Background:Rats are often used to prepare skin defect models.However,the skin defect sizes of the models prepared by researchers are different,and the lack of consensus on the critical-size defect makes it difficult t...Background:Rats are often used to prepare skin defect models.However,the skin defect sizes of the models prepared by researchers are different,and the lack of consensus on the critical-size defect makes it difficult to compare their research results.Methods:The time for wound closure was evaluated and recorded through gross observation.The regression equation between the healing time and the diameter of skin defect was established,which can be used to predict the healing time for a certain skin defect size in rats.Histochemical and immunohistochemical staining was used to observe the regeneration and reconstruction of skin appendages,and the functional skin repair was quantitatively scored.Results:The critical-size defect of rats was determined based on the maximum capacity of structural skin repair,and the functional skin repair was quantitatively scored based on the regeneration and reconstruction of skin appendages.The allowable range of critical-size skin defect of SD rats lies between 45 and 50 mm in diameter.The concept of structural repair and the category of functional repair of injured skin are put forward.The regression equation between the structural skin healing time and defect diameters is established.Conclusion:The allowable range of skin critical-size defect of SD rats lies between 45 and 50 mm in diameter.The regression equation between the structural skin healing time and defect diameters can be used to predict the healing time for a certain skin defect size in rats.展开更多
The exchange of information and materials between organelles plays a crucial role in regulating cellular physiological functions and metabolic levels.Mitochondria-associated endoplasmic reticulum membranes serve as ph...The exchange of information and materials between organelles plays a crucial role in regulating cellular physiological functions and metabolic levels.Mitochondria-associated endoplasmic reticulum membranes serve as physical contact channels between the endoplasmic reticulum membrane and the mitochondrial outer membrane,formed by various proteins and protein complexes.This microstructural domain mediates several specialized functions,including calcium(Ca^(2+))signaling,autophagy,mitochondrial morphology,oxidative stress response,and apoptosis.Notably,the dysregulation of Ca^(2+)signaling mediated by mitochondria-associated endoplasmic reticulum membranes is a critical factor in the pathogenesis of neurological diseases.Certain proteins or protein complexes within these membranes directly or indirectly regulate the distance between the endoplasmic reticulum and mitochondria,as well as the transduction of Ca^(2+)signaling.Conversely,Ca^(2+)signaling mediated by mitochondria-associated endoplasmic reticulum membranes influences other mitochondria-associated endoplasmic reticulum membraneassociated functions.These functions can vary significantly across different neurological diseases—such as ischemic stroke,traumatic brain injury,Alzheimer's disease,Parkinson's disease,amyotrophic lateral sclerosis,and Huntington's disease—and their respective stages of progression.Targeted modulation of these disease-related pathways and functional proteins can enhance neurological function and promote the regeneration and repair of damaged neurons.Therefore,mitochondria-associated endoplasmic reticulum membranes-mediated Ca^(2+)signaling plays a pivotal role in the pathological progression of neurological diseases and represents a significant potential therapeutic target.This review focuses on the effects of protein complexes in mitochondria-associated endoplasmic reticulum membranes and the distinct roles of mitochondria-associated endoplasmic reticulum membranes-mediated Ca^(2+)signaling in neurological diseases,specifically highlighting the early protective effects and neuronal damage that can result from prolonged mitochondrial Ca^(2+)overload or deficiency.This article provides a comprehensive analysis of the various mechanisms of Ca^(2+)signaling mediated by mitochondria-associated endoplasmic reticulum membranes in neurological diseases,contributing to the exploration of potential therapeutic targets for promoting neuroprotection and nerve repair.展开更多
Many eukaryotic genes are members of multi-gene families due to gene duplications, which generate new copies that allow functional divergence. However, the relationship between
Background: Many women suffer from sexual problems after anal sphincter tears due to obstetric trauma. Aim: The study aimed to assess changes in sexual function after anal sphincter repair. Methods: The study was a no...Background: Many women suffer from sexual problems after anal sphincter tears due to obstetric trauma. Aim: The study aimed to assess changes in sexual function after anal sphincter repair. Methods: The study was a non-randomized prospective observational cohort study. Inclusion of the study was done at the University Hospital, Uppsala, Sweden, between 2002 and 2007. Thirty-nine consecutive female patients admitted for anal sphincter repair were invited to the study. Twenty patients accepted and were included, four were lost to follow up and one was unevaluable (due to the formation of a stoma) leaving a study group of 15 patients. The patients were assessed with questionnaires before surgery and at three and 12 months after surgery. Outcomes: Change in reported sexual activity and dyspareunia. Results: Before surgery, 12/15 patients reported that their sexual life was impaired due to anal incontinence. The corresponding