205 research outputs found

    Period-doubling bifurcation and Neimark-Sacker bifurcation of a discrete predator-prey model with Allee effect and cannibalism

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    In this paper, a discrete predator-prey model incorporating Allee effect and cannibalism is derived from its continuous version by semidiscretization method. Not only the existence and local stability of fixed points of the discret system are investigated, but more important, the sufficient conditions for the occurrence of its period-doubling bifurcation and Neimark-Sacker bifurcation are obtained using the center manifold theorem and local bifurcation theory. Finally some numerical simulations are given to illustrate the existence of Neimark-Sacker bifurcation. The outcome of the study reveals that this discrete system undergoes various bifurcations including period-doubling bifurcation and Neimark-Sacker bifurcation

    Mutations in porin LamB contribute to ceftazidime-avibactam resistance in KPC-producing Klebsiella pneumoniae.

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    Ceftazidime-avibactam (CAZ-AVI) shows promising activity against carbapenem-resistant Klebsiella pneumoniae (CRKP), however, CAZ-AVI resistance have emerged recently. Mutations in KPCs, porins OmpK35 and/or OmpK36, and PBPs are known to contribute to the resistance to CAZ-AVI in CRKP. To identify novel CAZ-AVI resistance mechanism, we generated 10 CAZ-AVI-resistant strains from 14 CAZ-AVI susceptible KPC-producing K. pneumoniae (KPC-Kp) strains through in vitro multipassage resistance selection using low concentrations of CAZ-AVI. Comparative genomic analysis for the original and derived mutants identified CAZ-AVI resistance-associated mutations in KPCs, PBP3 (encoded by ftsI), and LamB, an outer membrane maltoporin. CAZ-AVI susceptible KPC-Kp strains became resistant when complemented with mutated blaKPC genes. Complementation experiments also showed that a plasmid borne copy of wild-type lamB or ftsI gene reduced the MIC value of CAZ-AVI in the induced resistant strains. In addition, blaKPC expression level increased in four of the six CAZ-AVI-resistant strains without KPC mutations, indicating a probable association between increased blaKPC expression and increased resistance in these strains. In conclusion, we here identified a novel mechanism of CAZ-AVI resistance associated with mutations in porin LamB in KPC-Kp

    Modelling the Effects of Climatic Factors on the Biomass and Rodent Distribution in a Tibetan Grassland Region in China

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    To identify the main climatic factors from 2007 to 2009 that influence biomass and rodent distribution, 576 fixed sample plots within 81 million km2 of different climatic grassland in Tibet were monitored. The aboveground biomass, the total burrows, the active burrows, the burrow index, and the rodent density in the plots were measured yearly in October. The monthly precipitation and the average temperatures from April to November were obtained for four successive years (2006-2009). Correlative and modelling analyses between the aboveground biomass, the rodent density, and the climatic factors were performed. The results showed that biomass and rodent density were significantly correlated with the climatic factors. Using ridge regression analyses, models of the biomass and rodent density with respect to the monthly precipitations and average temperatures of the previous year were developed. The raw testing data demonstrated that the models can be used approximately to predict biomass and rodent density

    Global emergence of a hypervirulent carbapenem-resistant <i>Escherichia coli </i>ST410 clone

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    Carbapenem-resistant Escherichia coli (CREC) ST410 has recently emerged as a major global health problem. Here, we report a shift in CREC prevalence in Chinese hospitals between 2017 and 2021 with ST410 becoming the most commonly isolated sequence type. Genomic analysis identifies a hypervirulent CREC ST410 clone, B5/H24RxC, which caused two separate outbreaks in a children's hospital. It may have emerged from the previously characterised B4/H24RxC in 2006 and has been isolated in ten other countries from 2015 to 2021. Compared with B4/H24RxC, B5/H24RxC lacks the blaOXA-181-bearing X3 plasmid, but carries a F-type plasmid containing blaNDM-5. Most of B5/H24RxC also carry a high pathogenicity island and a novel O-antigen gene cluster. We find that B5/H24RxC grew faster in vitro and is more virulent in vivo. The identification of this newly emerged but already globally disseminated hypervirulent CREC clone, highlights the ongoing evolution of ST410 towards increased resistance and virulence. </p

    Factors affecting costs and utilization of type 2 diabetes healthcare: a cross-sectional survey among 15 hospitals in urban China

