Diabetic retinopathy (DR) is one of the most prevalent complications of diabetes which could lead to vision impairment. Dysfunction of the retinal pigment epithelium (RPE) is an early pathogenic event, where various mechanisms may contribute to the disease progression. circular RNAs (circRNAs) have been reported to be important regulators in diabetic complications, acting as miRNA sponge, participating in the regulation of gene transcription or coding short peptides. Circular RNA microarray and RNA-seq were used to identify differentially expressed circRNAs in ARPE-19 cells in normal and high glucose treatments. The expression of cKIAA1462, miR-183-5p, and high mobility group box 1 (HMGB1) were determined using quantitative real-time polymerase chain reaction and Western blot. In vitro experiments, such as flow cytometry, Western blot, and Electron microscope (TEM) were conducted. The binding interaction was confirmed using dual-luciferase reporter and overexpression/inhibition experiments. cKIAA1462 was knocked down via intravitreal lentiviral injection in diabetic mice, followed by expression level detection, functional analysis and histological assessments. cKIAA1462 was significantly upregulated under high glucose conditions both in vitro and in vivo (in retinas of diabetic mice). It acted as a molecular sponge for miR-183-5p, increasing the expression of HMGB1. Elevated HMGB1 concurrently impaired autophagic flux (increased p62, decreased autophagosomes) and activated the NLRP3 inflammasome (upregulated NLRP3, ASC, caspase-1), promoting pyroptosis. Silencing cKIAA1462 in vivo restored autophagy, suppressed pyroptosis, improved retinal structure, and enhanced electroretinogram responses in diabetic mice. The cKIAA1462/miR-183-5p/HMGB1 axis plays a critical role in diabetic RPE injury by dual regulation of autophagy and pyroptosis. Targeting this pathway may offer a novel therapeutic strategy for early diabetic retinopathy.

BACKGROUND:Presently, the global prevalence of myopia and high myopia reaches approximately 1.95 billion and 277 million individuals, respectively. Projections suggest that by 2050, the number of people with myopia may rise to 4.758 billion and those with high myopia to 938 million. In highly myopic eyes, the occurrence of MF is reported to be as high as 8-33%. SUMMARY:This review comprehensively addresses the classification, pathogenesis, natural progression, concomitant pathologies, and therapeutic strategies for macular foveoschisis in highly myopic patients. KEY MESSAGES:In recent years, macular foveoschisis has emerged as a prevalent complication in individuals with high myopia, primarily resulting from the combination of inward traction by vitreoretinal adhesions and outward traction exerted by posterior scleral staphyloma on the retina. While some maintain partial visual stability over an extended period, others may progress to macular holes or even retinal detachment. For highly myopic patients with macular foveoschisis, the mainstay procedures are vitrectomy, macular buckle, and posterior scleral reinforcement. However, there is controversy about whether to perform inner limiting membrane peeling and gas filling.

Purpose: To describe surgical management and establish visual outcomes of open globe injury (OGI) in pediatric patients requiring vitrectomy. Methods: Forty-eight eyes of 48 pediatric patients underwent vitrectomy for OGI with secondary vitreoretinal complications in the eye center of Jilin University were included. Characteristics of patients, details of ocular examination and operation, presenting and final visual acuity were recorded. Results: Presenting visual acuity less than 20/400 was found in 44 eyes (91.7%), which included no light perception (NLP) in four eyes. At last visit, there was no eyes with visual acuity of NLP, and 19 eyes (39.6%) had a vision recovery to 20/400 or better. Mechanisms of injury, intraocular contents prolapse, presence of hyphema, intraocular foreign body, vitreous hemorrhage, retinal detachment, and total time from injury to PPV > 2 weeks were significant predictors of visual prognosis. Logistic regression analysis showed that hyphema was a significant predictive factor for poor visual outcome. Conclusion: Visual acuity was improved in most of the patients with OGI in this study. Hyphema is an important presenting ocular sign in estimating the post-vitrectomy visual outcome for OGI in children. Proper timing of vitrectomy is suggested, and in this study patients may benefit more with early vitrectomy as less proliferative vitreoretinopathy (PVR) was found together with a better visual acuity.

