BACKGROUND Cell division cyclin 25C(CDC25C)is a protein that plays a critical role in the cell cycle,specifically in the transition from the G2 phase to the M phase.Recent research has shown that CDC25C could be a pot...BACKGROUND Cell division cyclin 25C(CDC25C)is a protein that plays a critical role in the cell cycle,specifically in the transition from the G2 phase to the M phase.Recent research has shown that CDC25C could be a potential therapeutic target for cancers,particularly for hepatocellular carcinoma(HCC).However,the specific regulatory mechanisms underlying the role of CDC25C in HCC tumorigenesis and development remain incompletely understood.AIM To explore the impact of CDC25C on cell proliferation and apoptosis,as well as its regulatory mechanisms in HCC development.METHODS Hepa1-6 and B16 cells were transduced with a lentiviral vector containing shRNA interference sequences(LV-CDC25C shRNA)to knock down CDC25C.Subsequently,a xenograft mouse model was established by subcutaneously injecting transduced Hepa1-6 cells into C57BL/6 mice to assess the effects of CDC25C knockdown on HCC development in vivo.Cell proliferation and migration were evaluated using a Cell Counting Kit-8 cell proliferation assays and wound healing assays,respectively.The expression of endoplasmic reticulum(ER)stress-related molecules(glucose-regulated protein 78,X-box binding protein-1,and C/EBP homologous protein)was measured in both cells and subcutaneous xenografts using quantitative real-time PCR(qRT-PCR)and western blotting.Additionally,apoptosis was investigated using flow cytometry,qRT-PCR,and western blotting.RESULTS CDC25C was stably suppressed in Hepa1-6 and B16 cells through LV-CDC25C shRNA transduction.A xenograft model with CDC25C knockdown was successfully established and that downregulation of CDC25C expression significantly inhibited HCC growth in mice.CDC25C knockdown not only inhibited cell proliferation and migration but also significantly increased the ER stress response,ultimately promoting ER stress-induced apoptosis in HCC cells.CONCLUSION The regulatory mechanism of CDC25C in HCC development may involve the activation of ER stress and the ER stress-induced apoptosis signaling pathway.展开更多
AIM:To analyze the distribution of fibrovascular proliferative membranes(FVPMs)in proliferative diabetic retinopathy(PDR)patients that treated with pars plana vitrectomy(PPV),and to evaluate the outcomes separately.ME...AIM:To analyze the distribution of fibrovascular proliferative membranes(FVPMs)in proliferative diabetic retinopathy(PDR)patients that treated with pars plana vitrectomy(PPV),and to evaluate the outcomes separately.METHODS:This was a retrospective and cross-sectional study.Consecutive 25-gauge(25-G)PPV cases operated for PDR from May 2018 to April 2020.According to the FVPMs images outlined after operations,subjects were assigned into three groups:arcade type group,juxtapapillary type