Purpose: To report a case of interface fluid syndrome following small incision lenticule extraction (SMILE) and subsequent CIRCLE enhancement. Case Presentation: A 30-year-old female experienced progressively worsening vision following refractive enhancement surgery. The patient had experienced a transient increase in intraocular pressure (IOP) after SMILE, normalized poststeroid cessation. Three months after the enhancement, her best-corrected visual acuity deteriorated from 20/20 in both eyes before the surgery to 20/300. IOP measured by non-contact tonometry was 25.3 mmHg in the right eye and 26.7 mmHg in the left eye, while the measurements off the flap using iCare were 55.3 mmHg and 47.8 mmHg, respectively. Examination revealed moderate corneal edema, interface fluid pockets, and haze, which were confirmed by anterior segment optical coherence tomography. Treatment involved the discontinuation of steroids and the introduction of hypotensive medication, leading to significant symptom relief. Conclusion: This case highlights the importance of cautious and conservative steroid use, particularly in steroid-responsive patients. When steroids are administered in cases potentially involving diffuse lamellar keratitis and haze, monitoring peripheral IOP is essential.

Purpose: To report a case of interface fluid syndrome following small incision lenticule extraction (SMILE) and subsequent CIRCLE enhancement. Case Presentation: A 30-year-old female experienced progressively worsening vision following refractive enhancement surgery. The patient had experienced a transient increase in intraocular pressure (IOP) after SMILE, normalized poststeroid cessation. Three months after the enhancement, her best-corrected visual acuity deteriorated from 20/20 in both eyes before the surgery to 20/300. IOP measured by non-contact tonometry was 25.3 mmHg in the right eye and 26.7 mmHg in the left eye, while the measurements off the flap using iCare were 55.3 mmHg and 47.8 mmHg, respectively. Examination revealed moderate corneal edema, interface fluid pockets, and haze, which were confirmed by anterior segment optical coherence tomography. Treatment involved the discontinuation of steroids and the introduction of hypotensive medication, leading to significant symptom relief. Conclusion: This case highlights the importance of cautious and conservative steroid use, particularly in steroid-responsive patients. When steroids are administered in cases potentially involving diffuse lamellar keratitis and haze, monitoring peripheral IOP is essential.

视网膜静脉阻塞（retinal vein occlusion, RVO）是导致视力损害的主要眼底疾病之一，常引发视网膜缺血、出血、液体渗漏和黄斑水肿，从而导致视力下降甚至永久丧失。目前，RVO继发黄斑水肿的主要治疗方法是玻璃体腔内注射抗血管内皮生长因子（vascular endothelial growth factor, VEGF）药物。然而，RVO的病理机制不仅限于VEGF，还涉及血管生成素-2（angiopoietin-2, Ang-2）的作用。在病理状态下，Ang-2通过破坏血管稳定性，诱导新生血管形成，并加剧炎症反应，进一步促进RVO的病程进展。法瑞西单抗（Faricimab）作为一种双特异性抗体药物，能够同时抑制VEGF-A和Ang-2这两条关键的病理通路，显示出在改善患者视力方面的潜在优势。文章对Faricimab在RVO治疗中的作用机制、临床应用、相关治疗药物对比及未来发展前景进行了详细论述，为其在眼科领域的进一步应用提供了理论依据和参考。

Retinal vein occlusion (RVO) is one of the leading retinal diseases causing vision impairment and is often associated with retinal ischemia, hemorrhage, fluid leakage, and macular edema, ultimately resulting in decreased vision or even permanent vision loss. Currently, the primary treatment for RVO-associated macular edema is intravitreal injection of anti-vascular endothelial growth factor (VEGF) agents. However, the pathological mechanisms of RVO are not limited to VEGF alone, but also involve angiopoietin-2 (Ang-2). Under pathological conditions, Ang-2 disrupts vascular stability, induces neovascularization, and exacerbates inflammatory responses, thereby accelerating the progression of RVO. Faricimab, as a bispecific antibody, can simultaneously inhibit both VEGF-A and Ang-2 pathways, which are critical in RVO pathogenesis, and has shown potential advantages in improving visual outcomes. The article provides a detailed discussion on the mechanism of action, clinical applications, comparison with related therapeutic agents, and future development prospects of Faricimab in the treatment of RVO, offering a theoretical basis and reference for its further application in ophthalmology.

