Chronic stress induces psychiatric disorders, including depression and anxiety, yet effective therapies remain limited. Myelin in adult brains undergoes dynamic remodeling through oligodendrocyte precursor cells (OPCs) differentiation into oligodendrocytes (OLs) and the degeneration of pre-existing myelin. However, how chronic stress alters myelin dynamics and whether this represents a therapeutic target remains unclear. Here, adult mice subjected to 4-h daily restraint for 2 weeks exhibited significant anxiety, depression, and social deficits. Histological examinations revealed reduced OPC and OL density, decreased c-Fos-positive neurons, and loss of synaptic proteins in the brains exposed to chronic stress. To understand the dynamic changes of myelin, cell-lineage labeling and tracing demonstrated that chronic stress exposure remarkably inhibited oligodendrogenesis in the medial prefrontal cortex (mPFC), motor cortex, hippocampus, and amygdala, as revealed by the NG2CreERT; Tau-mGFP line, but did not significantly change pre-existing myelin as revealed by a newly generated line for mature OLs and myelin. To explore the role of myelinogenesis changes, adult myelin formation was inhibited by Olig2 conditional knockout in OPCs, resulting in decreased neuronal synaptic proteins and activity, accompanied by anxiety and depressive-like behaviors. Conversely, enhancing myelinogenesis through conditional deletion of the M1R in OPCs of stressed mice resulted in higher number of c-Fos-positive neurons, elevated synaptic protein expression, and a partial reversal of the behavioral deficits. Importantly, treating the stressed animal with the pro-myelination drug clemastine phenocopied the effects of M1R deletion on histological and behavioral disorders. Together, our findings demonstrate that enhancing oligodendrogenesis represents a promising strategy to rescue CRS-caused behavioral disorders.

Myelinogenesis is insufficient in numerous myelin-related diseases in the CNS, leading to functional impairments. Myelinogenesis couples with angiogenesis to ensure adequate need of oxygen and nutrients for oligodendrocyte (OL) differentiation. However, approaches to synchronize myelino-vascular coupling remain unavailable. We hypothesize the identification of shared signaling pathways in vascular cells and oligodendroglia may yield novel strategies to promote myelin repair through strengthening the blood vessel-myelination coupling. Here, single-cell sequencing and in situ hybridization revealed high expression of G-protein-coupled receptor 30 (Gpr30) in both vascular cells and oligodendroglia, with selective enrichment in pericytes and oligodendrocyte precursor cells (OPCs). Cell-specific deletion of GPR30 in pericytes driven by PDGFRβCreERT2 resulted in enhanced angiogenesis and myelination in developing brains. GPR30 deletion in OPCs or antagonizing GPR30 by G15 resulted in increased MBP-positive cell density and enhanced nanofiber wrapping capacity in vitro, thereby demonstrating an inhibiting role of GPR30 on OPC differentiation. To elucidate the coordinative role of GPR30 in both cell types, we employed NG2CreERT to induce a conditional knockout of GPR30 in both NG2-positive pericytes and OPCs. The conditional deletion of GPR30 enhanced myelination and increased vascular density in developing brains. Further, GPR30 cKO or G15 treatment enhanced myelin repair and functional recovery in the chronic neonatal hypoxia and lysolecithin-induced demyelination model, suggesting that antagonizing GPR30 is a promising strategy to synchronize angiogenesis with myelination to promote myelinogenesis. These findings establish GPR30 antagonism as a promising approach to enhance myelin repair through synchronizing pericyte-mediated angiogenesis and OPC differentiation.

