Objective Mitochondrial reactive oxygen species(mtROS)could cause damage to pancreaticβ-cells,rendering them susceptible to oxidative damage.Hence,investigating the potential of the mitochondriatargeted antioxidant(M...Objective Mitochondrial reactive oxygen species(mtROS)could cause damage to pancreaticβ-cells,rendering them susceptible to oxidative damage.Hence,investigating the potential of the mitochondriatargeted antioxidant(Mito-TEMPO)to protect pancreaticβ-cells from ferroptosis by mitigating lipid peroxidation becomes crucial.Methods MIN6 cells were cultured in vitro with 100μmol/L sodium palmitate(SP)to simulate diabetes.FerroOrange was utilized for the detection of Fe2+fluorescence staining,BODIPY581/591C11 for lipid reactive oxygen species,and MitoSox-Red for mtROS.Alterations in mitophagy levels were assessed through the co-localization of lysosomal and mitochondrial fluorescence.Western blotting was employed to quantify protein levels of Acsl4,GPX4,FSP1,FE,PINK1,Parkin,TOMM20,P62,and LC3.Subsequently,interventions were implemented using Mito-TEMPO and Carbonyl cyanide 3-chlorophenylhydrazone(CCCP)to observe changes in ferroptosis and mitophagy within MIN6 cells.Results We found that SP induced a dose-dependent increase in Fe2+and lipid ROS in MIN6 cells while decreasing the expression levels of GPX4 and FSP1 proteins.Through bioinformatics analysis,it has been uncovered that mitophagy assumes a crucial role within the ferroptosis pathway associated with diabetes.Additionally,SP decreased the expression of mitophagy-related proteins PINK1 and Parkin,leading to mtROS overproduction.Conversely,Mito-TEMPO effectively eliminated mtROS while activating the mitophagy pathways involving PINK1 and Parkin,thereby reducing the occurrence of ferroptosis in MIN6 cells.CCCP also demonstrated efficacy in reducing ferroptosis in MIN6 cells.Conclusion In summary,Mito-TEMPO proved effective in attenuating mtROS production and initiating mitophagy pathways mediated by PINK1 and Parkin in MIN6 cells.Consequently,this decreased iron overload and lipid peroxidation,ultimately safeguarding the cells from ferroptosis.展开更多
在对网格计算中现有的任务调度算法的研究基础上,仔细分析了调度算法中最经典的Min Min算法,指出了该算法中所存在的负载不平衡的缺点,并在该算法的基础上提出了一个改进模型来有效的平衡负载,同时给出了相应的Balance Min Min算法。最...在对网格计算中现有的任务调度算法的研究基础上,仔细分析了调度算法中最经典的Min Min算法,指出了该算法中所存在的负载不平衡的缺点,并在该算法的基础上提出了一个改进模型来有效的平衡负载,同时给出了相应的Balance Min Min算法。最后采用SimGrid工具包对所提出的算法进行仿真,验证了算法的合理性和高效性。展开更多
目的探讨彩色多普勒超声联合血清神经元特异性烯醇化酶(neuron-specific enolase,NSE)及5 min Apgar评分对新生儿颅内出血(intracranial hemorrhage,ICH)的诊断价值及影响ICH发生的危险因素。方法选取2019年2月至2021年3月承德市中心医...目的探讨彩色多普勒超声联合血清神经元特异性烯醇化酶(neuron-specific enolase,NSE)及5 min Apgar评分对新生儿颅内出血(intracranial hemorrhage,ICH)的诊断价值及影响ICH发生的危险因素。方法选取2019年2月至2021年3月承德市中心医院新生儿科收治的存在颅脑损伤危险因素的253例新生儿为研究对象,均接受彩色多普勒超声检查,根据是否存在ICH分为ICH组(n=99)和无ICH组(n=154)。观察并比较两组彩色多普勒超声参数[收缩期峰值流速(peak systolicvelocity,PSV)、阻力指数(resistance index,RI)、舒张末期流速(end diastolic velocity,EDV)]、血清NSE水平、5 min Apgar评分情况,分析血清NSE水平、Apgar评分与彩色多普勒超声参数的相关性及三者联合检测对新生儿ICH的诊断价值,并分析ICH发生的主要影响因素。