Coastal risk mitigation by green infrastructure in Latin America

This paper aims to highlight the prevailing experiences of Latin America and to clarify what ‘green infrastructure’ entails in addition to describing seven case studies from a range of coastal ecosystems (wetlands, coastal dunes, beaches and coral reefs) at scales varying from local to regional. The case studies are categorised according to their degree of naturalness (nature-based, engineered ecosystems, soft engineering, ecologically enhanced hard infrastructure and de-engineering). Generally, the implementation of green infrastructure projects aims to increase resilience, enhance the provision of ecosystem services, recover biodiversity, reduce the negative effects of hard infrastructure and implement corrective measures. The greatest benefits of these projects relate to the creation of multi-functional spaces, which often combine the above advantages with improved opportunities for recreation and/or economic activities. It is hoped that this paper will disseminate the experience in green infrastructure among academics and practitioners and stimulate wider adoption of green infrastructure projects and good practices

TRAIP promotes DNA damage response during genome replication and is mutated in primordial dwarfism.

DNA lesions encountered by replicative polymerases threaten genome stability and cell cycle progression. Here we report the identification of mutations in TRAIP, encoding an E3 RING ubiquitin ligase, in patients with microcephalic primordial dwarfism. We establish that TRAIP relocalizes to sites of DNA damage, where it is required for optimal phosphorylation of H2AX and RPA2 during S-phase in response to ultraviolet (UV) irradiation, as well as fork progression through UV-induced DNA lesions. TRAIP is necessary for efficient cell cycle progression and mutations in TRAIP therefore limit cellular proliferation, providing a potential mechanism for microcephaly and dwarfism phenotypes. Human genetics thus identifies TRAIP as a component of the DNA damage response to replication-blocking DNA lesions.This work was supported by funding from the Medical Research Council and the European Research Council (ERC, 281847) (A.P.J.), the Lister Institute for Preventative Medicine (A.P.J. and G.S.S.), Medical Research Scotland (L.S.B.), German Federal Ministry of Education and Research (BMBF, 01GM1404) and E-RARE network EuroMicro (B.W), Wellcome Trust (M. Hurles), CMMC (P.N.), Cancer Research UK (C17183/A13030) (G.S.S. and M.R.H), Swiss National Science Foundation (P2ZHP3_158709) (O.M.), AIRC (12710) and ERC/EU FP7 (CIG_303806) (S.S.), Cancer Research UK (C6/A11224) and ERC/EU FP7 (HEALTH-F2- 2010-259893) (A.N.B. and S.P.J.).This is the author accepted manuscript. The final version is available from NPG via http://dx.doi.org/10.1038/ng.345

HIV infection and sexual risk among men who have sex with men and women (MSMW): A systematic review and meta-analysis

Objectives: To estimate the number of men who have sex with men and women who are HIV-positive in the United States, and to compare HIV prevalence rates between men who have sex with men and women, men who have sex with men only, and men who have sex with women exclusively. Methods: Following PRISMA guidelines, we conducted a systematic review and meta-analysis of reports referencing HIV prevalence and men who have sex with men and women. We searched PubMed and Ovid PsycINFO for peer-reviewed, U.S.-based articles reporting on HIV prevalence among men who have sex with men and women. We conducted event rate, effect size, moderation and sensitivity analyses. Results: We estimate that 1.0% of U.S. males are bisexually-behaving, and that 121,800 bisexually-behaving men are HIV-positive. Men who have sex with men and women are less than half as likely to be HIV-positive as men who have sex with men only (16.9% vs. 33.3%; OR = 0.41, 95% CI: 0.31, 0.54), but more than five times as likely to be HIV-positive as men who have sex with women exclusively (18.3% vs. 3.5%; OR = 5.71, 95% CI: 3.47, 9.39). They are less likely to engage in unprotected receptive anal intercourse than men who have sex with men only (15.9% vs. 35.0%; OR = 0.36, 95% CI: 0.28, 0.46). Men who have sex with men and women in samples with high racial/ethnic minority proportions had significantly higher HIV prevalence than their counterparts in low racial/ethnic minority samples. Conclusions: This represents the first meta-analysis of HIV prevalence in the U.S. between men who have sex with men and women and men who have sex with men only. Data collection, research, and HIV prevention and care delivery specifically tailored to men who have sex with men and women are necessary to better quantify and ameliorate this population's HIV burden. © 2014 Friedman et al

Septic shock in pregnancy due to pyogenic sacroiliitis: a case report

This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

Reduced postprandial energy expenditure and increased exogenous fat oxidation in young woman after ingestion of test meals with a low protein content

