Impact of large-scale dynamic versus thermodynamic climate conditions on contrasting tropical cyclone genesis frequency

Significant advances have been made in understanding the key climate factors responsible for tropical cyclone (TC) activity, yet any theory that estimates likelihood of observed TC formation rates from mean climate states remains elusive. The present study investigates how the extremes of observed TC genesis (TCG) frequency during peak TC seasons are interrelated with distinct changes in the large-scale climate conditions over different ocean basins using the global International Best Track Archive for Climate Stewardship (IBTrACS) dataset and ERA-Interim for the period 1979–2014. Peak TC seasons with significantly high and low TCG frequency are identified for five major ocean basins, and their substantial spatial changes in TCG are noted with regionally distinct differences. To explore the possible climate link behind such changes, a suite of potentially relevant dynamic and thermodynamic climate conditions is analyzed. Results indicate that the observed changes in extreme TCG frequency are closely linked with distinct dominance of specific dynamic and thermodynamic climate conditions over different regions. While the combined influences of dynamic and thermodynamic climate conditions are found to be necessary for modulating TC formation rate over the North Atlantic, eastern Pacific, and southern Indian Oceans, significant changes in large-scale dynamic conditions appear to solely control the TCG frequency over the western Pacific and South Pacific basins. Estimation of the fractional changes in genesis-weighted climate conditions also indicates the coherent but distinct competing effects of different climate conditions on TCG frequency. The present study further points out the need for revising the existing genesis indices for estimating TCG frequency over individual basins

Real world and tropical cyclone world. Part I: high-resolution climate model verification

Recent global climate models with sufficient resolution and physics offer a promising approach for simulating real-world tropical cyclone (TC) statistics and their changing relationship with climate. In the first part of this study, we examine the performance of a high-resolution (;40-km horizontal grid) global climate model, the atmospheric component of the Australian Community Climate and Earth System Simulator (ACCESS) based on the Met Office Unified Model (UM8.5) Global Atmosphere (GA6.0). The atmospheric model is forced with observed sea surface temperature, and 20 years of integrations (1990–2009) are analyzed for evaluating the simulated TC statistics compared with observations. The model reproduces the observed climatology, geographical distribution, and interhemispheric asymmetry of global TC formation rates reasonably well. The annual cycle of regional TC formation rates over most basins is also well captured. However, there are some regional biases in the geographical distribution of TC formation rates. To identify the sources of these biases, a suite of model-simulated large-scale climate conditions that critically modulate TC formation rates are further evaluated, including the assessment of a multivariate genesis potential index. Results indicate that the model TC genesis biases correspond well to the inherent biases in the simulated large-scale climatic states, although the relative effects on TC genesis of some variables differs between basins. This highlights the model’s mean-state dependency in simulating accurate TC formation rates

NITROGEN, PHOSPHORUS, AND POTASSIUM RANGE OF VERMICOMPOST USING EISENIA FETIDA AND PERIONYX EXCAVATUS

The aim of the presentation is to produce vermicomposting from organic kitchen solid wastes using two types of earthworms such as Eisenia fetida and Perionyx excavatus and check the nitrogen, phosphorus, and potassium level between E. fetida and P. excavatus. This study examines the potential of the E. fetida and P. excavatus in the vermicompost of kitchen waste. As kitchen waste is rich in organic material. Physical and biochemical parameters were analyzed during the period of 60 days. Pre-decomposition is 15 days and subsequent vermicomposting is 60 days indicates, the rule of these species of vermitechnology increase was found in all the parameters such as total nitrogen (%), available phosphorus (%), and exchangeable potassium (%) while a decrease was found in pH and carbon-to-nitrogen ratio in E. fetida as the timing of vermicomposting increased from 0 days to 60 days

Time to death in the presence of E. coli: a mass-scale method for assaying pathogen resistance in Drosophila

This article does not have an abstract

Prognostic Value of Stress Myocardial Perfusion Positron Emission Tomography: Results From A Multicenter Observational Registry

