High Temperature in Combination with UV Irradiation Enhances Horizontal Transfer of stx2 Gene from E. coli O157:H7 to Non-Pathogenic E. coli

Background: Shiga toxin (stx) genes have been transferred to numerous bacteria, one of which is E. coli O157:H7. It is a common belief that stx gene is transferred by bacteriophages, because stx genes are located on lambdoid prophages in the E. coli O157:H7 genome. Both E. coli O157:H7 and non-pathogenic E. coli are highly enriched in cattle feedlots. We hypothesized that strong UV radiation in combination with high temperature accelerates stx gene transfer into nonpathogenic E. coli in feedlots. Methodology/Principal Findings: E. coli O157:H7 EDL933 strain were subjected to different UV irradiation (0 or 0.5 kJ/m 2) combination with different temperature (22, 28, 30, 32, and 37uC) treatments, and the activation of lambdoid prophages was analyzed by plaque forming unit while induction of Stx2 prophages was quantified by quantitative real-time PCR. Data showed that lambdoid prophages in E. coli O157:H7, including phages carrying stx2, were activated under UV radiation, a process enhanced by elevated temperature. Consistently, western blotting analysis indicated that the production of Shiga toxin 2 was also dramatically increased by UV irradiation and high temperature. In situ colony hybridization screening indicated that these activated Stx2 prophages were capable of converting laboratory strain of E. coli K12 into new Shiga toxigenic E. coli, which were further confirmed by PCR and ELISA analysis. Conclusions/Significance: These data implicate that high environmental temperature in combination with UV irradiatio

The Study of Rare Bc→Ds,d(∗)llˉB_c\rightarrow D^{(*)}_{s,d}l\bar{l} Decays

In this paper, we study rare decays $B_c\rightarrow D^{(*)}_{s,d}l\bar{l}$ within the Standard Model. The penguin, box, annihilation, color-favored cascade and color-suppressed cascade contributions are included. Based on our calculation, the annihilation and color-favored cascade diagrams play important roles in the differential branching fractions, forward-backward asymmetries, longitudinal polarizations of the final vector mesons and leptonic longitudinal polarization asymmetries. More importantly, color-favored cascade decays largely enhance the resonance cascade contributions. To avoid the resonance cascade contribution pollution, new cutting regions are put forward.Comment: 34 pages, 13 figure

Short hairpin RNA expression for enhancing the resistance of Bombyx mori (Bm) to nucleopolyhedrovirus in vitro and in vivo

A new paradigm of RNAi technology has been studied for enhancing the resistance to virus in plants and animals. Previous studies have shown that the Bombyx mori (Bm) U6 promoter based shRNA is an effective tool for inducing RNAi in Bombyx mori cell line. However, widespread knockdown and induction of phenotypes in Bm larvae have not been fully demonstrated. In this study, we examined Bm U6 promoter based shRNA expression for suppressing Bm nucleopolyhedrovirus (NPV) in the Bm cell line and silkworm larvae. We measured the relative expression level of replication genes of BmNPV in hemolymph of silkworm larvae and BmN cells transfected with recombinant targeting shRNA by quantitative real time polymerase chain reaction (PCR). These results indicated that the recombinant shRNA expression system was a useful tool for resistance to BmNPV in vivo and in vitro. The approach opens the door of RNAi technology as a wide range of strategies that offer a technically simpler, cheaper, and quicker gene-knockdown by recombinant shRNA for future genetics in silkworm Bm and other related species.Key words: RNA interference (RNAi), Silkworm Bombyx mori (Bm) cell line, short hairpin RNA (shRNA), Bm nucleopolyhedrovirus (BmNPV), quantitative real time polymerase chain reaction, Bm U6 promoter