<p>Abstract</p> <p>Background</p> <p>Macronutrient composition of diets can influence energy balance in humans. We tested the hypothesis whether low protein content in single meals may induce lower values of energy expenditure (EE) and fat oxidation (FO) as compared to adequate protein content.</p> <p>Methods</p> <p>Indirect calorimetry was combined with a breath test using naturally ¹³C-enriched corn oil to differentiate between postprandial exogenous and endogenous FO. Young women ingested single meals containing either 3.9% (low protein, LP) or 11.4% (adequate protein, AP) of total energy (~3100 kJ) as protein.</p> <p>Results</p> <p>Postprandial EE was 160 kJ/6 h lower (p < 0.01) after LP meals and diet induced thermogenesis (DIT) increased less (p < 0.001) as compared to AP meals. Total postprandial FO was not significantly different between meals (~17 g/6 h). However, exogenous postprandial FO was significantly (p < 0.01) higher (4.28 ± 1.57 g/6 h) after exposure to LP meals as compared to AP meals (1.87 ± 1.00 g/6 h). Less than 10% of ingested fat (50 g) was oxidized in the postprandial phase. The overall postprandial fat balance was approximately + 33 g.</p> <p>Conclusion</p> <p>Breath tests using naturally ¹³C-labeled corn oil mirror exogenous FO. Low protein meals resulted in reduced postprandial EE and increased exogenous FO as compared to adequate protein meals without differences in total FO.</p

Association between polymorphisms in RMI1, TOP3A, and BLM and risk of cancer, a case-control study

BACKGROUND: Mutations altering BLM function are associated with highly elevated cancer susceptibility (Bloom syndrome). Thus, genetic variants of BLM and proteins that form complexes with BLM, such as TOP3A and RMI1, might affect cancer risk as well. METHODS: In this study we have studied 26 tagged single nucleotide polymorphisms (tagSNPs) in RMI1, TOP3A, and BLM and their associations with cancer risk in acute myeloid leukemia/myelodysplatic syndromes (AML/MDS; N = 152), malignant melanoma (N = 170), and bladder cancer (N = 61). Two population-based control groups were used (N = 119 and N = 156). RESULTS: Based on consistency in effect estimates for the three cancer forms and similar allelic frequencies of the variant alleles in the control groups, two SNPs in TOP3A (rs1563634 and rs12945597) and two SNPs in BLM (rs401549 and rs2532105) were selected for analysis in breast cancer cases (N = 200) and a control group recruited from spouses of cancer patients (N = 131). The rs12945597 in TOP3A and rs2532105 in BLM showed increased risk for breast cancer. We then combined all cases (N = 584) and controls (N = 406) respectively and found significantly increased risk for variant carriers of rs1563634 A/G (AG carriers OR = 1.7 [95%CI 1.1-2.6], AA carriers OR = 1.8 [1.2-2.8]), rs12945597 G/A (GA carriers OR = 1.5 [1.1-1.9], AA carriers OR = 1.6 [1.0-2.5]), and rs2532105 C/T (CT+TT carriers OR = 1.8 [1.4-2.5]). Gene-gene interaction analysis suggested an additive effect of carrying more than one risk allele. For the variants of TOP3A, the risk increment was more pronounced for older carriers. CONCLUSION: These results further support a role of low-penetrance genes involved in BLM-associated homologous recombination for cancer risk

Role of Cell-to-Cell Variability in Activating a Positive Feedback Antiviral Response in Human Dendritic Cells

In the first few hours following Newcastle disease viral infection of human monocyte-derived dendritic cells, the induction of IFNB1 is extremely low and the secreted type I interferon response is below the limits of ELISA assay. However, many interferon-induced genes are activated at this time, for example DDX58 (RIGI), which in response to viral RNA induces IFNB1. We investigated whether the early induction of IFNBI in only a small percentage of infected cells leads to low level IFN secretion that then induces IFN-responsive genes in all cells. We developed an agent-based mathematical model to explore the IFNBI and DDX58 temporal dynamics. Simulations showed that a small number of early responder cells provide a mechanism for efficient and controlled activation of the DDX58-IFNBI positive feedback loop. The model predicted distributions of single cell responses that were confirmed by single cell mRNA measurements. The results suggest that large cell-to-cell variation plays an important role in the early innate immune response, and that the variability is essential for the efficient activation of the IFNB1 based feedback loop

A Spatio-Temporal Analysis of Matrix Protein and Nucleocapsid Trafficking during Vesicular Stomatitis Virus Uncoating