ObjectivesThe primary objective of this multicenter registry was to study the prognostic value of positron emission tomography (PET) myocardial perfusion imaging (MPI) and the improved classification of risk in a large cohort of patients with suspected or known coronary artery disease (CAD).BackgroundLimited prognostic data are available for MPI with PET.MethodsA total of 7,061 patients from 4 centers underwent a clinically indicated rest/stress rubidium-82 PET MPI, with a median follow-up of 2.2 years. The primary outcome of this study was cardiac death (n = 169), and the secondary outcome was all-cause death (n = 570). Net reclassification improvement (NRI) and integrated discrimination analyses were performed.ResultsRisk-adjusted hazard of cardiac death increased with each 10% myocardium abnormal with mildly, moderately, or severely abnormal stress PET (hazard ratio [HR]: 2.3 [95% CI: 1.4 to 3.8; p = 0.001], HR: 4.2 [95% CI: 2.3 to 7.5; p < 0.001], and HR: 4.9 [95% CI: 2.5 to 9.6; p < 0.0001], respectively [normal MPI: referent]). Addition of percent myocardium ischemic and percent myocardium scarred to clinical information (age, female sex, body mass index, history of hypertension, diabetes, dyslipidemia, smoking, angina, beta-blocker use, prior revascularization, and resting heart rate) improved the model performance (C-statistic 0.805 [95% CI: 0.772 to 0.838] to 0.839 [95% CI: 0.809 to 0.869]) and risk reclassification for cardiac death (NRI 0.116 [95% CI: 0.021 to 0.210]), with smaller improvements in risk assessment for all-cause death.ConclusionsIn patients with known or suspected CAD, the extent and severity of ischemia and scar on PET MPI provided powerful and incremental risk estimates of cardiac death and all-cause death compared with traditional coronary risk factors

TGF-beta 1 induces human alveolar epithelial to mesenchymal cell transition (EMT)

Background: Fibroblastic foci are characteristic features in lung parenchyma of patients with idiopathic pulmonary fibrosis (IPF). They comprise aggregates of mesenchymal cells which underlie sites of unresolved epithelial injury and are associated with progression of fibrosis. However, the cellular origins of these mesenchymal phenotypes remain unclear. We examined whether the potent fibrogenic cytokine TGF-β1 could induce epithelial mesenchymal transition (EMT) in the human alveolar epithelial cell line, A549, and investigated the signaling pathway of TGF-β1-mediated EMT. Methods: A549 cells were examined for evidence of EMT after treatment with TGF-β1. EMT was assessed by: morphology under phase-contrast microscopy; Western analysis of cell lysates for expression of mesenchymal phenotypic markers including fibronectin EDA (Fn-EDA), and expression of epithelial phenotypic markers including E-cadherin (E-cad). Markers of fibrogenesis, including collagens and connective tissue growth factor (CTGF) were also evaluated by measuring mRNA level using RT-PCR, and protein by immunofluorescence or Western blotting. Signaling pathways for EMT were characterized by Western analysis of cell lysates using monoclonal antibodies to detect phosphorylated Erk1/2 and Smad2 after TGF-β1 treatment in the presence or absence of MEK inhibitors. The role of Smad2 in TGF-β1-mediated EMT was investigated using siRNA. Results: The data showed that TGF-β1, but not TNF-α or IL-1β, induced A549 cells with an alveolar epithelial type II cell phenotype to undergo EMT in a time-and concentration-dependent manner. The process of EMT was accompanied by morphological alteration and expression of the fibroblast phenotypic markers Fn-EDA and vimentin, concomitant with a downregulation of the epithelial phenotype marker E-cad. Furthermore, cells that had undergone EMT showed enhanced expression of markers of fibrogenesis including collagens type I and III and CTGF. MMP-2 expression was also evidenced. TGF-β1-induced EMT occurred through phosphorylation of Smad2 and was inhibited by Smad2 gene silencing; MEK inhibitors failed to attenuate either EMT-associated Smad2 phosphorylation or the observed phenotypic changes. Conclusion: Our study shows that TGF-β1 induces A549 alveolar epithelial cells to undergo EMT via Smad2 activation. Our data support the concept of EMT in lung epithelial cells, and suggest the need for further studies to investigate the phenomenon

Calcium isotopes in scleractinian fossil corals since the Mesozoic: Implications for vital effects and biomineralization through time

