Pathological cardiac hypertrophy is an early and significant cardiac structural characteristic that contributes to the onset and progression of heart failure(HF).Its mainly structural feature is the abnormally enlarge...Pathological cardiac hypertrophy is an early and significant cardiac structural characteristic that contributes to the onset and progression of heart failure(HF).Its mainly structural feature is the abnormally enlarged cardiomyocyte.Effective intervention targets for abnormally enlarged cardiomyocyte remain to be identified.Previous studies have shown that the cellular shape and size can be regulated by the actin related protein 2/3(Arp2/3)complex,which is an actin-binding protein complex involved in the actin nucleation and assembly.However,the roles of the Arp2/3 complex in cardiomyocyte hypertrophy remain unknown.Here our study identifies its novel roles in the occurrence and development of cardiomyocyte hypertrophy.We found that mRNA levels of all subunits from the Arp2/3 complex are significantly upregulated(P<0.05)in the angiotensin Ⅱ(Ang Ⅱ)-induced neonatal rat primary and H9c2 cardiomyocyte hypertrophy.Further studies showed that siRNA-directed ARPC 2 silencing inhibits the reactivation of fetal genes and enlargement of cardiomyocyte area induced by Ang Ⅱ in neonatal rat primary cardiomyocytes(NRCMs)and H9c2 cells(P<0.05).In addition,the upstream activators of the Arp2/3 complex including SH3 protein interacting with Nck,90 kD(SPIN90)and Ras-related C3 botulinum toxin substrate 1(Rac1)/WASp family Verprolin-homologous protein-2(WAVE-2)are upregulated(P<0.05)in Ang Ⅱ-induced neonatal rat primary and H9c2 cardiomyocyte hypertrophy,indicating the excessive activation of the Arp2/3 complex.We further show that CK666,a specific Arp2/3 complex inhibitor,prevents the reactivation of fetal genes and the enlargement of cardiomyocyte area induced by Ang Ⅱ in NRCMs and H9c2 cells(P<0.05).Our results reveal that the Arp2/3 complex plays a crucial role in Ang Ⅱ-induced cardiomyocyte hypertrophy,which is beneficial to further studies about the molecular mechanisms by which the Arp2/3 complex regulates pathological cardiac hypertrophy.展开更多
目的分析脓毒症肺损伤患者中医证型分布状况与肺损伤相关指标及序贯性器官衰竭评分(sequential organ failure assessment,SOFA)、急性生理和慢性健康状况Ⅱ(Acute Physiology and Chronic Health EvaluationⅡ,APACHEⅡ)评分的相关性...目的分析脓毒症肺损伤患者中医证型分布状况与肺损伤相关指标及序贯性器官衰竭评分(sequential organ failure assessment,SOFA)、急性生理和慢性健康状况Ⅱ(Acute Physiology and Chronic Health EvaluationⅡ,APACHEⅡ)评分的相关性。方法选取2022年1月—2023年1月医院收治的脓毒症肺损伤患者80例,收集患者的一般资料、肺损伤相关指标[动脉血氧合指数(ratio of partial pressure of O_(2) in arterial blood to fraction of inspired oxygen,PaO_(2)/FiO_(2))、肺泡动脉氧分压差(alveolar-arterial oxygen gradient,P(A-a)O_(2))]及SOFA、APACHEⅡ评分情况,根据中医分型标准对脓毒症肺损伤患者进行分型,比较不同分型的脓毒症肺损伤患者以上各观察指标情况并分析相关性。结果脓毒症肺损伤患者以肺热壅痹证型占比最高、35.00%(28/80),其次为瘀血阻肺型27.50%(22/80),肺塞腑实型23.75%(19/80),水饮郁肺型13.75%(11/80)。不同证型的患者在性别、年龄方面差异均无统计学意义(P>0.05);不同证型的患者肺损伤指标PaO_(2)/FiO_(2)、P(A-a)O_(2)差异均有统计学意义(P<0.05);不同证型的患者SOFA、APACHEⅡ评分差异均有统计学意义(P<0.05)。肺热壅痹、瘀血阻肺、肺塞腑实、水饮郁肺证型与PaO_(2)/FiO_(2)呈显著负相关(P<0.05),与P(A-a)O_(2)、SOFA评分、APACHEⅡ评分呈显著正相关(P<0.05)。结论脓毒症肺损伤患者中医证型主要为肺热壅痹、瘀血阻肺、肺塞腑实、水饮郁肺,与肺损伤相关指标及SOFA、APACHEⅡ评分密切相关,掌握脓毒症肺损伤辨证分型特点并观察患者肺损伤相关指标及SOFA、APACHEⅡ评分变化,对疾病诊治及预后评估具有较高价值。展开更多
