Chemical and environmental vector control as a contribution to the elimination of visceral leishmaniasis on the Indian subcontinent: cluster randomized controlled trials in Bangladesh, India and Nepal

<p>Abstract</p> <p>Background</p> <p>Bangladesh, India and Nepal are working towards the elimination of visceral leishmaniasis (VL) by 2015. In 2005 the World Health Organization/Training in Tropical Diseases launched an implementation research programme to support integrated vector management for the elimination of VL from Bangladesh, India and Nepal. The programme is conducted in different phases, from proof-of-concept to scaling up intervention. This study was designed in order to evaluate the efficacy of the three different interventions for VL vector management: indoor residual spraying (IRS); long-lasting insecticide treated nets (LLIN); and environmental modification (EVM) through plastering of walls with lime or mud.</p> <p>Methods</p> <p>Using a cluster randomized controlled trial we compared three vector control interventions with a control arm in 96 clusters (hamlets or neighbourhoods) in each of the 4 study sites: Bangladesh (one), India (one) and Nepal (two). In each site four villages with high reported VL incidences were included. In each village six clusters and in each cluster five households were randomly selected for sand fly collection on two consecutive nights. Control and intervention clusters were matched with average pre-intervention vector densities.</p> <p>In each site six clusters were randomly assigned to each of the following interventions: indoor residual spraying (IRS); long-lasting insecticide treated nets (LLIN); environmental management (EVM) or control. All the houses (50-100) in each intervention cluster underwent the intervention measures. A reduction of intra-domestic sand fly densities measured in the study households by overnight US Centres for Disease Prevention and Control light trap captures (that is the number of sand flies per trap per night) was the main outcome measure.</p> <p>Results</p> <p>IRS, and to a lesser extent EVM and LLINs, significantly reduced sand fly densities for at least 5 months in the study households irrespective of type of walls or whether or not people shared their house with cattle. IRS was effective in all sites but LLINs were only effective in Bangladesh and India. Mud plastering did not reduce sand fly density (Bangladesh study); lime plastering in India and one Nepali site, resulted in a significant reduction of sand fly density but not in the second Nepali site.</p> <p>Conclusion</p> <p>Sand fly control can contribute to the regional VL elimination programme; IRS should be strengthened in India and Nepal but in Bangladesh, where vector control has largely been abandoned during the last decades, the insecticide treatment of existing bed nets (coverage above 90% in VL endemic districts) could bring about an immediate reduction of vector populations; operational research to inform policy makers about the efficacious options for VL vector control and programme performance should be strengthened in the three countries.</p

Phylogenetic analysis of Croatian orf viruses isolated from sheep and goats

<p>Abstract</p> <p>Background</p> <p>The <it>Orf virus </it>(ORFV) is the prototype of the parapoxvirus genus and it primarily causes contagious ecthyma in goats, sheep, and other ruminants worldwide. In this paper, we described the sequence and phylogenetic analysis of the B2L gene of ORFV from two natural outbreaks: i) in autochthonous Croatian Cres-breed sheep and ii) on small family goat farm.</p> <p>Results</p> <p>Sequence and phylogenetic analyses of the ORFV B2L gene showed that the Cro-Cres-12446/09 and Cro-Goat-11727/10 were not clustered together. Cro-Cres-12446/09 shared the highest similarity with ORFV NZ2 from New Zealand, and Ena from Japan; Cro-Goat-11727/10 was closest to the HuB from China and Taiping and Hoping from Taiwan.</p> <p>Conclusion</p> <p>Distinct ORFV strains are circulating in Croatia. Although ORFV infections are found ubiquitously wherever sheep and goats are farmed in Croatia, this is the first information on genetic relatedness of any Croatian ORFV with other isolates around the world.</p

Characterization of Mycosphaerellaceae species associated with citrus greasy spot in Panama and Spain

