Visual system is a critical sensory system in humans and a vital component of the central nervous system, which is responsible for over 80% of external information acquisition.Visual function is a key indicator of overall health.With socioeconomic development, the public has higher expectations for eye health, shifting the focus of eye health initiatives from disease treatment to comprehensive public eye health.Key scientific challenges include how to effectively prevent, diagnose, and treat blindness and visual impairment at an early stage; how to enhance the overall visual quality of patients to ensure not just sight but clear and comfortable vision; and how to meet the public's diverse and multi-tiered eye health needs.Visual science is an interdisciplinary field exploring the development of the visual system, the mechanisms of vision, and brain-related perceptual, cognitive and behavioral processes involving sight.Prioritizing and advancing visual science research is of great significance for promoting comprehensive eye health and implementing the Healthy China Strategy.This article first outlines the concept and research significance of visual science.It then highlights the key scientific questions in visual science pertaining to several major eye diseases, such as myopia, amblyopia, cataract, fundus diseases, glaucoma, and corneal diseases, reviews the historical foundation of visual science research in China, selectively summarizes key achievements and ongoing progress in this field, analyzes the landscape and challenges faced by domestic research, and proposes, to this end, strategies to advance visual science in China.These recommendations are designed to promote visual science research in China and ultimately advance comprehensive eye health.

Amblyopia is a neurodevelopmental disorder caused by abnormal visual experience during the critical period of visual development.During this critical period, the visual cortex exhibits high plasticity, enabling it to remodel neural circuits in response to visual input.However, this plasticity significantly declines with age, resulting in limited therapeutic efficacy in adult amblyopia patients.A core challenge in amblyopia treatment is reactivating plasticity in the adult visual cortex.Recent studies have identified perineuronal net (PNN) as key regulators of visual cortical plasticity.PNN are specialized extracellular matrix structures that envelop neurons and modulate synaptic plasticity through their unique molecular composition.Multiple studies suggest that manipulating the integrity or composition of PNN can alter cortical plasticity in adults.However, the precise molecular mechanisms and signaling pathways by which PNN regulate plasticity remain incompletely understood.This review summarizes recent advances in understanding how PNN modulate visual cortical plasticity, including potential molecular mechanisms and related signaling pathways, with the aim of providing theoretical insights for the development of novel amblyopia treatment strategies in adults.

Objective:To investigate the protective effect of PSD95 on neurobehavioral abnormalities and synaptic damage in cortex induced by hypoxia exposure in mice.Methods:The 3-week-old C57BL/6 male mice were injected with neuron-specific adeno-associated virus through stereotaxic brain after 7 days of normal environment adaptation.The mice were divided into normoxia group(AAV-NC-Nor),control hypoxia group(AAV-NC-Hyp),normal oxygen group with over-expression of postsynaptic density-95(PSD95)(AAV-PSD95-Nor),and hypoxia group with over-expression of PSD95(AAV-PSD95-Hyp).Using a hypobaric hypoxia chamber,PSD95-overexpressing mice were continuously ex-posed to hypoxic conditions for 14 days to establish a hypoxia exposure model.The open field,elevated cross maze and conditioned fear tests were used to detect the neurobehavioral activities of mice,and Golgi staining was used to observe the density of neuronal dendritic spines in cortex.The expression of PSD95,SYN1 and N-methyl-D-aspartate receptor subtype 2A(NMDAR2A)were detected by Western blot.Result:Compared with the normal oxygen group,the total distance and average speed of exercise in the open field experiment of mice in hypoxia group increased(P＜0.01),the rigidity time of mice in the conditioned fear box decreased(P＜0.01),and the density of dendritic spines in cortical region decreased(P＜0.05).The expressions of PSD95,SYN1 and NMDAR2A were decreased(P＜0.05).After the over-expression of PSD95,the autonomic activity of mice was reduced,the fear memory was relieved(P＜0.05),the dendrite density was reversed(P＜0.05),and the expression of synaptic related protein was increased(P＜0.05).Conclusion:Over-expression of PSD95 can alleviate neurobehavioral abnormalities and decline of fear memory induced under hypoxia exposure,protect neuronal dendritic spine injury in cortical region,and up-regulate the expression of syn-aptic protein.

