Phylogenetic relationships within Chrysogorgia (Alcyonacea: Octocorallia), a morphologically diverse genus of octocoral, revealed using a target enrichment approach

The octocoral genus Chrysogorgia (Duchassaing and Michelotti, 1864) contains 81 nominal species that are ecologically important components of benthic communities. Taxonomic examination of a large set of samples revealed many provisional new species, exhibiting a wide range of morphological variation. We established nine, distinct morphological groups of Chrysogorgia s.l. that were hypothesized to represent distinct genera. Here, we applied a recently developed universal target enrichment bait method for octocoral exons and ultraconserved elements (UCEs) on 96 specimens varying in morphology, collection ages and DNA quality and quantity to determine whether there was genetic support for these morphologically defined groups. Following Illumina sequencing and SPAdes assembly we recovered 1,682 of 1,700 targeted exon loci and 1,333 of 1,340 targeted UCE loci. Locus recovery per sample was highly variable and significantly correlated with time since specimen collection (2-60 years) and DNA quantity and quality. Phylogenetically informative sites in UCE and exon loci were ∼35% for 50% and 75% taxon-occupancy matrices. Maximum likelihood analyses recovered highly resolved trees with topologies supporting the recognition of 11 candidate genera, corresponding with morphological groups assigned a priori, nine of which are novel. Our results also demonstrate that this target-enrichment approach can be successfully applied to degraded museum specimens of up to 60 years old. This study shows that an integrative approach consisting of molecular and morphological methods will be essential to a proper revision of Chrysogorgia taxonomy and to understand regional diversity of these ecologically important corals

Alcohol use behaviors and risk of metabolic syndrome in South Korean middle-aged men

<p>Abstract</p> <p>Background</p> <p>It is thought that small volumes of alcohol may have positive effects on health. However, excessive drinking results in serious health problems. An accurate method to determine individual alcohol use behaviors are needed to assess objectively the extent to which drinking affects health. This study investigated the association between risk of metabolic syndrome (MetS) and alcohol use behaviors in middle-aged South Korean men using the Alcohol Use Disorders Identification Test.</p> <p>Methods</p> <p>This study used data from the South Korea National Health and Nutrition Examination (KNHANES) IV (2008), which extracted the standard survey household by using the proportional systematic sampling method. Data of 714 participants from KNHANES IV, 2008 were analyzed using Surveyfreq and Surveylogistic regression to investigate the association between MetS and alcohol use behaviors in middle-aged South Korean men.</p> <p>Results</p> <p>After adjustment for education, smoking, and physical activity, alcohol use behaviors were significantly associated with an increased risk of hypertension [odds ratio (OR) = 2.54, 95% confidence interval (CI) = 1.5-4.06 in the hazardous group; OR = 2.99, 95% CI = 1.84-4.92 in the problem group]; impaired fasting glucose (OR = 2.15, 95% CI = 1.16-3.99 in the hazardous group; OR = 2.48, 95% CI = 1.42-4.33 in the problem group); dyslipidemia (OR = 2.19, 95% CI = 1.38-3.47 in the problem group); abdominal obesity (OR = 1.93, 95% CI = 1.17-3.19 in the hazardous group; OR = 1.85, 95% CI = 1.17-2.92 in the problem group); and MetS (OR = 2.16, 95% CI = 1.24-3.77 in the hazardous group; OR = 2.54, 95% CI = 1.41-4.58 in problem group).</p> <p>Conclusions</p> <p>This study found that excessive alcohol use behaviors increased the risk of hypertension, diabetes, dyslipidemia, abdominal obesity, and MetS. Considering the rising rate of alcohol consumption and heavy drinking at single sittings, a culture of less risky alcohol consumption must be established to promote health among middle-aged men.</p

Evolutionary distinctiveness of fatty acid and polyketide synthesis in eukaryotes