This study investigated the protective effects of aldehyde dehydrogenase 2 (ALDH2) activation (via Alda-1), ALDH2 inhibition (via Daidzin), and the modulation of sirtuin 1 (SIRT1) and endoplasmic reticulum stress (ERS) on methyl-nitrosourea (MNU)-induced retinal damage in C57BL/6 mice. Seventy-two mice were randomly assigned to eight groups, including a control group, a MNU-alone group, and various treatment combination groups. Mice were administered with intraperitoneal injections of agonists and inhibitors targeting the ALDH2-SIRT1-ERS axis, respectively. Body weight, retinal layer thickness, and aldehyde metabolism biomarkers were assessed on the second and fourth day post-treatment. MNU administration induced retinal degeneration, resulting in significant body weight loss in all groups except the control. Treatment with Alda-1 attenuated retinal damage, while Daidzin exacerbated it. Pharmacological inhibition of SIRT1 (via EX-527) diminished the protective effects of Alda-1, and ERS induction (via TUN) nearly abolished its benefits. Conversely, SIRT1 activation (via SRT1720) mitigated the adverse effects of Daidzin, while ERS inhibition (via 4-PBA) partially alleviated Daidzin's impact. Furthermore, MNU increased levels of aldehyde metabolism markers (malondialdehyde [MDA] and 4-hydroxy-2-nonenal [4-HNE]), with Alda-1 reducing and Daidzin elevating these levels. Besides, pharmacological modulation of the SIRT1/ERS pathways intervened in the regulatory effects of Alda-1 and Daidzin on the aldehyde metabolism. Overall, ALDH2 activation protected retinal structure and regulated aldehyde metabolism, highlighting the critical role of the ALDH2-SIRT1/ERS signaling axis in mitigating retinal degeneration.

Abstract Objective This retrospective case-control study examined lipid and homocysteine (Hcy) patterns in Tibetan patients with acute ischemic stroke (AIS) in Xizang and developed an exploratory model to distinguish AIS cases from controls. Methods We enrolled 549 Tibetan AIS patients and 559 age- and sex-matched Tibetan controls. Clinical and biochemical indicators were compared between groups. XGBoost feature importance was used only for exploratory feature selection, and a random forest model was then constructed to evaluate the case-control discriminative ability of the selected indicators. Model performance was internally evaluated using AUC, recall rate, and F1 score. Results Compared with controls, AIS patients had lower high-density lipoprotein cholesterol (HDL), lower total cholesterol (TC), and higher Hcy levels. The combined lipid-Hcy imbalance pattern was defined as the co-occurrence of lower HDL and TC levels and higher Hcy levels in AIS patients than in controls. HDL, TC, and Hcy were consistently selected as AIS-associated indicators. The optimized random forest model based on these three indicators achieved an AUC of 0.924 in cross-validation and 0.887 in the test set. Conclusion HDL, TC, and Hcy were associated with AIS case-control status in Tibetan participants from Xizang and should be interpreted as associative markers rather than causal factors or diagnostic biomarkers. Because this was a retrospective case-control study and biomarkers were measured after AIS onset in cases, the model demonstrates only internal case-control discrimination and does not establish pre-onset predictive value. Prospective, multi-center external validation is needed before clinical use.

This study aimed to utilize Mendelian randomization (MR) analysis to investigate potential genetic targets related to aldehyde metabolism in the context of retinitis pigmentosa (RP) and to identify possible therapeutic options. Genome-wide association study data for RP were obtained for MR analysis. We employed various statistical methods, including inverse-variance weighted analysis, to evaluate potential causal associations with RP risk, followed by rigorous sensitivity analysis. Two-sample MR analysis identified a significant causal relationship between aflatoxin B1 (AFB1) aldehyde reductase and the risk of RP, with genetically predicted AFB1 aldehyde reductase contributing to a decreased risk of RP (odds ratio: 0.875; P = .008) based on inverse-variance weighted analysis. Sensitivity analysis suggested no evidence of heterogeneity or horizontal pleiotropy in the observed associations (P > .05). Additionally, the leave-one-out validation confirmed the robustness of these findings without significant alterations. The results from the reverse analysis for the causal relationship between the accidence of RP and AFB1 aldehyde reductase showed no significant statistical differences. Our findings highlighted the role of AFB1 aldehyde reductase in the pathogenesis of RP, proposing it as a promising protective measure for future treatment strategies.

