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      • KCI등재

        COVID‐19 and social work practice for older adults in China

        Lin Wenyi,Yin Wanxia 한국사회복지학회 2021 Asian Social Work and Policy Review Vol.15 No.1

        After the spread of COVID-19, the Chinese central government has issued a series of policies and regulations to guide the prevention and control of the epidemic in the elderly care industry. Social workers provided a series of services for older adults in nursing homes and in the community. All efforts made by government agencies and social workers have helped older adults go through the difficult time.

      • KCI등재

        Controllable synthesis of zone-distributed Pd over CeO2–ZrO2/Al2O3 as advanced three-way catalyst

        Li Lan,Shanhu Chen,Hongmei Li,Hanmei Li,Wanxia Wu,Jie Deng,Yaoqiang Chen 한국공업화학회 2018 Journal of Industrial and Engineering Chemistry Vol.58 No.-

        Two optimally designed catalysts (Ce0.7Zr0.3O2/Pd/Al2O3, Pd/Ce0.7Zr0.3O2/Pd/Al2O3) were synthesized and compared with conventional Pd/Ce0.7Zr0.3O2/Al2O3. The characterization results reveal that for Pd/Ce0.7Zr0.3O2/Al2O3, Pd species undergo severe agglomeration and encapsulation during thermal aging process, leading to dramatic catalyst deactivation. While for the two optimized catalysts, some Pd species initially distributed on Al2O3 would migrate to the surface of CexZr1−xO2(CZ) grains upon aging treatment, resulting in enhanced Pd–CZ interaction, thus the two aged samples possess higher dispersion, larger amount of oxidized Pd2+ species and more oxygen vacancies compared with conventional Pd/Ce0.7Zr0.3O2/Al2O3-a. Consequently, modified reducibility and improved three-way catalytic performance are obtained, especially for Pd/Ce0.7Zr0.3O2/Pd/Al2O3-a.

      • KCI등재

        The characteristic of the synonymous codon usage and phylogenetic analysis of hepatitis B virus

        Xiaoming Qi,Chaojun Wei,Yonghong Li,Yu Wu,Hui Xu,Rui Guo,Yanjuan Jia,Zhenhao Li,Zhenhong Wei,Wanxia Wang,Jing Jia,Yuanting Li,Anqi Wang,Xiaoling Gao 한국유전학회 2020 Genes & Genomics Vol.42 No.7

        Background Hepatitis B virus (HBV) infection is a crucial medical issue worldwide. The dependence of HBV replication on host cell machineries and their co-evolutionary interactions prompt the codon usage pattern of viral genes to translation selection and mutation pressure. Objective The evolutionary characteristics of HBV and the natural selection effects of the human genome on the codon usage characteristics were analyzed to provide a basis for medication development for HBV infection. Methods The codon usage pattern of sequences from different HBV genotypes of our isolates and reference HBV genome sequences downloaded from the National Center for Biotechnology Information (NCBI) database were analyzed by computing the relative synonymous codon usage (RSCU), nucleotide content, codon adaptation index (CAI) and the effective number of codons (ENC). Results The highest ENC values were observed in the C genotypes, followed by the B genotypes. The ENC values indicated a weak codon usage bias (CUB) in HBV genome. The number of codons differentially used between the three genotypes was markedly higher than that of similarly used codons. High CAI values indicated a good adaptability of HBV to its host. The ENC plot indicated the occurrence of mutational pressure in the three genotypes. The mean Ka/Ks ratios in the three genotypes were lower than 1, which indicated a negative selection pressure. The CAI and GC3% plot indicated the existence of CUB in the HBV genome. Conclusions Nucleotide composition, mutation bias, negative selection and mutational pressure are key factors influencing the CUB and phylogenetic diversity in HBV genotypes. The data provided here could be useful for developing drugs for HBV infection.

      • KCI등재

        SET8 suppression mediates high glucose-induced vascular endothelial inflammation via the upregulation of PTEN

        Shen Xuefang,Chen Xiangyuan,Wang Jing,Liu Jing,Wang Zhiyao,Hua Qing,Wu Qichao,Su Yanguang,He Huanzhong,Hu Yuqin,Meng Zhipeng,Xiong Wanxia,Zhu Minmin 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-

        Hyperglycemia-mediated endothelial inflammation participates in the pathogenesis of cardiovascular complications in subjects with diabetes. Previous studies reported that phosphatase and tensin homolog deleted on chromosome ten (PTEN) and SET8 participate in high glucose-mediated endothelial inflammation. In this study, we hypothesize that SET8 regulates PTEN expression, thus contributing to high glucose-mediated vascular endothelial inflammation. Our data indicated that plasma soluble intercellular adhesion molecule-1 (sICAM-1) and endothelial selectin (e-selectin) were increased in patients with diabetes and diabetic rats. PTEN expression was augmented in the peripheral blood mononuclear cells of patients with diabetes and in the aortic tissues of diabetic rats. Our in vitro study indicated that high glucose increased monocyte/endothelial adhesion, endothelial adhesion molecule expression and p65 phosphorylation in human umbilical vein endothelial cells (HUVECs). Moreover, high glucose led to endothelial inflammation via upregulation of PTEN. Furthermore, high glucose inhibited SET8 expression and histone H4 lysine 20 methylation (H4K20me1), a downstream target of SET8. SET8 overexpression reversed the effects of high-glucose treatment. shSET8-mediated endothelial inflammation was counteracted by siPTEN. Furthermore, SET8 was found to interact with FOXO1. siFOXO1 attenuated high glucose-mediated endothelial inflammation. FOXO1 overexpression-mediated endothelial inflammation was counteracted by siPTEN. H4K20me1 and FOXO1 were enriched in the PTEN promoter region. shSET8 increased PTEN promoter activity and augmented the positive effect of FOXO1 overexpression on PTEN promoter activity. Our in vivo study indicated that SET8 was downregulated and FOXO1 was upregulated in the peripheral blood mononuclear cells of patients with diabetes and the aortic tissues of diabetic rats. In conclusion, SET8 interacted with FOXO1 to modulate PTEN expression in vascular endothelial cells, thus contributing to hyperglycemia-mediated endothelial inflammation.

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