71 research outputs found

    Ionizing Radiation Resistance in Deinococcus Radiodurans

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    Deinococcus radiodurans is unmatched among all known species in its ability to resist ionizing radiation and other DNA-damaging factors. It is considered a model organism in the study of DNA damage and repair. Treatment of D. radiodurans with an acute dose of 5,000 Gy of ionizing radiation with almost no loss of viability, and an acute dose of 15,000 Gy with 37% viability. The extreme radiation resistance of this bacterium is due to efficient DNA repair capacity, high antioxidant activities, and unique cell structure. Based on the latest findings, the general characteristics and ionizing radiation resistance mechanisms of D. radiodurans are reviewed and discussed in this paper

    DUSP6: Potential interactions with FXR1P in the nervous system

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    229-237Fragile X syndrome (FXS) is a leading genetic cause of autism intellectual disorder and autism spectrum disorder (ASD), with either limited treatment options or incurable. Fragile X-related gene 1 (FXR1) is a homolog of the Fragile X mental retardation gene 1 (FMR1), the causative gene of FXS, and both are highly homologous and functionally identical. In FXS, both PI3K (AKT/mTOR signaling pathway) and ERK1/2 (MAPK signaling pathway) expression levels were abnormal. Dual specificity phosphatase 6 (DUSP6) is a member of the mitogen-activated protein kinases (MAPKs) that participates in the crosstalk between the two signaling systems of MEK/ERK and mTOR. By interacting with multiple nodes of MAPK and PI3K/AKT signaling pathways (including the mTOR complex), DUSP6 regulates cellular growth, proliferation, metabolism and participates in pathological processes of cancer and cognitive impairment. However, whether there is an interaction between FXR1P and DUSP6 and the effects of DUSP6 on the growth of SK-N-SH cells remains elusive. As demonstrated by our results, FXR1P was identified in the cytoplasm and nucleus of SK-N-SH cells co-localized with DUSP6, which might have regulated ERK1/2 signaling pathways in SK-N-SH cells. To a certain extent, FXR1P may reverse the negative regulation of ERK1/2 by DUSP6. Moreover, we discovered that not only does DUSP6 inhibit proliferation, but it also promotes the apoptosis of SK-N-SH cells

    Identification and comprehensive analyses of the CBL and CIPK gene families in wheat (Triticum aestivum L.)

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    The interaction analysis of wheat TaCBL and TaCIPK proteins were performed by Y2H method. (PDF 191 kb

    Severity of enterovirus A71 infection in a human SCARB2 knock-in mouse model is dependent on infectious strain and route

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    Enterovirus A71 (EV-A71) is a major etiological agent of human hand, foot and mouth disease, and it can cause severe neurological complications. Although several genotypes of EV-A71 strains are prevalent in different regions of the world, the genotype C4 has circulated in mainland China for more than 20 years. The pathogenicity of different EV-A71 clinical isolates varies and needs to be explored. In this study, hSCARB2 knock-in mice (N = 181) with a wide range of ages were tested for their susceptibility to two EV-A71 strains with the subgenotypes C4 and C2, and two infection routes (intracranial and venous) were compared. The clinical manifestations and pathology and their relationship to the measured viral loads in different tissues were monitored. We observed that 3 weeks is a crucial age, as mice younger than 3-week-old that were infected became extremely ill. However, mice older than 3 weeks displayed diverse clinical symptoms. Significant differences were observed in the pathogenicity of the two strains with respect to clinical signs, disease incidence, survival rate, and body weight change. We concluded that hSCARB2 knock-in mice are a sensitive model for investigating the clinical outcomes resulting from infection by different EV-A71 strains. The intracranial infection model appears to be suitable for evaluating EV-A71 neurovirulence, whereas the venous infection model is appropriate for studying the pathogenicity of EV-A71

    Innovating management mechanism to promote the development of curriculum of ideological and political education penetrating into all majors of medical corses

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    Ideological and political education is a process in which teachers of specialized courses integrate ideological and political education into classroom teaching and reform while imparting professional knowledge. It is the due meaning of medical education and the inevitable pursuit of medical colleges to carry out the fundamental task of cultivating people by virtue. How to integrate the ideological and political education into the teaching of medical professional knowledge needs teachers to play a leading role and to innovate the current teaching management mechanism. From the perspective view point of administrators, this paper puts forward some suggestions on how to improve the management mechanism and promote the development of ideological and political curriculum penetrating into all medical course

    DUSP6: Potential interactions with FXR1P in the nervous system

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    Fragile X syndrome (FXS) is a leading genetic cause of autism intellectual disorder and autism spectrum disorder (ASD), with either limited treatment options or incurable. Fragile X-related gene 1 (FXR1) is a homolog of the Fragile X mental retardation gene 1 (FMR1), the causative gene of FXS, and both are highly homologous and functionally identical. In FXS, both PI3K (AKT/mTOR signaling pathway) and ERK1/2 (MAPK signaling pathway) expression levels were abnormal. Dual specificity phosphatase 6 (DUSP6) is a member of the mitogen-activated protein kinases (MAPKs) that participates in the crosstalk between the two signaling systems of MEK/ERK and mTOR. By interacting with multiple nodes of MAPK and PI3K/AKT signaling pathways (including the mTOR complex), DUSP6 regulates cellular growth, proliferation, metabolism and participates in pathological processes of cancer and cognitive impairment. However, whether there is an interaction between FXR1P and DUSP6 and the effects of DUSP6 on the growth of SK-N-SH cells remains elusive. As demonstrated by our results, FXR1P was identified in the cytoplasm and nucleus of SK-N-SH cells co-localized with DUSP6, which might have regulated ERK1/2 signaling pathways in SK-N-SH cells. To a certain extent, FXR1P may reverse the negative regulation of ERK1/2 by DUSP6. Moreover, we discovered that not only does DUSP6 inhibit proliferation, but it also promotes the apoptosis of SK-N-SH cells

    Joint Selling of Complementary Components Under Brand and Retail Competition

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    Suppliers of complementary goods often package their items together when selling to downstream retailers. One motivation behind this behavior is to reduce double marginalization through coordinated pricing so that system efficiency is improved and individual members can also benefit. The objective of this paper is to understand how competition in supply chains would impact such joint selling partnerships among complementary suppliers. We first model competition at the supply level, which is generated from the existence of multiple partially substitutable brands (or suppliers) for a particular component. We then extend the analysis to a model that also involves retail competition caused by decentralization among retailers who assemble suppliers’ components into final products and sell to customers. The analysis of a model with two complementary components, one of which has multiple brands, indicates that the supply-level competition discourages joint selling of complementary goods. That is, when competing brands become more alike (or substitutable), complementary suppliers act more independently in pricing and selling their items. However, retail competition leads to an opposite effect: Competition among retailers would actually encourage complementary suppliers to package their goods together and act jointly
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