We employed an integrated bioinformatics screening approach along with Mendelian randomization (MR) analysis to explore potential genetic targets for varicose veins of lower extremities (VVs) and identify potential treatment options for VVs. Differential expression analysis was conducted using R software to identify differentially expressed genes (DEGs) of VVs from the Gene Expression Omnibus database. Weighted gene co-expression network analysis (WGCNA) was performed to identify co-expression networks. Functional enrichment analyses were conducted for the identified genes. A protein-protein interaction network was constructed to analyze the interactions among the identified genes. Additionally, genome-wide association studies data for VVs were downloaded for MR analysis. Various methods, including inverse-variance weighted, were employed to assess potential causal associations with VVs risk, followed by sensitivity analysis. The DEGs identified from the VVs Gene Expression Omnibus dataset included 180 upregulated genes and 335 downregulated genes. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analysis revealed that the downregulated DEGs were significantly associated with nuclear protein-containing complexes and nucleic acid binding (P < .05). WGCNA highlighted a highly significant "turquoise" module comprising 78 downregulated genes (P = 2e - 04). The protein-protein interaction network analysis of the significant DEGs and the WGCNA "turquoise" module identified 224 nodes and 491 edges, uncovering several hub genes such as BRCA1, NCBP2, GTPBP4, HDAC2, KHDRBS1, and HNRNPR. Detailed functional enrichment analysis indicated involvement in tumor-like cellular proliferation and differentiation processes, including protein acetylation, RNA splicing, and metabolic processes. MR analysis revealed a causal association between the tumor-related gene Ecto-NOX disulfide-thiol exchanger 2 (ENOX2) and the risk of VVs, with a statistical significance (odds ratio: 1.0016; 95% confidence interval: 1.0003-1.0029; P = .015) according to inverse-variance weighted analysis. Sensitivity analysis confirmed the absence of heterogeneity and horizontal pleiotropy in the observed associations (P > .05). "Leave-one-out" validation analysis did not indicate any changes. Our study unveils the involvement of ENOX2 and the related mechanisms in the pathogenesis of VVs, suggesting their potential as genetic targets for treatment.

Long-term spaceflight can lead to changes in eye structure and decreased visual function. At present, there are almost no effective methods to prevent and treat eye damage caused by microgravity environments. Oxidative stress has been identified as one of the contributing mechanisms of spaceflight-associated neuro-ocular syndrome (SANS), and hydrogen (H2) has demonstrated significant antioxidant and anti-inflammatory effects. The aim of this study was to determine whether hydrogen-rich water (HRW) has a protective effect against eye injury induced by tail-suspension simulated weightlessness in rats, and to elucidate the underlying mechanisms. In this experiment, we utilized an 8-week tail-suspension model to simulate weightlessness, and employed histopathology, visual electrophysiology, and biochemical indices to evaluate retinal structure, function, and related molecular mechanisms leading to retinal damage. We also assessed the therapeutic efficacy of HRW treatment. Results demonstrated that tail-suspension simulated weightlessness induced thinning of the retinal outer nuclear layer, decreased visual function, and promoted retinal inflammation, oxidative stress, and mitochondrial dysfunction in rats. HRW treatment effectively alleviated the degenerative changes in the retinal outer nuclear layer, improved retinal function, and reduced retinal inflammation in treated rats. Our findings revealed that HRW reduced the retinal oxidative stress response and enhanced mitochondrial function through the PI3K/Akt/Nrf2 signaling pathway. Overall, HRW may be a promising candidate for the treatment of eye injuries in simulated microgravity environments.