Objective:To investigate the effect of myo-inositol on the reactivation of ocular dominance plasticity in the visual cortex of adult mice and its mechanisms.Methods:Thirty-two male SPF-grade C57BL/6J mice at postnatal day 60 (P60) were randomly divided into four groups using a random number table: normal control group, monocular form deprivation (MD) group, myo-inositol group (myo-inositol administered to normal mice), and MD+ myo-inositol group (myo-inositol administered to MD mice), with 8 mice in each group.The right eyes of MD group and MD+ myo-inositol group received MD on P60.Mice in each group were housed until P64 when pattern visual evoked potential (P-VEP) recordings were performed in both eyes.The amplitude and peak time of P100 wave were measured, and the contralateral/ipsilateral ratio (C/I) was calculated to evaluate the shift of ocular dominance.Twenty-four mice were randomly divided into MD group and MD+ myo-inositol group using the random number table method, with 12 mice in each group.RNA was extracted from the visual cortex of the two groups of mice, and transcriptomic sequencing and bioinformatics analysis were performed to screen differentially expressed genes.Six mice were randomly divided into MD group and MD+ myo-inositol group using the random number table method, with 3 mice in each group, and the expression changes of differentially expressed genes cell communication network factor 1( CCN1), fatty acid binding protein 7( Fabp7) and galectin-3 binding protein ( Lgals3bp) were verified by real-time fluorescence quantitative PCR.This study adhered to the Regulations on the Administration of Laboratory Animals (2017 Edition), and the research protocol was approved by the Animal Ethics Committee of Tianjin Medical University (No.TMUaMEC2022004). Results:The P-VEP results showed that the right eye P100 amplitudes in the normal control, MD, myo-inositol and MD+ myo-inositol groups were (89.04±19.87), (83.04±9.42), (88.14±21.75) and (61.75±15.42)μV, and the P100 wave peak time were (102.40±5.64), (101.50±8.26), (101.33±8.66) and (111.30±7.17)ms, and C/I were 2.38±0.17, 2.35±0.22, 2.41±0.31, and 1.65±0.24, respectively, with statistically significant overall differences ( F=5.844, 2.221, 16.634; all P<0.05).Compared with the normal control group, MD group and myo-inositol group, the MD+ myo-inositol group had a significant decrease in the P100 wave amplitude in the right eye, a significant prolongation of the P100 wave peak time, and a significant decrease in the C/I, with statistically significant differences (all P<0.05).There was no significant difference in P100 wave amplitude or peak time in the left eyes among the normal control, MD, myo-inositol and MD+ myo-inositol groups ( F=0.249, 1.356; both P>0.05).The transcriptome sequencing results showed that there were significant differences in the expression of 93 genes between the MD+ myo-inositol group and the MD group, among which the differential expression of CCN1, Fabp7 and Lgals3bp genes related to visual plasticity was particularly significant.The real-time fluorescence quantitative PCR results verified that the expression of CCN1 in the MD+ myo-inositol group was significantly decreased, and the expression of Fabp7 and Lgals3bp was significantly increased, with statistically significant differences ( t=17.561, 9.237, 12.710; all P<0.001). Conclusions:Myo-inositol can effectively reactivate ocular dominance plasticity in the visual cortex in adult mice, and may mediate this process by regulating the expression of specific genes CCN1, Fabp7, and Lgals3bp.

Objective:To investigate the effect of monocular form deprivation (MD) during the pre-critical period of visual development on the density and morphology of dendritic spines in mouse primary visual cortex (V1) neurons.Methods:Twenty SPF male C57BL/6J mice with eyes opened on postnatal day 14 (P14) were selected and divided into MD and control groups using a random number table, with 10 mice in each group.The MD group was fed to P18 after 4 days of MD in the right eye, and the control group was raised to P18 under the same feeding conditions.All mice were decapitated after cardiac perfusion, and the sections were stained with the cell membrane fluorescent probe 1, 1′-dioctadecyl-3, 3′, 3′-tetramethylindocarbocyanine perchlorate, and imaged by laser scanning confocal microscopy to observe and compare the differences in density and morphology of dendritic spines in bilateral V1 neurons between the control group and the MD group.This study was approved by the Animal Ethics Committee of Tianjin Medical University (No.TMUaMEC2022004).Results:The total density of dendritic spines in the V1 area on the left side of the control group, the right side of the control group, the left side of the MD group, and the right side of the MD group were (7.57±0.25), (7.42±0.25), (6.54±0.18), and (7.51±0.29)spines/10 μm, respectively, with a statistically significant overall difference ( F=3.818, P<0.05).The total density of dendritic spines in the left V1 area of mice in the MD group was significantly lower than that in the left side of the control group and the right side of the MD group, and the differences were statistically significant (both P<0.05).There was a significant difference in the proportion of the four types of dendritic spines in V1 neurons on both sides between the two groups ( χ2=26.295, P=0.002).There was a significant difference in the proportion of the four types of dendritic spines between the left V1 of the MD group and the left and right V1 of the control group (both P<0.008 3).There was a significant difference in the filopodia-type dendritic spine density in bilateral V1 neurons between the two groups ( F=3.253, P<0.05).Compared with the left V1 area of the control group, the density of filopodia-type dendritic spines in the left V1 area of the MD group decreased significantly, with a statistical significance ( P<0.05).There was no significant difference in the density of thin-type, mushroom-type, and stubby-type dendritic spines in bilateral V1 area neurons between the two groups ( F=1.760, 2.618, 1.749; all P>0.05). Conclusions:MD during the pre-critical period of visual development can cause a decrease in the total density of dendritic spines and significant changes in the compositional proportions in the V1 contralateral to the deprived eye, and is mainly manifested by a decrease in the number of filopodia, suggesting that abnormal visual experience can cause plastic changes in the number and structure of synapses in the visual cortex during the pre-critical period of visual development.