© 2016 International Society for Microbial Ecology All rights reserved. Fatty acids, which are essential cell membrane constituents and fuel storage molecules, are thought to share a common evolutionary origin with polyketide toxins in eukaryotes. While fatty acids are primary metabolic products, polyketide toxins are secondary metabolites that are involved in ecologically relevant processes, such as chemical defence, and produce the adverse effects of harmful algal blooms. Selection pressures on such compounds may be different, resulting in differing evolutionary histories. Surprisingly, some studies of dinoflagellates have suggested that the same enzymes may catalyse these processes. Here we show the presence and evolutionary distinctiveness of genes encoding six key enzymes essential for fatty acid production in 13 eukaryotic lineages for which no previous sequence data were available (alveolates: dinoflagellates, Vitrella, Chromera; stramenopiles: bolidophytes, chrysophytes, pelagophytes, raphidophytes, dictyochophytes, pinguiophytes, xanthophytes; Rhizaria: chlorarachniophytes, haplosporida; euglenids) and 8 other lineages (apicomplexans, bacillariophytes, synurophytes, cryptophytes, haptophytes, chlorophyceans, prasinophytes, trebouxiophytes). The phylogeny of fatty acid synthase genes reflects the evolutionary history of the organism, indicating selection to maintain conserved functionality. In contrast, polyketide synthase gene families are highly expanded in dinoflagellates and haptophytes, suggesting relaxed constraints in their evolutionary history, while completely absent from some protist lineages. This demonstrates a vast potential for the production of bioactive polyketide compounds in some lineages of microbial eukaryotes, indicating that the evolution of these compounds may have played an important role in their ecological success

Distinct colonization patterns and cDNA-AFLP transcriptome profiles in compatible and incompatible interactions between melon and different races of Fusarium oxysporum f. sp. melonis

Background: Fusarium oxysporum f. sp. melonis Snyd. & Hans. (FOM) causes Fusarium wilt, the most important infectious disease of melon (Cucumis melo L.). The four known races of this pathogen can be distinguished only by infection on appropriate cultivars. No molecular tools are available that can discriminate among the races, and the molecular basis of compatibility and disease progression are poorly understood. Resistance to races 1 and 2 is controlled by a single dominant gene, whereas only partial polygenic resistance to race 1,2 has been described. We carried out a large-scale cDNA-AFLP analysis to identify host genes potentially related to resistance and susceptibility as well as fungal genes associated with the infection process. At the same time, a systematic reisolation procedure on infected stems allowed us to monitor fungal colonization in compatible and incompatible host-pathogen combinations. Results: Melon plants (cv. Charentais Fom-2), which are susceptible to race 1,2 and resistant to race 1, were artificially infected with a race 1 strain of FOM or one of two race 1,2 w strains. Host colonization of stems was assessed at 1, 2, 4, 8, 14, 16, 18 and 21 days post inoculation (dpi), and the fungus was reisolated from infected plants. Markedly different colonization patterns were observed in compatible and incompatible host-pathogen combinations. Five time points from the symptomless early stage (2 dpi) to obvious wilting symptoms (21 dpi) were considered for cDNA-AFLP analysis. After successful sequencing of 627 transcript-derived fragments (TDFs) differentially expressed in infected plants, homology searching retrieved 305 melon transcripts, 195 FOM transcripts expressed in planta and 127 orphan TDFs. RNA samples from FOM colonies of the three strains grown in vitro were also included in the analysis to facilitate the detection of in planta-specific transcripts and to identify TDFs differentially expressed among races/strains. Conclusion: Our data suggest that resistance against FOM in melon involves only limited transcriptional changes, and that wilting symptoms could derive, at least partially, from an active plant response. We discuss the pathogen-derived transcripts expressed in planta during the infection process and potentially related to virulence functions, as well as transcripts that are differentially expressed between the two FOM races grown in vitro. These transcripts provide candidate sequences that can be further tested for their ability to distinguish between races. Sequence data from this article have been deposited in GenBank, Accession Numbers: HO867279-HO867981

Risk propensity in the foreign direct investment location decision of emerging multinationals