figure at 12 months was 9/15 (p = 0.43). Three patients remained sexually inactive throughout the study, five patients increased their sexual activity and one had decreased activity. Out of the 12 who were active, four stated dyspareunia at baseline, and only one reported dyspareunia at 12 months. The mean Miller incontinence scores at baseline and 12 months were 10.1 and 8.7, respectively. The change in incontinence score did not differ between those with decreased, stable or increased sexual activity. However, there was a definite correlation (r = 0.54 - 0.60, p 0.05) between change in sexual function and deferring time for stool. Clinical Implications: Operative management of anal sphincter tears alone is not curative for sexual problems due to anal incontinence but can be a part of the treatment. Strengths and Limitations: The study is a prospective study of sexual function. The limitations are that the questionnaires were not validated due to lack of such questionnaires at the time of the study and that the study population is quite small. Conclusion: Patients with a sphincter injury and fecal incontinence often have an impaired sexual function. Increased deferring time for stools after surgery increases the likelihood of improved sexual function.展开更多
背景:规律的体育运动可以改善免疫功能,促进身体健康。免疫细胞如何通过炎症调节、代谢协同等机制提升运动表现,现有研究尚未形成系统性理论支撑。目的:梳理免疫细胞在肌肉修复、能量代谢与疲劳恢复中的作用,构建“免疫调控-运动表现”...背景:规律的体育运动可以改善免疫功能,促进身体健康。免疫细胞如何通过炎症调节、代谢协同等机制提升运动表现,现有研究尚未形成系统性理论支撑。目的:梳理免疫细胞在肌肉修复、能量代谢与疲劳恢复中的作用,构建“免疫调控-运动表现”的理论框架。方法:检索PubMed、Web of Science、Embase和中国知网等中英文数据库,围绕运动表现与免疫主题进行系统检索,检索日期截至2025-03-01。筛选近年发表的免疫功能调控运动表现的相关研究与综述文献,结合文献主题归纳与机制分析,探讨免疫运动的协同机制。结果与结论:运动训练所引发的应激过程中,免疫细胞借助调控炎症反应促进肌纤维恢复,维持代谢的平稳状态;免疫应答的时序性、组织特异性及其与训练负荷的匹配情况,是影响运动能力提升表现的关键因素;免疫系统在运动适应中不仅承担健康防御职能,而且在调控运动表现上也起到关键作用,未来研究应结合细胞组学、空间转录组与免疫代谢学等技术,为制定免疫调节影响训练干预策略提供依据。展开更多
Axonal junction defects and an inhibitory environment after spinal cord injury seriously hinder the regeneration of damaged tissues and neuronal functions. At the site of spinal cord injury, regenerative biomaterials ...Axonal junction defects and an inhibitory environment after spinal cord injury seriously hinder the regeneration of damaged tissues and neuronal functions. At the site of spinal cord injury, regenerative biomaterials can fill cavities, deliver curative drugs, and provide adsorption sites for transplanted or host cells. Some regenerative biomaterials can also inhibit apoptosis, inflammation and glial scar formation, or further promote neurogenesis, axonal growth and angiogenesis. This review summarized a variety of biomaterial scaffolds made of natural, synthetic, and combined materials applied to spinal cord injury repair. Although these biomaterial scaffolds have shown a certain therapeutic effect in spinal cord injury repair, there are still many problems to be resolved, such as product standards and material safety and effectiveness.展开更多
Resident and inflammatory macrophages are essential effectors of the innate immune system. These cells provide innate immune defenses and regulate tissue and organ homeostasis. In addition to their roles in diseases s...Resident and inflammatory macrophages are essential effectors of the innate immune system. These cells provide innate immune defenses and regulate tissue and organ homeostasis. In addition to their roles in diseases such as cancer, obesity and osteoarthritis, they play vital roles in tissue repair and disease rehabilitation. Macrophages and other inflammatory cells are recruited to tissue injury sites where they promote changes in the microenvironment. Among the inflammatory cell types, only macrophages have both pro-inflammatory (Ml) and anti-inflammatory (M2) actions, and M2 macrophages have four subtypes. The co-action of Ml and M2 subtypes can create a favorable microenvironment, releasing cytokines for damaged tissue repair. In this review, we discuss the activation of macrophages and their roles in severe peripheral nerve injury. We also describe the therapeutic potential of macrophages in nerve tissue engineering treatment and highlight approaches for enhancing M2 cell-mediated nerve repair and regeneration.展开更多
基金National Key Research and Development Program of China,Grant/Award Number:2023YFC2410403。
文摘Background:Rats are often used to prepare skin defect models.However,the skin defect sizes of the models prepared by researchers are different,and the lack of consensus on the critical-size defect makes it difficult to compare their research results.Methods:The time for wound closure was evaluated and recorded through gross observation.The regression equation between the healing time and the diameter of skin defect was established,which can be used to predict the healing time for a certain skin defect size in rats.Histochemical and immunohistochemical staining was used to observe the regeneration and reconstruction of skin appendages,and the functional skin repair was quantitatively scored.Results:The critical-size defect of rats was determined based on the maximum capacity of structural skin repair,and the functional skin repair was quantitatively scored based on the regeneration and reconstruction of skin appendages.The allowable range of critical-size skin defect of SD rats lies between 45 and 50 mm in diameter.The concept of structural repair and the category of functional repair of injured skin are put forward.The regression equation between the structural skin healing time and defect diameters is established.Conclusion:The allowable range of skin critical-size defect of SD rats lies between 45 and 50 mm in diameter.The regression equation between the structural skin healing time and defect diameters can be used to predict the healing time for a certain skin defect size in rats.