统计学方法采用独立样本t检验、χ^(2)检验、Pearson相关性分析、Logistic回归分析及受试者操作特征(receiver operating characteristic,ROC)曲线分析。结果ICH组与无ICH组PSV[(6.4±1.2)cm/s与(10.1±1.4)cm/s,t=21.628]、RI(0.6±0.1与0.7±0.1,t=8.144)、EDV[(2.5±0.4)cm/s与(3.1±0.4)cm/s,t=13.216]以及5 min Apgar评分[(6.5±1.7)分与(8.8±1.0)分,t=13.308]比较,ICH组均显著低于无ICH组(P值均<0.001);血清NSE水平显著高于无ICH组[(149.1±10.6)μg/L与(95.2±10.4)μg/L,t=40.015,P<0.001]。ICH组血清NSE水平与彩色多普勒超声参数PSV、RI、EDV呈负相关(r值分为-0.573、-0.520、-0.536,P值均<0.05);5 min Apgar评分与彩色多普勒超声参数PSV、RI、EDV呈正相关(r值分别为0.601、0.529、0.505,P值均<0.05)。ROC曲线结果发现,彩色多普勒超声、血清NSE水平、5 min Apgar评分联合诊断新生儿ICH的曲线下面积(area under the curve,AUC)最大,为0.861。单因素分析显示,与无ICH组比较,ICH组患儿的胎龄更小,出生体质量、5 min Apgar评分更低,出生窒息、应用多巴胺、应用机械通气比例及血清NSE水平更高,差异有统计学意义(P值均<0.05)。多因素Logistic回归分析结果显示,胎龄<32周、出生体质量<1500 g、血清NSE水平>117.95μg/L、5 min Apgar评分<7分是诱发ICH的独立危险因素。结论彩色多普勒超声联合血清NSE及5 min Apgar评分可提高ICH的诊断价值;胎龄<32周、出生体质量<1500 g、血清NSE水平>117.95μg/L、5 min Apgar评分<7分是诱发ICH的独立危险因素。展开更多
基金supported by a grant from the Science and Technology Tackling Programme Project of Xinjiang Production and Construction Corps(2021AB030).
文摘Objective Mitochondrial reactive oxygen species(mtROS)could cause damage to pancreaticβ-cells,rendering them susceptible to oxidative damage.Hence,investigating the potential of the mitochondriatargeted antioxidant(Mito-TEMPO)to protect pancreaticβ-cells from ferroptosis by mitigating lipid peroxidation becomes crucial.Methods MIN6 cells were cultured in vitro with 100μmol/L sodium palmitate(SP)to simulate diabetes.FerroOrange was utilized for the detection of Fe2+fluorescence staining,BODIPY581/591C11 for lipid reactive oxygen species,and MitoSox-Red for mtROS.Alterations in mitophagy levels were assessed through the co-localization of lysosomal and mitochondrial fluorescence.Western blotting was employed to quantify protein levels of Acsl4,GPX4,FSP1,FE,PINK1,Parkin,TOMM20,P62,and LC3.Subsequently,interventions were implemented using Mito-TEMPO and Carbonyl cyanide 3-chlorophenylhydrazone(CCCP)to observe changes in ferroptosis and mitophagy within MIN6 cells.Results We found that SP induced a dose-dependent increase in Fe2+and lipid ROS in MIN6 cells while decreasing the expression levels of GPX4 and FSP1 proteins.Through bioinformatics analysis,it has been uncovered that mitophagy assumes a crucial role within the ferroptosis pathway associated with diabetes.Additionally,SP decreased the expression of mitophagy-related proteins PINK1 and Parkin,leading to mtROS overproduction.Conversely,Mito-TEMPO effectively eliminated mtROS while activating the mitophagy pathways involving PINK1 and Parkin,thereby reducing the occurrence of ferroptosis in MIN6 cells.CCCP also demonstrated efficacy in reducing ferroptosis in MIN6 cells.Conclusion In summary,Mito-TEMPO proved effective in attenuating mtROS production and initiating mitophagy pathways mediated by PINK1 and Parkin in MIN6 cells.Consequently,this decreased iron overload and lipid peroxidation,ultimately safeguarding the cells from ferroptosis.
