195 research outputs found

    Cognitive diversity and innovative work behaviour:The mediating roles of task reflexivity and relationship conflict and the moderating role of perceived support

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    Previous research has merely explored the positive relationship between cognitive diversity and creativity, but the potential negative side of cognitive diversity might also prevail and should be examined together with its positive side. To address this gap, our study, drawing on the categorization–elaboration model framework, explored both the positive and negative effects of cognitive diversity on creativity/innovation in a single model. Using data collected from 101 teams (including both team leaders and team members) in 10 Chinese manufacturing companies, we identified a dual pathway – namely, task reflexivity (i.e., positive pathway) and relationship conflict (i.e., negative pathway) – in the linkage of cognitive diversity and innovative work behaviour (i.e., IWB). Cognitive diversity encouraged IWB via the task reflexivity pathway, but impeded IWB via the relationship conflict pathway. We further demonstrated that perceived support for innovation moderated the relationships between cognitive diversity and task reflexivity/relationship conflict, with cognitive diversity more related to task reflexivity and less related to relationship conflict when perceived support for innovation was high. Moderated mediation effects also indicated that the positive indirect effect of cognitive diversity on IWB through task reflexivity existed only when support for innovation was high and that the negative indirect effect of cognitive diversity on IWB through relationship conflict occurred only when support for innovation was low

    Phylogenetic analysis of porcine parvoviruses from swine samples in China

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    <p>Abstract</p> <p>Background</p> <p>Porcine parvovirus (PPV) usually causes reproductive failure in sows. The objective of the present study was to analyze the phylogenetic distribution and perform molecular characterization of PPVs isolated in China, as well as to identify two field strains, LZ and JY. The data used in this study contained the available sequences for NS1 and VP2 from GenBank, as well as the two aforementioned Chinese strains.</p> <p>Results</p> <p>Phylogenetic analysis shows that the PPV sequences are divided into four groups. The early Chinese PPV isolates are Group I viruses, and nearly all of the later Chinese PPV isolates are Group II viruses. LZ belongs to group II, whereas the JY strain is a Group III virus. This is the first report on the isolation of a Group III virus in China. The detection of selective pressures on the PPV genome shows that the NS1 and VP2 genes are under purifying selection and positive selection, respectively. Moreover, the amino acids in the VP2 capsid are highly variable because of the positive selection.</p> <p>Conclusions</p> <p>Our study provides new molecular data on PPV strains in China, and emphasizes the importance of etiological studies of PPV in pigs.</p

    In-vitro and in-vivo phenotype of type Asia 1 foot-and-mouth disease viruses utilizing two non-RGD receptor recognition sites

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    <p>Abstract</p> <p>Background</p> <p>Foot-and-mouth disease virus (FMDV) uses a highly conserved Arg-Gly-Asp (RGD) triplet for attachment to host cells and this motif is believed to be essential for virus viability. Previous sequence analyses of the 1D-encoding region of an FMDV field isolate (Asia1/JS/CHA/05) and its two derivatives indicated that two viruses, which contained an Arg-Asp-Asp (RDD) or an Arg-Ser-Asp (RSD) triplet instead of the RGD integrin recognition motif, were generated serendipitously upon short-term evolution of field isolate in different biological environments. To examine the influence of single amino acid substitutions in the receptor binding site of the RDD-containing FMD viral genome on virus viability and the ability of non-RGD FMDVs to cause disease in susceptible animals, we constructed an RDD-containing FMDV full-length cDNA clone and derived mutant molecules with RGD or RSD receptor recognition motifs. Following transfection of BSR cells with the full-length genome plasmids, the genetically engineered viruses were examined for their infectious potential in cell culture and susceptible animals.</p> <p>Results</p> <p>Amino acid sequence analysis of the 1D-coding region of different derivatives derived from the Asia1/JS/CHA/05 field isolate revealed that the RDD mutants became dominant or achieved population equilibrium with coexistence of the RGD and RSD subpopulations at an early phase of type Asia1 FMDV quasispecies evolution. Furthermore, the RDD and RSD sequences remained genetically stable for at least 20 passages. Using reverse genetics, the RDD-, RSD-, and RGD-containing FMD viruses were rescued from full-length cDNA clones, and single amino acid substitution in RDD-containing FMD viral genome did not affect virus viability. The genetically engineered viruses replicated stably in BHK-21 cells and had similar growth properties to the parental virus. The RDD parental virus and two non-RGD recombinant viruses were virulent to pigs and bovines that developed typical clinical disease and viremia.</p> <p>Conclusions</p> <p>FMDV quasispecies evolving in a different biological environment gained the capability of selecting different receptor recognition site. The RDD-containing FMD viral genome can accommodate substitutions in the receptor binding site without additional changes in the capsid. The viruses expressing non-RGD receptor binding sites can replicate stably in vitro and produce typical FMD clinical disease in susceptible animals.</p

