BACKGROUND： An animal model of chronic optic nerve injury is necessary to further understand the pathological mechanisms involved. OBJECTIVE： To establish a stabilized, chronic, optic nerve crush model, which is sim...BACKGROUND： An animal model of chronic optic nerve injury is necessary to further understand the pathological mechanisms involved. OBJECTIVE： To establish a stabilized, chronic, optic nerve crush model, which is similar to the clinical situation to explore histopathological and optic electrophysiological changes involved in this injury. DESIGN, TIME AND SETTING： A randomized and controlled animal trial was performed at Shanghai Institute of Neurosurgery from May to October 2004, MATERIALS： A BAL3XRAY undetachable balloon and Magic-BD catheter were provided by BLAT, France; JX-2000 biological signal processing system by Second Military Medical University of Chinese PLA, China; inverted phase contrast microscopy by Olympus, Japan. METHODS： A total of twenty normal adult cats were randomly assigned to control （n = 5） and model （n = 15） groups, according to different doses of contrast agent injected through balloons as follows： 0.2 mL injection, 0.25 mL injection, and 0.35 mL injection, with each group containing 5 animals. Imitating the clinical pterion approach, the optic nerves were exposed using micro-surgical methods. An engorged undetachable balloon was implanted beneath the nerve and connected to a catheter. Balloon size was controlled with a contrast agent injection （0.1 mL/10 min） to form an occupying lesion model similar to sellar tumors. MAIN OUTCOME MEASURES： The visually evoked potential examination was used to study optical electrophysiology changes in pre-post chronic optical nerve injury. Ultrastructural pathological changes to the optic nerve were analyzed by electron microscopy. RESULTS： During the early period （day 11 after modeling）, visually evoked potential demonstrated no significant changes. In the late period （day 51 after modeling）, recorded VEP demonstrated that P1 wave latency was prolonged and P1 wave amplitude was obviously reduced. Following injury, the endoneurium, myelin sheath, lamella, axolemma, and axon appeared disordered. CONCLUSION： Results demonstrated that the chronic, intracranial, optical nerve crush model was stable and could simulate optic nerve lesions induced by sellar tumors. Under the condition of chronic optical nerve crush, visually evoked potentials were aggravated.展开更多
Systemic lupus erythematosus(SLE),a chronic autoimmune disease,is marked by impaired immune tolerance and heightened activity in both innate and adaptive immune systems.Hallmarks of SLE include elevated type I interfe...Systemic lupus erythematosus(SLE),a chronic autoimmune disease,is marked by impaired immune tolerance and heightened activity in both innate and adaptive immune systems.Hallmarks of SLE include elevated type I interferons and autoantibody production,though the exact causes of SLE remain elusive despite advances in research techniques.Crucial to SLE research is understanding its pathogenesis and developing effective diagnostic and therapeutic methods.Recent studies have highlighted a significant link between mitochondrial abnormalities and SLE's development and progression.Mitochondrial dysfunction plays a key role in SLE pathogenesis through various mechanisms such as mitochondrial DNA mutations,oxidative stress,immune metabolic reprogramming,and cellular death.These factors collectively contribute to the loss of self-tolerance,increased autoantibody production,and impaired clearance of immune complexes,leading to their deposition.This triggers sustained inflammatory responses and damages multiple organs.This review focuses on the diagnostic and therapeutic approaches related to mitochondrial abnormalities in SLE.Targeting mitochondrial pathways presents a promising strategy for treating SLE,potentially improving prognosis and quality of life for those affected.Future research should further investigate the role of mitochondria in the onset and progression of SLE,providing new avenues for understanding and managing this complex disease.展开更多
To the Editor,Lupus nephritis(LN),a renal symptom of systemic lupus erythematosus(SLE),frequently causes severe organ damage in SLE patients.1 There is no consensus on the definition of refractory LN,which has been su...To the Editor,Lupus nephritis(LN),a renal symptom of systemic lupus erythematosus(SLE),frequently causes severe organ damage in SLE patients.1 There is no consensus on the definition of refractory LN,which has been suggested to occur when remission is not achieved after 3–12 months of combined glucocorticoids and immunosuppressive therapy.2 Podocytic infolding glomerulopathy(PIG),a rare type of glomerular morphological alteration,is primarily characterized by the presence of microspheres,microtubular structures,or a combination of the two,which are associated with podocyte infolding into the glomerular basement membrane(GBM).3,4 The exact pathogenesis of PIG remains unclear,but it may be associated with autoimmune diseases like SLE and Sjögren's syndrome.The occurrence of refractory LN complicated by PIG is rare and poses significant challenges in management.Here,we endeavor to provide the patient with benefits by employing a novel treatment,Telitacicept,which has demonstrated the potential to achieve complete renal remission in such cases.展开更多
