Alien plant species that invade high elevations are generalists : support for the directional ecological filtering hypothesis

QUESTIONS : The richness of invasive alien plant species tends to decrease with increasing elevation. This pattern may be due to alien plant species requiring traits allowing survival at high elevations (the Abiotic Limitation Hypothesis; ALH). In contrast, the more recent Directional Ecological Filtering Hypothesis (DEFH) suggests that only species with broad environmental tolerances will successfully spread from lowlands (where most introductions occur) to high elevations. Here we test the support for the DEFH and the ALH along an elevational gradient by asking: First, are alien species that occur at higher elevations generalists? Second, do alien species occurring at higher elevations exhibit traits that distinguishes them from lowland alien species? LOCATION : Sani Pass, Maloti-Drakensberg Transfrontier Conservation Area, South Africa.METHODS : A nestedness analysis was conducted to test whether alien species were nested along the elevational gradient, and ANOVA and Chi2 tests (supplemented by resampling procedures) were used to determine if functional traits differed between high and low elevation alien species.RESULTS : Significant nestedness of the alien flora indicates that alien species occurring at high elevations are generalists, being widespread across the elevational gradient. Compared to low elevation aliens, plant height was lower and cold tolerance weaker for high elevation species. CONCLUSION : We found support for the DEFH with the majority of high elevation aliens being widespread generalists. Overall only two of the 11 functional traits differed between high and low elevation alien species, with only one trait supporting the ALH: shorter plant stature found at higher elevations. Therefore, complementing nestedness analyses with trait data provides a more nuanced insight into the determinants of alien richness patterns along elevational gradients and highlights how the two contemporary hypotheses might not be mutually exclusive.http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1654-11032018-03-31hb2017Plant Production and Soil Scienc

Socioeconomic and psychosocial gradients in cardiovascular pathogen burden and immune response: the multi-ethnic study of atherosclerosis.

BACKGROUND: The biologic mechanisms linking socioeconomic position and psychosocial factors to cardiovascular disease (CVD) are not well understood. Immune response to persistent pathogens may be one of these mechanisms. METHODS: We analyzed cross-sectional data from the multi-ethnic study of atherosclerosis (N=999) composed of adults age 45-84. Log-binomial regression and ordinal logistic regression models were used to examine associations of socioeconomic factors and psychosocial factors with pathogen burden and immune response among those infected. Pathogen burden was assessed based on seroprevalence of Helicobacter pylori, cytomegalovirus, herpes simplex virus-1, and Chlamydia pneumoniae and antibody levels were used to characterize high immune response to all four pathogens. RESULTS: Low education was a strong and significant independent predictor of higher pathogen burden after adjustment for covariates (adjusted odds ratio (OR) 95% confidence interval (CI) 1.37, 1.19-1.57). Among subjects seropositive for all four pathogens, low education and a higher level of chronic psychosocial stress showed a positive association with higher antibody response, although associations were no longer significant in models with all covariates included (OR=1.64, 95% CI 0.82-3.31 for lowest vs. highest educational category and OR=1.29, 95% CI 0.96-1.73 for a one level increase in chronic stress). CONCLUSION: Pathogen burden and heightened immune response may represent a biological pathway by which low socioeconomic position and chronic stress are related to increased rates of cardiovascular disease.http://deepblue.lib.umich.edu/bitstream/2027.42/78523/1/AielloDiezRoux2009_BrainBehavioImmunology.pd

A functional genomic and proteomic perspective of sea urchin calcium signaling and egg activation

