Stony Coral Tissue Loss Disease and Other Diseases Affect Adults and Recruits of Major Reef Builders at Different Spatial Scales in the Dominican Republic

Monitoring programs can help understand coral disease dynamics. Here, we present results from a national program in the Dominican Republic (DR) aimed at evaluating coral diseases 3 times a year following a nested spatial design. Prevalence of coral diseases in DR varied from sites to regions, suggesting that disease dynamics can be driven by local processes and/or across larger spatial scales. Three diseases were common: Dark Spot (DSD), Yellow Band (YBD) and Stony Coral Tissue Loss Disease (SCTLD). DSD and YBD were more prevalent across the western coast (north and south), whereas SCTLD was restricted for the study period to the northern coast. SCTLD has become endemic in the northwestern coast, epizootic in the northeastern, and absent in other sites across DR. SCTLD prevalence in the northwest was below 10% across sites, whereas in the northeast it varied from 2.13±3.69% (mean± sd) to 38.7±13.55% in Galeras and from 1.9±0.99% to 38.5±19.8% in Samaná. Over 10 coral species were affected by SCTLD in DR, with Pseudodiploria spp, Dendrogyra cylindrus, Eusmilia fastigiata, Siderastrea siderea, Montastraea cavernosa and Meandrina spp, being the most susceptible. We observed SCTLD affecting recruits and juvenile corals with 5% prevalence on average. Furthermore, we observed Oreaster reticulatus climbing on 1% healthy and 27% SCTLD P. strigosa colonies in Samaná. We conclude that SCTLD is a serious problem in DR, producing rapid loss of coral cover of major reef builders that are locally used for propagation efforts. This monitoring plan will provide future insights to design more effective disease responses

HTLV-1 infection in solid organ transplant donors and recipients in Spain

Background: HTLV-1 infection is a neglected disease, despite infecting 10–15 million people worldwide and severe illnesses develop in 10% of carriers lifelong. Acknowledging a greater risk for developing HTLV-1 associated illnesses due to immunosuppression, screening is being widely considered in the transplantation setting. Herein, we report the experience with universal HTLV testing of donors and recipients of solid organ transplants in a survey conducted in Spain. Methods: All hospitals belonging to the Spanish HTLV network were invited to participate in the study. Briefly, HTLV antibody screening was performed retrospectively in all specimens collected from solid organ donors and recipients attended since the year 2008. Results: A total of 5751 individuals were tested for HTLV antibodies at 8 sites. Donors represented 2312 (42.2%), of whom 17 (0.3%) were living kidney donors. The remaining 3439 (59.8%) were recipients. Spaniards represented nearly 80%. Overall, 9 individuals (0.16%) were initially reactive for HTLV antibodies. Six were donors and 3 were recipients. Using confirmatory tests, HTLV-1 could be confirmed in only two donors, one Spaniard and another from Colombia. Both kidneys of the Spaniard were inadvertently transplanted. Subacute myelopathy developed within 1 year in one recipient. The second recipient seroconverted for HTLV-1 but the kidney had to be removed soon due to rejection. Immunosuppression was stopped and 3 years later the patient remains in dialysis but otherwise asymptomatic. Conclusion: The rate of HTLV-1 is low but not negligible in donors/recipients of solid organ transplants in Spain. Universal HTLV screening should be recommended in all donor and recipients of solid organ transplantation in Spain. Evidence is overwhelming for very high virus transmission and increased risk along with the rapid development of subacute myelopath

Rapid subacute myelopathy following kidney transplantation from HTLV-1 donors: role of immunosuppresors and failure of antiretrovirals

Two kidney transplant recipients from a single donor became infected with HTLV-1 (human T-lymphotropic virus type 1) in Spain. One developed myelopathy 8 months following surgery despite early prescription of antiretroviral therapy. The allograft was removed from the second recipient at month 8 due to rejection and immunosuppressors discontinued. To date, 3 years later, this patient remains infected but asymptomatic. HTLV-1 infection was recognized retrospectively in the donor, a native Spaniard who had sex partners from endemic regions. Our findings call for a reappraisal of screening policies on donor-recipient organ transplantation. Based on the high risk of disease development and the large flux of persons from HTLV-1 endemic regions, pre-transplant HTLV-1 testing should be mandatory in Spain

Gas phase Elemental abundances in Molecular cloudS (GEMS) : III. Unlocking the CS chemistry: the CS plus O reaction