Objective:To investigate the protective effect of PSD95 on neurobehavioral abnormalities and synaptic damage in cortex induced by hypoxia exposure in mice.Methods:The 3-week-old C57BL/6 male mice were injected with neuron-specific adeno-associated virus through stereotaxic brain after 7 days of normal environment adaptation.The mice were divided into normoxia group(AAV-NC-Nor),control hypoxia group(AAV-NC-Hyp),normal oxygen group with over-expression of postsynaptic density-95(PSD95)(AAV-PSD95-Nor),and hypoxia group with over-expression of PSD95(AAV-PSD95-Hyp).Using a hypobaric hypoxia chamber,PSD95-overexpressing mice were continuously ex-posed to hypoxic conditions for 14 days to establish a hypoxia exposure model.The open field,elevated cross maze and conditioned fear tests were used to detect the neurobehavioral activities of mice,and Golgi staining was used to observe the density of neuronal dendritic spines in cortex.The expression of PSD95,SYN1 and N-methyl-D-aspartate receptor subtype 2A(NMDAR2A)were detected by Western blot.Result:Compared with the normal oxygen group,the total distance and average speed of exercise in the open field experiment of mice in hypoxia group increased(P＜0.01),the rigidity time of mice in the conditioned fear box decreased(P＜0.01),and the density of dendritic spines in cortical region decreased(P＜0.05).The expressions of PSD95,SYN1 and NMDAR2A were decreased(P＜0.05).After the over-expression of PSD95,the autonomic activity of mice was reduced,the fear memory was relieved(P＜0.05),the dendrite density was reversed(P＜0.05),and the expression of synaptic related protein was increased(P＜0.05).Conclusion:Over-expression of PSD95 can alleviate neurobehavioral abnormalities and decline of fear memory induced under hypoxia exposure,protect neuronal dendritic spine injury in cortical region,and up-regulate the expression of syn-aptic protein.

Objective:To investigate the status and influencing factors of teaching competence of clinical teachers in the affiliated hospitals of University of Chinese Medicine, and provide a reference for improving the teaching competency of clinical teachers.Methods:Using both objective sampling and random sampling methods, 330 clinical teachers from 3 affiliated hospitals of Beijing University of Chinese Medicine were investigated using the Clinical Teaching Competence Scale for Clinical Teachers in Affiliated Hospitals of TCM Universities from January 22 to February 6, 2024. The main statistical analysis methods included statistical description, non-parametric test, and multivariable linear regression.Results:The total score of clinical teachers' teaching competence was (176.83±22.84) points, with a scoring rate of 84.20%. Regression analysis revealed that teaching title ( β=0.053), age ( β=0.003), general self-efficacy ( β=0.009), and the agreeableness ( β=0.012) and openness ( β=0.010) of the Big Five personality traits were the main influencing factors of teaching competence of clinical teachers ( P<0.05). Conclusions:The clinical teachers in the surveyed medical institutions showed relatively high overall teaching competence, but there is still a need to strengthen their teaching abilities. Colleges and universities should adopt measures to comprehensively enhance their teaching competence, such as paying attention to the growth needs of clinical teachers with low professional titles, increasing the motivation for clinical teachers with high professional titles to improve their teaching abilities, establishing mentorship systems for early-career teachers, encouraging clinical teachers to develop self-efficacy, and focusing on cultivating the personality traits of agreeableness and openness in clinical teachers.