A distinguishing feature of emerging economy multinationals is their apparent tolerance for host country institutional risk. Employing behavioral decision theory and quasi-experimental data, we find that managers’ domestic experience satisfaction increases their relative risk propensity regarding controllable risk (legally protectable loss), but decreases their tendency to accept non-controllable risk (e.g., political instability). In contrast, firms’ potential slack reduces relative risk propensity regarding controllable risk, yet amplifies the tendency to take non-controllable risk. We suggest that these counterbalancing effects might help explain observation that risk-taking in FDI location decisions is influenced by firm experience and context. The study provides a new understanding of why firms exhibit heterogeneous responses to host country risks, and the varying effects of institutions

HCV Induces Oxidative and ER Stress, and Sensitizes Infected Cells to Apoptosis in SCID/Alb-uPA Mice

Hepatitis C virus (HCV) is a blood-borne pathogen and a major cause of liver disease worldwide. Gene expression profiling was used to characterize the transcriptional response to HCV H77c infection. Evidence is presented for activation of innate antiviral signaling pathways as well as induction of lipid metabolism genes, which may contribute to oxidative stress. We also found that infection of chimeric SCID/Alb-uPA mice by HCV led to signs of hepatocyte damage and apoptosis, which in patients plays a role in activation of stellate cells, recruitment of macrophages, and the subsequent development of fibrosis. Infection of chimeric mice with HCV H77c also led an inflammatory response characterized by infiltration of monocytes and macrophages. There was increased apoptosis in HCV-infected human hepatocytes in H77c-infected mice but not in mice inoculated with a replication incompetent H77c mutant. Moreover, TUNEL reactivity was restricted to HCV-infected hepatocytes, but an increase in FAS expression was not. To gain insight into the factors contributing specific apoptosis of HCV infected cells, immunohistological and confocal microscopy using antibodies for key apoptotic mediators was done. We found that the ER chaperone BiP/GRP78 was increased in HCV-infected cells as was activated BAX, but the activator of ER stress–mediated apoptosis CHOP was not. We found that overall levels of NF-κB and BCL-xL were increased by infection; however, within an infected liver, comparison of infected cells to uninfected cells indicated both NF-κB and BCL-xL were decreased in HCV-infected cells. We conclude that HCV contributes to hepatocyte damage and apoptosis by inducing stress and pro-apoptotic BAX while preventing the induction of anti-apoptotic NF-κB and BCL-xL, thus sensitizing hepatocytes to apoptosis

Pneumocystis murina colonization in immunocompetent surfactant protein A deficient mice following environmental exposure

<p>Abstract</p> <p>Background</p> <p><it>Pneumocystis spp</it>. are opportunistic pathogens that cause pneumonia in immunocompromised humans and animals. <it>Pneumocystis </it>colonization has also been detected in immunocompetent hosts and may exacerbate other pulmonary diseases. Surfactant protein A (SP-A) is an innate host defense molecule and plays a role in the host response to <it>Pneumocystis</it>.</p> <p>Methods</p> <p>To analyze the role of SP-A in protecting the immunocompetent host from <it>Pneumocystis </it>colonization, the susceptibility of immunocompetent mice deficient in SP-A (KO) and wild-type (WT) mice to <it>P. murina </it>colonization was analyzed by reverse-transcriptase quantitative PCR (qPCR) and serum antibodies were measured by enzyme-linked immunosorbent assay (ELISA).</p> <p>Results</p> <p>Detection of <it>P. murina </it>specific serum antibodies in immunocompetent WT and KO mice indicated that the both strains of mice had been exposed to <it>P. murina </it>within the animal facility. However, P. <it>murina </it>mRNA was only detected by qPCR in the lungs of the KO mice. The incidence and level of the mRNA expression peaked at 8–10 weeks and declined to undetectable levels by 16–18 weeks. When the mice were immunosuppressed, <it>P. murina </it>cyst forms were also only detected in KO mice. <it>P. murina </it>mRNA was detected in <it>SCID </it>mice that had been exposed to KO mice, demonstrating that the immunocompetent KO mice are capable of transmitting the infection to immunodeficient mice. The pulmonary cellular response appeared to be responsible for the clearance of the colonization. More CD4+ and CD8+ T-cells were recovered from the lungs of immunocompetent KO mice than from WT mice, and the colonization in KO mice depleted CD4+ cells was not cleared.</p> <p>Conclusion</p> <p>These data support an important role for SP-A in protecting the immunocompetent host from <it>P. murina </it>colonization, and provide a model to study <it>Pneumocystis </it>colonization acquired via environmental exposure in humans. The results also illustrate the difficulties in keeping mice from exposure to <it>P. murina </it>even when housed under barrier conditions.</p

