Nonspecific orbital inflammation(NSOI)is an orbital inflammation that is not associated with an infection. Even though it's often considered the most common diagnosis in orbital biopsies, it's still an exclusionary diagnosis that means systemic illnesses and other possible causes have to be ruled out. Though it is always an excluded clinical diagnosis, acute orbital symptoms such discomfort, exophthalmos, periorbital edema, chemosis, diplopia, and vision impairment are commonly associated with NSOI. Clinical diagnosis and management of NSOI provide a substantial difficulty. There are presently no recognized diagnostic criteria or standard treatment strategy for NSOI, and the clinical symptoms and histological features show significant variation. This guide was formulated under the auspices of the Ocular Oncology Committee of the Opthalmology Branch of the Chinese Medical Doctor Association, Opthalmology Committee of International Association of Intelligent Medicine, Opthalmology Committee of International Association of Translational Medicine making a detailed summary of the definition, classification, diagnosis and treatment of the NSOI, with a view to aiding clinicians to improve diagnostic efficiency and formulate a better treatment plan for patients.

AIM:To investigate the value of optical coherence tomography angiography(OCTA)indicators in the diagnosis of diabetic retinopathy(DR), and to provide patients with diabetic nephropathy(DN)with more sensitive OCTA screening indicators to detect concurrent DR at an early stage.METHODS: A total of 200 patients who treated in the ophthalmology department of the Seventh Affiliated Hospital, Sun Yat-sen University from 2022 to 2023 were included, including 95 first-diagnosed DR patients and 105 patients without DR, and all patients underwent OCTA examination and a collection of demographics and renal function parameters. After a quality check, automated measurements of the foveal avascular zone area, vessel density(VD), and perfusion density(PD)of both 3 mm×3 mm and 6 mm×6 mm windows were obtained.RESULTS: Using random forest and multivariate Logistic regression methods, we developed a diagnostic model for DR based on 12 variables(age, FBG, SBP, DBP, HbA1c, ALT, ALP, urea/Scr, DM duration, HUA, DN, and CMT). Adding specific OCTA parameters enhanced the efficacy of the existing diagnostic model for DR(outer vessel density in 6 mm×6 mm window, AUC=0.837 vs 0.819, P=0.03). In the study of DN patients, the parameters in the 6 mm×6 mm window improved the diagnostic efficacy of DR(inner VD; outer VD; full VD; outer PD; full PD).CONCLUSION:The outer VD in the 6 mm×6 mm window can enhance the efficacy of the traditional DR diagnostic model. Meanwhile, compared with the 3 mm×3 mm window, the microvascular parameters in the 6 mm× 6 mm window focusing on DN patients can be more sensitive to diagnosing the occurrence of DR.

AIM: To investigate and clarify the intervention mechanism of trigonelline(TRG)in preventing ferroptosis in ARPE-19 cells based on the Nrf2/HO-1/GPX4 pathway.METHODS: The ARPE-19 cells were cultured and subsequently treated with varying concentrations of trigonelline to ascertain the most effective concentration for modulating the cells. Then the cells were categorized into distinct groups, including normal control(NC)group, high glucose(HG)group, Fer-1 group, TRG group based on the determined concentration. Samples from each group were then gathered to assess relevant indicators. The intracellular levels of glutathione(GSH), malondialdehyde(MDA), and Ferrion were quantified in accordance with the protocols provided by the GSH, MDA, and Ferrion detection kits. Flow cytometry was employed to measure the ROS levels within each group. Additionally, Western blot analysis was conducted to examine the expression of nuclear factor erythroid 2-related factor 2(Nrf2), heme oxygenase-1(HO-1), glutathione peroxidase(GPX4), and acyl-CoA synthetase long-chain family member 4(ACSL4)across the different groups.RESULTS: The preconditioning intervention with 40 μg/mL TRG effectively mitigated the decline in cell activity induced by high glucose levels. The levels of reactive oxygen species(ROS)and MDA in the HG group were markedly elevated compared to the NC group; and the TRG group exhibited significantly reduced levels of ROS and MDA compared to those of the HG group, with the antioxidant stress index GSH showing opposite trends to those of ROS and MDA across all the groups. Whereas the Fer-1 and TRG groups showed decreased expression levels of ACSL4 protein and iron ions, and the expression levels of Nrf2, HO-1 and GPX4 in the Fer-1 and TRG groups were increased.CONCLUSION: TRG protects ARPE-19 cells from the detrimental effects of high glucose by targeting the Nrf2/HO-1/GPX4 signaling pathway to counter ferroptosis.