Although the effects of noise-induced hearing loss (NIHL) on cognitive functions have been widely investigated, the cognitive effects of noise-induced hidden hearing loss (NIHHL), particularly its impact on memory, remain poorly understood. The Dnah11 gene, which encodes a dynein motor protein involved in synaptic development, may play a role in NIHHL-related cognitive impairment. We aimed to investigate whether NIHHL induces memory impairment and explore the role of Dnah11 expression in this process. Behavioral experiments identified the peak of memory impairment at 1 month following noise exposure. To elucidate molecular changes, hippocampal gene expression was analyzed using transcriptomic sequencing, reverse transcription quantitative polymerase chain reaction (RT-qPCR), and immunofluorescence. RNA sequencing revealed significant Dnah11 upregulation, with immunofluorescence confirming DNAH11 overexpression in hyperactivated CaMKIIα-positive excitatory neurons. Stereotaxic injection of recombinant adeno-associated virus (rAAV) vectors to knock down hippocampal Dnah11 expression improved memory performance in NIHHL mice without improving hearing loss. This cognitive improvement was accompanied by partial restoration of synaptic plasticity-related proteins, including SYN and PSD95. These findings indicate that Dnah11 upregulation in hippocampal excitatory neurons contributes to NIHHL-induced memory impairment, and targeting Dnah11 may offer a therapeutic strategy for memory impairment associated with hidden hearing loss. • NIHHL induced significant memory impairment in mice at 1 month after noise exposure. • Overexpression of DNAH11 in hyperactivation of CaMKIIα-positive excitatory neurons of the hippocampus was associated with memory impairment via disrupted synaptic plasticity. • Dnah11 knockdown in CaMKIIα-positive excitatory neurons rescued memory impairment and restored synaptic plasticity. Noise-induced hidden hearing loss (NIHHL) can lead to memory impairment in mice through disruption of synaptic plasticity. This effect may be associated with upregulated DNAH11 expression in hyperactivated CaMKIIα-positive excitatory neurons in the hippocampus. Knockdown of the Dnah11 gene in the hippocampus ameliorated memory impairment and restored synaptic plasticity in mice.

JOURNAL/nrgr/04.03/01300535-202507000-00032/figure1/v/2024-09-09T124005Z/r/image-tiff A microgravity environment has been shown to cause ocular damage and affect visual acuity, but the underlying mechanisms remain unclear. Therefore, we established an animal model of weightlessness via tail suspension to examine the pathological changes and molecular mechanisms of retinal damage under microgravity. After 4 weeks of tail suspension, there were no notable alterations in retinal function and morphology, while after 8 weeks of tail suspension, significant reductions in retinal function were observed, and the outer nuclear layer was thinner, with abundant apoptotic cells. To investigate the mechanism underlying the degenerative changes that occurred in the outer nuclear layer of the retina, proteomics was used to analyze differentially expressed proteins in rat retinas after 8 weeks of tail suspension. The results showed that the expression levels of fibroblast growth factor 2 (also known as basic fibroblast growth factor) and glial fibrillary acidic protein, which are closely related to Müller cell activation, were significantly upregulated. In addition, Müller cell regeneration and Müller cell gliosis were observed after 4 and 8 weeks, respectively, of simulated weightlessness. These findings indicate that Müller cells play an important regulatory role in retinal outer nuclear layer degeneration during weightlessness.

目的 探索三叉神经脊束核尾侧亚核(Vc)神经元内Panx1参与脉冲电磁场(PEMF)对三叉神经痛(TN)的镇痛效应及其潜在机制.方法 将雄性C57BL/6J小鼠随机分为假手术组、TN组及TN+PEMF组,每组10只.建立眶下神经结扎模型构建TN小鼠,并对TN+PEMF组小鼠施加脉冲电磁场刺激(15 Hz,5 Gauss,2 h/d,7 d).采用Von Frey纤维丝测定各组小鼠触须垫区域机械性痛阈值变化,并用视频记录分析小鼠口面部单侧不对称理毛持续时长以检测自发性痛觉过敏行为;通过免疫荧光染色技术检测对侧的Vc内Panx1的分布水平;使用Western blotting检测Panx1、p-Src及NR1的表达量变化.结果 TN组小鼠与假手术组相比,触须垫区域机械痛阈值显著降低(P＜0.05),面部理毛活动持续时长明显增加(P＜0.05),Panx1、p-Src及NR1蛋白的表达均显著升高(P＜0.01);TN+PEMF组小鼠与TN组相比,机械痛阈值显著升高(P＜0.05),面部理毛活动持续时长明显减少(P＜0.05),Panx1、p-Src及NR1的表达均显著降低(P＜0.01).结论 PEMF可显著缓解TN小鼠口面部机械痛及自发痛,抑制NR1-Src-Panx1通路的激活.