文摘在对网格计算中现有的任务调度算法的研究基础上,仔细分析了调度算法中最经典的Min Min算法,指出了该算法中所存在的负载不平衡的缺点,并在该算法的基础上提出了一个改进模型来有效的平衡负载,同时给出了相应的Balance Min Min算法。最后采用SimGrid工具包对所提出的算法进行仿真,验证了算法的合理性和高效性。
文摘目的探讨彩色多普勒超声联合血清神经元特异性烯醇化酶(neuron-specific enolase,NSE)及5 min Apgar评分对新生儿颅内出血(intracranial hemorrhage,ICH)的诊断价值及影响ICH发生的危险因素。方法选取2019年2月至2021年3月承德市中心医院新生儿科收治的存在颅脑损伤危险因素的253例新生儿为研究对象,均接受彩色多普勒超声检查,根据是否存在ICH分为ICH组(n=99)和无ICH组(n=154)。观察并比较两组彩色多普勒超声参数[收缩期峰值流速(peak systolicvelocity,PSV)、阻力指数(resistance index,RI)、舒张末期流速(end diastolic velocity,EDV)]、血清NSE水平、5 min Apgar评分情况,分析血清NSE水平、Apgar评分与彩色多普勒超声参数的相关性及三者联合检测对新生儿ICH的诊断价值,并分析ICH发生的主要影响因素。统计学方法采用独立样本t检验、χ^(2)检验、Pearson相关性分析、Logistic回归分析及受试者操作特征(receiver operating characteristic,ROC)曲线分析。结果ICH组与无ICH组PSV[(6.4±1.2)cm/s与(10.1±1.4)cm/s,t=21.628]、RI(0.6±0.1与0.7±0.1,t=8.144)、EDV[(2.5±0.4)cm/s与(3.1±0.4)cm/s,t=13.216]以及5 min Apgar评分[(6.5±1.7)分与(8.8±1.0)分,t=13.308]比较,ICH组均显著低于无ICH组(P值均<0.001);血清NSE水平显著高于无ICH组[(149.1±10.6)μg/L与(95.2±10.4)μg/L,t=40.015,P<0.001]。ICH组血清NSE水平与彩色多普勒超声参数PSV、RI、EDV呈负相关(r值分为-0.573、-0.520、-0.536,P值均<0.05);5 min Apgar评分与彩色多普勒超声参数PSV、RI、EDV呈正相关(r值分别为0.601、0.529、0.505,P值均<0.05)。ROC曲线结果发现,彩色多普勒超声、血清NSE水平、5 min Apgar评分联合诊断新生儿ICH的曲线下面积(area under the curve,AUC)最大,为0.861。单因素分析显示,与无ICH组比较,ICH组患儿的胎龄更小,出生体质量、5 min Apgar评分更低,出生窒息、应用多巴胺、应用机械通气比例及血清NSE水平更高,差异有统计学意义(P值均<0.05)。多因素Logistic回归分析结果显示,胎龄<32周、出生体质量<1500 g、血清NSE水平>117.95μg/L、5 min Apgar评分<7分是诱发ICH的独立危险因素。结论彩色多普勒超声联合血清NSE及5 min Apgar评分可提高ICH的诊断价值;胎龄<32周、出生体质量<1500 g、血清NSE水平>117.95μg/L、5 min Apgar评分<7分是诱发ICH的独立危险因素。
文摘空间聚类是空间数据挖掘的重要手段之一。本文研究了一种基于质心点距离的Max-min distance空间聚类算法:通过加载园地图斑数据,计算其园地图斑质心,判断聚类中心之间的距离,并将符合条件的园地图斑进行聚类,最终将聚类结果可视化表达。本文的算法是利用Visual Studio 2017实验平台和ArcGIS Engine组件式开发环境,采用C#语言进行编写。实验结果表明:1)Max-mindistance聚类通过启发式的选择簇中心,克服了K-means选择簇中心过于邻近的缺点,能够适应嵩口镇等山区丘陵地区空间分布呈破碎的园地数据集分布,有效地实现园地的合理聚类;2)根据连片面积将园地空间聚类结果分为大中小三类,未来嵩口镇可以重点发展园地连片规模较大的村庄,形成规模化的青梅种植园。
