BACKGROUND： Some previous studies have shown that exercise is an important factor that affects the latencies of visual-evoked potentials （VEPs）. OBJECTIVE： To investigate the effects of spending a period of time u...BACKGROUND： Some previous studies have shown that exercise is an important factor that affects the latencies of visual-evoked potentials （VEPs）. OBJECTIVE： To investigate the effects of spending a period of time undergoing tennis training on the latencies of VEPs by comparing the latencies of VEPs before tennis training with those after 8 weeks of tennis training. DESIGN, TIME AND SETTING： The non-randomly concurrent controlled experiment was performed in the Department of Human Movement Sciences, Physical Education College, Shandong Normal University from April to June 2007. PARTICIPANTS： In total, 45 healthy volunteers from Shandong Normal University were selected as subjects, including 31 students majoring in physical education （11 males and 5 females participated in the tennis training plan for 8 weeks）, and 14 students from other subjects. Informed consent was obtained. According to whether they were majoring in physical education or not, and whether or not they took part in tennis training, the students were divided into 3 groups： a tennis group of physical education students （n = 16） a non-tennis group of physical education students （n =15） and a non-tennis group of non-physical education students （n = 14）. METHODS： The subjects in the tennis group took part in a regular tennis training plan of 2 hours a day and 3 days per week, for 8 weeks, while the subjects in two non-tennis groups were not in the tennis training plan The NDI-200 neural electricity tester （Shanghai Haishen Medical Electronic Instrument Co., Ltd.） was used to measure VEPs before and after the experiment in all three groups, and to compare the latencies of VEPs recorded before training with those recorded after training. MAIN OUTCOME MEASURES： Comparison of the changes in latencies of VEPs before and after 8 weeks of tennis training. RESULTS： All 45 subjects finished the test and datas from all were included in the statistical analysis. There were no significant differences among all the three groups before tennis training, but the female subjects in each group showed significantly shorter N75 latencies than male subjects of the same group （P 〈 0.05）. Comparing the latencies of VEPs after training with those recorded before training, the N75, P100 and N145 latencies were all found to be significantly shorter than before training in the tennis group （P 〈 0.05）, but the N75, P100 and N145 latencies were unaffected in the two non-tennis groups （P 〉 0.05）; some latencies were even significantly longer than the before-training values. CONCLUSION： Special tennis training for 8 weeks can make the subjects＇ VEP latencies significantly shorter. Thus, VEP latencies can change with tennis training.展开更多
Objective To systemically explore the range of visual angles that affect visual acuity, and to establish the relationship between the P 1 component （peak latency -100 ms） of the pattern-reversal visual-evoked potent...Objective To systemically explore the range of visual angles that affect visual acuity, and to establish the relationship between the P 1 component （peak latency -100 ms） of the pattern-reversal visual-evoked potential （PRVEP） and the visual acuity at particular visual angles. Methods Two hundred and ten volunteers were divided into seven groups, according to visual acuity as assessed by the standard logarithmic visual acuity chart （SLD-II）. For each group, the PRVEP components were elicited in response to visual angle presentations at 8°, 4°, 2°, 1°/60＇, 30＇, 15＇, and 7.5＇, in the whiteblack chess-board reversal mode with a contrast level of 100% at a frequency of 2 Hz. Visual stimuli were presented monocularly, and 200 presentations were averaged for each block of trials. The early and stable component P1 was recorded at the mid-line of the occipital region （Oz） and analyzed with SPSS 13.00. Results （1） Oz had the maximum Pl amplitude; there was no significant difference between genders or for interocular comparison in normal controls and subjects with optic myopia. （2） The P1 latency decreased slowly below 30＇, then increased rapidly. The P1 amplitude initially increased with check size, and was maximal at -1° and -30＇. （3） The P1 latency in the group with visual acuity 〈0.2 was signifi- cantly different at 8°, 15＇ and 7.5＇, while the amplitude differed at all visual angles, compared with the group with normal vision. Differences in P1 for the groups with 0.5 and 0.6 acuity were only present at visual angles 〈1°. （4） Regression analysis showed that the P1 latency and amplitude were associated with visual acuity over the full range of visual angles. There was a moderate correlation at visual angles 〈30＇. Regression equations were calculated for the P1 components and visual acuity, based on visual angle. Conclusion （1） Visual angle should be taken into consideration when exploring the function of the visual pathway, especially visual acuity. A visual angle -60＇ might be appropriate when using PRVEP com- ponents to evaluate poor vision and to identify malingerers. （2） Increased P1 amplitude and decreased P1 latency were as- sociated with increasing visual acuity, and the P1 components displayed a linear correlation with visual acuity, especially in the range of optimal visual angles. Visual acuity can be deduced from P 1 based on visual angle.展开更多