[EN] Greasy spot of citrus, caused by Zasmidium citri-griseum (= Mycosphaerella citri), is widely distributed in the Caribbean Basin, inducing leaf spots, premature defoliation, and yield loss. Greasy spot-like symptoms were frequently observed in humid citrus-growing regions in Panama as well as in semi-arid areas in Spain, but disease aetiology was unknown. Citrus-growing areas in Panama and Spain were surveyed and isolates of Mycosphaerellaceae were obtained from citrus greasy spot lesions. A selection of isolates from Panama (n = 22) and Spain (n = 16) was assembled based on their geographical origin, citrus species, and affected tissue. The isolates were characterized based on multi-locus DNA (ITS and EF-1 alpha) sequence analyses, morphology, growth at different temperatures, and independent pathogenicity tests on the citrus species most affected in each country. Reference isolates and sequences were also included in the analysis. Isolates from Panama were identified as Z. citri-griseum complex, and others from Spain attributed to Amycosphaerella africana. Isolates of the Z. citri-griseum complex had a significantly higher optimal growth temperature (26.8 degrees C) than those of A. africana (19.3 degrees C), which corresponded well with their actual biogeographical range. The isolates of the Z. citri-griseum complex from Panama induced typical greasy spot symptoms in 'Valencia' sweet orange plants and the inoculated fungi were reisolated. No symptoms were observed in plants of the 'Ortanique' tangor inoculated with A. africana. These results demonstrate the presence of citrus greasy spot, caused by Z. citri-griseum complex, in Panama whereas A. africana was associated with greasy spot-like symptoms in Spain.Research was partially funded by 'Programa de Formacion de los INIA Iberoamerica' and INIA RTA2010-00105-00-00-FEDER to Vidal Aguilera Cogley.. We thank J. Martinez-Minaya (UV) for assistance with INLAAguilera-Cogley, VA.; Berbegal Martinez, M.; Català, S.; Collison Brentu, F.; Armengol Fortí, J.; Vicent Civera, A. (2017). Characterization of Mycosphaerellaceae species associated with citrus greasy spot in Panama and Spain. PLoS ONE. 12(12):1-19. https://doi.org/10.1371/journal.pone.0189585S1191212Crous, P. W., Summerell, B. A., Carnegie, A. J., Wingfield, M. J., Hunter, G. C., Burgess, T. I., … Groenewald, J. Z. (2009). Unravelling Mycosphaerella: do you believe in genera? Persoonia - Molecular Phylogeny and Evolution of Fungi, 23(1), 99-118. doi:10.3767/003158509x479487Mondal, S. N., & Timmer, L. W. (2006). Greasy Spot, a Serious Endemic Problem for Citrus Production in the Caribbean Basin. Plant Disease, 90(5), 532-538. doi:10.1094/pd-90-0532Whiteside, J. O. (1970). Etiology and Epidemiology of Citrus Greasy Spot. Phytopathology, 60(10), 1409. doi:10.1094/phyto-60-1409Huang, F., Groenewald, J. Z., Zhu, L., Crous, P. W., & Li, H. (2015). Cercosporoid diseases of Citrus. Mycologia, 107(6), 1151-1171. doi:10.3852/15-059Wellings, C. R. (1981). Pathogenicity of fungi associated with citrus greasy spot in New South Wales. Transactions of the British Mycological Society, 76(3), 495-499. doi:10.1016/s0007-1536(81)80080-0Marco, G. M. (1986). A Disease Similar to Greasy Spot but of Unknown Etiology on Citrus Leaves in Argentina. Plant Disease, 70(11), 1074a. doi:10.1094/pd-70-1074aVidal Aguilera-Cogley, & Antonio Vicent. (2015). FUNGAL DISEASES OF CITRUS IN PANAMA. Acta Horticulturae, (1065), 947-952. doi:10.17660/actahortic.2015.1065.118Honger J. Aetiology and importance of foliage diseases affecting citrus in the nursery at the Agricultural Research Station (ARS). PhD Thesis. Accra: University of Ghana; 2004.Vicent A, Álvarez A, León M, García-Jiménez J. Mycosphaerella sp. asociada a manchas foliares de cítricos en España. In: Proceedings of the 13th Congress of the Spanish Phytopathological Society. 