group,and central type group.All patients were followed up for over one year.General characteristics,operation-related variables,postoperative parameters and complications were recorded.RESULTS:Among 103 eyes recruited,the FVPMs distribution of nasotemporal and inferiosuperioral was significantly different(both P<0.01),with 95(92.23%)FVPMs located in the nasal quadrants,and 74(71.84%)in the inferior.The eyes with a central FVPM required the longest operation time,with silicon oil used in most patients,generally combined with tractional retinal detachment(RD)and rhegmatogenous RD,the worst postoperative bestcorrected visual acuity(BCVA)and the highest rates of recurrent RD(all P<0.05).FVPM type,age of onset diabetes mellitus,preoperative BCVA,and combined with tractional RD and rhegmatogenous RD were significantly associated with BCVA improvement(all P<0.05).Compared with the central type group,the arcade type group had higher rates of BCVA improvement.CONCLUSION:FVPMs are more commonly found in the nasal and inferior mid-peripheral retina in addition to the area of arcade vessels.Performing 25-G PPV for treating PDR eyes with central FVPM have relatively worse prognosis.展开更多
目的分析2型糖尿病患者25-羟维生素D[25(OH)D]水平,初步了解血清25(OH)D水平与2型糖尿病患者糖化血红蛋白(HbA1c)、胰岛功能等代谢指标的相关性。方法选择新乡市第一人民医院内分泌科2020年1月至2020年12月收治的459例2型糖尿病患者为...目的分析2型糖尿病患者25-羟维生素D[25(OH)D]水平,初步了解血清25(OH)D水平与2型糖尿病患者糖化血红蛋白(HbA1c)、胰岛功能等代谢指标的相关性。方法选择新乡市第一人民医院内分泌科2020年1月至2020年12月收治的459例2型糖尿病患者为研究对象。收集患者的临床资料,包括性别、年龄、血清25(OH)D、空腹胰岛素、C肽、HbA1c、空腹血糖、餐后血糖、尿微量白蛋白、尿白蛋白肌酐比值、血钙、血尿酸(UA)、三酰甘油(TG)、总胆固醇(TCH)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)等。根据血清25(OH)D水平将患者分为充足组[n=20,25(OH)D≥30μg·L^(-1)]、不足组[n=95,20μg·L^(-1)≤25(OH)D<30μg·L^(-1)]、缺乏组[n=231,10μg·L^(-1)≤25(OH)D<20μg·L^(-1)]、严重缺乏组[n=113,25(OH)D<10μg·L^(-1)]。比较4组患者各代谢指标的差异,采用Pearson相关分析25(OH)D与各代谢指标的相关性。结果2型糖尿病患者血清25(OH)D水平为3.00~46.59(15.75±0.35)μg·L^(-1),男性患者的血清25(OH)D水平显著高于女性患者(P<0.05)。2型糖尿病患者25(OH)D缺乏的患病率为74.9%(344/459),25(OH)D缺乏主要发生在1、2、3、4、11、12月份。不足组、缺乏组和严重缺乏组患者HbA1c显著高于充足组(P<0.05),缺乏组和严重缺乏组患者HbA1c显著高于不足组(P<0.05);缺乏组和严重缺乏组患者HbA1c比较差异无统计学意义(P>0.05)。充足组与不足组、缺乏组与严重缺乏组患者空腹血糖比较差异无统计学意义(P>0.05);缺乏组和严重缺乏组患者空腹血糖显著高于充足组、不足组(P<0.05)。充足组、不足组、缺乏组患者空腹胰岛素、尿微量白蛋白、日尿白蛋白总量、尿白蛋白肌酐比值比较差异无统计学意义(P>0.05);严重缺乏组患者空腹胰岛素显著低于充足组、不足组和缺乏组,尿微量白蛋白、日尿白蛋白总量、尿白蛋白肌酐比值显著高于充足组、不足组和缺乏组(P<0.05)。4组患者的稳态模型评估的胰岛素抵抗指数(HOMA-IR)、血清白蛋白、血肌酐、餐后1 h血糖、餐后2 h血糖、餐后3 h血糖、空腹C肽、餐后1 h C肽、餐后2 h C肽、餐后3 h C肽、TG、TCH、LDL、HDL、血UA、血钙比较差异均无统计学意义(P>0.05)。Pearson相关性分析结果显示,2型糖尿病患者血清25(OH)D水平与HbA1c、尿微量白蛋白、尿白蛋白肌酐比值呈负相关(r=-0.093、-0.166、-0.157,P<0.05),与空腹胰岛素呈正相关(r=0.089,P<0.05)。2型糖尿病患者血清25(OH)D水平与空腹血糖、HOMA-IR、血清白蛋白、血肌酐、餐后1 h血糖、餐后2 h血糖、餐后3 h血糖、空腹C肽、餐后1 h C肽、餐后2 h C肽、餐后3 h C肽、TG、TCH、LDL、HDL、血UA、血钙等无相关性(P>0.05)。结论2型糖尿病患者25(OH)D缺乏与不足普遍存在,女性患者缺乏更明显。2型糖尿病患者25(OH)D水平与空腹胰岛素呈正相关,与HbA1c、尿微量白蛋白、尿白蛋白肌酐比值呈负相关,25(OH)D缺乏的2型糖尿病患者主要分布在1、2、3、4、11、12月份。展开更多
基金Supported by Natural Science Foundation of Guangxi Zhuang Autonomous Region,China,No.2023GXNSFAA026070 and No.2018GXNSFAA281071.