AIM: To investigate the effects of insulin-like growth factor 1(IGF-1)on the secretion of transforming growth factor β2(TGF-β2), matrix metalloproteinase 2(MMP-2)and hypoxia-inducible factor 1α(HIF-1α)in human scleral fibroblasts(HSF)and their mechanism.METHODS: The cells were cultured with IGF-1 and PI3K/AKT pathway inhibitor LY294002, respectively. CCK-8 method was used to detect cell viability and determine the optimal concentration and time of drug action. Cell migration activity was observed by cell scratch method. To determine the effects of IGF-1 on HSF cells and the regulatory role of PI3K/AKT pathway, HSF cells were divided into control group(without drugs), IGF-1(80 μg/L)group, IGF-1+LY294002(80 μg/L+5 mmol/L)group, and LY294002(5 mmol/L)group, and were cultured for 24 h; the protein expression levels of TGF-β2, MMP-2, HIF-1α, PI3K and AKT were detected by Western blot; the fluorescence expression of TGF-β2, MMP-2 and HIF-1α was detected by cellular immunofluorescence.RESULTS: The results of CCK-8 showed that the cell viability of the 80 μg/L IGF-1 group cultured with different concentrations of IGF-1 was the highest(all P<0.05), and the cell viability of the 80 μg/L IGF-1 group at 24 h was the highest under different culture times. Therefore, the concentration of IGF-1 was selected as 80 μg/L for 24 h. The viability of cells cultured with different concentrations of LY294002 gradually decreased from 6 h(all P<0.05). According to the IC50 value, therefore, the concentration of LY294002 was selected as 5 mmol/L for 24 h. The cell scratch results showed that compared with the control group, the cell mobility of 40 μg/L and 80 μg/L IGF-1 groups was increased(all P<0.05). Compared with the control group, cell mobility in the 2.5 and 5 mmol/L LY294002 groups was decreased(all P<0.05). Western blot results showed that compared with the control group, the protein expressions of TGF-β2, MMP-2, HIF-1α, PI3K and AKT in the IGF-1 group were increased, while those in the LY294002 group were decreased(all P<0.05). Compared with the IGF-1 group, the expression levels of TGF-β2, MMP-2, HIF-1α, PI3K and AKT in the IGF-1+LY294002 group were decreased(all P<0.05). The results of cell immunofluorescence showed that compared with the control group, the fluorescence expressions of TGF-β2, MMP-2 and HIF-1α in the IGF-1 group were increased, while those in the LY294002 group were decreased(all P<0.05). Compared with the IGF-1 group, the fluorescence expressions of TGF-β2, MMP-2 and HIF-1α in the IGF-1+LY294002 group were significantly decreased(all P<0.05).CONCLUSION: IGF-1 promoted the proliferation and migration of human HSF. IGF-1 may up-regulate the expression of TGF-β2, MMP-2 and HIF-1α in HSF through the PI3K/AKT signaling pathway, and participate in the occurrence and development of myopia.