Dominant optic atrophy (DOA) is an inherited optic neuropathy and more than 75% of DOA patients harbor pathogenic mutations in OPA1. We reported a 39-year-old female harboring c.2119G>T mutation of OPA1 and manifested progressive visual impairment after hydroxychloroquine (HCQ) therapy. The patient’s visual impairment remained stable for 10 years until she began to take HCQ 13 months ago. She complained about progressively decreased vision in both eyes. Bilateral pale temporal optic disc was similar with that of 11 years ago. Optical coherence tomography showed bilateral moderate retinal nerve fiber layer thinning other than the nasal quadrant and general thinning of the inner retina in the macular. Microcystic macular edema was noted in nasal macular in both eyes. Visual field testing showed paracentral scotoma and microperimetry showed decrease sensitivity in the macular in both eyes. After the patient stopped taking HCQ, her functional tests including visual acuity, field testing and microperimetry testing was stable compared with those of 2 years ago. However, progressive inner macular and RNFL thinning was shown by OCT. OPA1 c.2119 G>T found in this patient was a mutation that had been rarely reported in previous studies. The patient has been followed up for over 10 years and her visual acuity stayed stable for decades long until she took HCQ for 13 months. Her vision decline terminated after she stopped taking HCQ. Although HCQ toxicity is highly related to the duration and daily dose, HCQ may aggravate visual impairment in certain individuals harboring OPA1 mutation. Patients with DOA should avoid using neurotoxic HCQ and other medications that may interfere mitochondrial metabolism.

Dominant optic atrophy (DOA) is an inherited optic neuropathy and more than 75% of DOA patients harbor pathogenic mutations in OPA1. We reported a 39-year-old female harboring c.2119G>T mutation of OPA1 and manifested progressive visual impairment after hydroxychloroquine (HCQ) therapy. The patient’s visual impairment remained stable for 10 years until she began to take HCQ 13 months ago. She complained about progressively decreased vision in both eyes. Bilateral pale temporal optic disc was similar with that of 11 years ago. Optical coherence tomography showed bilateral moderate retinal nerve fiber layer thinning other than the nasal quadrant and general thinning of the inner retina in the macular. Microcystic macular edema was noted in nasal macular in both eyes. Visual field testing showed paracentral scotoma and microperimetry showed decrease sensitivity in the macular in both eyes. After the patient stopped taking HCQ, her functional tests including visual acuity, field testing and microperimetry testing was stable compared with those of 2 years ago. However, progressive inner macular and RNFL thinning was shown by OCT. OPA1 c.2119 G>T found in this patient was a mutation that had been rarely reported in previous studies. The patient has been followed up for over 10 years and her visual acuity stayed stable for decades long until she took HCQ for 13 months. Her vision decline terminated after she stopped taking HCQ. Although HCQ toxicity is highly related to the duration and daily dose, HCQ may aggravate visual impairment in certain individuals harboring OPA1 mutation. Patients with DOA should avoid using neurotoxic HCQ and other medications that may interfere mitochondrial metabolism.

目的：应用广角扫频源光学相干断层扫描成像(swept-source optical coherence tomography, SS-OCT)的en face结构投射图研究玻璃体早期液化特征。方法：使用SS-OCT进行18 mm×18 mm 的容积（Cube）扫描，创建并分析健康未成年人（年龄5~18岁）70眼的系列玻璃体en face结构投射图。 结果：在未成年人中，视网膜前的玻璃体包含4种液化结构，分别为后皮质前玻璃体囊袋（posterior precortical vitreous pocket, PPVP）、视盘前Martegiani区（the area of Martegiani, AM）、血管前液化裂隙（prevascular vitreous fissures，PVF）和液化池（cistern）。所有研究眼均能检出PPVP、AM和PVF，其中22眼（31.4%）的PPVP和AM连通。41眼（58.6%）可检出液化池，且其年龄大于未检出液化池的个体（P =0.01），液化池的发生与年龄呈正相关（r_s=0.315，P =0.008）。液化池的象限空间分布频率依次为颞上（90.2%）、鼻上（58.5%）、颞下（36.6%）、鼻下（24.4%），最常累及颞上象限（P＜0.001）。 结论：PPVP、AM和PVF是健康人群视网膜前玻璃体早期液化过程中均出现的特征。液化池的发生与年龄呈正相关，最常出现在颞上象限，可能是年龄相关性玻璃体液化变性的结果。