2006; Murcia; Spain.Abdelfattah, A., Cacciola, S. O., Mosca, S., Zappia, R., & Schena, L. (2016). Analysis of the Fungal Diversity in Citrus Leaves with Greasy Spot Disease Symptoms. Microbial Ecology, 73(3), 739-749. doi:10.1007/s00248-016-0874-xQuaedvlieg, W., Binder, M., Groenewald, J. Z., Summerell, B. A., Carnegie, A. J., Burgess, T. I., & Crous, P. W. (2014). Introducing the Consolidated Species Concept to resolve species in the Teratosphaeriaceae. Persoonia - Molecular Phylogeny and Evolution of Fungi, 33(1), 1-40. doi:10.3767/003158514x681981Edgar, R. C. (2004). MUSCLE: multiple sequence alignment with high accuracy and high throughput. Nucleic Acids Research, 32(5), 1792-1797. doi:10.1093/nar/gkh340Darriba, D., Taboada, G. L., Doallo, R., & Posada, D. (2012). jModelTest 2: more models, new heuristics and parallel computing. Nature Methods, 9(8), 772-772. doi:10.1038/nmeth.2109Ronquist, F., Teslenko, M., van der Mark, P., Ayres, D. L., Darling, A., Höhna, S., … Huelsenbeck, J. P. (2012). MrBayes 3.2: Efficient Bayesian Phylogenetic Inference and Model Choice Across a Large Model Space. Systematic Biology, 61(3), 539-542. doi:10.1093/sysbio/sys029Rambaut A. FigTree v1. 4.0, a graphical viewer of phylogenetic trees. Edinburgh, Scotland: University of Edinburgh; 2016.Spiegelhalter, D. J., Best, N. G., Carlin, B. P., & van der Linde, A. (2002). Bayesian measures of model complexity and fit. Journal of the Royal Statistical Society: Series B (Statistical Methodology), 64(4), 583-639. doi:10.1111/1467-9868.00353Rue, H., Martino, S., & Chopin, N. (2009). Approximate Bayesian inference for latent Gaussian models by using integrated nested Laplace approximations. Journal of the Royal Statistical Society: Series B (Statistical Methodology), 71(2), 319-392. doi:10.1111/j.1467-9868.2008.00700.xChristensen RH. Ordinal—regression models for ordinal data. R package version 2015.1–21. 2015. http://www.cran.r-project.org/package=ordinal/ Accessed 8 May 2017.Hunter, G. C., Wingfield, B. D., Crous, P. W., & Wingfield, M. J. (2006). A multi-gene phylogeny for species of Mycosphaerella occurring on Eucalyptus leaves. Studies in Mycology, 55, 147-161. doi:10.3114/sim.55.1.147Braun, U., & Urtiaga, R. (2013). New species and new records of cercosporoid hyphomycetes from Cuba and Venezuela (Part 2). Mycosphere, 4(2), 172-214. doi:10.5943/mycosphere/4/2/3Braun, U., Crous, P. W., & Nakashima, C. (2014). Cercosporoid fungi (Mycosphaerellaceae) 2. Species on monocots (Acoraceae to Xyridaceae, excluding Poaceae). IMA Fungus, 5(2), 203-390. doi:10.5598/imafungus.2014.05.02.04Aptroot A. Mycosphaerella and its anamorphs: conspectus of Mycosphaerella CBS Biodiversity Series 5. Utrecht: CBS-KNAW Fungal Biodiversity Centre; 2006.Crous, P. W., & Wingfield, M. J. (1996). Species of Mycosphaerella and Their Anamorphs Associated with Leaf Blotch Disease of Eucalyptus in South Africa. Mycologia, 88(3), 441. doi:10.2307/3760885Aguín, O., Sainz, M. J., Ares, A., Otero, L., & Pedro Mansilla, J. (2013). Incidence, severity and causal fungal species of Mycosphaerella and Teratosphaeria diseases in Eucalyptus stands in Galicia (NW Spain). Forest Ecology and Management, 302, 379-389. doi:10.1016/j.foreco.2013.03.021Maxwell, A., Dell, B., Neumeister-Kemp, H. G., & Hardy, G. E. S. J. (2003). Mycosphaerella species associated with Eucalyptus in south-western Australia: new species, new records and a key. Mycological Research, 107(3), 351-359. doi:10.1017/s0953756203007354Otero L, Aguín O, Mansilla J, Hunter G, Wingfield M. Identificación de especies de Mycosphaerella en Eucalyptus globulus y E. nitens en Galicia. In: Proceedings of the 13th Congress of the Spanish Phytopathological Society; 2006; Murcia, Spain.ZHAN, J., & McDONALD, B. A. (2011). 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Observation of the Baryonic Flavor-Changing Neutral Current Decay Lambda_b -> Lambda mu+ mu-