Neuromyelitis optica spectrum disorder-related optic neuritis involves various cellular responses to inflammation and degeneration.In most patients,the primary mechanism underlying neuromyelitis optica spectrum disord...Neuromyelitis optica spectrum disorder-related optic neuritis involves various cellular responses to inflammation and degeneration.In most patients,the primary mechanism underlying neuromyelitis optica spectrum disorder-related optic neuritis is the interaction of aquaporin-4 antibodies with the aquaporin-4 protein present on astrocytes within posterior optic nerve.This binding subsequently initiates a cascade of events leading to secondary demyelination of the optic nerve,ultimately culminating in optic nerve degeneration.Earlier studies on this disorder primarily used systemic-induced animal models,which often require prior activation of a systemic immune response.This can result in primary demyelination of the optic nerve,complicating the interpretation of experimental results.Such methodologies hinder the ability to isolate immune responses triggered by specific antibodies.Additionally,the lack of a detailed profile of disease progression over time limits our capacity to identify potential intervention windows.Therefore,constructing a targeted optic neuritis animal model induced by specific antibodies and elucidate the disease progression arecrucial for exploring the mechanisms underlying neuromyelitis optica spectrum disorder-related optic neuritis.In this study,specific antibodies against aquaporin-4 were precisely injected into the retrobulbar optic nerve of mice to induce a targeted inflammatory response in the posterior optic nerve,resulting in a more representative mouse model of neuromyelitis optica spectrum disorder-related optic neuritis than current models.The progression of the disease was then dynamically observed from both histological and functional perspectives over the course of 1 month following the induction of inflammation.By the first week,astrocytes were damaged,as evidenced by the loss of aquaporin-4 and glial fibrillary acidic protein,the activation of microglia,and the upregulation of microglia-related cytokines,including tumor necrosis factor,interleukin-6,interleukin-1β,C-X-C motif ligand 10,and brain-derived neurotrophic factor.Starting from the second week,there were signs of optic nerve demyelination and significant damage to axonal fibers and retinal ganglion cell bodies.Visual-evoked potentials and dark adaptation threshold responses in electroretinogram both indicated dysfunction in the visual pathway and retina,while optical coherence tomography revealed thinning of the retinal nerve fiber layer in live mice.In summary,in this study we conducted a dynamic exploration of the occurrence and progression of neuromyelitis optica spectrum disorder-related optic neuritis triggered by specific antibodies.Our results show pathological changes at various stages and correlate histological and molecular alterations with in vivo structural and functional deterioration.The findings from this study lay an important foundation for further research on neuromyelitis optica spectrum disorder-related optic neuritis.展开更多
文摘BACKGROUND： Some previous studies have shown that exercise is an important factor that affects the latencies of visual-evoked potentials （VEPs）. OBJECTIVE： To investigate the effects of spending a period of time undergoing tennis training on the latencies of VEPs by comparing the latencies of VEPs before tennis training with those after 8 weeks of tennis training. DESIGN, TIME AND SETTING： The non-randomly concurrent controlled experiment was performed in the Department of Human Movement Sciences, Physical Education College, Shandong Normal University from April to June 2007. PARTICIPANTS： In total, 45 healthy volunteers from Shandong Normal University were selected as subjects, including 31 students majoring in physical education （11 males and 5 females participated in the tennis training plan for 8 weeks）, and 14 students from other subjects. Informed consent was obtained. According to whether they were majoring in physical education or not, and whether or not they took part in tennis training, the students were divided into 3 groups： a tennis group of physical education students （n = 16） a non-tennis group of physical education students （n =15） and a non-tennis group of non-physical education students （n = 14）. METHODS： The subjects in the tennis group took part in a regular tennis training plan of 2 hours a day and 3 days per week, for 8 weeks, while the subjects in two non-tennis groups were not in the tennis training plan The NDI-200 neural electricity tester （Shanghai Haishen Medical Electronic Instrument Co., Ltd.） was used to measure VEPs before and after the experiment in all three groups, and to compare the latencies of VEPs recorded before training with those recorded after training. MAIN OUTCOME MEASURES： Comparison of the changes in latencies of VEPs before and after 8 weeks of tennis training. RESULTS： All 45 subjects finished the test and datas from all were included in the statistical analysis. There were no significant differences among all the three groups before tennis training, but the female subjects in each group showed significantly shorter N75 latencies than male subjects of the same group （P 〈 0.05）. Comparing the latencies of VEPs after training with those recorded before training, the N75, P100 and N145 latencies were all found to be significantly shorter than before training in the tennis group （P 〈 0.05）, but the N75, P100 and N145 latencies were unaffected in the two non-tennis groups （P 〉 0.05）; some latencies were even significantly longer than the before-training values. CONCLUSION： Special tennis training for 8 weeks can make the subjects＇ VEP latencies significantly shorter. Thus, VEP latencies can change with tennis training.
