Ankle snapping occurs when tendons or retinacular structures abruptly move or slip over adjacent anatomical structures,often due to anatomical variations,pathological conditions,or acute injury.This phenomenon can cau...Ankle snapping occurs when tendons or retinacular structures abruptly move or slip over adjacent anatomical structures,often due to anatomical variations,pathological conditions,or acute injury.This phenomenon can cause pain and discomfort,ranging from mild irritation to debilitating symptoms that potentially disrupt daily activities and athletic pursuits.Considering the anatomy of the ankle,these snapping phenomena can be categorized into four regional groups:(1)Lateral;(2)Medial;(3)Anterior;and(4)Posterior.Lateral ankle snapping,a common occurrence,typically results from peroneal tendon subluxation due to compromise of the superior and inferior peroneal retinacula,or from intrasheath subluxation,characterized by abnormal tendon motion within an otherwise intact retromalleolar groove and retinaculum.Medial ankle snapping primarily affects the posterior tibial tendon and can involve the flexor digitorum longus tendon.Anterior ankle snapping results from abnormal gliding of the tibialis anterior tendon,extensor digitorum longus tendon,peroneus tertius tendon,and inferior extensor retinaculum.Posterior ankle snapping typically involves the plantaris tendon and flexor hallucis longus(hallux saltans).This mini-review comprehensively explores these snapping phenomena and their related pathologies in the foot and ankle,emphasizing the crucial roles of anatomical knowledge,thorough clinical assessment,and appropriate diagnostic and treatment approaches.展开更多
This is a correction to:Isabela R R Moraes,Mariana Antunes,Laura S Lopez-Greco,Fernando Jose Zara,Antonio Leao Castilho,Functional reproductive morphology of the snapping shrimp genus Synalpheus Spence Bate,1888(Decap...This is a correction to:Isabela R R Moraes,Mariana Antunes,Laura S Lopez-Greco,Fernando Jose Zara,Antonio Leao Castilho,Functional reproductive morphology of the snapping shrimp genus Synalpheus Spence Bate,1888(Decapoda,Alpheidae),Current Zoology,2024,71,338-352;https:/doi.org/10.1093/cz/zoae053.展开更多
BACKGROUND Hepatic ischemia-reperfusion(I/R)injury related to liver transplantation and hepatic resection remains a challenge in clinical practice.Accumulating evidence indicates that mitochondrial dysfunction is a cr...BACKGROUND Hepatic ischemia-reperfusion(I/R)injury related to liver transplantation and hepatic resection remains a challenge in clinical practice.Accumulating evidence indicates that mitochondrial dysfunction is a critical cause of I/R injury.The protein 4-nitrophenylphosphatase domain and non-neuronal SNAP25-like protein homolog 1(NIPSNAP1)is involved in the regulation of mitophagy and the recruitment of autophagy receptor proteins independent of PTEN induced putative kinase 1.AIM To clarify the protective mechanism of NIPSNAP1 against hepatic I/R,with a focus on mitophagy and mitochondrial dynamics,as well as the potential mechanism by which n6-methyladenosine(m6A)modification regulates NIPSNAP1.METHODS Mice were administered an adeno-associated virus in vivo and a hepatic I/R model was established via portal vein interruption followed by reperfusion to explore the effect of NIPSNAP1 on hepatic I/R.HepG2 cells were subjected to hypoxia/reoxygenation treatment in vitro.RESULTS We observed a significant downregulation of both NIPSNAP1 and insulin-like growth factor 2 mRNA-binding protein 2(IGF2BP2)expression in vivo and in vitro.NIPSNAP1 knockdown impaired mitophagy and disrupted mitochondrial dynamics;in contrast,NIPSNAP1 overexpression resulted in the opposite effects.Further studies revealed that IGF2BP2 functions as an m6A reader that targets and binds NIPSNAP1,thereby regulating its mRNA stability.CONCLUSION NIPSNAP1 prevents hepatic I/R injury by promoting mitophagy and maintaining mitochondrial homeostasis,serving as a novel target of the m6A reader IGF2BP2.Therefore,targeting the IGF2BP2/NIPSNAP1 axis may facilitate the development of better therapeutics for hepatic I/R.展开更多