AIM: To assess the stability of the tear film and the characteristics of corneal nerves in patients with Parkinson's disease(PD).METHODS: This cross-sectional observational study included 72 PD patients and 50 healthy controls. Disease severity was determined using the Hoehn-Yahr(H-Y)scale, dividing patients into mild and moderate PD groups. Dry eye symptoms were evaluated via the ocular surface disease index(OSDI)questionnaire, while tear secretion was quantified using the Schirmer I test. Ocular surface damage was assessed through staining scores, and comprehensive ocular examinations were performed utilizing the LipiView ocular surface interferometer and an ocular surface analyzer. Corneal nerve parameters were examined using corneal confocal microscopy in conjunction with automated analysis software ACCMetrics, with correlations drawn between these parameters, PD course, and severity.RESULTS: PD patients exhibited significantly elevated OSDI scores, indicative of more pronounced dry eye symptoms compared to the control group(F=70.290, P<0.01). Tear film stability was markedly compromised, with significantly shorter tear film breakup time and increased corneal fluorescein staining, both showing statistically significant differences relative to controls(all P<0.01). Tear secretion indices, including Schirmer I test results and tear meniscus height, were significantly reduced in PD patients(all P<0.01), whereas lipid secretion indices, such as lipid layer thickness and meibomian gland dropout score, did not show significant variation. Corneal nerve analysis revealed significant reductions in corneal nerve fiber density, nerve branch density, fiber length, and total branch density in PD patients compared to controls(all P<0.01). Furthermore, blink frequency was markedly prolonged(F=62.353, P<0.01). Correlation analysis demonstrated a significant relationship between alterations in tear film stability and both disease duration and H-Y scores.CONCLUSION: PD patients have obvious dry eye manifestations in the early stage of the disease, including the reduction of tear film stability and corneal nerve fiber density, and gradually aggravate with the progress of the disease. Neurodegenerative disease-related dry eye needs to be diagnosed early and actively treated.

AIM: To investigate the alterations in corneal aberration and relative refractive power following the reduction of back optic zone diameters(BOZD)of orthokeratology lenses.METHODS: Myopic children aged 8-12 years, deemed suitable and willing to wear orthokeratology lenses, were randomly allocated to wear lenses with a 6.0 mm BOZD or a 5.0 mm BOZD. Data collection included changes in higher-order aberrations, relative refractive power and the treatment zone diameter of the two groups after wearing lenses for 1 d, 1 wk, 1, and 3 mo. The correlation of increase in corneal higher-order aberrations with refractive power was analyzed.RESULTS: The increases in total higher-order aberrations, spherical aberrations and coma aberrations varied over time following lens wear(all P<0.001), and there were no statistically significant differences in the changes of total higher-order aberrations and coma aberrations between the two groups of patients(all P>0.05). A significant difference was observed in the increment of spherical aberrations in the 5 mm range between the two groups of patients, which varied over time(Ftime=40.179, Ptime<0.001; Fgroup=11.948, Pgroup=0.001; Finteraction=3.262, Pinteraction=0.03). A significant difference was observed in the increment of spherical aberrations in the 4 mm range between the two patient groups(Ftime=34.462, Ptime<0.001; Fgroup=13.094, Pgroup<0.001; Finteraction=1.372, Pinteraction=0.25). There was no statistically significant distinction in relative refractive power between the two groups(Fgroup=0.048, Pgroup=0.83; Finteraction=1.208, Pinteraction=0.31); however, relative refractive power changed over time(Ftime=40.030, Ptime<0.001). The difference in treatment zone diameter between the two groups was statistically significant, with changes over time(Ftime=11.212, Ptime<0.001; Fgroup=74.073, Pgroup<0.001; Finteraction=0.312, Pinteraction=0.82). The total higher-order aberrations, spherical aberrations, and coma aberrations in 4, 5 and 6 mm range showed a positive correlation with relative refractive power values(all P<0.001). Statistically significant difference was observed in the axial length between the two groups after wearing lenses for 3, 6 and 12 mo(Ftime=185.398, Ptime<0.001; Fgroup=5.618, Pgroup=0.02; Finteraction=2.315, Pinteraction=0.11).CONCLUSION: Orthokeratology lenses leaded to elevated higher-order aberrations. Orthokeratology lenses with smaller BOZD produced significantly greater spherical aberrations at 4 and 5 mm range and smaller treatment zone diameters. The corneal total higher-order aberration was positively correlated with relative refractive power. Wearing orthokeratology lenses with a smaller BOZD can cause slower axial growth and better myopia control.