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    <p>Abstract</p> <p>Background</p> <p>Type 2 Diabetes mellitus (T2DM) affects persons of all ages, while also placing heavy economic burdens on national economies and healthcare systems. The study aims to investigate the determinants of direct medical cost (DMC), out-of-pocket (OOP) proportion of the cost, and healthcare utilization associated with T2DM.</p> <p>Methods</p> <p>This cross-sectional study was conducted in four major cities in China. Eligible subjects were adult outpatients who received treatment at one of 15 sampled secondary or tertiary hospitals and consecutively enrolled between March 2007 and May 2007. Generalized estimating equations were used to determine impact factors associated with DMC and healthcare utilization.</p> <p>Results</p> <p>Insurance schemes and receiving insulin therapy were significantly associated with a higher annual DMC of T2DM. For each increase in number of complications, there was about 33% increase in annual DMC. Insurance schemes were significantly associated with the proportions of DMC from pocket. A 7% significantly lower proportion of DMC was paid and 23% more clinic visits (AOR = 1.232, P < 0.001) were made by patients admitted at secondary hospitals than tertiary hospitals. The group with higher income (> 2000 CNY/month) paid 23% less from their pocket, compared with the lower income group. The number of complications also significantly increased the outpatient visits (AOR = 1.064, P < 0.001).</p> <p>Conclusions</p> <p>It implies that preventing complications through the use of more effective treatment regimens is important in order to control the healthcare expenditures of the diseases. Healthcare reform needs to be focused on the medical insurance system and redistribution of patients in hospitals of different levels.</p

    Dufulin Activates HrBP1 to Produce Antiviral Responses in Tobacco

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    BACKGROUND: Dufulin is a new antiviral agent that is highly effective against plant viruses and acts by activating systemic acquired resistance (SAR) in plants. In recent years, it has been used widely to prevent and control tobacco and rice viral diseases in China. However, its targets and mechanism of action are still poorly understood. METHODOLOGY/PRINCIPAL FINDINGS: Here, differential in-gel electrophoresis (DIGE) and classical two-dimensional electrophoresis (2-DE) techniques were combined with mass spectrometry (MS) to identify the target of Dufulin. More than 40 proteins were found to be differentially expressed (≥1.5 fold or ≤1.5 fold) upon Dufulin treatment in Nicotiana tabacum K(326). Based on annotations in the Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) databases, these proteins were found to be related to disease resistance. Directed acyclic graph (DAG) analysis of the various pathways demonstrated harpin binding protein-1 (HrBP1) as the target of action of Dufulin. Additionally, western blotting, semi-quantitative reverse transcription polymerase chain reaction (RT-PCR), and real time PCR analyses were also conducted to identify the specific mechanism of action of Dufulin. Our results show that activation of HrBP1 triggers the salicylic acid (SA) signaling pathway and thereby produces antiviral responses in the plant host. A protective assay based on lesion counting further confirmed the antiviral activity of Dufulin. CONCLUSION: This study identified HrBP1 as a target protein of Dufulin and that Dufulin can activate the SA signaling pathway to induce host plants to generate antiviral responses

    Adult-Age Inflammatory Pain Experience Enhances Long-Term Pain Vigilance in Rats

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    Background: Previous animal studies have illustrated a modulatory effect of neonatal pain experience on subsequent painrelated behaviors. However, the relationship between chronic pain status in adulthood and future pain perception remains unclear. Methodology/Principal Findings: In the current study, we investigated the effects of inflammatory pain experience on subsequent formalin-evoked pain behaviors and fear conditioning induced by noxious stimulation in adult rats. Our results demonstrated an increase of the second but not the first phase of formalin-induced pain behaviors in animals with a history of inflammatory pain that have recovered. Similarly, rats with persistent pain experience displayed facilitated acquisition and prolonged retention of pain-related conditioning. These effects of prior pain experience on subsequent behavior were prevented by repeated morphine administration at an early stage of inflammatory pain. Conclusions/Significance: These results suggest that chronic pain diseases, if not properly and promptly treated, may have a long-lasting impact on processing and perception of environmental threats. This may increase the susceptibility of patients to subsequent pain-related disorders, even when chronic pain develops in adulthood. These data highlight th

    QKI is a critical pre-mRNA alternative splicing regulator of cardiac myofibrillogenesis and contractile function

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    The RNA-binding protein QKI belongs to the hnRNP K-homology domain protein family, a well-known regulator of pre-mRNA alternative splicing and is associated with several neurodevelopmental disorders. Qki is found highly expressed in developing and adult hearts. By employing the human embryonic stem cell (hESC) to cardiomyocyte differentiation system and generating QKI-deficient hESCs (hESCs-QKIdel) using CRISPR/Cas9 gene editing technology, we analyze the physiological role of QKI in cardiomyocyte differentiation, maturation, and contractile function. hESCs-QKIdel largely maintain normal pluripotency and normal differentiation potential for the generation of early cardiogenic progenitors, but they fail to transition into functional cardiomyocytes. In this work, by using a series of transcriptomic, cell and biochemical analyses, and the Qki-deficient mouse model, we demonstrate that QKI is indispensable to cardiac sarcomerogenesis and cardiac function through its regulation of alternative splicing in genes involved in Z-disc formation and contractile physiology, suggesting that QKI is associated with the pathogenesis of certain forms of cardiomyopathies
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