目的:探究浮针配合再灌注活动治疗压力性尿失禁(stress urinary incontinence,SUI)的临床效果。方法:选择赣州市立医院2020年5月—2022年6月收治的女性SUI患者84例为观察对象,按照随机数字表法分成两组。对照组(n=42)予以普通针刺治疗,...目的:探究浮针配合再灌注活动治疗压力性尿失禁(stress urinary incontinence,SUI)的临床效果。方法:选择赣州市立医院2020年5月—2022年6月收治的女性SUI患者84例为观察对象,按照随机数字表法分成两组。对照组(n=42)予以普通针刺治疗,观察组(n=42)则予以浮针配合再灌注活动治疗,均持续治疗4周。对比分析两组治疗前、治疗后1个月的尿失禁严重程度、盆底肌肌力、性生活质量,并观察两组康复治疗效果。结果:治疗后1个月,两组国际尿失禁咨询委员会尿失禁问卷简表(international consulation on incontinence questionnaire short form,ICI-Q-SF)评分较治疗前均降低,且观察组较对照组更低,差异均有统计学意义(P<0.05);治疗后1个月,两组Ⅰ、Ⅱ类肌纤维肌电较治疗前均升高,且观察组较对照组均更高,差异均有统计学意义(P<0.05);治疗后1个月,两组盆腔脏器脱垂/尿失禁性功能问卷(pelvic organ prolapse/urinary incontinence sexual function questionnaire-12,PISQ-12)评分较治疗前均升高,且观察组较对照组更高,差异均有统计学意义(P<0.05);观察组的总有效率[85.71%(36/42)]高于对照组[61.90%(26/42)],差异有统计学意义(P<0.05)。结论:SUI患者予以浮针配合再灌注活动治疗具有显著效果,能更好地促进尿失禁症状改善,还能强化患者盆底肌肌力,提升患者性生活质量。展开更多
Background and Aims:Hepatic ischemia-reperfusion injury(HIRI)is a prevalent complication of liver transplantation,partial hepatectomy,and severe infection,necessitating the development of more effective clinical strat...Background and Aims:Hepatic ischemia-reperfusion injury(HIRI)is a prevalent complication of liver transplantation,partial hepatectomy,and severe infection,necessitating the development of more effective clinical strategies.Receptor activity–modifying protein 1(RAMP1),a member of the G protein–coupled receptor adapter family,has been implicated in numerous physiological and pathological processes.The study aimed to investigate the pathogenesis of RAMP1 in HIRI.Methods:We established a 70%liver ischemia-reperfusion model in RAMP1 knockout(KO)and wild-type mice.Liver and blood samples were collected after 0,6,and 24 h of hypoxia/reperfusion.Liver histological and serological analyses were performed to evaluate liver damage.We also conducted in-vitro and in-vivo experiments to explore the molecular mechanism underlying RAMP1 function.Results:Liver injury was exacerbated in RAMP1-KO mice compared with the sham group,as evidenced by increased cell death and elevated serum transaminase and inflammation levels.HIRI was promoted in RAMP1-KO mice via the induction of hepatocyte apoptosis and inhibition of proliferation.The absence of RAMP1 led to increased activation of the extracellular signal–regulated kinase(ERK)/mitogen-activated protein kinase(MAPK)pathway and yes-associated protein(YAP)phosphorylation,ultimately promoting apoptosis.SCH772984,an ERK/MAPK phosphorylation inhibitor,and PY-60,a YAP phosphorylation inhibitor,reduced apoptosis in in-vitro and in-vivo experiments.Conclusions:Our findings suggest that RAMP1 protects against HIRI by inhibiting ERK and YAP phosphorylation signal transduction,highlighting its potential as a therapeutic target for HIRI and providing a new avenue for intervention.展开更多
文摘目的:探究浮针配合再灌注活动治疗压力性尿失禁(stress urinary incontinence,SUI)的临床效果。方法:选择赣州市立医院2020年5月—2022年6月收治的女性SUI患者84例为观察对象,按照随机数字表法分成两组。对照组(n=42)予以普通针刺治疗,观察组(n=42)则予以浮针配合再灌注活动治疗,均持续治疗4周。对比分析两组治疗前、治疗后1个月的尿失禁严重程度、盆底肌肌力、性生活质量,并观察两组康复治疗效果。结果:治疗后1个月,两组国际尿失禁咨询委员会尿失禁问卷简表(international consulation on incontinence questionnaire short form,ICI-Q-SF)评分较治疗前均降低,且观察组较对照组更低,差异均有统计学意义(P<0.05);治疗后1个月,两组Ⅰ、Ⅱ类肌纤维肌电较治疗前均升高,且观察组较对照组均更高,差异均有统计学意义(P<0.05);治疗后1个月,两组盆腔脏器脱垂/尿失禁性功能问卷(pelvic organ prolapse/urinary incontinence sexual function questionnaire-12,PISQ-12)评分较治疗前均升高,且观察组较对照组更高,差异均有统计学意义(P<0.05);观察组的总有效率[85.71%(36/42)]高于对照组[61.90%(26/42)],差异有统计学意义(P<0.05)。结论:SUI患者予以浮针配合再灌注活动治疗具有显著效果,能更好地促进尿失禁症状改善,还能强化患者盆底肌肌力,提升患者性生活质量。
基金supported by:The National Natural Science Foundation of China(82270688,81402426)The Natural Science Foundation.of Guangdong Province(2021A1515010726,2022A1515012650,2020A1515010302)+1 种基金The Cultivation Project of National Natural Science Foundationof the Third Affliated Hospital of Sun Yat-sen University(No.2020GzRPYMS09)Science and Technology ProjectsinGuangzhou(No.202102010310,202201020427).
文摘Background and Aims:Hepatic ischemia-reperfusion injury(HIRI)is a prevalent complication of liver transplantation,partial hepatectomy,and severe infection,necessitating the development of more effective clinical strategies.Receptor activity–modifying protein 1(RAMP1),a member of the G protein–coupled receptor adapter family,has been implicated in numerous physiological and pathological processes.The study aimed to investigate the pathogenesis of RAMP1 in HIRI.Methods:We established a 70%liver ischemia-reperfusion model in RAMP1 knockout(KO)and wild-type mice.Liver and blood samples were collected after 0,6,and 24 h of hypoxia/reperfusion.Liver histological and serological analyses were performed to evaluate liver damage.We also conducted in-vitro and in-vivo experiments to explore the molecular mechanism underlying RAMP1 function.Results:Liver injury was exacerbated in RAMP1-KO mice compared with the sham group,as evidenced by increased cell death and elevated serum transaminase and inflammation levels.HIRI was promoted in RAMP1-KO mice via the induction of hepatocyte apoptosis and inhibition of proliferation.The absence of RAMP1 led to increased activation of the extracellular signal–regulated kinase(ERK)/mitogen-activated protein kinase(MAPK)pathway and yes-associated protein(YAP)phosphorylation,ultimately promoting apoptosis.SCH772984,an ERK/MAPK phosphorylation inhibitor,and PY-60,a YAP phosphorylation inhibitor,reduced apoptosis in in-vitro and in-vivo experiments.Conclusions:Our findings suggest that RAMP1 protects against HIRI by inhibiting ERK and YAP phosphorylation signal transduction,highlighting its potential as a therapeutic target for HIRI and providing a new avenue for intervention.
