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RISS 인기검색어
- 검색키워드
- 저자 : Zhibin Ye (검색결과 4 건)
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Wang, Jianli,Song, Yilin,Zhang, Cheng,Ye, Zhibin,Liu, Hui,Lee, Myong-Hoon,Wang, Dehai,Ji, Jianbing WILEY-VCH Verlag 2008 Macromolecular Chemistry and Physics Vol.209 No.14
<P>A novel alternating copolymer of sulfonated poly(ether ether ketone-benzimidazole)s (SPEEK-BI) was synthesized by polycondensation of aromatic bisphenol containing benzimidazole and a mixture of sulfonated and non-sulfonated difluorobenzophenones. By varying the amount of two difluorobenzophenones, the ratio of sulfonic acid unit to imidazole base was controlled straightforwardly. The polymer structure was characterized by <SUP>1</SUP>H NMR and IR spectroscopy. Two different methods of ion exchange capacity measurement supported a strong inter- and intra-molecular interaction between acid and base units, which resulted in an improved mechanical strength as well as avoiding phase separation. Tough membranes with good mechanical stability in hot water (80 °C) and alcohol were obtained by solution casting, which is potential for applications in polymer electrolyte membrane fuel cells and membranes for separation of liquids or gases.</P><P> <img src='wiley_img/10221352-2008-209-14-MACP200700610-gra001.gif' alt='wiley_img/10221352-2008-209-14-MACP200700610-gra001'> </P>
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Ying Xu,Xun Zhou,Yuqi Zheng,Haochen Guan,Chensheng Fu,Jing Xiao,Zhibin Ye 대한고혈압학회 2020 Clinical Hypertension Vol.26 No.2
Background: To analyze the association between hypertension and urinary uric acid excretion in patients with chronic kidney disease (CKD). Methods: We screened 87 patients who had been admitted at the Dept of Nephrology, Huadong hospital between April 2017 to April 2019 who had completed 24-h ambulatory blood pressure monitoring and retained 24-h urine biochemical test specimens, thirty adult patients (age ≤ 65 years) with CKD 1–2 stages were recruited in the study. Pearson’s correlation analysis and multiple linear regression analysis were used to study the correlation of urinary uric acid excretion with ambulatory blood pressure values and the association of morning mean diastolic pressure (mMDP), night mean diastolic pressure (nMDP) and CV of dMSP (coefficient of variation of day mean systolic pressure) with fractional excretion of uric acid (FEua) and uric acid clearance rate (Cur). Independent T test was used to compare the differences of blood pressure values in FEua1 (FEua< 6.0%) and FEua2 (FEua≥6.0%) or Cur1 (Cur < 6.2 ml/min/1.73 m2 ) and Cur2 (Cur ≥ 6.2 ml/min/1.73m2 ) groups according to the median of FEua or Cur, respectively. Results: After adjusting for confounding factors, multiple linear regression analysis showed that FEua was positively associated with the mMDP and nMDP, Cur was positively associated with CV of dMSP. Levels of mMDP and nMDP in FEua1 group was lower than that in FEua2 group (both P < 0.05), level of CV of dMSP in Cur2 group were higher than that in Cur1 group (P < 0.01). Conclusions: We demonstrated that there is a positive correlation of FEua with morning and night mean diastolic pressure separately and Cur is positively related to CV of dMSP in CKD population. Monitoring the trend of urinary uric acid, may have a role in the early detection for hypertension or relative risks in the population of CKD.
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Jing Xiao,Xiaoli Zhang,Chensheng Fu,Qingmei Yang,Ying Xie,Zhenxing Zhang,Zhibin Ye 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Hyperuricemia contributes to renal inflammation. We aimed to investigate the role of Na+–K+–ATPase (NKA) in hyperuricemiainduced renal tubular injury. Human primary proximal tubular epithelial cells (PTECs) were incubated with uric acid (UA) at increasing doses or for increasing lengths of time. PTECs were then stimulated by pre-incubation with an NKA α1 expression vector or small interfering RNA before UA (100 μg ml−1, 48 h) stimulation. Hyperuricemic rats were induced by gastric oxonic acid and treated with febuxostat (Feb). ATP levels, the activity of NKA and expression of its α1 subunit, Src, NOD-like receptor pyrin domain-containing protein 3 (NLRP3) and interleukin 1β (IL-1β) were measured both in vitro and in vivo. Beginning at concentrations of 100 μg ml−1, UA started to dose-dependently reduce NKA activity. UA at a concentration of 100 μg ml−1 time-dependently affected the NKA activity, with the maximal increased NKA activity at 24 h, but the activity started to decrease after 48 h. This inhibitory effect of UA on NKA activity at 48 h was in addition to a decrease in NKA α1 expression in the cell membrane, but an increase in lysosomes. This process also involved the subsequent activation of Src kinase and NLRP3, promoting IL-1β processing. In hyperuricemic rats, renal cortex NKA activity and its α1 expression were upregulated at the 7th week and both decreased at the 10th week, accompanied with increased renal cortex expression of Src, NLRP3 and IL-1β. The UA levels were reduced and renal tubular injuries in hyperuricemic rats were alleviated in the Feb group. Our data suggested that the impairment of NKA and its consequent regulation of Src, NLRP3 and IL-1β in the renal proximal tubule contributed to hyperuricemia-induced renal tubular injury.
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Jing Xiao,Sibo Zhu,Haochen Guan,Haochen Guan,Fengqin Li,Xiaoli Zhang,Hui Guo,Xiaojun Wang,Zhibin Ye 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
One of the mechanisms in hyperuricemia (HUA)-induced renal tubular injury is the impairment of Na+-K+-ATPase (NKA) signaling, which further triggers inflammation, autophagy, and mitochondrial dysfunction and leads to cell injury. Here, we used RNA sequencing to screen the most likely regulators of NKA signaling and found that the liver kinase B1(LKB1)/adenosine monophosphate (AMP)-activated protein kinase (AMPK)/ mammalian target of rapamycin (mTOR) pathway was the most abundantly enriched pathway in HUA. AMPK is a key regulator of cell energy metabolism; hence, we examined the effect of AMPK on HUA-induced dysregulation of NKA signaling and cell injury. We first detected AMPK activation in high uric acid (UA)-stimulated proximal tubular epithelial cells (PTECs). We further found that sustained treatment with the AMPK activator 5-aminoimidazole-4-carboxamide 1-β-d-ribofuranoside (AICAR), but not the AMPK inhibitor Compound C, significantly alleviated UA-induced reductions in NKA activity and NKA α1 subunit expression on the cell membrane by reducing NKA degradation in lysosomes; sustained AICAR treatment also significantly alleviated activation of the NKA downstream molecules Src and interleukin-1β (IL-1β) in PTECs. AICAR further alleviated high UA-induced apoptosis, autophagy, and mitochondrial dysfunction. Although AMPK activation by metformin did not reduce serum UA levels in hyperuricemic rats, it significantly alleviated HUAinduced renal tubular injury and NKA signaling impairment in vivo with effects similar to those of febuxostat. Our study suggests that AMPK activation may temporarily compensate for HUA-induced renal injury. Sustained AMPK activation could reduce lysosomal NKA degradation and maintain NKA function, thus alleviating NKA downstream inflammation and protecting tubular cells from high UA-induced renal tubular injury.
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