细胞自噬是将细胞内受损、变性、衰老的蛋白质或细胞器清除的过程,是细胞本身的代谢需要,也是某些细胞器的更新。自噬过程涉及膜融合。可溶性N-乙基马来酰亚胺敏感的融合蛋白附着蛋白受体(soluble N-ethylmaleimide-sensitive factor at...细胞自噬是将细胞内受损、变性、衰老的蛋白质或细胞器清除的过程,是细胞本身的代谢需要,也是某些细胞器的更新。自噬过程涉及膜融合。可溶性N-乙基马来酰亚胺敏感的融合蛋白附着蛋白受体(soluble N-ethylmaleimide-sensitive factor attachment protein receptor,SNARE)之间相互作用形成SNARE复合体参与膜融合。突触样相关蛋白25(synaptosomal-associated protein of 25 kDa,SNAP25)亚家族成员包括SNAP25、SNAP23、SNAP47和SNAP29,可与其他SNARE相互作用形成SNARE复合体从而参与自噬。本文着重对SNAP25亚家族中各成员如何参与自噬,以及在自噬中所起的作用进行综述,进而为SNAP25亚家族作为疾病治疗的新靶点提供策略。展开更多
目的:引进中文版注意缺陷多动障碍SNAP-Ⅳ评定量表-父母版(Chinese version of Swan-son Nolan and Pelham,Version IV Scale-parent form,SNAP-IV)并检验其信效度。方法:对31名符合美国精神障碍诊断与统计手册第4版诊断标准的注意缺陷...目的:引进中文版注意缺陷多动障碍SNAP-Ⅳ评定量表-父母版(Chinese version of Swan-son Nolan and Pelham,Version IV Scale-parent form,SNAP-IV)并检验其信效度。方法:对31名符合美国精神障碍诊断与统计手册第4版诊断标准的注意缺陷多动障碍(ADHD)门诊患儿和231名正常儿童进行中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版、中文版Conners父母用症状问卷(PSQ)及中文版Achenbach儿童行为量表(CBCL)评估,以检验校标效度。对27名受试者(ADHD组3人,正常组24人)1周内再次进行中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版评估,以检验重测信度。结果:中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版全量表内部一致性信度Cronbachα系数为0.95,注意力不集中、多动冲动、对立违抗3个分量表Cronbachα系数分别为0.90、0.89、0.88。重测信度组内相关系数(ICC)为0.68,3个分量表的重测信度ICC分别为0.75、0.76、0.24。中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版与PSQ及CBCL对应各因子得分之间相关系数分别介于0.29～0.73、0.30～0.74,验证性因子分析显示中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版的3因子及4因子模型均合理。中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版诊断ADHD敏感度为0.87,特异度为0.79。结论:中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版具有良好的信度与效度。展开更多
文摘Ankle snapping occurs when tendons or retinacular structures abruptly move or slip over adjacent anatomical structures,often due to anatomical variations,pathological conditions,or acute injury.This phenomenon can cause pain and discomfort,ranging from mild irritation to debilitating symptoms that potentially disrupt daily activities and athletic pursuits.Considering the anatomy of the ankle,these snapping phenomena can be categorized into four regional groups:(1)Lateral;(2)Medial;(3)Anterior;and(4)Posterior.Lateral ankle snapping,a common occurrence,typically results from peroneal tendon subluxation due to compromise of the superior and inferior peroneal retinacula,or from intrasheath subluxation,characterized by abnormal tendon motion within an otherwise intact retromalleolar groove and retinaculum.Medial ankle snapping primarily affects the posterior tibial tendon and can involve the flexor digitorum longus tendon.Anterior ankle snapping results from abnormal gliding of the tibialis anterior tendon,extensor digitorum longus tendon,peroneus tertius tendon,and inferior extensor retinaculum.Posterior ankle snapping typically involves the plantaris tendon and flexor hallucis longus(hallux saltans).This mini-review comprehensively explores these snapping phenomena and their related pathologies in the foot and ankle,emphasizing the crucial roles of anatomical knowledge,thorough clinical assessment,and appropriate diagnostic and treatment approaches.
文摘This is a correction to:Isabela R R Moraes,Mariana Antunes,Laura S Lopez-Greco,Fernando Jose Zara,Antonio Leao Castilho,Functional reproductive morphology of the snapping shrimp genus Synalpheus Spence Bate,1888(Decapoda,Alpheidae),Current Zoology,2024,71,338-352;https:/doi.org/10.1093/cz/zoae053.