Measurement of W+W− production in association with one jet in proton–proton collisions at sqrt(s) = 8TeV with the ATLAS detector

The production of W boson pairs in association with one jet in pp collisions at View the MathML sources=8 TeV is studied using data corresponding to an integrated luminosity of 20.3 fb−1 collected by the ATLAS detector during 2012 at the CERN Large Hadron Collider. The cross section is measured in a fiducial phase-space region defined by the presence of exactly one electron and one muon, missing transverse momentum and exactly one jet with a transverse momentum above 25 GeV and a pseudorapidity of |η|<4.5|η|<4.5. The leptons are required to have opposite electric charge and to pass transverse momentum and pseudorapidity requirements. The fiducial cross section is found to be View the MathML sourceσWWfid,1-jet=136±6(stat)±14(syst)±3(lumi) fb. In combination with a previous measurement restricted to leptonic final states with no associated jets, the fiducial cross section of WW production with zero or one jet is measured to be View the MathML sourceσWWfid,≤1-jet=511±9(stat)±26(syst)±10(lumi) fb. The ratio of fiducial cross sections in final states with one and zero jets is determined to be 0.36±0.050.36±0.05. Finally, a total cross section extrapolated from the fiducial measurement of WW production with zero or one associated jet is reported. The measurements are compared to theoretical predictions and found in good agreement

Search for squarks and gluinos in final states with jets and missing transverse momentum using 139 fb−1 of s√ = 13 TeV pp collision data with the ATLAS detector

A search for the supersymmetric partners of quarks and gluons (squarks and gluinos) in final states containing jets and missing transverse momentum, but no electrons or muons, is presented. The data used in this search were recorded by the ATLAS experiment in proton-proton collisions at a centre-of-mass energy of s√ = 13 TeV during Run 2 of the Large Hadron Collider, corresponding to an integrated luminosity of 139 fb−1. The results are interpreted in the context of various R-parity-conserving models where squarks and gluinos are produced in pairs or in association and a neutralino is the lightest supersymmetric particle. An exclusion limit at the 95% confidence level on the mass of the gluino is set at 2.30 TeV for a simplified model containing only a gluino and the lightest neutralino, assuming the latter is massless. For a simplified model involving the strong production of mass-degenerate first- and second-generation squarks, squark masses below 1.85 TeV are excluded if the lightest neutralino is massless. These limits extend substantially beyond the region of supersymmetric parameter space excluded previously by similar searches with the ATLAS detector

Measurement of Azimuthal Anisotropy of Muons from Charm and Bottom Hadrons in pp Collisions at √s = 13 TeV with the ATLAS Detector

The elliptic flow of muons from the decay of charm and bottom hadrons is measured in p p collisions at √ s = 13     TeV using a data sample with an integrated luminosity of 150     pb − 1 recorded by the ATLAS detector at the LHC. The muons from heavy-flavor decay are separated from light-hadron decay muons using momentum imbalance between the tracking and muon spectrometers. The heavy-flavor decay muons are further separated into those from charm decay and those from bottom decay using the distance-of-closest-approach to the collision vertex. The measurement is performed for muons in the transverse momentum range 4–7 GeV and pseudorapidity range | η | < 2.4 . A significant nonzero elliptic anisotropy coefficient v 2 is observed for muons from charm decays, while the v 2 value for muons from bottom decays is consistent with zero within uncertainties