To study VSV entry and the fate of incoming matrix (M) protein during virus uncoating we used recombinant viruses encoding M proteins with a C-terminal tetracysteine tag that could be fluorescently labeled using biarsenical (Lumio) compounds. We found that uncoating occurs early in the endocytic pathway and is inhibited by expression of dominant-negative (DN) Rab5, but is not inhibited by DN-Rab7 or DN-Rab11. Uncoating, as defined by the separation of nucleocapsids from M protein, occurred between 15 and 20 minutes post-entry and did not require microtubules or an intact actin cytoskeleton. Unexpectedly, the bulk of M protein remained associated with endosomal membranes after uncoating and was eventually trafficked to recycling endosomes. Another small, but significant fraction of M distributed to nuclear pore complexes, which was also not dependent on microtubules or polymerized actin. Quantification of fluorescence from high-resolution confocal micrographs indicated that after membrane fusion, M protein diffuses across the endosomal membrane with a concomitant increase in fluorescence from the Lumio label which occurred soon after the release of RNPs into the cytoplasm. These data support a new model for VSV uncoating in which RNPs are released from M which remains bound to the endosomal membrane rather than the dissociation of M protein from RNPs after release of the complex into the cytoplasm following membrane fusion

Effect of dioxins on regulation of tyrosine hydroxylase gene expression by aryl hydrocarbon receptor: a neurotoxicology study

<p>Abstract</p> <p>Background</p> <p>Dioxins and related compounds are suspected of causing neurological disruption. Epidemiological studies indicated that exposure to these compounds caused neurodevelopmental disturbances such as learning disability and attention deficit hyperactivity disorder, which are thought to be closely related to dopaminergic dysfunction. Although the molecular mechanism of their actions has not been fully investigated, a major participant in the process is aryl hydrocarbon receptor (AhR). This study focused on the effect of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) exposure on the regulation of TH, a rate-limiting enzyme of dopamine synthesis, gene expression by AhR.</p> <p>Methods</p> <p>N2a-Rβ cells were established by transfecting murine neuroblastoma Neuro2a with the rat AhR cDNA. TH expression induced by TCDD was assessed by RT-PCR and Western blotting. Participation of AhR in TCDD-induced TH gene expression was confirmed by suppressing AhR expression using the siRNA method. Catecholamines including dopamine were measured by high-performance liquid chromatography. A reporter gene assay was used to identify regulatory motifs in the promoter region of TH gene. Binding of AhR with the regulatory motif was confirmed by an electrophoretic mobility shift assay (EMSA).</p> <p>Results</p> <p>Induction of TH by TCDD through AhR activation was detected at mRNA and protein levels. Induced TH protein was functional and its expression increased dopamine synthesis. The reporter gene assay and EMSA indicated that AhR directly regulated TH gene expression. Regulatory sequence called aryl hydrocarbon receptor responsive element III (AHRE-III) was identified upstream of the TH gene from -285 bp to -167 bp. Under TCDD exposure, an AhR complex was bound to AHRE-III as well as the xenobiotic response element (XRE), though AHRE-III was not identical to XRE, the conventional AhR-binding motif.</p> <p>Conclusion</p> <p>Our results suggest TCDD directly regulate the dopamine system by TH gene transactivation via an AhR-AHRE-III-mediated pathway. The AhR- mediated pathway could have a particular AhR-mediated genomic control pathway transmitting the effects of TCDD action to target cells in the development of dopaminergic disabilities.</p

A healthy mistrust: how worldview relates to attitudes about breast cancer screening in a cross-sectional survey of low-income women

<p>Abstract</p> <p>Background</p> <p>Perceived racial discrimination is one factor which may discourage ethnic minorities from using healthcare. However, existing research only partially explains why some persons do accept health promotion messages and use preventive care, while others do not. This analysis explores 1) the psychosocial characteristics of those, within disadvantaged groups, who identify their previous experiences as racially discriminatory, 2) the extent to which perceived racism is associated with broader perspectives on societal racism and powerlessness, and 3) how these views relate to disadvantaged groups' expectation of mistreatment in healthcare, feelings of mistrust, and motivation to use care.</p> <p>Methods</p> <p>Using survey data from 576 African-American women, we explored the prevalence and predictors of beliefs and experiences related to social disengagement, racial discrimination, desired and actual racial concordance with medical providers, and fear of medical research. We then used both sociodemographic characteristics, and experiences and attitudes about disadvantage, to model respondents' scores on an index of personal motivation to receive breast cancer screening, measuring screening knowledge, rejection of fatalistic explanatory models of cancer, and belief in early detection, and in collaborative models of patient-provider responsibility.</p> <p>Results</p> <p>Age was associated with lower motivation to screen, as were depressive symptoms, anomie, and fear of medical research. Motivation was low among those more comfortable with African-American providers, regardless of current provider race. However, greater awareness of societal racism positively predicted motivation, as did talking to others when experiencing discrimination. Talking was most useful for women with depressive symptoms.</p> <p>Conclusion</p> <p>Supporting the Durkheimian concepts of both anomic and altruistic suicide, both disengagement (depression, anomie, vulnerability to victimization, and discomfort with non-Black physicians) as well as over-acceptance (low awareness of discrimination in society) predict poor health maintenance attitudes in disadvantaged women. Women who recognize their connection to other African-American women, and who talk about negative experiences, appear most motivated to protect their health.</p