We report the first observation of the baryonic flavor-changing neutral current decay Lambda_b -> Lambda mu+ mu- with 24 signal events and a statistical significance of 5.8 Gaussian standard deviations. This measurement uses ppbar collisions data sample corresponding to 6.8fb-1 at sqrt{s}=1.96TeV collected by the CDF II detector at the Tevatron collider. The total and differential branching ratios for Lambda_b -> Lambda mu+ mu- are measured. We find B(Lambda_b -> Lambda mu+ mu-) = [1.73+-0.42(stat)+-0.55(syst)] x 10^{-6}. We also report the first measurement of the differential branching ratio of B_s -> phi mu+ mu- using 49 signal events. In addition, we report branching ratios for B+ -> K+ mu+ mu-, B0 -> K0 mu+ mu-, and B -> K*(892) mu+ mu- decays.Comment: 8 pages, 2 figures, 4 tables. Submitted to Phys. Rev. Let

Anti-α-Internexin Autoantibody from Neuropsychiatric Lupus Induce Cognitive Damage via Inhibiting Axonal Elongation and Promote Neuron Apoptosis

Neuropsychiatric systemic lupus erythematosus (NPSLE) is a major complication for lupus patients, which often leads to cognitive disturbances and memory loss and contributes to a significant patient morbidity and mortality. The presence of anti-neuronal autoantibodies (aAbs) has been identified; as examples, anti-NMDA receptors and anti-Ribsomal P aAbs have been linked to certain pathophysiological features of NPSLE.In the current study, we used a proteomic approach to identify an intermediate neurofilament alpha-internexin (INA) as a pathogenetically relevant autoantigen in NPSLE. The significance of this finding was then validated in an expanded of a cohort of NPSLE patients (n = 67) and controls (n = 270) by demonstrating that high titers of anti-INA aAb was found in both the serum and cerebrospinal fluid (CSF) of ∼50% NPSLE. Subsequently, a murine model was developed by INA immunization that resulted in pronounced cognitive dysfunction that mimicked features of NPSLE. Histopathology in affected animals displayed cortical and hippocampal neuron apoptosis. In vitro studies further demonstrated that anti-INA Ab mediated neuronal damage via inhibiting axonal elongation and eventually driving the cells to apoptosis.Taken together, this study identified a novel anti-neurofilament aAb in NPSLE, and established a hitherto undescribed mechanism of aAb-mediated neuron damage that could have relevance to the pathophysiology of NPSLE

Elevated risk of stillbirth in males: systematic review and meta-analysis of more than 30 million births

Background Stillbirth rates have changed little over the last decade, and a high proportion of cases are unexplained. This meta-analysis examined whether there are inequalities in stillbirth risks according to sex. Methods A systematic review of the literature was conducted, and data were obtained on more than 30 million birth outcomes reported in observational studies. The pooled relative risk of stillbirth was estimated using random-effects models. Results The crude mean rate (stillbirths/1,000 total births) was 6.23 for males and 5.74 for females. The pooled relative risk was 1.10 (95% confidence interval (CI): 1.07-1.13). The attributable fraction in the whole population was 4.2% (95% CI: 3.70-4.63), and the attributable fraction among male fetuses was 7.8% (95% CI: 7.0-8.66). Study populations from countries with known sex-biased sex selection issues had anomalous stillbirth sex ratios and higher overall stillbirth risks than other countries, reflecting increased mortality among females. Conclusions Risk of stillbirth in males is elevated by about 10%. The population-attributable risk is comparable to smoking and equates to approximately 100,000 stillbirths per year globally. The pattern is consistent across countries of varying incomes. Given current difficulties in reducing stillbirth rates, work to understand the causes of excess male risk is warranted. We recommend that stillbirths are routinely recorded by sex. This will also assist in exposing prenatal sex selection as elevated or equal risks of stillbirth in females would be readily apparent and could therefore be used to trigger investigation