文摘BACKGROUND Cell division cyclin 25C(CDC25C)is a protein that plays a critical role in the cell cycle,specifically in the transition from the G2 phase to the M phase.Recent research has shown that CDC25C could be a potential therapeutic target for cancers,particularly for hepatocellular carcinoma(HCC).However,the specific regulatory mechanisms underlying the role of CDC25C in HCC tumorigenesis and development remain incompletely understood.AIM To explore the impact of CDC25C on cell proliferation and apoptosis,as well as its regulatory mechanisms in HCC development.METHODS Hepa1-6 and B16 cells were transduced with a lentiviral vector containing shRNA interference sequences(LV-CDC25C shRNA)to knock down CDC25C.Subsequently,a xenograft mouse model was established by subcutaneously injecting transduced Hepa1-6 cells into C57BL/6 mice to assess the effects of CDC25C knockdown on HCC development in vivo.Cell proliferation and migration were evaluated using a Cell Counting Kit-8 cell proliferation assays and wound healing assays,respectively.The expression of endoplasmic reticulum(ER)stress-related molecules(glucose-regulated protein 78,X-box binding protein-1,and C/EBP homologous protein)was measured in both cells and subcutaneous xenografts using quantitative real-time PCR(qRT-PCR)and western blotting.Additionally,apoptosis was investigated using flow cytometry,qRT-PCR,and western blotting.RESULTS CDC25C was stably suppressed in Hepa1-6 and B16 cells through LV-CDC25C shRNA transduction.A xenograft model with CDC25C knockdown was successfully established and that downregulation of CDC25C expression significantly inhibited HCC growth in mice.CDC25C knockdown not only inhibited cell proliferation and migration but also significantly increased the ER stress response,ultimately promoting ER stress-induced apoptosis in HCC cells.CONCLUSION The regulatory mechanism of CDC25C in HCC development may involve the activation of ER stress and the ER stress-induced apoptosis signaling pathway.
基金Supported by the Program for Qinhuangdao Self-financing Science and Technology Plan of 2008 (No.201805A143).
文摘AIM:To analyze the distribution of fibrovascular proliferative membranes(FVPMs)in proliferative diabetic retinopathy(PDR)patients that treated with pars plana vitrectomy(PPV),and to evaluate the outcomes separately.METHODS:This was a retrospective and cross-sectional study.Consecutive 25-gauge(25-G)PPV cases operated for PDR from May 2018 to April 2020.According to the FVPMs images outlined after operations,subjects were assigned into three groups:arcade type group,juxtapapillary type group,and central type group.All patients were followed up for over one year.General characteristics,operation-related variables,postoperative parameters and complications were recorded.RESULTS:Among 103 eyes recruited,the FVPMs distribution of nasotemporal and inferiosuperioral was significantly different(both P<0.01),with 95(92.23%)FVPMs located in the nasal quadrants,and 74(71.84%)in the inferior.The eyes with a central FVPM required the longest operation time,with silicon oil used in most patients,generally combined with tractional retinal detachment(RD)and rhegmatogenous RD,the worst postoperative bestcorrected visual acuity(BCVA)and the highest rates of recurrent RD(all P<0.05).FVPM type,age of onset diabetes mellitus,preoperative BCVA,and combined with tractional RD and rhegmatogenous RD were significantly associated with BCVA improvement(all P<0.05).Compared with the central type group,the arcade type group had higher rates of BCVA improvement.CONCLUSION:FVPMs are more commonly found in the nasal and inferior mid-peripheral retina in addition to the area of arcade vessels.Performing 25-G PPV for treating PDR eyes with central FVPM have relatively worse prognosis.