Plant genetic diversity affects multiple trophic levels and trophic interactions

: Intraspecific genetic diversity is an important component of biodiversity. A substantial body of evidence has demonstrated positive effects of plant genetic diversity on plant performance. However, it has remained unclear whether plant genetic diversity generally increases plant performance by reducing the pressure of plant antagonists across trophic levels for different plant life forms, ecosystems and climatic zones. Here, we analyse 4702 effect sizes reported in 413 studies that consider effects of plant genetic diversity on trophic groups and their interactions. We found that that increasing plant genetic diversity decreased the performance of plant antagonists including invertebrate herbivores, weeds, plant-feeding nematodes and plant diseases, while increasing the performance of plants and natural enemies of herbivores. Structural equation modelling indicated that plant genetic diversity increased plant performance partly by reducing plant antagonist pressure. These results reveal that plant genetic diversity often influences multiple trophic levels in ways that enhance natural pest control in managed ecosystems and consumer control of plants in natural ecosystems for sustainable plant production

Sca-1+ cardiac fibroblasts promote development of heart failure

The causative effect of GM-CSF produced by cardiac fibroblasts to development of heart failure has not been shown. We identified the pathological GM-CSF-producing cardiac fibroblast subset and the specific deletion of IL-17A signaling to these cells attenuated cardiac inflammation and heart failure. We describe here the CD45−CD31−CD29+mEFSK4+PDGFRα+Sca-1+periostin+ (Sca-1+) cardiac fibroblast subset as the main GM-CSF producer in both experimental autoimmune myocarditis and myocardial infarction mouse models. Specific ablation of IL-17A signaling to Sca-1+periostin+ cardiac fibroblasts (PostnCreIl17rafl/fl) protected mice from post-infarct heart failure and death. Moreover, PostnCreIl17rafl/fl mice had significantly fewer GM-CSF-producing Sca-1+ cardiac fibrob-lasts and inflammatory Ly6Chi monocytes in the heart. Sca-1+ cardiac fibroblasts were not only potent GM-CSF producers, but also exhibited plasticity and switched their cytokine production profiles depending on local microenvironments. Moreover, we also found GMCSF-positive cardiac fibroblasts in cardiac biopsy samples from heart failure patients of myocarditis or ischemic origin. Thus, this is the first identification of a pathological GMCSF-producing cardiac fibroblast subset in human and mice hearts with myocarditis and ischemic cardiomyopathy. Sca-1+ cardiac fibroblasts direct the type of immune cells infiltrating the heart during cardiac inflammation and drive the development of heart failure

The Roles of E93 and Kr-h1 in Metamorphosis of Nilaparvata lugens

Metamorphosis is a crucial process in insect development. Ecdysone-induced protein 93 (E93) is a determinant that promotes adult metamorphosis in both hemimetabolous and holometabolous insects. Krüppel-homolog 1 (Kr-h1), an early juvenile hormone (JH)-inducible gene, participates in JH signaling pathway controlling insect metamorphosis. In the current study, an E93 cDNA (NlE93) and two Kr-h1 cDNA variants (NlKr-h1-a and NlKr-h1-b) were cloned from Nilaparvata lugens (Stål), one of the most destructive hemimetabolous insect pests on rice. Multiple sequence alignment showed that both NlE93 and NlKr-h1 share high identity with their orthologs from other insects. The expression patterns revealed that decreasing NlKr-h1 mRNA levels were correlated with increasing NlE93 mRNA levels and vice versa. Moreover, RNA interference (RNAi) assays showed that the knockdown of one of the two genes resulted in significantly upregulated expression of the other. Correspondingly, phenotypical observation of the RNAi insects revealed that depletion of NlE93 prevented nymph–adult transition (causing a supernumerary nymphal instar), while depletion of NlKr-h1 triggered precocious formation of incomplete adult features. The results suggest that Nlkr-h1 and NlE93 are mutual repressors, fitting into the MEKRE93 pathway. The balance between these two genes plays a critical role in the metamorphosis of N. lugens determining the proper timing for activating metamorphosis during the nymphal stage

ABSCISIC ACID-INSENSITIVE 5-KIP-RELATED PROTEIN 1-SHOOT MERISTEMLESS modulates reproductive development of Arabidopsis