AbstractThe sea urchin egg has a rich history of contributions to our understanding of fundamental questions of egg activation at fertilization. Within seconds of sperm–egg interaction, calcium is released from the egg endoplasmic reticulum, launching the zygote into the mitotic cell cycle and the developmental program. The sequence of the Strongylocentrotus purpuratus genome offers unique opportunities to apply functional genomic and proteomic approaches to investigate the repertoire and regulation of Ca2+ signaling and homeostasis modules present in the egg and zygote. The sea urchin “calcium toolkit” as predicted by the genome is described. Emphasis is on the Ca2+ signaling modules operating during egg activation, but the Ca2+ signaling repertoire has ramifications for later developmental events and adult physiology as well. Presented here are the mechanisms that control the initial release of Ca2+ at fertilization and additional signaling components predicted by the genome and found to be expressed and operating in eggs at fertilization. The initial release of Ca2+ serves to coordinate egg activation, which is largely a phenomenon of post-translational modifications, especially dynamic protein phosphorylation. Functional proteomics can now be used to identify the phosphoproteome in general and specific kinase targets in particular. This approach is described along with findings to date. Key outstanding questions regarding the activation of the developmental program are framed in the context of what has been learned from the genome and how this knowledge can be applied to functional studies

Small Molecule Inhibitors of Staphylococcus aureus RnpA Alter Cellular mRNA Turnover, Exhibit Antimicrobial Activity, and Attenuate Pathogenesis

Methicillin-resistant Staphylococcus aureus is estimated to cause more U.S. deaths annually than HIV/AIDS. The emergence of hypervirulent and multidrug-resistant strains has further amplified public health concern and accentuated the need for new classes of antibiotics. RNA degradation is a required cellular process that could be exploited for novel antimicrobial drug development. However, such discovery efforts have been hindered because components of the Gram-positive RNA turnover machinery are incompletely defined. In the current study we found that the essential S. aureus protein, RnpA, catalyzes rRNA and mRNA digestion in vitro. Exploiting this activity, high through-put and secondary screening assays identified a small molecule inhibitor of RnpA-mediated in vitro RNA degradation. This agent was shown to limit cellular mRNA degradation and exhibited antimicrobial activity against predominant methicillin-resistant S. aureus (MRSA) lineages circulating throughout the U.S., vancomycin intermediate susceptible S. aureus (VISA), vancomycin resistant S. aureus (VRSA) and other Gram-positive bacterial pathogens with high RnpA amino acid conservation. We also found that this RnpA-inhibitor ameliorates disease in a systemic mouse infection model and has antimicrobial activity against biofilm-associated S. aureus. Taken together, these findings indicate that RnpA, either alone, as a component of the RNase P holoenzyme, and/or as a member of a more elaborate complex, may play a role in S. aureus RNA degradation and provide proof of principle for RNA catabolism-based antimicrobial therapy

Circulating pancreatic polypeptide concentrations predict visceral and liver fat content

CONTEXT AND OBJECTIVE: No current biomarker can reliably predict visceral and liver fat content, both of which are risk factors for cardiovascular disease. Vagal tone has been suggested to influence regional fat deposition. Pancreatic polypeptide (PP) is secreted from the endocrine pancreas under vagal control. We investigated the utility of PP in predicting visceral and liver fat. PATIENTS AND METHODS: Fasting plasma PP concentrations were measured in 104 overweight and obese subjects (46 men and 58 women). In the same subjects, total and regional adipose tissue, including total visceral adipose tissue (VAT) and total subcutaneous adipose tissue (TSAT), were measured using whole-body magnetic resonance imaging. Intrahepatocellular lipid content (IHCL) was quantified by proton magnetic resonance spectroscopy. RESULTS: Fasting plasma PP concentrations positively and significantly correlated with both VAT (r = 0.57, P < .001) and IHCL (r = 0.51, P < .001), but not with TSAT (r = 0.02, P = .88). Fasting PP concentrations independently predicted VAT after controlling for age and sex. Fasting PP concentrations independently predicted IHCL after controlling for age, sex, body mass index (BMI), waist-to-hip ratio, homeostatic model assessment 2-insulin resistance, (HOMA2-IR) and serum concentrations of triglyceride (TG), total cholesterol (TC), and alanine aminotransferase (ALT). Fasting PP concentrations were associated with serum ALT, TG, TC, low- and high-density lipoprotein cholesterol, and blood pressure (P < .05). These associations were mediated by IHCL and/or VAT. Fasting PP and HOMA2-IR were independently significantly associated with hepatic steatosis (P < .01). CONCLUSIONS: Pancreatic polypeptide is a novel predictor of visceral and liver fat content, and thus a potential biomarker for cardiovascular risk stratification and targeted treatment of patients with ectopic fat deposition