先天性白内障是造成儿童视力下降甚至致盲的常见疾病之一,其致病因素多样,其中遗传因素占1/3左右且多数源于基因突变.该病的遗传方式分为常染色体显性遗传(AD)、常染色体隐性遗传(AR)和性染色体连锁遗传,有较大的遗传与表型异质性.基于现代科学技术的不断发展和学者们对先天性白内障的研究,本文主要对遗传性先天性白内障致病基因的研究进展进行综述.

A series of recent studies suggested that miR-143 might involve in the tumorigenesis and metastasis of various cancer types. However, the biological function and underlying mechanisms of miR-143 in human epithelial ovarian carcinoma (EOC) remain unknown. Therefore, this study aimed to investigate the miR-143 expression and its clinical diagnosis significance in patients suffering EOC and to analyze its role and underlying molecular mechanism in EOC. Our result showed that the expression levels of miR-143 were downregulated in EOC tissues and cell lines, was associated with International Federation of Gynaecology and Obstetrics (FIGO) stage, pathological grade and lymph node metastasis (all P < 0.01) . Overexpression of miR-143 significantly inhibited EOC cell proliferation, migration, and invasion. Furthermore, computational algorithm combined with luciferase reporter assays identified connective tissue growth factor (CTGF) as the direct target of miR-143 in EOC cells. The expression level of CTGF was significantly increased in EOC tissues, was inversely correlated with miR-143 expression in clinical EOC tissues. Knockdown of CTGF mimicked the suppression effect induced by miR-143 overexpression. Restoration of CTGF expression partially reversed the suppression effect induced by miR-143 overexpression. These results suggested that miR-143 inhibited EOC cell proliferation, migration, and invasion, at least in part, via suppressing CTGF expression.

Correction of astigmatism is an important part of refractive cataract surgery.Currently,methods of combined corneal astigmatism correction in cataract surgery mainly include keratotomy and Toric intraocular lens (IOL) implantation.Whether it is a scalpel or femtosecond laser keratotomy,the effects of astigmatism correction is related to the position,shape,length and depth of the incisions,configuration,and distance between incisions and optic axis.Moreover,the pattern and material of Toric IOL can affect its rotation stability and effects of astigmatism correction.This article reviewed recent progress of correcting corneal astigmatism in cataract surgery,which provided reference for ophthalmologists in clinical.

AIM:To investigate the function of Pentacam in accurately selecting the model and axial position of Toric artificial lens. METHODS: Totally 53 eyes of 46 cataract patients who were scheduled to receive phacoemulsification from January 2018 to December 2018 were selected in our hospital. Before the operation, corneal astigmatism was greater than 1.0D according to the examination results by AL-Scan and automatic corneal curvature instrument, and Pentacam was used to evaluate the corneal astigmatism to guide the accurate selection of Toric IOL model and the axial position to be implanted. Surgery was done by the same doctor. After operation, the patients were traced and visited for 3mo to collect the uncorrected visual acuity(UCVA), the best corrected visual acuity(BCVA), the whole-eye astigmatism, the corneal curvature and target induced astigmatism(TIA)before and after the operation as well as the postoperative astigmatism, the rate not relying on the glasses, visual quality assessment and so on. RESULTS: There was no obvious change on patients' corneal astigmatism before and after the operation. The whole-eye astigmatism was reduced and UCVA and BCVA were obviously improved. The difference was statistically meaningful(P&lt;0.05). The postoperative residual astigmatism and TIA were statistically tested, and the results showed no statistical significance(P&gt;0.05). The rate of distant vision defecation and visual quality were significantly improved. CONCLUSION: Pentacam can evaluate the corneal astigmatism more comprehensively and accurately, which is helpful to guide the accurate selection of Toric artificial lens model, and to improve the postoperative expected effect.