文摘目的分析2型糖尿病患者25-羟维生素D[25(OH)D]水平,初步了解血清25(OH)D水平与2型糖尿病患者糖化血红蛋白(HbA1c)、胰岛功能等代谢指标的相关性。方法选择新乡市第一人民医院内分泌科2020年1月至2020年12月收治的459例2型糖尿病患者为研究对象。收集患者的临床资料,包括性别、年龄、血清25(OH)D、空腹胰岛素、C肽、HbA1c、空腹血糖、餐后血糖、尿微量白蛋白、尿白蛋白肌酐比值、血钙、血尿酸(UA)、三酰甘油(TG)、总胆固醇(TCH)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)等。根据血清25(OH)D水平将患者分为充足组[n=20,25(OH)D≥30μg·L^(-1)]、不足组[n=95,20μg·L^(-1)≤25(OH)D<30μg·L^(-1)]、缺乏组[n=231,10μg·L^(-1)≤25(OH)D<20μg·L^(-1)]、严重缺乏组[n=113,25(OH)D<10μg·L^(-1)]。比较4组患者各代谢指标的差异,采用Pearson相关分析25(OH)D与各代谢指标的相关性。结果2型糖尿病患者血清25(OH)D水平为3.00~46.59(15.75±0.35)μg·L^(-1),男性患者的血清25(OH)D水平显著高于女性患者(P<0.05)。2型糖尿病患者25(OH)D缺乏的患病率为74.9%(344/459),25(OH)D缺乏主要发生在1、2、3、4、11、12月份。不足组、缺乏组和严重缺乏组患者HbA1c显著高于充足组(P<0.05),缺乏组和严重缺乏组患者HbA1c显著高于不足组(P<0.05);缺乏组和严重缺乏组患者HbA1c比较差异无统计学意义(P>0.05)。充足组与不足组、缺乏组与严重缺乏组患者空腹血糖比较差异无统计学意义(P>0.05);缺乏组和严重缺乏组患者空腹血糖显著高于充足组、不足组(P<0.05)。充足组、不足组、缺乏组患者空腹胰岛素、尿微量白蛋白、日尿白蛋白总量、尿白蛋白肌酐比值比较差异无统计学意义(P>0.05);严重缺乏组患者空腹胰岛素显著低于充足组、不足组和缺乏组,尿微量白蛋白、日尿白蛋白总量、尿白蛋白肌酐比值显著高于充足组、不足组和缺乏组(P<0.05)。4组患者的稳态模型评估的胰岛素抵抗指数(HOMA-IR)、血清白蛋白、血肌酐、餐后1 h血糖、餐后2 h血糖、餐后3 h血糖、空腹C肽、餐后1 h C肽、餐后2 h C肽、餐后3 h C肽、TG、TCH、LDL、HDL、血UA、血钙比较差异均无统计学意义(P>0.05)。Pearson相关性分析结果显示,2型糖尿病患者血清25(OH)D水平与HbA1c、尿微量白蛋白、尿白蛋白肌酐比值呈负相关(r=-0.093、-0.166、-0.157,P<0.05),与空腹胰岛素呈正相关(r=0.089,P<0.05)。2型糖尿病患者血清25(OH)D水平与空腹血糖、HOMA-IR、血清白蛋白、血肌酐、餐后1 h血糖、餐后2 h血糖、餐后3 h血糖、空腹C肽、餐后1 h C肽、餐后2 h C肽、餐后3 h C肽、TG、TCH、LDL、HDL、血UA、血钙等无相关性(P>0.05)。结论2型糖尿病患者25(OH)D缺乏与不足普遍存在,女性患者缺乏更明显。2型糖尿病患者25(OH)D水平与空腹胰岛素呈正相关,与HbA1c、尿微量白蛋白、尿白蛋白肌酐比值呈负相关,25(OH)D缺乏的2型糖尿病患者主要分布在1、2、3、4、11、12月份。