Objective: Microgravity contributes to ocular injury yet the underlying mechanism remains unclear. This study aims to elucidate the mechanism behind choroidal circulation disorder and outer retinal degeneration in rats with simulated weightlessness.Methods: Optical coherence tomography angiography (OCTA) was used to evaluate choroidal circulation and retinal morphological alterations in rats with weightlessness simulation. Electroretinogram and transmission electron microscopy were used to examine the ultrastructure and function of the choroid and outer retina. Furthermore, histological and terminal deoxynucleotidyl transferase deoxyuridine dUTP nick-end labeling (TUNEL) staining was used to monitor retinal morphology. Western blotting was performed to analyze the expressions of blood-retinal outer barrier function-related proteins (Cx43, ZO-1, and occludin).Results: The choroidal thickening was observed from the fourth week of simulated weightlessness (p < 0.05), and choroidal capillary density started to decline by the fifth week (p < 0.05). Transmission electron microscopy revealed that the choroidal vessels were open and operating well by the fourth week. However, most of the mitochondria within the vascular endothelium underwent mild swelling, and by the fifth week, the choroidal vessels had various degrees of erythrocyte aggregation, mitochondrial swelling, and apoptosis. Additionally, ERG demonstrated a decline in retinal function beginning in the fifth week (p < 0.05). TUNEL staining revealed a significantly higher apoptotic index in the outer nuclear layer of the retina (p < 0.05). At the sixth week weeks of simulated weightlessness, OCTA and hematoxylin and eosin (HE) staining of retinal sections revealed that the outer nuclear layer of the retina started to become thin (p < 0.05). Results from western blotting revealed that Cx43, ZO-1, and occludin exhibited decreased expression (p < 0.05).Conclusion: Based on our findings in a rat model of simulated weightlessness, choroidal circulation disturbance induced by choroidal congestion is the initial cause of outer retinal degeneration. Blood-retinal barrier disruption is significant in this process.

Ethnopharmacological relevance: Mudan granule (MuD), a patent compound traditional Chinese medicine (TCM), is broadly clinically used for diabetic peripheral neuropathy (DPN) treatment in China. Since diabetic retinopathy (DR) and DPN are both 'Qi deficiency' and collaterals obstruction syndrome in TCM theory, it is worthwhile to investigate the specific pharmacological effects of MuD on DR.Aim of the study: DR is a serious neurovascular complication of diabetic mellitus (DM). The present study is to investigate the effects of MuD on DR, and further explore the potential therapeutic targets.Materials and methods: Diabetic mice model was induced by the intraperitoneal injection of 60 mg/kg streptozotocin for five consecutive days. 8 weeks later, MuD was administered to diabetic mice (MuD group), while the untreated diabetic mellitus mice (DM group) and age-matched healthy mice (CON group) were administered with the equal volume saline. After 6-week intervention, the retinal function and morphological changes were observed. Then the molecule profiling of the ocular tissues was systematically analyzed through TMT-based proteomics. Furthermore, western blotting and immunofluorescence staining detections were applied to validate the differentially expressed proteins.Results: The MuD treatment in DR mice actively protected retinal function and inhibited the retinal thickness decreasing. 109 differentially expressed proteins were screened in DM compared to CON, 56 of which were up-regulated and 53 were down-regulated (fold change > 1.2, p < 0.05). MuD significantly regulated 70 biomarkers of diabetic retinal damage. Bioinformatics analysis showed that these proteins were significantly enriched in the TNF/TNFR/NF-κB signaling pathway which was related to inflammatory reaction. Interestingly, our study revealed that fibrillin 2 (FBN2) was the key diminished biomarker in DM retina compared to CON (0.36 times), and the most significantly upregulated (3.26 times) differential protein in the MuD group compared to DM. Molecular biological methods further confirmed that MuD could depress inflammation (TNF-α, NFκB and IL-6) and impede retinal neovascularization and fibrogenesis by upregulation of FBN2 level and down-regulation of TGF-β/VEGFA axis.Conclusion: MuD could ameliorate diabetic mice retinal dysfunction through strengthening FBN2 activation and inhibiting TNF signaling pathway. The suppression of the neoangiogenesis and fibrogenesis triggered by the FBN2/TGF-β/VEGFA signaling pathway, and the inflammatory reactions activated by the TNF-α/NF-κB/IL-6 signaling pathway might provide effective targets for pharmacological intervention treating DR.