Background As a common ocular complication of diabetes mellitus, diabetic cataract is becoming a leading cause of visual impairment. The progression of diabetic cataract progression involves epithelial-to-mesenchymal transition (EMT), the precise role of which remains to be investigated. As microRNAs (miRNAs) are suggested to be involved in the pathogenesis of many diseases, identification of aberrantly expressed miRNAs in diabetic lens epithelial cells (LECs) and their targets may provide insights into our understanding of diabetic cataract and potential therapeutic targets. Methods Diabetic cataract capsules and LECs exposed to high glucose (25 mmol/L, 1–5 days) were used to mimic the model. Quantitative RT-PCR was performed to evaluate the differential expression of miRNA. Dual luciferase reporter assay was used to identify the binding target of miR-199a-5p. The expression of EMT-associated proteins was determined by immunofluorescence and Western blot analysis. Results Our results showed the differential expression of miR-9, -16, -22, -199a and -204. MiR-199a was downregulated in diabetic cataract capsule and hyperglycemia-conditioned human LECs. Specific protein 1 could be directly targeted and regulated by miR-199a in LECs and inhibit EMT in diabetic LECs. Conclusion Our findings implied miR-199a could be a therapeutic target by regulating SP1 directly to affect EMT in diabetic cataract and provided novel insights into the pathogenesis of diabetic cataract.

Background: As a disorder occurs in the eyes, keratoconus (KC) is induced by the thinning of the corneal stroma. This study was designed to reveal the key long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and mRNAs involved in the mechanisms of KC. Methods: Transcriptome RNA-seq data set GSE112155 was acquired from the Gene Expression Omnibus database, which contained 10 KC samples and 10 myopic control samples. Using the edgeR package, the differentially expressed (DE)-mRNAs between KC and control samples were screened. The DE-lncRNAs and DE-miRNAs in this data set were identified using the HUGO Gene Nomenclature Committee (HGNC). Using the pheatmap package, bidirectional hierarchical clustering of the DE-RNAs was conducted. Then, an enrichment analysis of the DE-mRNAs was performed using the DAVID tool. Moreover, a competitive endogenous RNA (ceRNA) regulatory network was built using the Cytoscape software. After KC-associated pathways were searched within the Comparative Toxicogenomics Database, a KC-associated ceRNA regulatory network was constructed. Results: There were 282 DE-lncRNAs (192 upregulated and 90 downregulated), 40 DE-miRNAs (29 upregulated and 11 downregulated), and 910 DE-mRNAs (554 upregulated and 356 downregulated) between the KC and control samples. A total of 34 functional terms and 9 pathways were enriched for the DE-mRNAs. In addition, 6 mRNAs (including PPARG, HLA-B, COL4A1, and COL4A2), 5 miRNAs (including miR-181a), 9 lncRNAs (including XIST), and the XIST-miR-181a-COL4A1 axis were involved in the KC-associated ceRNA regulatory network. Conclusions: PPARG, HLA-B, COL4A1, COL4A2, miR-181a, and XIST might be correlated with the development of KC. Further, the XIST-miR-181a-COL4A1 axis might be implicated in the pathogenesis of KC.

The long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) is reportedly involved in the initiation and progression of cancers of several types. However, the role, expression status, and the detailed mechanism of NEAT1 in retinoblastoma (RB) yet need to be unraveled. We explored the role and the mechanism of NEAT1 activity in RB. Our data show enhanced NEAT1 expression in RB-affected tissues compared with the corresponding control. Functional experiments reveal that a NEAT1 knockdown in RB cells significantly inhibits proliferation, cycle progression, and facilitates apoptosis and caspase-3 and -9 activities. Besides that, miR-124 was predicted to be a target of NEAT1 and its reduced expression, as well as the inverse correlation of NEAT1 with miR-124, was observed in RB-affected tissues. Further, luciferase and RNA immunoprecipitation (RIP) assays confirmed the interaction between NEAT1 and miR-124. Rescue experiments confirmed that the inhibition of miR-124 could reverse the effect of NEAT1 on RB cell proliferation, cycle arrest, apoptosis, and caspase-3 and -9 activities. Thus, NEAT1 promotes RB progression by sponging miR-124, providing a therapeutic target for RB.