Objective: To investigate the early vitreous liquefaction characteristics using en face structural projection images obtained by wide-angle swept-source optical coherence tomography (SS-OCT). Methods: SS-OCT was employed to perform 18*18mm volumetric (Cube) scans. A series of en face structural projection images of the vitreous were created and analyzed for 70 eyes from healthy minors aged between 5 and 18 years. Results: In minors, four types of vitreous liquefaction structures were identified anterior to the retina: pre-posterior vitreous pocket (PPVP), the preoptic area of Martegiani (AM), pre-vascular liquefaction fissures (PVF), and cisterns. PPVP, AM, and PVF were detectable in all studied eyes, with PPVP and AM being interconnected in 22 eyes (31.4%). Cisterns were observed in 41 eyes (58.6%), and the mean age of individuals with cisterns was higher than those without (P =0.01). The occurrence of cisterns positively correlated with age (r=0.315; P=0.008). The frequency of cistern quadrant distribution was highest in the superotemporal quadrant (90.2%), followed by the superonasal quadrant (58.5%), inferotemporal quadrant (36.6%), and inferonasal quadrant (24.4%). The superotemporal quadrant was the most frequently affected (P <0.001). Conclusion: PPVP, AM, and PVF are features consistently observed in the early vitreous liquefaction process anterior to the retina in healthy individuals. The occurrence of cisterns positively correlates with age and is most common in the superotemporal quadrant, possibly representing the result of age-related vitreous liquefaction degeneration. These findings provide a theoretical foundation for studying the pathogenesis of vitreoretinal interface diseases. 

内源性真菌性眼内炎(endogenous fungal endophtalmitis, EFE)是最具破坏性的眼部感染之一，在临床上较少见。如诊断和治疗不及时，可严重损害患者视力，甚至需摘除眼球。由于EFE发病隐匿，病程较长，病原学涂片和培养阳性率较低，早期临床症状与葡萄膜炎相似，极易被误诊和漏诊，延误治疗时机。EFE最常见的感染灶来源为肝脏、肺、尿路、脑膜炎、胃肠道、心内膜以及骨髓。文章报道了一例腰椎感染致双眼内源性念珠菌性眼内炎的男性患者，66岁，因“右眼视力下降1周”首诊于眼科，专科检查见右眼玻璃体炎性混浊，初诊为右眼葡萄膜炎，予抗炎等治疗症状无好转，右眼视力持续下降，右眼前房穿刺抽液送检提示：热带念珠菌感染，之后左眼视力也逐渐下降，加之患者近期于骨科住院，术中腰椎间盘退变的纤维软骨组织DNA-病原微生物宏基因组检测结果示热带念珠菌，考虑双眼EFE，予全身及局部使用抗真菌药物联合双眼玻璃体切割手术，治疗后患者视力恢复良好，随访1年无复发。该病例及相关文献回顾，有助于加深临床医生对此类疾病的认识，为今后临床诊疗提供一定思路，也起到一定警示作用。