    Effect of Sciadonic Acid on Hepatic Lipid Metabolism in Obese Mice Induced by A High-fat Diet

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    Objective: To investigate the potential beneficial effects of sciadonic acid (SA) on improving obesity induced by a high-fat diet in mice. Methods: Forty-eight male C57BL/6 mice were adaptively fed for one week and then randomly divided into the following groups: Control group (C), positive control group (S), model group (M), low-dose sciadonic acid group (LSA), medium-dose sciadonic acid group (MSA), and high-dose sciadonic acid group (HSA). The modeling process lasted for 16 weeks, and the low and high-dose groups were orally administered different doses of SA solution at a fixed time each day. After the modeling period, potential mechanisms of SA in regulating lipid metabolism in obese mice were explored, including aspects such as blood lipid metabolism, hepatic fat metabolism, hepatic oxidative stress, hepatic lipid synthesis, and expression of metabolism-related genes. Results: The high-dose SA intervention in obese mice significantly decreased the levels of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) in serum, while increasing high-density lipoprotein cholesterol (HDL-C) (P<0.05). It inhibited weight gain, reduced epididymal fat accumulation, and improved liver tissue damage. Additionally, SA significantly increased the activities of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in mice (P<0.05), and significantly reduced the production of oxidative end products MDA (P<0.05), alleviated oxidative stress in vivo, and inhibited lipid synthesis by regulating the expression of genes related to lipid metabolism to improve lipid metabolism. Conclusion: SA could improve lipid metabolism disorders in obese mice by suppressing fat accumulation, alleviate oxidative stress, regulate lipid synthesis and metabolism

    TL1A–DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease

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    T helper type 17 (Th17) cells play an important pathogenic function in autoimmune diseases; their regulation, however, is not well understood. We show that the expression of a tumor necrosis factor receptor family member, death receptor 3 (DR3; also known as TNFRSF25), is selectively elevated in Th17 cells, and that TL1A, its cognate ligand, can promote the proliferation of effector Th17 cells. To further investigate the role of the TL1A–DR3 pathway in Th17 regulation, we generated a TL1A-deficient mouse and found that TL1A−/− dendritic cells exhibited a reduced capacity in supporting Th17 differentiation and proliferation. Consistent with these data, TL1A−/− animals displayed decreased clinical severity in experimental autoimmune encephalomyelitis (EAE). Finally, we demonstrated that during EAE disease progression, TL1A was required for the optimal differentiation as well as effector function of Th17 cells. These observations thus establish an important role of the TL1A–DR3 pathway in promoting Th17 cell function and Th17-mediated autoimmune disease

    Biodiversity promotes ecosystem functioning despite environmental change

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    Three decades of research have demonstrated that biodiversity can promote the functioning of ecosystems. Yet, it is unclear whether the positive effects of biodiversity on ecosystem functioning will persist under various types of global environmental change drivers. We conducted a meta-analysis of 46 factorial experiments manipulating both species richness and the environment to test how global change drivers (i.e. warming, drought, nutrient addition or CO2 enrichment) modulated the effect of biodiversity on multiple ecosystem functions across three taxonomic groups (microbes, phytoplankton and plants). We found that biodiversity increased ecosystem functioning in both ambient and manipulated environments, but often not to the same degree. In particular, biodiversity effects on ecosystem functioning were larger in stressful environments induced by global change drivers, indicating that high-diversity communities were more resistant to environmental change. Using a subset of studies, we also found that the positive effects of biodiversity were mainly driven by interspecific complementarity and that these effects increased over time in both ambient and manipulated environments. Our findings support biodiversity conservation as a key strategy for sustainable ecosystem management in the face of global environmental change