基金supported by grants from the National Nature Science Foundation of China(30872666,81172911 and 81271379)Shanghai Key Lab of Forensic Medicine(KF1005)
文摘Objective To systemically explore the range of visual angles that affect visual acuity, and to establish the relationship between the P 1 component （peak latency -100 ms） of the pattern-reversal visual-evoked potential （PRVEP） and the visual acuity at particular visual angles. Methods Two hundred and ten volunteers were divided into seven groups, according to visual acuity as assessed by the standard logarithmic visual acuity chart （SLD-II）. For each group, the PRVEP components were elicited in response to visual angle presentations at 8°, 4°, 2°, 1°/60＇, 30＇, 15＇, and 7.5＇, in the whiteblack chess-board reversal mode with a contrast level of 100% at a frequency of 2 Hz. Visual stimuli were presented monocularly, and 200 presentations were averaged for each block of trials. The early and stable component P1 was recorded at the mid-line of the occipital region （Oz） and analyzed with SPSS 13.00. Results （1） Oz had the maximum Pl amplitude; there was no significant difference between genders or for interocular comparison in normal controls and subjects with optic myopia. （2） The P1 latency decreased slowly below 30＇, then increased rapidly. The P1 amplitude initially increased with check size, and was maximal at -1° and -30＇. （3） The P1 latency in the group with visual acuity 〈0.2 was signifi- cantly different at 8°, 15＇ and 7.5＇, while the amplitude differed at all visual angles, compared with the group with normal vision. Differences in P1 for the groups with 0.5 and 0.6 acuity were only present at visual angles 〈1°. （4） Regression analysis showed that the P1 latency and amplitude were associated with visual acuity over the full range of visual angles. There was a moderate correlation at visual angles 〈30＇. Regression equations were calculated for the P1 components and visual acuity, based on visual angle. Conclusion （1） Visual angle should be taken into consideration when exploring the function of the visual pathway, especially visual acuity. A visual angle -60＇ might be appropriate when using PRVEP com- ponents to evaluate poor vision and to identify malingerers. （2） Increased P1 amplitude and decreased P1 latency were as- sociated with increasing visual acuity, and the P1 components displayed a linear correlation with visual acuity, especially in the range of optimal visual angles. Visual acuity can be deduced from P 1 based on visual angle.
基金The study was partially supported by the General Research Fund(GRF)from the Research Grants Council(RGC)of the Hong Kong Special Administrative Region,China,No.15103522(to ST)the Internal Research Grant from the Hong Kong Polytechnic University 2021-23,No.P0035512(to ST)and P0035375(to HHLC)+1 种基金the Innovation and Technology Commission of the Hong Kong Special Administrative Region(ITC InnoHK CEVR Project)The Hong Kong Polytechnics University Research Center for Sharp Vision,No.P0039595.
文摘Neuromyelitis optica spectrum disorder-related optic neuritis involves various cellular responses to inflammation and degeneration.In most patients,the primary mechanism underlying neuromyelitis optica spectrum disorder-related optic neuritis is the interaction of aquaporin-4 antibodies with the aquaporin-4 protein present on astrocytes within posterior optic nerve.This binding subsequently initiates a cascade of events leading to secondary demyelination of the optic nerve,ultimately culminating in optic nerve degeneration.Earlier studies on this disorder primarily used systemic-induced animal models,which often require prior activation of a systemic immune response.This can result in primary demyelination of the optic nerve,complicating the interpretation of experimental results.Such methodologies hinder the ability to isolate immune responses triggered by specific antibodies.Additionally,the lack of a detailed profile of disease progression over time limits our capacity to identify potential intervention windows.Therefore,constructing a targeted optic neuritis animal model induced by specific antibodies and elucidate the disease progression arecrucial for exploring the mechanisms underlying neuromyelitis optica spectrum disorder-related optic neuritis.In this study,specific antibodies against aquaporin-4 were precisely injected into the retrobulbar optic nerve of mice to induce a targeted inflammatory response in the posterior optic nerve,resulting in a more representative mouse model of neuromyelitis optica spectrum disorder-related optic neuritis than current models.The progression of the disease was then dynamically observed from both histological and functional perspectives over the course of 1 month following the induction of inflammation.By the first week,astrocytes were damaged,as evidenced by the loss of aquaporin-4 and glial fibrillary acidic protein,the activation of microglia,and the upregulation of microglia-related cytokines,including tumor necrosis factor,interleukin-6,interleukin-1β,C-X-C motif ligand 10,and brain-derived neurotrophic factor.Starting from the second week,there were signs of optic nerve demyelination and significant damage to axonal fibers and retinal ganglion cell bodies.Visual-evoked potentials and dark adaptation threshold responses in electroretinogram both indicated dysfunction in the visual pathway and retina,while optical coherence tomography revealed thinning of the retinal nerve fiber layer in live mice.In summary,in this study we conducted a dynamic exploration of the occurrence and progression of neuromyelitis optica spectrum disorder-related optic neuritis triggered by specific antibodies.Our results show pathological changes at various stages and correlate histological and molecular alterations with in vivo structural and functional deterioration.The findings from this study lay an important foundation for further research on neuromyelitis optica spectrum disorder-related optic neuritis.