在人类基因组中,编码蛋白质的序列仅占2%[1],绝大部分的DNA不具备编码功能,这些DNA转录后形成的产物即为非编码RNA（Noncoding RNA,ncRNA）。起初发现时,受研究条件的限制,ncRNA长期被认为是RNA聚合酶Ⅱ转录的副产物,被称作无生物学功能的转录噪音或基因组

Purpose: This study was aimed at identifying differentially expressed genes (DEGs) in bacterial and fungal keratitis. The candidate genes can be selected and quantified to distinguish between causative agents of infectious keratitis to improve therapeutic outcomes. Methods: The expression profile of bacterial or fungal infection, and normal corneal tissues were downloaded from the Gene Expression Omnibus. The limma package in R was used to screen DEGs in bacterial and fungal keratitis. The Co-Express tool was used to calculate correlation coefficients of co-expressed genes. The "Advanced network merge" function of Cytoscape tool was applied to obtain a fusional co-expression network based on bacterial and fungal keratitis DEGs. Finally, functional enrichment analysis by DAVID software and KEGG analysis by KOBAS of DEGs in fusion network were performed. Results: In total, 451 DEGs in bacterial keratitis and 353 DEGs in fungal keratitis were screened, among which 148 DEGs were found only in bacterial keratitis and 50 DEGs only in fungal keratitis. Besides, 117 co-expressed gene pairs were identified among bacterial keratitis DEGs and 87 pairs among fungal keratitis DEGs. In total, nine biological pathways and seven KEGG pathways were screened by analyzing DEGs in the fusional co-expression network. Conclusion: TLR4 is the representative DEG specific to bacterial keratitis, and SOD2 is the representative DEG specific to fungal keratitis, both of which are promising candidate genes to distinguish between bacterial and fungal keratitis.

Dioscin is a typical saponin with multiple pharmacological activities. The past few years have seen an emerging interest in and growing research on this pleiotropic saponin. Here, we review the emerging pharmacological activities reported recently, with foci on its antitumor, antimicrobial, anti-inflammatory, antioxidative, and tissue-protective properties. The potential use of dioscin in therapies of diverse clinical disorders is also discussed.

Objective: The objective of this study was to investigate expression of interleukin-2 (IL-2), IL-6, IL-10, and IL-1 beta in rats with fungal keratitis. Methods: Rat models of fungal keratitis were established in vitro and divided into the blank control group, the injury control group and the fungal experimental group. The modeling results were detected via hematoxylin-eosin (HE) staining. The expression levels of IL-2, IL-6, IL-10, and IL-1 beta in corneal epithelial tissues were detected via immunohistochemistry at 24 hours after modeling, and the optical density of staining was analyzed. Moreover, relative expression levels of IL-2, IL-6, IL-10, and IL-1 beta messenger ribonucleic acid (mRNA) in corneal epithelial tissues were detected via reverse transcription-polymerase chain reaction (RT-PCR) at 4, 8, 16 and 24 hours after modeling. Results: At 24 hours after fungal infection, edema occurred in the corneal epithelium and stroma, and there was infiltration of a large number of inflammatory cells in the corneal limbus and stroma. IL-2, IL-6, IL-10, and IL-1 beta were hardly expressed in the control group, little expressed in the injury control group and highly expressed in the fungal experimental group. Optical density analyses showed that there were statistically significant differences among the three groups (P< 0.05). At 4, 8, 16 and 24 hours after modeling, relative expression levels of IL-2, IL-6, IL-10, and IL-1 beta mRNA in corneal epithelial tissues were gradually increased. There were statistically significant differences in relative expression levels of mRNA at each time point between the fungal experimental group and the injury control group (P< 0.05), and relative expression levels of mRNA at the same time point also had statistically significant differences between the two groups (P< 0.05). Conclusion: In this study, the expression of IL-2, IL-6, IL-10, and IL-1 beta began to increase gradually after modeling, and they were increased remarkably at 24 hours, suggesting that changes in expression of IL-2, IL-6, IL-10, and IL-1 beta may be involved in the occurrence and development of fungal keratitis in rats.

