightful comments and also to the editor of the journal.Saz Rubio, MMD. (2019). The pragmatic-semiotic construction of male identities in contemporary advertising of male grooming products. Discourse & Communication. 13(2):192-227. https://doi.org/10.1177/1750481318817621S192227132Alexander, S. M. (2003). Stylish Hard Bodies: Branded Masculinity in Men’s Health Magazine. Sociological Perspectives, 46(4), 535-554. doi:10.1525/sop.2003.46.4.535Attwood, F. (2005). ‘Tits and ass and porn and fighting’. International Journal of Cultural Studies, 8(1), 83-100. doi:10.1177/1367877905050165Rubio, M. D. 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Novel and Conserved Protein Macoilin Is Required for Diverse Neuronal Functions in Caenorhabditis elegans

Neural signals are processed in nervous systems of animals responding to variable environmental stimuli. This study shows that a novel and highly conserved protein, macoilin (MACO-1), plays an essential role in diverse neural functions in Caenorhabditis elegans. maco-1 mutants showed abnormal behaviors, including defective locomotion, thermotaxis, and chemotaxis. Expression of human macoilin in the C. elegans nervous system weakly rescued the abnormal thermotactic phenotype of the maco-1 mutants, suggesting that macoilin is functionally conserved across species. Abnormal thermotaxis may have been caused by impaired locomotion of maco-1 mutants. However, calcium imaging of AFD thermosensory neurons and AIY postsynaptic interneurons of maco-1 mutants suggest that macoilin is required for appropriate responses of AFD and AIY neurons to thermal stimuli. Studies on localization of MACO-1 showed that C. elegans and human macoilins are localized mainly to the rough endoplasmic reticulum. Our results suggest that macoilin is required for various neural events, such as the regulation of neuronal activity

Hypoxia and the Hypoxic Response Pathway Protect against Pore-Forming Toxins in C. elegans

Pore-forming toxins (PFTs) are by far the most abundant bacterial protein toxins and are important for the virulence of many important pathogens. As such, cellular responses to PFTs critically modulate host-pathogen interactions. Although many cellular responses to PFTs have been recorded, little is understood about their relevance to pathological or defensive outcomes. To shed light on this important question, we have turned to the only genetic system for studying PFT-host interactions—Caenorhabditis elegans intoxication by Crystal (Cry) protein PFTs. We mutagenized and screened for C. elegans mutants resistant to a Cry PFT and recovered one mutant. Complementation, sequencing, transgenic rescue, and RNA interference data demonstrate that this mutant eliminates a gene normally involved in repression of the hypoxia (low oxygen response) pathway. We find that up-regulation of the C. elegans hypoxia pathway via the inactivation of three different genes that normally repress the pathway results in animals resistant to Cry PFTs. Conversely, mutation in the central activator of the hypoxia response, HIF-1, suppresses this resistance and can result in animals defective in PFT defenses. These results extend to a PFT that attacks mammals since up-regulation of the hypoxia pathway confers resistance to Vibrio cholerae cytolysin (VCC), whereas down-regulation confers hypersusceptibility. The hypoxia PFT defense pathway acts cell autonomously to protect the cells directly under attack and is different from other hypoxia pathway stress responses. Two of the downstream effectors of this pathway include the nuclear receptor nhr-57 and the unfolded protein response. In addition, the hypoxia pathway itself is induced by PFT, and low oxygen is protective against PFT intoxication. These results demonstrate that hypoxia and induction of the hypoxia response protect cells against PFTs, and that the cellular environment can be modulated via the hypoxia pathway to protect against the most prevalent class of weapons used by pathogenic bacteria

Smad phosphoisoform signals in acute and chronic liver injury: similarities and differences between epithelial and mesenchymal cells

Hepatocellular carcinoma (HCC) usually arises from hepatic fibrosis caused by chronic inflammation. In chronic liver damage, hepatic stellate cells undergo progressive activation to myofibroblasts (MFB), which are important extracellular-matrix-producing mesenchymal cells. Concomitantly, perturbation of transforming growth factor (TGF)-β signaling by pro-inflammatory cytokines in the epithelial cells of the liver (hepatocytes) promotes both fibrogenesis and carcinogenesis (fibro-carcinogenesis). Insights into fibro-carcinogenic effects on chronically damaged hepatocytes have come from recent detailed analyses of the TGF-β signaling process. Smad proteins, which convey signals from TGF-β receptors to the nucleus, have intermediate linker regions between conserved Mad homology (MH) 1 and MH2 domains. TGF-β type I receptor and pro-inflammatory cytokine-activated kinases differentially phosphorylate Smad2 and Smad3 to create phosphoisoforms phosphorylated at the COOH-terminal, linker, or both (L/C) regions. After acute liver injury, TGF-β-mediated pSmad3C signaling terminates hepatocytic proliferation induced by the pro-inflammatory cytokine-mediated mitogenic pSmad3L pathway; TGF-β and pro-inflammatory cytokines synergistically enhance collagen synthesis by activated hepatic stellate cells via pSmad2L/C and pSmad3L/C pathways. During chronic liver disease progression, pre-neoplastic hepatocytes persistently affected by TGF-β together with pro-inflammatory cytokines come to exhibit the same carcinogenic (mitogenic) pSmad3L and fibrogenic pSmad2L/C signaling as do MFB, thereby accelerating liver fibrosis while increasing risk of HCC. This review of Smad phosphoisoform-mediated signals examines similarities and differences between epithelial and mesenchymal cells in acute and chronic liver injuries and considers Smad linker phosphorylation as a potential target for the chemoprevention of fibro-carcinogenesis