横波可控震源振动器平板作为页岩气勘探中的关键部件,其疲劳寿命直接影响可控震源的使用寿命和勘探精度。然而,传统的振动器平板疲劳寿命优化方法未考虑平板与平板齿间焊接残余应力的影响,导致平板结构在抗疲劳优化设计方面效果不佳。为...横波可控震源振动器平板作为页岩气勘探中的关键部件,其疲劳寿命直接影响可控震源的使用寿命和勘探精度。然而,传统的振动器平板疲劳寿命优化方法未考虑平板与平板齿间焊接残余应力的影响,导致平板结构在抗疲劳优化设计方面效果不佳。为此,使用局部灵敏度法对平板疲劳寿命进行敏感性分析,确定了焊接残余应力为影响疲劳寿命的关键因素。随后,建立了平板的各向最大焊接残余应力与焊接速度和焊接层间温度之间的数学模型,并以各向最大焊接残余应力为约束,以疲劳寿命为优化目标,建立相应的优化模型。最后,利用NSGA-Ⅱ(nondominated sorting genetic algorithm-Ⅱ,非支配排序遗传算法-Ⅱ)获取Pareto解集,并结合熵权法和TOPSIS(technique for order preference by similarity to ideal solution,逼近理想解排序)法确定最佳优化方案:焊接速度为10.23 mm/s,焊接层间温度为105℃。结果表明,优化后平板的疲劳寿命为10.23年,相比优化前提高了17.72%。研究结果可为横波可控震源振动器平板的疲劳寿命优化提供科学有效的理论方法和工程指导。展开更多
文摘Pathological cardiac hypertrophy is an early and significant cardiac structural characteristic that contributes to the onset and progression of heart failure(HF).Its mainly structural feature is the abnormally enlarged cardiomyocyte.Effective intervention targets for abnormally enlarged cardiomyocyte remain to be identified.Previous studies have shown that the cellular shape and size can be regulated by the actin related protein 2/3(Arp2/3)complex,which is an actin-binding protein complex involved in the actin nucleation and assembly.However,the roles of the Arp2/3 complex in cardiomyocyte hypertrophy remain unknown.Here our study identifies its novel roles in the occurrence and development of cardiomyocyte hypertrophy.We found that mRNA levels of all subunits from the Arp2/3 complex are significantly upregulated(P<0.05)in the angiotensin Ⅱ(Ang Ⅱ)-induced neonatal rat primary and H9c2 cardiomyocyte hypertrophy.Further studies showed that siRNA-directed ARPC 2 silencing inhibits the reactivation of fetal genes and enlargement of cardiomyocyte area induced by Ang Ⅱ in neonatal rat primary cardiomyocytes(NRCMs)and H9c2 cells(P<0.05).In addition,the upstream activators of the Arp2/3 complex including SH3 protein interacting with Nck,90 kD(SPIN90)and Ras-related C3 botulinum toxin substrate 1(Rac1)/WASp family Verprolin-homologous protein-2(WAVE-2)are upregulated(P<0.05)in Ang Ⅱ-induced neonatal rat primary and H9c2 cardiomyocyte hypertrophy,indicating the excessive activation of the Arp2/3 complex.We further show that CK666,a specific Arp2/3 complex inhibitor,prevents the reactivation of fetal genes and the enlargement of cardiomyocyte area induced by Ang Ⅱ in NRCMs and H9c2 cells(P<0.05).Our results reveal that the Arp2/3 complex plays a crucial role in Ang Ⅱ-induced cardiomyocyte hypertrophy,which is beneficial to further studies about the molecular mechanisms by which the Arp2/3 complex regulates pathological cardiac hypertrophy.