Obese patients after gastric bypass surgery have lower brain-hedonic responses to food than after gastric banding

Objectives Roux-en-Y gastric bypass (RYGB) has greater efficacy for weight loss in obese patients than gastric banding (BAND) surgery. We hypothesise that this may result from different effects on food hedonics via physiological changes secondary to distinct gut anatomy manipulations. Design We used functional MRI, eating behaviour and hormonal phenotyping to compare body mass index (BMI)-matched unoperated controls and patients after RYGB and BAND surgery for obesity. Results Obese patients after RYGB had lower brain-hedonic responses to food than patients after BAND surgery. RYGB patients had lower activation than BAND patients in brain reward systems, particularly to high-calorie foods, including the orbitofrontal cortex, amygdala, caudate nucleus, nucleus accumbens and hippocampus. This was associated with lower palatability and appeal of high-calorie foods and healthier eating behaviour, including less fat intake, in RYGB compared with BAND patients and/or BMI-matched unoperated controls. These differences were not explicable by differences in hunger or psychological traits between the surgical groups, but anorexigenic plasma gut hormones (GLP-1 and PYY), plasma bile acids and symptoms of dumping syndrome were increased in RYGB patients. Conclusions The identification of these differences in food hedonic responses as a result of altered gut anatomy/physiology provides a novel explanation for the more favourable long-term weight loss seen after RYGB than after BAND surgery, highlighting the importance of the gut–brain axis in the control of reward-based eating behaviour

Erratum: Author Correction: Identification of genes required for eye development by high-throughput screening of mouse knockouts.

[This corrects the article DOI: 10.1038/s42003-018-0226-0.]

Modulation of enhancer looping and differential gene targeting by Epstein-Barr virus transcription factors directs cellular reprogramming

Epstein-Barr virus (EBV) epigenetically reprogrammes B-lymphocytes to drive immortalization and facilitate viral persistence. Host-cell transcription is perturbed principally through the actions of EBV EBNA 2, 3A, 3B and 3C, with cellular genes deregulated by specific combinations of these EBNAs through unknown mechanisms. Comparing human genome binding by these viral transcription factors, we discovered that 25% of binding sites were shared by EBNA 2 and the EBNA 3s and were located predominantly in enhancers. Moreover, 80% of potential EBNA 3A, 3B or 3C target genes were also targeted by EBNA 2, implicating extensive interplay between EBNA 2 and 3 proteins in cellular reprogramming. Investigating shared enhancer sites neighbouring two new targets (WEE1 and CTBP2) we discovered that EBNA 3 proteins repress transcription by modulating enhancer-promoter loop formation to establish repressive chromatin hubs or prevent assembly of active hubs. Re-ChIP analysis revealed that EBNA 2 and 3 proteins do not bind simultaneously at shared sites but compete for binding thereby modulating enhancer-promoter interactions. At an EBNA 3-only intergenic enhancer site between ADAM28 and ADAMDEC1 EBNA 3C was also able to independently direct epigenetic repression of both genes through enhancer-promoter looping. Significantly, studying shared or unique EBNA 3 binding sites at WEE1, CTBP2, ITGAL (LFA-1 alpha chain), BCL2L11 (Bim) and the ADAMs, we also discovered that different sets of EBNA 3 proteins bind regulatory elements in a gene and cell-type specific manner. Binding profiles correlated with the effects of individual EBNA 3 proteins on the expression of these genes, providing a molecular basis for the targeting of different sets of cellular genes by the EBNA 3s. Our results therefore highlight the influence of the genomic and cellular context in determining the specificity of gene deregulation by EBV and provide a paradigm for host-cell reprogramming through modulation of enhancer-promoter interactions by viral transcription factors

a systematic analysis from the WHO/ILO Joint Estimates of the Work-related Burden of Disease and Injury