    ADAMTS16 activates latent TGF-β, accentuating fibrosis and dysfunction of the pressure-overloaded heart

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    AIMS: Cardiac fibrosis is a major cause of heart failure (HF), and mediated by the differentiation of cardiac fibroblasts into myofibroblasts. However, limited tools are available to block cardiac fibrosis. ADAMTS16 is a member of the ADAMTS superfamily of extracellular protease enzymes involved in extracellular matrix (ECM) degradation and remodelling. In this study, we aimed to establish ADAMTS16 as a key regulator of cardiac fibrosis. METHODS AND RESULTS: Western blot and qRT-PCR analyses demonstrated that ADAMTS16 was significantly up-regulated in mice with transverse aortic constriction (TAC) associated with left ventricular hypertrophy and HF, which was correlated with increased expression of Mmp2, Mmp9, Col1a1, and Col3a1. Overexpression of ADAMTS16 accelerated the AngII-induced activation of cardiac fibroblasts into myofibroblasts. Protein structural analysis and co-immunoprecipitation revealed that ADAMTS16 interacted with the latency-associated peptide (LAP)-transforming growth factor (TGF)-β via a RRFR motif. Overexpression of ADAMTS16 induced the activation of TGF-β in cardiac fibroblasts; however, the effects were blocked by a mutation of the RRFR motif to IIFI, knockdown of Adamts16 expression, or a TGF-β-neutralizing antibody (ΝAb). The RRFR tetrapeptide, but not control IIFI peptide, blocked the interaction between ADAMTS16 and LAP-TGF-β, and accelerated the activation of TGF-β in cardiac fibroblasts. In TAC mice, the RRFR tetrapeptide aggravated cardiac fibrosis and hypertrophy by up-regulation of ECM proteins, activation of TGF-β, and increased SMAD2/SMAD3 signalling, however, the effects were blocked by TGF-β-NAb. CONCLUSION: ADAMTS16 promotes cardiac fibrosis, cardiac hypertrophy, and HF by facilitating cardiac fibroblasts activation via interacting with and activating LAP-TGF-β signalling. The RRFR motif of ADAMTS16 disrupts the interaction between ADAMTS16 and LAP-TGF-β, activates TGF-β, and aggravated cardiac fibrosis and hypertrophy. This study identifies a novel regulator of TGF-β signalling and cardiac fibrosis, and provides a new target for the development of therapeutic treatment of cardiac fibrosis and HF

    Biological control of the vernal population increase of Calanus finmarchicus on Georges Bank

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    Author Posting. © Elsevier B.V., 2006. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Deep Sea Research Part II: Topical Studies in Oceanography 53 (2006): 2632-2655, doi:10.1016/j.dsr2.2006.08.011.An adjoint data assimilation approach was used to quantify the physical and biological controls on Calanus finmarchicus N3 to C stages on Georges Bank and its nearby environs. The mean seasonal cycle of vertically-averaged distributions, from 5 years of the GLOBEC Georges Bank Broad-Scale Surveys between January and June, was assimilated into a physical-biological model based on the climatological circulation. Large seasonal and spatial variability is present in the inferred supply sources, mortality rates, computed molting fluxes, and physical transports. Estimated mortalities fall within the range of observed rates, and exhibit stage structure that is consistent with earlier findings. Inferred off-bank initial conditions indicate that the deep basins in the Gulf of Maine are source regions of early-stage nauplii and late-stage copepodids in January. However, the population increase on Georges Bank from January to April is controlled mostly by local biological processes. Magnitudes of the physical transport terms are nearly as large as the mortality and molting fluxes, but their bank-wide averages are small in comparison to the biological terms. The hypothesis of local biological control is tested in a sensitivity experiment in which upstream sources are set to zero. In that solution, the lack of upstream sources is compensated by a decrease in mortality that is much smaller than the uncertainty in observational estimates.This work was supported by the US GLOBEC Georges Bank program: Integration and Synthesis of Georges Bank Broad-Scale Survey Results, sponsored by NSF (OCE-0233800) and NOAA (NA17RJ1223)