基金the National Natural Science Foundation of China,No.30271333
文摘BACKGROUND： An animal model of chronic optic nerve injury is necessary to further understand the pathological mechanisms involved. OBJECTIVE： To establish a stabilized, chronic, optic nerve crush model, which is similar to the clinical situation to explore histopathological and optic electrophysiological changes involved in this injury. DESIGN, TIME AND SETTING： A randomized and controlled animal trial was performed at Shanghai Institute of Neurosurgery from May to October 2004, MATERIALS： A BAL3XRAY undetachable balloon and Magic-BD catheter were provided by BLAT, France; JX-2000 biological signal processing system by Second Military Medical University of Chinese PLA, China; inverted phase contrast microscopy by Olympus, Japan. METHODS： A total of twenty normal adult cats were randomly assigned to control （n = 5） and model （n = 15） groups, according to different doses of contrast agent injected through balloons as follows： 0.2 mL injection, 0.25 mL injection, and 0.35 mL injection, with each group containing 5 animals. Imitating the clinical pterion approach, the optic nerves were exposed using micro-surgical methods. An engorged undetachable balloon was implanted beneath the nerve and connected to a catheter. Balloon size was controlled with a contrast agent injection （0.1 mL/10 min） to form an occupying lesion model similar to sellar tumors. MAIN OUTCOME MEASURES： The visually evoked potential examination was used to study optical electrophysiology changes in pre-post chronic optical nerve injury. Ultrastructural pathological changes to the optic nerve were analyzed by electron microscopy. RESULTS： During the early period （day 11 after modeling）, visually evoked potential demonstrated no significant changes. In the late period （day 51 after modeling）, recorded VEP demonstrated that P1 wave latency was prolonged and P1 wave amplitude was obviously reduced. Following injury, the endoneurium, myelin sheath, lamella, axolemma, and axon appeared disordered. CONCLUSION： Results demonstrated that the chronic, intracranial, optical nerve crush model was stable and could simulate optic nerve lesions induced by sellar tumors. Under the condition of chronic optical nerve crush, visually evoked potentials were aggravated.
基金Key Research and Development Program of Jiangxi Municipal Science and Technology Department,Grant/Award Number:20192BBGL70024Science and Technology Program of Department of Health of Jiangxi Province,Grant/Award Number:20204254National Key Research and Development Program of China,Grant/Award Number:2021YFC2501304。
文摘Systemic lupus erythematosus(SLE),a chronic autoimmune disease,is marked by impaired immune tolerance and heightened activity in both innate and adaptive immune systems.Hallmarks of SLE include elevated type I interferons and autoantibody production,though the exact causes of SLE remain elusive despite advances in research techniques.Crucial to SLE research is understanding its pathogenesis and developing effective diagnostic and therapeutic methods.Recent studies have highlighted a significant link between mitochondrial abnormalities and SLE's development and progression.Mitochondrial dysfunction plays a key role in SLE pathogenesis through various mechanisms such as mitochondrial DNA mutations,oxidative stress,immune metabolic reprogramming,and cellular death.These factors collectively contribute to the loss of self-tolerance,increased autoantibody production,and impaired clearance of immune complexes,leading to their deposition.This triggers sustained inflammatory responses and damages multiple organs.This review focuses on the diagnostic and therapeutic approaches related to mitochondrial abnormalities in SLE.Targeting mitochondrial pathways presents a promising strategy for treating SLE,potentially improving prognosis and quality of life for those affected.Future research should further investigate the role of mitochondria in the onset and progression of SLE,providing new avenues for understanding and managing this complex disease.
基金National Key Research and Development Program of China(2021YFC2501304)Science and Technology Program of Department of Health of Jiangxi Province(20204254)Key Research and Development Program of Jiangxi Municipal Science and Technology Department(20192BBGL70024).
文摘To the Editor,Lupus nephritis(LN),a renal symptom of systemic lupus erythematosus(SLE),frequently causes severe organ damage in SLE patients.1 There is no consensus on the definition of refractory LN,which has been suggested to occur when remission is not achieved after 3–12 months of combined glucocorticoids and immunosuppressive therapy.2 Podocytic infolding glomerulopathy(PIG),a rare type of glomerular morphological alteration,is primarily characterized by the presence of microspheres,microtubular structures,or a combination of the two,which are associated with podocyte infolding into the glomerular basement membrane(GBM).3,4 The exact pathogenesis of PIG remains unclear,but it may be associated with autoimmune diseases like SLE and Sjögren's syndrome.The occurrence of refractory LN complicated by PIG is rare and poses significant challenges in management.Here,we endeavor to provide the patient with benefits by employing a novel treatment,Telitacicept,which has demonstrated the potential to achieve complete renal remission in such cases.