Fungal endophthalmitis is one of the most destructive eye infections and is relatively rare in clinical practice.If not diagnosed and treated promptly, it can severely damage vision and even lead to enucleation.Due to its insidious onset, long course, low positive rates in smears and cultures, and early clinical symptoms similar to uveitis, it is prone to misdiagnosis and missed diagnosis, leading to delayed treatment. A review of the literature indicates that the most common sources of EFE infection are the liver, lung, urinary tract, meningitis, gastrointestinal tract, endocarditis and osteomyelitis.In this paper, we report a case of lumbar spine infection causing bilateral candidal endophthalmitis in a 66-year-old male patient.He initially presented to the ophthalmology department of our hospital with a one-week history of decreased vision in the right eye, specialized examination revealed inflammatory opacity in the vitreous of the right eye, initially diagnosed as uveitis and treated with anti-inflammatory therapy without improvement.As the vision in the right eye continued to decline, aqueous humor aspiration from the anterior chamber of the right eye indicated infection with tropical Candida.Subsequently, the vision in the left eye also gradually decreased.Considering the recent hospitalization in the orthopedic department for lumbar disc degeneration, metagenomics analysis of fibrous cartilage tissue DNA during surgery detected tropical Candida, suggesting bilateral endogenous fungal endophthalmitis,The patient was treated with systemic and local antifungal medications in combination with bilateral vitrectomy surgery.After treatment, the vision recovered well, and there was no recurrence during a one-year follow-up.The objective of this thesis is to deepen the understanding of clinicians on this type of disease by reporting this case and reviewing relevant literature, providing some insights for future clinical diagnosis and treatment, and serving as a warning.

先天性晶状体脱位(congenital ectopia lentis, CEL)是一种罕见的遗传相关性疾病，其主要临床特征是晶状体悬韧带先天性发育异常，导致晶状体偏离正常解剖位置。随着病情的进展，CEL可引起高度屈光不正甚至弱视外，还可能导致继发性青光眼和视网膜脱离等严重的并发症。目前，手术仍是改善CEL患儿视觉质量及防治并发症的主要手段。常用的手术方式包括晶状体摘除术、前房型人工晶状体(intraocular lens, IOL)植入术、囊袋支撑装置联合IOL植入术及经巩膜IOL固定术等，这些手术方式各具特点，但目前最佳手术方式仍未有定论。既往大量文献表明，手术能够显著改善CEL患儿视力，但随着眼球的生长发育，CEL患儿术后屈光状态常出现近视漂移。此外，术后并发症如缝线暴露，IOL瞳孔夹持、IOL脱位、视网膜脱离等仍有可能发生，需要长期的严密随访。这些因素都使得CEL的治疗具有挑战性。为此，文章就CEL的手术方式、视力预后、术后屈光变化及术后并发症进行综述，旨在为该疾病的临床诊断及治疗提供更为全面和深入的理解。

Congenital ectopia lentis (CEL) is a rare genetic disorder characterized by the displacement of the lens from its normal anatomical position due to abnormalities in the lens zonular. As the progression of the disease, CEL can lead to high refractive error, even amblyopia, as well as other serious complications such as secondary glaucoma and retinal detachment. Currently, surgical intervention remains the primary method to improve the visual quality and prevent complications in children with CEL.Common surgical options include lens extraction, anterior chamber intraocular lens (IOL) implantation, IOL implantation combined with capsular tension devices, and transcleral fixation of IOL. Each surgical approach has its own characteristics, but there is currently no consensus on the best surgical method. Previous literature has shown that surgery can significantly improve vision in children with CEL; however, due to the growth of the eye, postoperative refractive status often experiences myopic shift. Additionally, complications such as suture exposure, IOL pupil capture, IOL dislocation, and retinal detachment may still occur, necessitating long-term close follow-up. These factors make the treatment of CEL challenging. This article reviews the surgical approaches, visual prognosis, postoperative refractive changes, and postoperative complications associated with CEL, aiming to provide a more comprehensive and in-depth understanding for the clinical diagnosis and treatment of this disease.

马方综合征 (Marfan syndrome, MFS) 是一种由原纤维蛋白-1(fibrillin-1,FBN-1)突变引起的全身性遗传性疾病，FBN-1基因突变与MFS相关表型的联系相关，目前已报道的MFS常见的眼部表现包括角膜扁平、长眼轴、晶状体异位以及视网膜病变等异常，这些眼部异常将对MFS患者的视力产生影响，如角膜异常可影响角膜高阶像差的异常，可能导致近视或散光等屈光状态异常，从而影响视觉质量，损害视力清晰度。此外，MFS的眼底血管病变，也可能导致MFS患者的视力丧失，研究发现，MFS视网膜血管及脉络膜血管的密度较正常人减少，并与最佳矫正视力相关，由于光感受器的代谢与营养供应与视网膜及脉络膜血管息息相关，血管异常可能与视力损失相关。由于MFS患者存在视力损害的风险，其早期诊断和治疗尤为重要，因此，了解MFS眼部病变的特点及其对视力的影响，对制定针对MFS眼病的治疗方案具有重要的意义。另外，由于MFS眼部异常与FBN1基因突变相关，其基因突变类型多样，致病机制复杂，总结MFS眼部特点对其发病机制的继续探索有一定的指导作用，因此，文章拟就MFS患者眼部生物学参数特点及其对视力的影响这一领域国内外的相关研究进展进行综述。