Soil (or plant) water deficit accelerates plant reproduction. However, the underpinning molecular mechanisms remain unknown. By modulating cell division/number, ABSCISIC ACID-INSENSITIVE 5 (ABI5), a key bZIP (basic (region) leucine zippers) transcription factor, regulates both seed development and abiotic stress responses. The KIP-RELATED PROTEIN (KRP) cyclin-dependent kinases (CDKs) play an essential role in controlling cell division, and SHOOT MERISTEMLESS (STM) plays a key role in the specification of flower meristem identity. Here, our findings show that abscisic acid (ABA) signaling and/or metabolism in adjust reproductive outputs (such as rosette leaf number and open flower number) under water-deficient conditions in Arabidopsis (Arabidopsis thaliana) plants. Reproductive outputs increased under water-sufficient conditions but decreased under water-deficient conditions in the ABA signaling/metabolism mutants abscisic acid2-1 (aba2-1), aba2-11, abscisic acid insensitive3-1 (abi3-1), abi4-1, abi5-7, and abi5-8. Further, under water-deficient conditions, ABA induced-ABI5 directly bound to the promoter of KRP1, which encodes a CDK that plays an essential role in controlling cell division, and this binding subsequently activated KRP1 expression. In turn, KRP1 physically interacted with STM, which functions in the specification of flower meristem identity, promoting STM degradation. We further demonstrate that reproductive outputs are adjusted by the ABI5–KRP1–STM molecular module under water-deficient conditions. Together, our findings reveal the molecular mechanism by which ABA signaling and/or metabolism regulate reproductive development under water-deficient conditions. These findings provide insights that may help guide crop yield improvement under water deficiency

A systematic review and meta-analysis of cold exposure and cardiovascular disease outcomes

BackgroundCold exposure has been considered an essential risk factor for the global disease burden, while its role in cardiovascular diseases is still underappreciated. The increase in frequency and duration of extreme cold weather events like cold spells makes it an urgent task to evaluate the effects of ambient cold on different types of cardiovascular disease and to understand the factors contributing to the population's vulnerability.MethodsIn the present systematic review and meta-analysis, we searched PubMed, Scopus, and Cochrane. We included original research that explored the association between cold exposure (low temperature and cold spell) and cardiovascular disease outcomes (mortality and morbidity). We did a random-effects meta-analysis to pool the relative risk (RR) of the association between a 1°C decrease in temperature or cold spells and cardiovascular disease outcomes.ResultsIn total, we included 159 studies in the meta-analysis. As a result, every 1°C decrease in temperature increased cardiovascular disease-related mortality by 1.6% (RR 1.016; [95% CI 1.015–1.018]) and morbidity by 1.2% (RR 1.012; [95% CI 1.010–1.014]). The most pronounced effects of low temperatures were observed in the mortality of coronary heart disease (RR 1.015; [95% CI 1.011–1.019]) and the morbidity of aortic aneurysm and dissection (RR 1.026; [95% CI 1.021–1.031]), while the effects were not significant in hypertensive disease outcomes. Notably, we identified climate zone, country income level and age as crucial influential factors in the impact of ambient cold exposure on cardiovascular disease. Moreover, the impact of cold spells on cardiovascular disease outcomes is significant, which increased mortality by 32.4% (RR 1.324; [95% CI 1.2341.421]) and morbidity by 13.8% (RR 1.138; [95% CI 1.015–1.276]).ConclusionCold exposure could be a critical risk factor for cardiovascular diseases, and the cold effect varies between disease types and climate zones.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO, identifier: CRD42022347247

Rational design of Bi-doped rGO/Co3O4 nanohybrids for ethanol sensing

Gas sensors based on metal oxide semiconductors (MOSCs) and reduced graphene oxide (rGO) for sensing of organic volatile compounds often suffer from high operation temperature, low responses, poor selectivity, or narrow detection range. Herein, we design and fabricate Bi-doped rGO/Co3O4 (BGCO) nanohybrids with a flower morphology, which have been applied as a sensing layer for an ethanol sensor. This BGCO sensor exhibits a maximum p-type response of 178.1 towards 500 ppm ethanol at an optimum working temperature of 120 °C. The sensor’s detection range for the ethanol concentration is from 500 ppb to 500 ppm, and the sensor has an excellent selectivity to ethanol compared to other types of organic volatile gases and oxidizing gas such as NO2. The enhanced ethanol sensing mechanism is attributed to the increased conductivity of Bi doped rGO/Co3O4 material. Additionally, incorporation of Bi dopant can promote the redox reaction, and the rGO/Co3O4 act as the catalyst