Müller cells(MCs)are the most common glial cells in the human retina. They provide homeostatic, metabolic, and functional support to neurons. MCs play a critical role in regulating extracellular space volume, ion and water homeostasis, and maintaining the blood-retinal barrier. They release gliotransmitters and other neuroactive molecules, influencing synaptic activity through neurotransmitter recycling. All these functions directly or indirectly alter neuronal activity. MCs support the survival of photoreceptors and neurons, are responsible for the structural stability of the retina, and act as regulators of immune and inflammatory responses. They are activated in response to almost all pathogenic stimuli. Reactive MCs have neuroprotective effects, but excessive activation of MCs under pathological conditions can withdraw neuronal protection and lead to neuronal degeneration. Thus, MCs may play a double-edged sword role in the pathogenesis of macular edema due to retinal vein occlusion(RVO-ME). Understanding the response of MCs to pathological stimuli and their protective and damaging effects on the retina and macula is crucial for studying the pathogenesis and guiding the treatment of RVO-ME. This article reviews the role of MCs in RVO-ME, aiming to provide new strategies for the treatment of RVO-ME.

The sirtuin 1(SIRT1)is an important NAD+-dependent deacetylase that has attracted much attention in ophthalmic research in recent years. This is because the expression of SIRT1 in ocular tissues and its function are inextricably linked to the pathogenesis and progression of many ocular diseases, including dry eye, glaucoma, cataract and diabetic retinopathy. Through in-depth investigations, we have found that SIRT1, as a key regulatory protein, has a profound impact on the pathophysiological processes of ocular diseases through a variety of mechanisms, such as regulating apoptotic programs, modulating oxidative stress, mediating inflammatory responses and maintaining normal mitochondrial function. These findings indicate that SIRT1 plays an important protective role in ocular diseases. The aim of this article is to comprehensively review the latest research findings on SIRT1 in ophthalmic diseases in recent years, and hopes to provide new ideas and methods for the prevention and treatment of ophthalmic diseases by thoroughly analyzing the mechanism of action of SIRT1.

Fungal keratitis represents a significant cause of blindness, with current therapeutic approaches yielding limited success. The disease's onset and progression are primarily driven by fungal virulence factors and the host's immune response. The innate immune system is the first to respond, with neutrophils playing a pivotal role in the antifungal defense. Although neutrophils are critical for pathogen clearance, their excessive or abnormal activation can lead to tissue damage, exacerbating the disease. Thus, elucidating the mechanisms underlying neutrophil activity in fungal keratitis is crucial for refining treatment strategies. This article aims to systematically review the principal antimicrobial mechanisms employed by neutrophils, including phagocytosis, degranulation, and the formation of neutrophil extracellular traps(NETs). Furthermore, it explores the crosstalk between neutrophils and macrophages, alongside their collective impact and underlying mechanisms in the context of fungal keratitis. Exploration of the mechanisms of fungal keratitis facilitates precise intervention and enhances the efficacy of treatment.

Exosomes are ubiquitous in all types of body fluids, exhibiting a high degree of abundance and diversity. Given their distinctive structure and function, exosomes are involved in a range of life activities, including intercellular communication, material transport, and immune regulation. An increasing number of studies have identified exosomes as a source of diagnostic markers for diabetic retinopathy. Furthermore, exosomes represent a novel avenue for therapeutic intervention, with promising clinical applications. This paper examines the diagnostic and therapeutic mechanisms of exosomes in diabetic retinopathy, reviews the advancements in exosomes-based diagnostics and therapeutics for diabetic retinopathy, and aims to enhance the precision and efficiency of clinical diagnosis and treatment of diabetic retinopathy.