文摘目的分析脓毒症肺损伤患者中医证型分布状况与肺损伤相关指标及序贯性器官衰竭评分(sequential organ failure assessment,SOFA)、急性生理和慢性健康状况Ⅱ(Acute Physiology and Chronic Health EvaluationⅡ,APACHEⅡ)评分的相关性。方法选取2022年1月—2023年1月医院收治的脓毒症肺损伤患者80例,收集患者的一般资料、肺损伤相关指标[动脉血氧合指数(ratio of partial pressure of O_(2) in arterial blood to fraction of inspired oxygen,PaO_(2)/FiO_(2))、肺泡动脉氧分压差(alveolar-arterial oxygen gradient,P(A-a)O_(2))]及SOFA、APACHEⅡ评分情况,根据中医分型标准对脓毒症肺损伤患者进行分型,比较不同分型的脓毒症肺损伤患者以上各观察指标情况并分析相关性。结果脓毒症肺损伤患者以肺热壅痹证型占比最高、35.00%(28/80),其次为瘀血阻肺型27.50%(22/80),肺塞腑实型23.75%(19/80),水饮郁肺型13.75%(11/80)。不同证型的患者在性别、年龄方面差异均无统计学意义(P>0.05);不同证型的患者肺损伤指标PaO_(2)/FiO_(2)、P(A-a)O_(2)差异均有统计学意义(P<0.05);不同证型的患者SOFA、APACHEⅡ评分差异均有统计学意义(P<0.05)。肺热壅痹、瘀血阻肺、肺塞腑实、水饮郁肺证型与PaO_(2)/FiO_(2)呈显著负相关(P<0.05),与P(A-a)O_(2)、SOFA评分、APACHEⅡ评分呈显著正相关(P<0.05)。结论脓毒症肺损伤患者中医证型主要为肺热壅痹、瘀血阻肺、肺塞腑实、水饮郁肺,与肺损伤相关指标及SOFA、APACHEⅡ评分密切相关,掌握脓毒症肺损伤辨证分型特点并观察患者肺损伤相关指标及SOFA、APACHEⅡ评分变化,对疾病诊治及预后评估具有较高价值。
文摘横波可控震源振动器平板作为页岩气勘探中的关键部件,其疲劳寿命直接影响可控震源的使用寿命和勘探精度。然而,传统的振动器平板疲劳寿命优化方法未考虑平板与平板齿间焊接残余应力的影响,导致平板结构在抗疲劳优化设计方面效果不佳。为此,使用局部灵敏度法对平板疲劳寿命进行敏感性分析,确定了焊接残余应力为影响疲劳寿命的关键因素。随后,建立了平板的各向最大焊接残余应力与焊接速度和焊接层间温度之间的数学模型,并以各向最大焊接残余应力为约束,以疲劳寿命为优化目标,建立相应的优化模型。最后,利用NSGA-Ⅱ(nondominated sorting genetic algorithm-Ⅱ,非支配排序遗传算法-Ⅱ)获取Pareto解集,并结合熵权法和TOPSIS(technique for order preference by similarity to ideal solution,逼近理想解排序)法确定最佳优化方案:焊接速度为10.23 mm/s,焊接层间温度为105℃。结果表明,优化后平板的疲劳寿命为10.23年,相比优化前提高了17.72%。研究结果可为横波可控震源振动器平板的疲劳寿命优化提供科学有效的理论方法和工程指导。