    Effects of obesity with reduced 25(OH)D levels on bone health in elderly Chinese people: a nationwide cross-sectional study

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    BackgroundObesity is often accompanied by lower 25(OH)D levels, whereas these two parameters exhibit opposite effects on bone health. It is uncertain what are the effects of lower 25(OH)D levels in obesity on bone health in elderly Chinese people.MethodsA nationally representative cross-sectional analysis of China Community-based Cohort of Osteoporosis (CCCO) was performed from 2016 to 2021, which consisted of 22,081 participants. Demographic data, disease history, Body mass index (BMI), bone mineral density (BMD), the levels of the biomarkers of vitamin D status and those of bone metabolism markers were measured for all participants (N = 22,081). The genes (rs12785878, rs10741657, rs4588, rs7041, rs2282679 and rs6013897) related to 25(OH)D transportation and metabolism were performed in a selected subgroup (N = 6008).ResultsObese subjects exhibited lower 25(OH)D levels (p &lt; 0.05) and higher BMD (p &lt; 0.001) compared with those of normal subjects following adjustment. The genotypes and allele frequency of rs12785878, rs10741657, rs6013897, rs2282679, rs4588 and rs7041 indicated no significant differences among three BMI groups following correction by the Bonferroni’s method (p &gt; 0.05). The levels of total 25(OH)D (ToVD) were significantly different among the GC1F, GC1S and GC2 haplotype groups (p &lt; 0.05). Correlation analysis indicated that ToVD levels were significantly correlated with parathyroid hormone levels, BMD, risk of osteoporosis (OP) and the concentration levels of other bone metabolism markers (p &lt; 0.05). Generalized varying coefficient models demonstrated that the increasing BMI, ToVD levels and their interactions were positively associated with BMD outcomes (p &lt; 0.001), whereas the reduced levels of ToVD and BMI increased the risk of OP, which was noted notably for the subjects with reduced ToVD levels (less than 20.69 ng/ml) combined with decreased BMI (less than 24.05 kg/m2).ConclusionThere was a non-linear interaction of BMI and 25(OH)D. And higher BMI accompanied by decreased 25(OH)D levels is associated with increased BMD and decreased incidence of OP, optimal ranges exist for BMI and 25(OH)D levels. The cutoff value of BMI at approximately 24.05 kg/m2 combined with an approximate value of 25(OH)D at 20.69 ng/ml are beneficial for Chinese elderly subjects

    Globe-LFMC 2.0, an enhanced and updated dataset for live fuel moisture content research

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    Globe-LFMC 2.0, an updated version of Globe-LFMC, is a comprehensive dataset of over 280,000 Live Fuel Moisture Content (LFMC) measurements. These measurements were gathered through field campaigns conducted in 15 countries spanning 47 years. In contrast to its prior version, Globe-LFMC 2.0 incorporates over 120,000 additional data entries, introduces more than 800 new sampling sites, and comprises LFMC values obtained from samples collected until the calendar year 2023. Each entry within the dataset provides essential information, including date, geographical coordinates, plant species, functional type, and, where available, topographical details. Moreover, the dataset encompasses insights into the sampling and weighing procedures, as well as information about land cover type and meteorological conditions at the time and location of each sampling event. Globe-LFMC 2.0 can facilitate advanced LFMC research, supporting studies on wildfire behaviour, physiological traits, ecological dynamics, and land surface modelling, whether remote sensing-based or otherwise. This dataset represents a valuable resource for researchers exploring the diverse LFMC aspects, contributing to the broader field of environmental and ecological research
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