基金Supported by the National Natural Science Foundation of China,No.82200658.
文摘BACKGROUND Hepatic ischemia-reperfusion(I/R)injury related to liver transplantation and hepatic resection remains a challenge in clinical practice.Accumulating evidence indicates that mitochondrial dysfunction is a critical cause of I/R injury.The protein 4-nitrophenylphosphatase domain and non-neuronal SNAP25-like protein homolog 1(NIPSNAP1)is involved in the regulation of mitophagy and the recruitment of autophagy receptor proteins independent of PTEN induced putative kinase 1.AIM To clarify the protective mechanism of NIPSNAP1 against hepatic I/R,with a focus on mitophagy and mitochondrial dynamics,as well as the potential mechanism by which n6-methyladenosine(m6A)modification regulates NIPSNAP1.METHODS Mice were administered an adeno-associated virus in vivo and a hepatic I/R model was established via portal vein interruption followed by reperfusion to explore the effect of NIPSNAP1 on hepatic I/R.HepG2 cells were subjected to hypoxia/reoxygenation treatment in vitro.RESULTS We observed a significant downregulation of both NIPSNAP1 and insulin-like growth factor 2 mRNA-binding protein 2(IGF2BP2)expression in vivo and in vitro.NIPSNAP1 knockdown impaired mitophagy and disrupted mitochondrial dynamics;in contrast,NIPSNAP1 overexpression resulted in the opposite effects.Further studies revealed that IGF2BP2 functions as an m6A reader that targets and binds NIPSNAP1,thereby regulating its mRNA stability.CONCLUSION NIPSNAP1 prevents hepatic I/R injury by promoting mitophagy and maintaining mitochondrial homeostasis,serving as a novel target of the m6A reader IGF2BP2.Therefore,targeting the IGF2BP2/NIPSNAP1 axis may facilitate the development of better therapeutics for hepatic I/R.
文摘细胞自噬是将细胞内受损、变性、衰老的蛋白质或细胞器清除的过程,是细胞本身的代谢需要,也是某些细胞器的更新。自噬过程涉及膜融合。可溶性N-乙基马来酰亚胺敏感的融合蛋白附着蛋白受体(soluble N-ethylmaleimide-sensitive factor attachment protein receptor,SNARE)之间相互作用形成SNARE复合体参与膜融合。突触样相关蛋白25(synaptosomal-associated protein of 25 kDa,SNAP25)亚家族成员包括SNAP25、SNAP23、SNAP47和SNAP29,可与其他SNARE相互作用形成SNARE复合体从而参与自噬。本文着重对SNAP25亚家族中各成员如何参与自噬,以及在自噬中所起的作用进行综述,进而为SNAP25亚家族作为疾病治疗的新靶点提供策略。
文摘目的:引进中文版注意缺陷多动障碍SNAP-Ⅳ评定量表-父母版(Chinese version of Swan-son Nolan and Pelham,Version IV Scale-parent form,SNAP-IV)并检验其信效度。方法:对31名符合美国精神障碍诊断与统计手册第4版诊断标准的注意缺陷多动障碍(ADHD)门诊患儿和231名正常儿童进行中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版、中文版Conners父母用症状问卷(PSQ)及中文版Achenbach儿童行为量表(CBCL)评估,以检验校标效度。对27名受试者(ADHD组3人,正常组24人)1周内再次进行中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版评估,以检验重测信度。结果:中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版全量表内部一致性信度Cronbachα系数为0.95,注意力不集中、多动冲动、对立违抗3个分量表Cronbachα系数分别为0.90、0.89、0.88。重测信度组内相关系数(ICC)为0.68,3个分量表的重测信度ICC分别为0.75、0.76、0.24。中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版与PSQ及CBCL对应各因子得分之间相关系数分别介于0.29～0.73、0.30～0.74,验证性因子分析显示中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版的3因子及4因子模型均合理。中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版诊断ADHD敏感度为0.87,特异度为0.79。结论:中文版注意缺陷多动障碍SNAP-Ⅳ评定量表父母版具有良好的信度与效度。