目的:基于网络药理学及实验验证探讨枸杞子治疗干眼(DE)的作用机制.方法:以"枸杞子"为关键词,通过采用TCMSP数据库与分析平台,搜索枸杞子的药物活性成分及作用靶点,以GeneCards和OMIM数据库搜索Dry eye(DE)相关的基因靶点,将枸杞子与DE的靶点基因导入Venn软件,可获得两者交集的靶点图,后将数据导入String数据库获得PPI蛋白与蛋白相互作用网络图,借助于Cytoscape3.7.2软件构建枸杞子活性成分-作用靶点-相关疾病的网络图;再利用Bioconductor平台及R语言GO富集分析、KEGG富集分析;通过实验验证干眼发病机制中的关键靶标.结果:通过TCMSP数据库与分析平台筛选得到枸杞子的有效化学成分45种,活性成分对应的靶点基因174个,与DE共同的靶点基因131个,根据"药物-成分-疾病-靶点"网络拓扑图,枸杞子治疗DE的主要有效成分27个.分析PPI网络,根据度值较高,即枸杞子治疗DE的关键靶点主要包括AKT1、VEGFA、CASP3、IL1B、JUN、PTGS2、CXCL8等,根据GO富集分析获得枸杞子治疗DE的166种生物学功能与过程,KEGG富集分析显示涉及31条信号通路,此外,通过实验验证发现DE模型组的结膜组织中AKT1、IL-6、TNF-α及IL-17蛋白表达量显著升高.结论:枸杞子治疗DE是多成分-多靶点-多途径的复杂过程,且枸杞子治疗DE主要通过抗炎及抑制细胞凋亡相关分子参与调控.

目的 研究不同模拟飞行光环境下,不同视力受试者动态视力(DVA)的差异,为保障飞行安全提供试验依据.方法 招募24名受试者,其中6名视力正常者为1.0/1.0视力组(小数视力),18名近视受试者随机分为0.8/0.8视力组、0.6/0.6视力组和0.4/0.4视力组,每组6人.在模拟日光、迎光、背光、曙暮光和云上光环境下,通过观察3.0、4.5、6.0、7.5 km/h运动速度的视标检测DVA.采用具有2个重复测量因素的三因素重复测量方差分析,比较不同光环境对不同视力者DVA的影响.结果 光环境、静态视力和运动速度3个因素间不存在交互作用(P>0.05).通过进一步两因素交互作用检验,分析发现光环境和静态视力存在交互作用(P<0.05),运动速度和静态视力存在交互作用(P<0.05),光环境和运动速度不存在交互作用(P>0.05).与日光环境相比,所有视力组受试者在背光下的DVA显著提高(P<0.001),在曙暮光、迎光下的DVA均显著下降(P<0.001).除0.4/0.4视力组外,其余视力组在云上光环境下的DVA显著低于日光(P<0.05).在相同的模拟光环境下,1.0/1.0视力组DVA最高,0.8/0.8视力组高于0.6/0.6视力组,0.4/0.4视力组最低,差异有统计学意义(P<0.05).对于3.0、4.5、6.0 km/h运动速度的视标,1.0/1.0视力组DVA最高,0.8/0.8视力组高于0.6/0.6视力组,0.4/0.4视力组最低,差异有统计学意义(P<0.05).1.0/1.0视力组观察7.5 km/h运动速度视标的DVA显著高于低视力组(P<0.05),0.4/0.4视力组低于0.8/0.8和0.6/0.6视力组,差异有统计学意义(P<0.05).所有视力组受试者DVA均随目标运动速度的增加而显著下降(P<0.05).结论 光环境和静态视力水平、运动速度和静态视力水平对DVA水平的作用相互影响.近视者在不利光环境(如迎光、云上光和曙暮光)下观察快速运动目标时,DVA严重下降,应引起飞行人员和航空医学工作者的重视.