The Effect of ACACB cis-Variants on Gene Expression and Metabolic Traits

Acetyl Coenzyme A carboxylase β (ACACB) is the rate-limiting enzyme in fatty acid oxidation, and continuous fatty acid oxidation in Acacb knock-out mice increases insulin sensitivity. Systematic human studies have not been performed to evaluate whether ACACB variants regulate gene expression and insulin sensitivity in skeletal muscle and adipose tissues. We sought to determine whether ACACB transcribed variants were associated with ACACB gene expression and insulin sensitivity in non-diabetic African American (AA) and European American (EA) adults.ACACB transcribed single nucleotide polymorphisms (SNPs) were genotyped in 105 EAs and 46 AAs whose body mass index (BMI), lipid profiles and ACACB gene expression in subcutaneous adipose and skeletal muscle had been measured. Allelic expression imbalance (AEI) was assessed in lymphoblast cell lines from heterozygous subjects in an additional EA sample (n = 95). Selected SNPs were further examined for association with insulin sensitivity in a cohort of 417 EAs and 153 AAs.ACACB transcribed SNP rs2075260 (A/G) was associated with adipose ACACB messenger RNA expression in EAs and AAs (p = 3.8×10(-5), dominant model in meta-analysis, Stouffer method), with the (A) allele representing lower gene expression in adipose and higher insulin sensitivity in EAs (p = 0.04). In EAs, adipose ACACB expression was negatively associated with age and sex-adjusted BMI (r = -0.35, p = 0.0002).Common variants within the ACACB locus appear to regulate adipose gene expression in humans. Body fat (represented by BMI) may further regulate adipose ACACB gene expression in the EA population

Pleiotropic Roles of a Ribosomal Protein in Dictyostelium discoideum

The cell cycle phase at starvation influences post-starvation differentiation and morphogenesis in Dictyostelium discoideum. We found that when expressed in Saccharomyces cerevisiae, a D. discoideum cDNA that encodes the ribosomal protein S4 (DdS4) rescues mutations in the cell cycle genes cdc24, cdc42 and bem1. The products of these genes affect morphogenesis in yeast via a coordinated moulding of the cytoskeleton during bud site selection. D. discoideum cells that over- or under-expressed DdS4 did not show detectable changes in protein synthesis but displayed similar developmental aberrations whose intensity was graded with the extent of over- or under-expression. This suggested that DdS4 might influence morphogenesis via a stoichiometric effect – specifically, by taking part in a multimeric complex similar to the one involving Cdc24p, Cdc42p and Bem1p in yeast. In support of the hypothesis, the S. cerevisiae proteins Cdc24p, Cdc42p and Bem1p as well as their D. discoideum cognates could be co-precipitated with antibodies to DdS4. Computational analysis and mutational studies explained these findings: a C-terminal domain of DdS4 is the functional equivalent of an SH3 domain in the yeast scaffold protein Bem1p that is central to constructing the bud site selection complex. Thus in addition to being part of the ribosome, DdS4 has a second function, also as part of a multi-protein complex. We speculate that the existence of the second role can act as a safeguard against perturbations to ribosome function caused by spontaneous variations in DdS4 levels

Bioaccumulation and ecotoxicity of carbon nanotubes

Carbon nanotubes (CNT) have numerous industrial applications and may be released to the environment. In the aquatic environment, pristine or functionalized CNT have different dispersion behavior, potentially leading to different risks of exposure along the water column. Data included in this review indicate that CNT do not cross biological barriers readily. When internalized, only a minimal fraction of CNT translocate into organism body compartments. The reported CNT toxicity depends on exposure conditions, model organism, CNT-type, dispersion state and concentration. In the ecotoxicological tests, the aquatic organisms were generally found to be more sensitive than terrestrial organisms. Invertebrates were more sensitive than vertebrates. Single-walled CNT were found to be more toxic than double-/multi-walled CNT. Generally, the effect concentrations documented in literature were above current modeled average environmental concentrations. Measurement data are needed for estimation of environmental no-effect concentrations. Future studies with benchmark materials are needed to generate comparable results. Studies have to include better characterization of the starting materials, of the dispersions and of the biological fate, to obtain better knowledge of the exposure/effect relationships