Marfan syndrome (MFS) is a systemic hereditary disease caused by fibrillin-1 (FBN-1) mutations. FBN-1 gene mutations are associated with MFS-related phenotypes. Common ocular manifestations of MFS reported so far include corneal flattening, long axial length, ectopia lentis, and retinal abnormalities. These ocular abnormalities will affect the vision of MFS patients. For example, corneal abnormalities can affect abnormalities in corneal higher-order aberrations, which may lead to abnormal refractive states such as myopia or astigmatism, thereby affecting visual quality and compromising visual acuity. In addition, retinal vascular abnormalities may also lead to vision loss in MFS patients. Studies have found that the density of retinal and choroidal blood vessels in MFS patients is lower than that in normal individuals and is associated with best corrected visual acuity. Given the close relationship between the metabolism and nutrient supply of photoreceptors and retinal and choroidal vasculature, vascular abnormalities may be linked to visual impairment. Since MFS patients are at risk of visual impairment, early diagnosis and treatment are particularly important. Therefore, understanding the characteristics of ocular manifestations in MFS and their impact on vision is crucial for devising effective treatment strategies for MFS-related ocular conditions. Additionally, as ocular abnormalities in MFS are linked to mutations in the FBN1 gene, which exhibit diverse mutation types and complex pathogenic mechanisms, summarizing the ocular features of MFS can provide valuable insights for further exploration into its pathogenesis. Therefore, this article aims to review the progress of domestic and international research on the ocular biological parameters of MFS patients and their impact on vision.

Autoimmune uveitis is one of the most common inflammatory eye diseases leading to blindness globally. Its etiology is primarily associated with autoimmune responses. Patients with this condition often exhibit complex and chronic disease courses, with a high propensity for recurrence. Current treatments mainly involve corticosteroids and immunosuppressive agents, which, despite their effectiveness, entail significant side effects that severely impact patients' vision and quality of life. There are still unresolved questions regarding the etiology and immunopathogenesis of autoimmune uveitis, and traditional high-throughput sequencing techniques fall short of adequately elucidatingits pathogenic mechanisms at the cellular level. With the continuous advancement of single-cell sequencing technology, an increasing number of studies are leveraging this approach to deeply investigate the pathogenesis of autoimmune uveitis, thereby offering new insights for identifying novel diagnostic and therapeutic targets. This paper reviews the latest applications of single-cell sequencing technology in exploring the pathogenesis of autoimmune uveitis. Through the utilization of this technology, researchers can gain a more comprehensive understanding of cellular-level changes in patients, providing robust support for the search for new therapeutic avenues. These studies offer new directions for the diagnosis and treatment of autoimmune uveitis and provide valuable information for the development of future therapeutic strategies and approaches.

Autoimmune uveitis is one of the most common inflammatory eye diseases leading to blindness globally. Its etiology is primarily associated with autoimmune responses. Patients with this condition often exhibit complex and chronic disease courses, with a high propensity for recurrence. Current treatments mainly involve corticosteroids and immunosuppressive agents, which, despite their effectiveness, entail significant side effects that severely impact patients' vision and quality of life. There are still unresolved questions regarding the etiology and immunopathogenesis of autoimmune uveitis, and traditional high-throughput sequencing techniques fall short of adequately elucidatingits pathogenic mechanisms at the cellular level. With the continuous advancement of single-cell sequencing technology, an increasing number of studies are leveraging this approach to deeply investigate the pathogenesis of autoimmune uveitis, thereby offering new insights for identifying novel diagnostic and therapeutic targets. This paper reviews the latest applications of single-cell sequencing technology in exploring the pathogenesis of autoimmune uveitis. Through the utilization of this technology, researchers can gain a more comprehensive understanding of cellular-level changes in patients, providing robust support for the search for new therapeutic avenues. These studies offer new directions for the diagnosis and treatment of autoimmune uveitis and provide valuable information for the development of future therapeutic strategies and approaches.