目的 比较同一体质量区间不同品系大鼠、小鼠眼轴的差别.方法 选用野生型(SD)大鼠、实验室现有的不同品系大鼠和小鼠:先天性静止性夜盲(CSNB)大鼠、卷毛(HL)大鼠、视网膜锥细胞失功能(RCD)大鼠、C57BL/6小鼠、锥体光感受器功能丧失 1(cpfl1)小鼠、锥体光感受器功能丧失 3(cpfl3)小鼠、先天性静止性夜盲(Nob2)小鼠,按照体质量划分为不同组别(大鼠以 50 g为一区间分为 10 组,小鼠以 10 g为一区间共分为两组),测量其眼轴,在同一体质量区间比较不同品系大鼠和小鼠之间的眼轴区别.结果 大鼠与小鼠眼轴长度随体质量增加而增长,在不同品系之间存在差异.其中 100～150 g体质量的 CSNB大鼠眼轴长度大于 SD大鼠(P<0.05).150～200 g体质量的 RCD大鼠眼轴长度大于 SD 大鼠(P<0.01),但 SD 与 CSNB 大鼠之间不具有统计学差异;200～250 g、450～500 g、500～550 g体质量的 HL与 RCD大鼠眼轴较 SD大鼠长(P<0.05),但 SD 与 CSNB 大鼠之间没有统计差异;250～300 g与 300～350 g体质量的三种品系大鼠眼轴均长于 SD 大鼠(P<0.01);350～400 g 体质量的 CSNB与 RCD大鼠眼轴长于 SD大鼠(P<0.01),但 SD大鼠与 HL 大鼠之间无统计学差异;400～450 g 体质量的四种品系大鼠眼轴均无统计学差异;550～600 g体质量的 HL大鼠眼轴较 SD大鼠长(P<0.05),CSNB与 SD 大鼠之间无统计差异.全部体质量的 C57BL/6 小鼠眼轴长度短于其余 3 个品系的小鼠(P<0.01);结论 不同体质量区间,各基因突变大鼠或小鼠眼轴长于对照鼠(SD大鼠 C57BL/6 小鼠)眼轴,且在大鼠中,此差异在发育期更为明显.

Background To develop machine learning models for objectively evaluating visual acuity (VA) based on pattern-reversal visual evoked potentials (PRVEPs) and other related visual parameters. Methods Twenty-four volunteers were recruited and forty-eight eyes were divided into four groups of 1.0, 0.8, 0.6, and 0.4 (decimal vision). The relationship between VA, peak time, or amplitude of P100 recorded at 5.7°, 2.6°, 1°, 34′, 15′, and 7′ check sizes were analyzed using repeated-measures analysis of variance. Correlations between VA and P100, contrast sensitivity (CS), refractive error, wavefront aberrations, and visual field were analyzed by rank correlation. Based on meaningful P100 peak time, P100 amplitude, and other related visual parameters, four machine learning algorithms and an ensemble classification algorithm were used to construct objective assessment models for VA. Receiver operating characteristic (ROC) curves were used to compare the efficacy of different models by repeated sampling comparisons and ten-fold cross-validation. Results The main effects of P100 peak time and amplitude between different VA and check sizes were statistically significant (all P < 0.05). Except amplitude at 2.6° and 5.7°, VA was negatively correlated with peak time and positively correlated with amplitude. The peak time initially shortened with increasing check size and gradually lengthened after the minimum value was reached at 1°. At the 1° check size, there were statistically significant differences when comparing the peak times between the vision groups with each other (all P < 0.05), and the amplitudes of the vision reduction groups were significantly lower than that of the 1.0 vision group (all P < 0.01). The correlations between peak time, amplitude, and visual acuity were all highest at 1° ( r s = − 0.740, 0.438). VA positively correlated with CS and spherical equivalent (all P < 0.001). There was a negative correlation between VA and coma aberrations ( P < 0.05). For different binarization classifications of VA, the classifier models with the best assessment efficacy all had the mean area under the ROC curves (AUC) above 0.95 for 500 replicate samples and above 0.84 for ten-fold cross-validation. Conclusions Machine learning models established by meaning visual parameters related to visual acuity can assist in the objective evaluation of VA.

航空医疗救援是借助航空器作为交通工具,运用医学手段救助受困对象的活动,在救灾救援任务中发挥着举足轻重的作用.本文主要探讨了航空医疗救援活动中,航空特殊环境的特点及可能带来的危害;常见危重疾病的机上救治和护理要点.这有助于减少因医疗操作不当造成的损伤,从而使航空医疗救援活动安全、有序、高效地展开.