MicroRNA-218 (miR-218) has been implicated in the development and progression of multiple cancers. We investigated the role of miR-218 in ovarian cancer progression. We found that miR-218 expression levels were lower in ovarian cancer tissues and cell lines than in adjacent normal tissues or a normal ovarian cell line.miR-218 levels associated with International Federation of Gynecology and Obstetrics (FIGO) stage and lymph node metastasis. Exogenous expression of miR-218 inhibited cell proliferation, colony formation, migration, and invasion in vitro and suppressed tumor growth in a tumor-bearing nude mouse model. Runt-related transcription factor 2 (RUNX2) was identified as a direct functional target of miR-218, and its expression was inversely correlated with miR-218 expression in ovarian cancer tissues. RUNX2 overexpression rescued the suppressive effect of miR-218 on ovarian cancer cell proliferation, colony formation, migration, and invasion. These findings highlight an important role played bymiR-218 in the regulation of cancer growth and metastasis, in part by repressing RUNX2, and revealed the potential of miR-218 as a new therapeutic target inovarian cancer.

A growing body of evidence suggests that microRNA-494 (miR-494) could act as tumor-suppressive or oncogenic microRNAs (miRNAs) in different types of tumors. However, the biological roles and underlying mechanisms of miR-494 remain unknown in human epithelial ovarian carcinoma (EOC). Therefore, the aims of this study were to investigate the miR-494 expression and the significance of its clinical diagnosis in patients suffering EOC and to analyze its role and underlying molecular mechanism on the carcinogenesis of EOC. Here, we found that miR-494 was significantly decreased in EOC cell lines and tissues and its expression was negatively correlated with advanced International Federation of Gynecology and Obstetrics (FIGO) stage, high pathological grade, and lymph node metastasis (all P < 0.01). Functional studies showed that overexpression of miR-494 in EOC cells could remarkably inhibit proliferation, colony formation, migration, and invasion and induce cell apoptosis, G0/G1 phase arrest. An in vivo analysis revealed that the overexpression of miR-494 suppressed tumor growth in a nude mouse xenograft model system. Bioinformatic assay and dual-luciferase assay confirmed that insulin-like growth factor 1 receptor (IGF1R) was as a direct target of miR-494 in EOC cells. Western blot assay showed that overexpression of miR-494 inhibited IGF1R expression and its downstream signal protein expression. In addition, downregulation of IGF1R has similar effects with miR-494 overexpression on EOC cells and overexpression of IGF1R effectively rescued the inhibition of overexpressed miR-494 in EOC cells. These data suggested that miR-494 functions as a tumor suppressor in EOC by targeting IGF1R.

目的：评价透明晶状体摘除联合后房型折叠人工晶状体植入术矫正中老年超高度近视的有效性及安全性。方法对32例60只超高度近视眼在表面麻醉下行透明晶状体皮质吸出联合后房型折叠人工晶状体植入术。患者年龄40～65〔平均（52．33±11．19）〕岁。双眼28例，单眼4例，随访3～18个月。眼轴长平均（30．03±2．04）mm。比较术前术后视力、最佳矫正视力、散光度数，随访术后并发症情况。结果患眼术后3个月视力≥0．5者32眼（53．3％）；最佳矫正视力≥0．5者46眼（76．7％）。术中无1例发生后囊破裂。术后无1例发生网脱，术后有8例14眼（23．3％）发生后囊混浊，行钕：钇－铝－石榴石激光（ Nd：YAG）后囊切开术。随访期内未发现黄斑水肿、出血、青光眼、人工晶状体偏心等并发症。结论透明晶状体摘除治疗中老年超高度近视术后效果满意、安全，但熟练掌握超声乳化技术及术前完善的预防性治疗工作至关重要，是开展此项技术的关键，并且术后需长期随访，注意远期并发症的发生。

This is to review the current state of knowledge on the functional and clinical aspects of bestrophin 1, a prominent member of a family of proteins involved in the control and properties of the light peak of the EOG. Initially human bestrophin 1 gene (BEST1) mutations were identified to underlie Best vitelliform macular dystrophy (VMD), a dominantly inherited, juvenile-onset form of macular degeneration. In the recent past the phenotypical spectrum of retinal disorders associated with BEST1 mutations has been extended and the term bestrophinopathies was coined. The physiological role of bestrophin 1 is still not completely understood but has been linked to the generation of a transepithelial chloride current by controlling voltage-dependent calcium channels (VDCC). Dysfunction of bestrophin 1 may result in abnormal ion and fluid transport by the retinal pigment epithelium (RPE) disturbing and even disrupting direct interactions between the RPE and the photoreceptors.