We present a Cenozoic record of δ^(44/40)Ca from well preserved scleractinian fossil corals, as well as fossil coral δ^(44/40)Ca data from two time periods during the Mesozoic (84 and 160 Ma). To complement the coral data, we also extend existing bulk pelagic carbonate records back to ∼80 Ma. The same fossil corals used for this study were previously shown to be excellently preserved, and to be faithful archives of past seawater Mg/Ca and Sr/Ca since ∼200 Ma (Gothmann et al., 2015). We find that the δ^(44/40)Ca compositions of bulk pelagic carbonates from ODP Site 807 (Ontong Java Plateau) and DSDP Site 516 (Rio Grande Rise) have not varied by more than ∼±0.20‰ over the last ∼80 Myr. In contrast, the δ^(44/40)Ca compositions of Mesozoic and Early Cenozoic fossil corals are ∼1‰ lighter than those of modern corals. The observed change in coral δ^(44/40)Ca does not likely reflect secular variations in seawater δ^(44/40)Ca. Instead, we propose that it reflects a vital effect of calcification – specifically, a sensitivity of coral Ca isotope discrimination to changing seawater [Ca] and/or pH. Support for this hypothesis comes from the presence of an empirical correlation between our coral δ^(44/40)Ca record and records of seawater [Ca] and pH since the Mesozoic (Lowenstein et al., 2003 and Hönisch et al., 2012). We explore various mechanisms that could give rise to such a vital effect, including: (1) changes in calcification rate, (2) changes in proton pumping in exchange for Ca^(2+), (3) variable Rayleigh distillation from an isolated calcifying fluid, and (4) changes in the calcium mass balance of the extracellular calcifying fluid (termed here the “leaky Ca model”). We test for the dependence of seawater δ^(44/40)Ca on external seawater [Ca] by measuring the δ^(44/40)Ca of cultured corals grown in seawater solutions with [Ca] ranging from 10 to 15 mmol/kg. Corals grown under elevated [Ca] conditions show a slight, ∼0.15‰ depletion of δ^(44/40)Ca at higher seawater [Ca] – a supportive but not definitive result

Animal model integration to AutDB, a genetic database for autism

<p>Abstract</p> <p>Background</p> <p>In the post-genomic era, multi-faceted research on complex disorders such as autism has generated diverse types of molecular information related to its pathogenesis. The rapid accumulation of putative candidate genes/loci for Autism Spectrum Disorders (ASD) and ASD-related animal models poses a major challenge for systematic analysis of their content. We previously created the Autism Database (AutDB) to provide a publicly available web portal for ongoing collection, manual annotation, and visualization of genes linked to ASD. Here, we describe the design, development, and integration of a new module within AutDB for ongoing collection and comprehensive cataloguing of ASD-related animal models.</p> <p>Description</p> <p>As with the original AutDB, all data is extracted from published, peer-reviewed scientific literature. Animal models are annotated with a new standardized vocabulary of phenotypic terms developed by our researchers which is designed to reflect the diverse clinical manifestations of ASD. The new Animal Model module is seamlessly integrated to AutDB for dissemination of diverse information related to ASD. Animal model entries within the new module are linked to corresponding candidate genes in the original "Human Gene" module of the resource, thereby allowing for cross-modal navigation between gene models and human gene studies. Although the current release of the Animal Model module is restricted to mouse models, it was designed with an expandable framework which can easily incorporate additional species and non-genetic etiological models of autism in the future.</p> <p>Conclusions</p> <p>Importantly, this modular ASD database provides a platform from which data mining, bioinformatics, and/or computational biology strategies may be adopted to develop predictive disease models that may offer further insights into the molecular underpinnings of this disorder. It also serves as a general model for disease-driven databases curating phenotypic characteristics of corresponding animal models.</p

Face recognition and visual search strategies in autism spectrum disorders: Amending and extending a recent review by Weigelt et al.

The purpose of this review was to build upon a recent review by Weigelt et al. which examined visual search strategies and face identification between individuals with autism spectrum disorders (ASD) and typically developing peers. Seven databases, CINAHL Plus, EMBASE, ERIC, Medline, Proquest, PsychInfo and PubMed were used to locate published scientific studies matching our inclusion criteria. A total of 28 articles not included in Weigelt et al. met criteria for inclusion into this systematic review. Of these 28 studies, 16 were available and met criteria at the time of the previous review, but were mistakenly excluded; and twelve were recently published. Weigelt et al. found quantitative, but not qualitative, differences in face identification in individuals with ASD. In contrast, the current systematic review found both qualitative and quantitative differences in face identification between individuals with and without ASD. There is a large inconsistency in findings across the eye tracking and neurobiological studies reviewed. Recommendations for future research in face recognition in ASD were discussed