基金supported by Yunnan Province Innovation Team of Prevention and Treatment for Brain Disease with Acupuncture and Tuina,No.202405AS350007Youth Top Talent Project of 10-thousand Talent Plan in Yunnan Province,No.YNWR-QNBJ-2018-345+3 种基金the National Natural Science Foundation of China,No.81960731Joint Special Project of Traditional Chinese Medicine in Science and Technology Department of Yunnan Province,Nos.2019FF002[-008],202001AZ070001-002 and 202001AZ070001-030Yunnan Province University Innovation Team Projects No.2019YGC04Yunnan Province Project Education Fund,Nos.2024Y406,2024Y414(all to PZ)。
文摘The exchange of information and materials between organelles plays a crucial role in regulating cellular physiological functions and metabolic levels.Mitochondria-associated endoplasmic reticulum membranes serve as physical contact channels between the endoplasmic reticulum membrane and the mitochondrial outer membrane,formed by various proteins and protein complexes.This microstructural domain mediates several specialized functions,including calcium(Ca^(2+))signaling,autophagy,mitochondrial morphology,oxidative stress response,and apoptosis.Notably,the dysregulation of Ca^(2+)signaling mediated by mitochondria-associated endoplasmic reticulum membranes is a critical factor in the pathogenesis of neurological diseases.Certain proteins or protein complexes within these membranes directly or indirectly regulate the distance between the endoplasmic reticulum and mitochondria,as well as the transduction of Ca^(2+)signaling.Conversely,Ca^(2+)signaling mediated by mitochondria-associated endoplasmic reticulum membranes influences other mitochondria-associated endoplasmic reticulum membraneassociated functions.These functions can vary significantly across different neurological diseases—such as ischemic stroke,traumatic brain injury,Alzheimer's disease,Parkinson's disease,amyotrophic lateral sclerosis,and Huntington's disease—and their respective stages of progression.Targeted modulation of these disease-related pathways and functional proteins can enhance neurological function and promote the regeneration and repair of damaged neurons.Therefore,mitochondria-associated endoplasmic reticulum membranes-mediated Ca^(2+)signaling plays a pivotal role in the pathological progression of neurological diseases and represents a significant potential therapeutic target.This review focuses on the effects of protein complexes in mitochondria-associated endoplasmic reticulum membranes and the distinct roles of mitochondria-associated endoplasmic reticulum membranes-mediated Ca^(2+)signaling in neurological diseases,specifically highlighting the early protective effects and neuronal damage that can result from prolonged mitochondrial Ca^(2+)overload or deficiency.This article provides a comprehensive analysis of the various mechanisms of Ca^(2+)signaling mediated by mitochondria-associated endoplasmic reticulum membranes in neurological diseases,contributing to the exploration of potential therapeutic targets for promoting neuroprotection and nerve repair.