Funding Information: Countries provided feedback on the estimates through WHO's consultation of its 194 Member States. We specially acknowledge the ILO for its strategic contributions, as well as its sharing of data and contributions to the production of the estimates. Eurostat produced and shared the transition probabilities for exposure to UVR assigned via proxy of occupation for 27 countries in the European Region. Dr Yuka Ujita (ILO) and then Dr Halim Hamzaoui (ILO) were the ILO focal point for the WHO/ILO Joint Estimates. Marion McFeedy (consultant to the ILO) contributed to initial database development, and Dr Bochen Cao (WHO) shared WHO Global Health Estimates. Dr Claudine Backes (WHO) and Dr Emilie van Deventer (WHO) contributed to the early development of the estimation approach. Jessica CY Ho (WHO), Wahyu R Mahanani (WHO), Dr Bálint Náfrádi (ILO), Dr Annette M Prüss (WHO) and Dr Yuka Ujita provided feedback on an earlier version of the manuscript. Dr Ivan D Ivanov (WHO), Nancy Leppink (ILO), Franklin Muchiri (ILO), Dr Maria P Neira (WHO), Vera L Isaac Paquete-Perdigão (ILO) and Joaquim P Pintado Nunes (ILO) contributed to the WHO/ILO Joint Estimates of the Work-related Burden of Disease and Injury. Dr Maria P Neira and Vera L Isaac Paquete-Perdigão provided overall guidance. Funding Information: This modelling study was prepared with financial support to WHO from: the National Institute for Occupational Safety and Health of the Centers for Disease Control and Prevention of the United States of America (Grant 1E11OH0010676-02, Grant 6NE11OH010461-02-01 and Grant 5NE11OH010461-03-00); the German Federal Ministry of Health (BMG Germany) under the BMG-WHO Collaboration Programme 2020–2023 (WHO specified award ref. 70672); and the Spanish Agency for International Cooperation (AECID) (WHO specified award ref. 71208). The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript. Publisher Copyright: © 2023 International Labour Organization, World Health OrganizationBackground: A World Health Organization (WHO) and International Labour Organization (ILO) systematic review reported sufficient evidence for higher risk of non-melanoma skin cancer (NMSC) amongst people occupationally exposed to solar ultraviolet radiation (UVR). This article presents WHO/ILO Joint Estimates of global, regional, national and subnational occupational exposures to UVR for 195 countries/areas and the global, regional and national attributable burdens of NMSC for 183 countries, by sex and age group, for the years 2000, 2010 and 2019. Methods: We calculated population-attributable fractions (PAFs) from estimates of the population occupationally exposed to UVR and the risk ratio for NMSC from the WHO/ILO systematic review. Occupational exposure to UVR was modelled via proxy of occupation with outdoor work, using 166 million observations from 763 cross-sectional surveys for 96 countries/areas. Attributable NMSC burden was estimated by applying the PAFs to WHO's estimates of the total NMSC burden. Measures of inequality were calculated. Results: Globally in 2019, 1.6 billion workers (95 % uncertainty range [UR] 1.6–1.6) were occupationally exposed to UVR, or 28.4 % (UR 27.9–28.8) of the working-age population. The PAFs were 29.0 % (UR 24.7–35.0) for NMSC deaths and 30.4 % (UR 29.0–31.7) for disability-adjusted life years (DALYs). Attributable NMSC burdens were 18,960 deaths (UR 18,180–19,740) and 0.5 million DALYs (UR 0.4–0.5). Men and older age groups carried larger burden. Over 2000–2019, attributable deaths and DALYs almost doubled. Conclusions: WHO and the ILO estimate that occupational exposure to UVR is common and causes substantial, inequitable and growing attributable burden of NMSC. Governments must protect outdoor workers from hazardous exposure to UVR and attributable NMSC burden and inequalities.publishersversionpublishe