Context. Carbon monosulphide (CS) is among the most abundant gas-phase S-bearing molecules in cold dark molecular clouds. It is easily observable with several transitions in the millimeter wavelength range, and has been widely used as a tracer of the gas density in the interstellar medium in our Galaxy and external galaxies. However, chemical models fail to account for the observed CS abundances when assuming the cosmic value for the elemental abundance of sulfur. Aims. The CS+O -> CO + S reaction has been proposed as a relevant CS destruction mechanism at low temperatures, and could explain the discrepancy between models and observations. Its reaction rate has been experimentally measured at temperatures of 150-400 K, but the extrapolation to lower temperatures is doubtful. Our goal is to calculate the CS+O reaction rate at temperatures Methods. We performed ab initio calculations to obtain the three lowest potential energy surfaces (PES) of the CS+O system. These PESs are used to study the reaction dynamics, using several methods (classical, quantum, and semiclassical) to eventually calculate the CS + O thermal reaction rates. In order to check the accuracy of our calculations, we compare the results of our theoretical calculations for T similar to 150-400 K with those obtained in the laboratory. Results. Our detailed theoretical study on the CS+O reaction, which is in agreement with the experimental data obtained at 150-400 K, demonstrates the reliability of our approach. After a careful analysis at lower temperatures, we find that the rate constant at 10 K is negligible, below 10(-15) cm(3) s(-1), which is consistent with the extrapolation of experimental data using the Arrhenius expression. Conclusions. We use the updated chemical network to model the sulfur chemistry in Taurus Molecular Cloud 1 (TMC 1) based on molecular abundances determined from Gas phase Elemental abundances in Molecular CloudS (GEMS) project observations. In our model, we take into account the expected decrease of the cosmic ray ionization rate, zeta(H2), along the cloud. The abundance of CS is still overestimated when assuming the cosmic value for the sulfur abundance.Peer reviewe

Identifying susceptibility genes for primary ovarian insufficiency on the high-risk genetic background of a fragile X premutation

This is the final version. Available on open access from Elsevier via the DOI in this recordObjective: To identify modifying genes that explains the risk of fragile X-associated primary ovarian insufficiency (FXPOI). Design: Gene-based, case/control association study, followed by a functional screen of highly ranked genes using a Drosophila model. Setting: Participants were recruited from academic and clinical settings. Patient(s): Women with a premutation (PM) who experienced FXPOI at the age of 35 years or younger (n = 63) and women with a PM who experienced menopause at the age of 50 years or older (n = 51) provided clinical information and a deoxyribonucleic acid sample for whole genome sequencing. The functional screen was on the basis of Drosophila TRiP lines. Intervention(s): Clinical information and a DNA sample were collected for whole genome sequencing. Main Outcome Measures: A polygenic risk score derived from common variants associated with natural age at menopause was calculated and associated with the risk of FXPOI. Genes associated with the risk of FXPOI were identified on the basis of the P-value from gene-based association test and an altered level of fecundity when knocked down in the Drosophila PM model. Results: The polygenic risk score on the basis of common variants associated with natural age at menopause explained approximately 8% of the variance in the risk of FXPOI. Further, SUMO1 and KRR1 were identified as possible modifying genes associated with the risk of FXPOI on the basis of an untargeted gene analysis of rare variants. Conclusions: In addition to the large genetic effect of a PM on ovarian function, the additive effects of common variants associated with natural age at menopause and the effect of rare modifying variants appear to play a role in FXPOI risk.Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)Fundacion Merck Salu

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Schadevergoeding bij overlijden: een stoel die een soort tafeltje is

In het aansprakelijkheidsrecht heeft een benadeelde in beginsel recht op volledige vergoeding van zijn schade. De gevolgen van de schadetoebrengende gebeurtenis dienen zoveel als mogelijk te worden weggenomen of te worden gecompenseerd. Daarbij wordt gekeken naar de situatie waarin de benadeelde zou hebben verkeerd indien de schadetoebrengende gebeurtenis niet zou hebben plaatsgevonden. Dat is bij overlijden per definitie problematisch. Er is iemand weggevallen, wat vele gevolgen heeft. De schade als gevolg van het overlijden komt maar beperkt voor vergoeding in aanmerking. In artikel 6:108 BW is een drietal beperkingen te vinden. Het gaat hier om beperkingen ten aanzien van de aard van de schade, de kring van gerechtigden en de omvang van de schade. Daarbij hinkt het recht op schadevergoeding bij overlijden op twee gedachten. Aan de ene kant is er het aansprakelijkheidsrecht, maar de geleden schade komt niet volledig voor vergoeding in aanmerking. Aan de andere kant is er het recht op alimentatie uit het familierecht, maar dat wordt bij overlijden niet consequent toegepast. De motieven voor de beperkingen van het recht op schadevergoeding zijn achterhaald en niet (langer) overtuigend. Het recht is niet bij de tijd, het sluit niet aan bij de maatschappelijke ontwikkelingen. De beperkingen die het recht op schadevergoeding bij overlijden in de huidige samenleving met zich meebrengt zorgen voor complexe methoden om de nabestaanden tegemoet te komen en oogsten daardoor veel kritiek. In deze bijdrage wordt die kritiek besproken. De bijdrage wordt afgesloten met enkele denkrichtingen voor nader onderzoek

Search for the production of dark matter in association with top-quark pairs in the single-lepton final state in proton-proton collisions at √s=8 TeV

Peer reviewe

Search for massive resonances in dijet systems containing jets tagged as W or Z boson decays in pp collisions at √s=8 TeV

Peer reviewe