糖基化是一种重要的蛋白质翻译后修饰，通常发生在内质网和高尔基体的特定位置。N-糖基化和O-糖基化是最常见的糖基化修饰类型。与其他翻译后修饰相比，糖基化具有独特的生物学意义，包括结构的复杂多样性，生物功能的重要性以及进化上的保守性。糖基化修饰对于蛋白质稳定性、细胞黏附与识别、细胞内信号传导和表观遗传学具有重要影响，从而参与调节细胞生物学和发病机制。近年来，越来越多的研究揭示了糖基化参与眼部疾病的发生和发展，包括眼表疾病、圆锥角膜、青光眼、年龄相关性黄斑变性、视网膜色素变性、糖尿病视网膜病变等。眼部蛋白糖基化异常可通过诱发新生血管形成、炎症反应、氧化应激、异常免疫应答等改变细胞的结构与功能，进而影响各种眼病的发生发展。通过深入研究糖基化在不同眼部疾病中的作用机制，可以为相关眼部疾病的早期诊断和治疗提供新的思路和方法。现综述糖基化在眼部疾病的研究进展，以探究调控蛋白质糖基化对眼部疾病的诊疗意义。

Glycosylation is an important post-translational modification of proteins that usually occurs at specific locations within the endoplasmic reticulum and Golgi apparatus. N-glycosylation and O-glycosylation are the most common types of glycosylation modifications. Compared to other post-translational modifications, glycosylation has unique biological significance, including structural complexity and diversity, crucial biological functions, and evolutionary conservation. Glycosylation modifications significantly impact protein stability, cell adhesion and recognition, intracellular signal transduction, and epigenetics, thereby regulating cellular biology and pathogenesis. In recent years, an increasing amount of research has revealed the involvement of glycosylation in the occurrence and development of ocular diseases, including ocular surface diseases, keratoconus, glaucoma, age-related macular degeneration, retinitis pigmentosa, and diabetic retinopathy. Abnormal glycosylation of ocular proteins can induce changes in cell structure and function through mechanisms such as neovascularization, inflammatory response, oxidative stress, and abnormal immune response, thereby influencing the occurrence and development of various eye diseases. By deeply studying the mechanisms of glycosylation in different ocular diseases, new insights and methods can be provided for the early diagnosis and treatment of related ocular diseases. This review summarizes the research progress of glycosylation in ocular diseases to explore the diagnostic and therapeutic significance of regulating protein glycosylation in ocular diseases.

白内障是世界范围内致盲的主要原因之一，占中低收入国家致盲病例的50%。随着人口老龄化程度的加深，到2050年中国白内障致盲病例预计达到2 000万。卫生支出占比低、医疗设备及眼科医生紧缺、筛查费用昂贵仍是中低收入国家无法开展大规模白内障筛查的主要原因。人工智能(artificial intelligence，AI)协助白内障诊断具有便捷、低成本、可远程进行等优点，有望减少甚至避免白内障致盲的发生。文章将对AI通过结合裂隙灯眼前节图像、眼底照片及扫频源光学相干层析图像进行白内障自动诊断等研究进行简要综述。

Cataract is a primary cause of blindness globally, particularly accounting for 50% of blindness cases in low- and middle- income countries. As the population ages, it is predicated that cataract blindness cases in China will rise to 20 million by 2050. However, low health expenditures, scarcity of medical equipment and ophthalmologists, and high screening costs continue to hinder mass cataract screening in these countries. Artificial intelligence(AI)-assisted cataract diagnosis offers significant advantages, including convenience, cost-effectiveness, and remote accessibility, potentially reducing or even eliminating cataract blindness. This review aims to concisely summarize the research on automatic cataract diagnosis utilizing AI, incorporating slit lamp images of anterior eye segment, fundus photographs, and swept source optical coherence tomography images.