The traditional methods for the control of myopia development are optical correction, orthokeratology lens, defocus glasses and other methods, however, these approaches are poor. At present, it has been demonstrated that outdoor activities and the application of low concentration atropine had a positive effect on preventing the occurrence of myopia and controlling the growth of myopia diopter. The occurrence and development of axial myopia was related to scleral remodeling toward myopic direction, but the mechanism remains unclear. In addition, true myopia caused by the axial growth was irreversible. After long-term spaceflight, astronauts had posterior eyeball flattening, axial shortening, and hyperopic displacement of refractive state, indicating that stress environment could cause sclera remodeling. Therefore, the combination of appropriate exercise to promote the transfer of blood head and increase the hydrostatic pressure gradient of the head and eye tissue might affect the local scleral remodeling and shorten the axial direction of the eye, or delay the trend of axial growth, which could provide a new idea for the prevention and control of myopia.

AIM: To study the effects of the specific simulated luminous environment on the visual performance of people with different vision, so as to provide an experimental basis for revising pilots' vision standards. METHODS: A controlled randomized trial was conducted. Twenty-four volunteers were recruited and divided into four groups(1.0/1.0, 0.8/0.8, 0.6/0.6 and 0.4/0.4, decimal vision)according to right/left eye visual acuity, with six subjects in each group. Each subject was tested for static distant vision, kinetic visual acuity, color vision, depth perception error and visual search time under the simulated luminous environments of sunlight, twilight, and on-cloud, respectively, to compare changes in the impact of distinctive luminous surroundings on the visual performance indicators of human beings with different vision.RESULTS: There were main effect differences in static distant vision, kinetic visual acuity, color error, depth perception error and visual search time under different light environments(all P<0.01). The binocular static distant visual acuity, abilities of color discrimination, depth perception and visual search in simulated sunlight environment were higher than those in simulated twilight and on-cloud environments. In the 0.4/0.4 vision group, kinetic vision in simulated twilight and on-cloud environments were significantly lower than that in simulated sunlight environment(P<0.01). There were main effect differences in binocular static distant vision, kinetic visual acuity, depth perception error and visual search time among subjects with different vision(all P<0.05). Compared with 1.0/1.0 vision group, those with 0.6/0.6 and 0.4/0.4 vision had significant decrease in kinetic visual acuity, depth perception ability and visual search ability(all P<0.05). CONCLUSION: Different luminous environments have a great impact on the visual performance of people with low vision, which poses a potential threat to flight safety.

目的 比较大动物心脏手术实验中氯胺酮肌注和异氟烷吸入全身麻醉诱导的优劣,探索更适合大动物心脏手术的围术期麻醉管理策略,以提高实验质量、促进临床转化.?方法 选取体外循环下主动脉瓣置换术的小尾寒羊36只,随机均分为两组.分别给予肌肉注射8 mg/kg氯胺酮诱导和2％异氟烷面罩吸入诱导,合理追加剂量直至气管插管成功.术中麻醉维持均采用一致的静吸复合麻醉方案.收集插管期间的心率、血压指标,记录麻醉诱导时间、手术时长、体外循环时长、体外循环前及结束后的血气指标、麻醉药物总用量和动物死亡数量等.?结果 相较于氯胺酮组,异氟烷组的麻醉诱导时间明显缩短,差异有统计学意义(t=4.842,P<0.01);与气管插管前的心率相比,异氟烷组插管即刻增加的更少,差异有统计学意义(t=3.904,P<0.01),且插管后3 min恢复的更快,差异有统计学意义(t=2.794,P<0.01);与气管插管前的血压相比,异氟烷组插管即刻变化更大,具有统计学差异(t=4.858,P<0.01),插管后3 min降低更快,差异有统计学意义(t=2.996,P<0.01).两组术中麻醉药物总用量、手术时长、体外循环时长、气管导管拔除所需时间和动物死亡数量差异无统计学意义(P>0.05).?结论 异氟烷吸入麻醉诱导时间短、血流动力学稳定,创伤小、动物依从性高,更安全有效,可提高大动物体外循环下心脏手术实验质量.