文摘Many eukaryotic genes are members of multi-gene families due to gene duplications, which generate new copies that allow functional divergence. However, the relationship between
文摘Background: Many women suffer from sexual problems after anal sphincter tears due to obstetric trauma. Aim: The study aimed to assess changes in sexual function after anal sphincter repair. Methods: The study was a non-randomized prospective observational cohort study. Inclusion of the study was done at the University Hospital, Uppsala, Sweden, between 2002 and 2007. Thirty-nine consecutive female patients admitted for anal sphincter repair were invited to the study. Twenty patients accepted and were included, four were lost to follow up and one was unevaluable (due to the formation of a stoma) leaving a study group of 15 patients. The patients were assessed with questionnaires before surgery and at three and 12 months after surgery. Outcomes: Change in reported sexual activity and dyspareunia. Results: Before surgery, 12/15 patients reported that their sexual life was impaired due to anal incontinence. The corresponding figure at 12 months was 9/15 (p = 0.43). Three patients remained sexually inactive throughout the study, five patients increased their sexual activity and one had decreased activity. Out of the 12 who were active, four stated dyspareunia at baseline, and only one reported dyspareunia at 12 months. The mean Miller incontinence scores at baseline and 12 months were 10.1 and 8.7, respectively. The change in incontinence score did not differ between those with decreased, stable or increased sexual activity. However, there was a definite correlation (r = 0.54 - 0.60, p 0.05) between change in sexual function and deferring time for stool. Clinical Implications: Operative management of anal sphincter tears alone is not curative for sexual problems due to anal incontinence but can be a part of the treatment. Strengths and Limitations: The study is a prospective study of sexual function. The limitations are that the questionnaires were not validated due to lack of such questionnaires at the time of the study and that the study population is quite small. Conclusion: Patients with a sphincter injury and fecal incontinence often have an impaired sexual function. Increased deferring time for stools after surgery increases the likelihood of improved sexual function.
文摘背景:规律的体育运动可以改善免疫功能,促进身体健康。免疫细胞如何通过炎症调节、代谢协同等机制提升运动表现,现有研究尚未形成系统性理论支撑。目的:梳理免疫细胞在肌肉修复、能量代谢与疲劳恢复中的作用,构建“免疫调控-运动表现”的理论框架。方法:检索PubMed、Web of Science、Embase和中国知网等中英文数据库,围绕运动表现与免疫主题进行系统检索,检索日期截至2025-03-01。筛选近年发表的免疫功能调控运动表现的相关研究与综述文献,结合文献主题归纳与机制分析,探讨免疫运动的协同机制。结果与结论:运动训练所引发的应激过程中,免疫细胞借助调控炎症反应促进肌纤维恢复,维持代谢的平稳状态;免疫应答的时序性、组织特异性及其与训练负荷的匹配情况,是影响运动能力提升表现的关键因素;免疫系统在运动适应中不仅承担健康防御职能,而且在调控运动表现上也起到关键作用,未来研究应结合细胞组学、空间转录组与免疫代谢学等技术,为制定免疫调节影响训练干预策略提供依据。
基金supported by the National Natural Science Foundation of China,No.81571213(to BW),No.81800583(to YYX)the 13~(th) Six Talent Peaks Project(C type)of Jiangsu Province of China(to BW)+1 种基金the Medical Science and Technique Development Foundation of Nanjing of China,No.QRX17006(to BW)the Medical Science and Innovation Platform of Nanjing of China,No.ZDX16005(to BW)
文摘Axonal junction defects and an inhibitory environment after spinal cord injury seriously hinder the regeneration of damaged tissues and neuronal functions. At the site of spinal cord injury, regenerative biomaterials can fill cavities, deliver curative drugs, and provide adsorption sites for transplanted or host cells. Some regenerative biomaterials can also inhibit apoptosis, inflammation and glial scar formation, or further promote neurogenesis, axonal growth and angiogenesis. This review summarized a variety of biomaterial scaffolds made of natural, synthetic, and combined materials applied to spinal cord injury repair. Although these biomaterial scaffolds have shown a certain therapeutic effect in spinal cord injury repair, there are still many problems to be resolved, such as product standards and material safety and effectiveness.
基金supported by the National Natural Science Foundation of China,No.31771052(to YW)the National Key Research&Development Program of China,No.2017YFA0104701,2017YFA0104702 and 2016YFC1101601+2 种基金the National Basic Research Program of China(973 Program),No.2014CB542201(to JP)the Natural Science Foundation of Beijing,No.7172202(to YW)the PLA Youth Training Project for Medical Science,No.16QNP144(to YW)
文摘Resident and inflammatory macrophages are essential effectors of the innate immune system. These cells provide innate immune defenses and regulate tissue and organ homeostasis. In addition to their roles in diseases such as cancer, obesity and osteoarthritis, they play vital roles in tissue repair and disease rehabilitation. Macrophages and other inflammatory cells are recruited to tissue injury sites where they promote changes in the microenvironment. Among the inflammatory cell types, only macrophages have both pro-inflammatory (Ml) and anti-inflammatory (M2) actions, and M2 macrophages have four subtypes. The co-action of Ml and M2 subtypes can create a favorable microenvironment, releasing cytokines for damaged tissue repair. In this review, we discuss the activation of macrophages and their roles in severe peripheral nerve injury. We also describe the therapeutic potential of macrophages in nerve tissue engineering treatment and highlight approaches for enhancing M2 cell-mediated nerve repair and regeneration.