The visual cortex is an essential part of the brain for processing visual information. It exhibits structural and functional plasticity, which is crucial for adapting to complex visual environments. The quintessential manifestation of visual cortical plasticity is ocular dominance plasticity during the critical period, which involves numerous cellular and molecular events. While previous studies have emphasized the role of visual cortical neurons and their associated functional molecules in visual plasticity, recent findings have revealed that structural factors such as the extracellular matrix and glia are also involved. Investigating how these molecules interact to form a complex network that facilitates plasticity in the visual cortex is crucial to our understanding of the development of the visual system and the advancement of therapeutic strategies for visual disorders like amblyopia.
Neuronal Plasticity/physiology* ; Dominance, Ocular/physiology* ; Visual Cortex/physiology* ; Humans ; Animals ; Neurons/physiology*

This study aimed to comprehensively examine the association of gallstones, cholecystectomy, and cancer risk. Multivariable logistic regressions were performed to estimate the observational associations of gallstones and cholecystectomy with cancer risk, using data from a nationwide cohort involving 239 799 participants. General and gender-specific two-sample Mendelian randomization (MR) analysis was further conducted to assess the causalities of the observed associations. Observationally, a history of gallstones without cholecystectomy was associated with a high risk of stomach cancer (adjusted odds ratio (aOR)=2.54, 95% confidence interval (CI) 1.50-4.28), liver and bile duct cancer (aOR=2.46, 95% CI 1.17-5.16), kidney cancer (aOR=2.04, 95% CI 1.05-3.94), and bladder cancer (aOR=2.23, 95% CI 1.01-5.13) in the general population, as well as cervical cancer (aOR=1.69, 95% CI 1.12-2.56) in women. Moreover, cholecystectomy was associated with high odds of stomach cancer (aOR=2.41, 95% CI 1.29-4.49), colorectal cancer (aOR=1.83, 95% CI 1.18-2.85), and cancer of liver and bile duct (aOR=2.58, 95% CI 1.11-6.02). MR analysis only supported the causal effect of gallstones on stomach, liver and bile duct, kidney, and bladder cancer. This study added evidence to the causal effect of gallstones on stomach, liver and bile duct, kidney, and bladder cancer, highlighting the importance of cancer screening in individuals with gallstones.
Humans ; Mendelian Randomization Analysis ; Gallstones/complications* ; Female ; Male ; Cholecystectomy/statistics & numerical data* ; Middle Aged ; Risk Factors ; Aged ; Adult ; Neoplasms/etiology* ; Stomach Neoplasms/epidemiology*

Objective:To investigate the effect of monocular form deprivation (MD) on the distribution density of neuregulin-1 (NRG1) + and NRG1 - parvalbumin (PV) neurons in the primary visual cortex of mice during the critical period of visual development. Methods:Twelve healthy 28-day-old SPF male C57BL/6J mice were randomly divided into control group and MD group by the random number table method, with 6 mice in each group.After MD on postnatal day (P) 28, the MD group was fed until P32, while the control group was fed normally until P32.All mice were sacrificed by cervical dislocation after cardiac perfusion, and brain tissues were quickly collected.After fixation overnight, brain slices were subjected to PV and NRG1 immunofluorescence staining to observe and compare the differences in the distribution density of PV + , PV + /NRG1 + and PV + /NRG1 - neurons in both sides of the primary visual cortex (V1) area of the two groups.This study was conducted in accordance with the Regulations on the Administration of Experimental Animals (2017 Revision), and the study protocol was approved by the Institutional Animal Care and Use Committee of Tianjin Medical University (No.TMUaMEC2022004). Results:Immunofluorescence staining showed that the density of PV + and PV + /NRG1 + neurons was (137.8±4.3), (108.8±4.1), (137.4±4.0)/mm 2 in the contralateral V1 area of the control group, MD group and the ipsilateral V1 area of the MD group, and that of PV + /NRG1 + neurons was (112.0±4.6), (82.1±4.7) and (113.6±5.7)/mm 2, respectively, with statistically significant overall differences ( F=15.88, 12.53; both P<0.001).PV + neuron density and PV + /NRG1 + neuron density in the contralateral V1 area of the MD group were significantly lower than in the control group and in the ipsilateral V1 area of the MD group (all P<0.001).There was no difference in PV + /NRG1 - neuron density between the two groups ( F=0.20, P>0.05). Conclusions:PV + /NRG1 + neurons may be the main cell type regulating the development of primary visual cortex during the critical period.