Evaluating the global impact of low physical activity on type 2 diabetes: Insights from the global burden of disease 2019 study.

AIM: We aimed to assess the global implications of low physical activity (LPA) on type 2 diabetes mellitus (T2DM) by utilizing data from the Global Burden of Disease (GBD) 2019. METHODS: The analysis was conducted by examining the age-standardized disability-adjusted life years (DALYs) rates over a 30-year period. To assess the trends, we utilized estimated annual percentage changes (EAPCs). RESULTS: The study revealed a notable increase in the burden of DALYs attributable to T2DM resulting from LPA, with an EAPC of 0.84 (95% confidence interval 0.78-0.89). Among the regions examined, Oceania showed the highest burden, whereas Eastern Europe exhibited the lowest burden. Specifically, within the Central Asia region, a considerable increase in T2DM-LPA DALYs was observed, with an EAPC of 3.18 (95% confidence interval 3.01-3.36). The burden associated with T2DM-LPA DALYs was found to be similar between genders and increased across all age groups, peaking in the 80-84 years. Furthermore, there was a clear association between the socio-demographic index (SDI) and the age-standardized DALYs rate. Regions categorized as low-middle and middle SDI experienced a substantial rise in burden. CONCLUSION: This study highlights a substantial increase in the T2DM-LPA DALYs in low-middle and middle SDI regions, as well as among individuals aged 80-84 years. These findings emphasize the importance of implementing comprehensive global health interventions that promote physical activity, particularly targeting high-risk populations and regions.

Inhibition of acetylcholinesterase attenuated retinal inflammation via suppressing NF-κB activation.

Elevated inflammatory cytokines contribute to the pathogenesis of various retinal diseases such as diabetic retinopathy, retinal vasculitis and retinitis. However, the underlying mechanism of retinal inflammation remains largely unknown. Recent studies demonstrated that acetylcholinesterase (ACHE) is an inflammatory indicator in central neural system. This study was aimed to dissect the role of ACHE in retinal inflammation, and its mechanism of action. Retinal inflammation was induced by intravitreal injection of tumor necrosis factor-α (TNF-α) in heterozygous ACHE knockdown mice (ACHE+/-) and wild type mice (ACHE+/+). Donepezil, a well-known ACHE inhibitor, was administrated by daily gavage. Expression of ACHE and intercellular adherent molecule-1 (ICAM-1), infiltration of CD11b+ inflammatory cells, retinal leukostasis and vascular leakage was determined in both ACHE+/- and ACHE+/+ mice. ARPE-19 cells, a human retinal pigment epithelial cell line, were cultured for in vitro assay. Knockdown of ACHE was achieved by lipofectamine-mediated siRNA transfection and pharmaceutical suppression of ACHE was manipulated by donepezil. Cellular expression and distribution of ACHE, ICAM-1, and phosphorylation of NF-κB, IκB and IKKα/ß were detected by western-blot analysis or immunocytochemistry. Retinal expression of ACHE was dramatically upregulated, in parallel with increased ICAM-1 expression, enhanced leukostasis and augmented CD11b+ inflammatory cell infiltration as well as vascular hyperpermeability in ACHE+/+ mice injected with TNF-α. However, TNF-α-injected ACHE+/- mice showed lower level of ICAM-1, less leukostasis and fewer infiltrated CD11b+ cells. Moreover, TNF-α-induced retinal vascular leakage was significantly reduced in ACHE+/- mice. Similarly, TNF-α-induced retinal inflammatory response were also attenuated by donepezil intervention. In addition, TNF-α treatment resulted in significant induction of ACHE, upregulation of ICAM-1 and nuclear translocation of NF-κB, phosphorylation of IκB and IKKα/ß in ARPE-19 cells. However, inhibition of ACHE reduced TNF-α-induced phosphorylation of NF-κB, IκB and IKKα/ß in ARPE-19 cells. The present study reveals a pivotal role of ACHE in retinal inflammation. Inhibition of ACHE attenuates retinal inflammation and retinal leakage likely through suppressing NF-κB signaling activation.

Salutary effect of fenofibrate on type 1 diabetic retinopathy via inhibiting oxidative stress-mediated Wnt/ß-catenin pathway activation.

Fenofibrate has been shown to have therapeutic effects on diabetic retinopathy (DR). Our previous studies demonstrated that the oxidative stress-activated Wnt/ß-catenin pathway plays a pathogenic role in diabetic complications. In the present study, we evaluate the effect and mechanism of fenofibrate on regulating the oxidative stress-activated Wnt/ß-catenin pathway by using the genetic type 1 diabetes model of C57BL/6J-Ins2Akita mice and high glucose (HG)-treated ARPE-19. Our results demonstrated that retinal phosphorylation of LRP6 and nuclear ß-catenin were increased in C57BL/6J-Ins2Akita mice suggesting activation of Wnt/ß-catenin signaling. Meanwhile, C57BL/6J-Ins2Akita showed upregulation of oxidant enzyme Nox4 and Nox2 and downregulation of antioxidant enzyme SOD1 and SOD2. All these alterations were reversed in C57BL/6J-Ins2Akita mice with fenofibrate treatment. Moreover, fenofibrate significantly ameliorated diabetes-induced retinal vascular leakage in C57BL/6J-Ins2Akita mice. In cultured ARPE-19, fenofibrate decreased HG-induced Nox2 and Nox4 upregulation, attenuated SOD1 and SOD2 downregulation and inhibited LRP6 phosphorylation. Moreover, activation of Wnt/ß-catenin by Wnt3a conditional medium (WCM) reduced SOD1 and SOD2 and did not affect Nox2 and Nox4. Fenofibrate suppressed WCM-induced LRP6 phosphorylation and reversed SOD downregulation. Importantly, Nox4 overexpression directly phosphorylated LPR6 in ARPE19; conversely, Nox4 knockdown suppressed HG-induced LPR6 phosphorylation. Taken together, Nox-mediated oxidative stress contributes to Wnt/ß-catenin activation in DR. Fenofibrate ameliorated DR through coordinate attenuation of oxidative stress and blockade of Wnt/ß-catenin signaling.

The role of Cdk5-mediated Drp1 phosphorylation in Aß1-42 induced mitochondrial fission and neuronal apoptosis.

Alzheimer's disease, one of the most common neurodegenerative diseases, is pathologically characterized by Amyloid beta containing plaques and neurofibrillary tangles. Amyloid beta (Aß) induces neuronal apoptosis through the intracellular Ca2+ increase, subsequent hyperactivation of cyclin-dependent kinase 5 (Cdk5) and mitochondrial abnormality. Recently, Cdk5 was identified as an upstream regulator of mitochondrial fission during neuronal apoptosis, but the underlying mechanism remains unclear. Here, in vitro phosphorylation assays showed that Cdk5 could phosphorylate the recombinant Drp1 at Serine 579. Aß1-42 stimulation increased the phosphorylation level of Drp1 at Serine 579 in mouse cortical neurons. Cdk5 inhibitor roscovitine and knockdown of Cdk5 by a lentiviral vector expressing shRNA targeting Cdk5 (Lenti-Cdk5-shRNA) efficiently prevented Aß1-42 induced Drp1 phosphorylation in neurons. In addition, Aß1-42 stimulation induced markedly mitochondrial fission in neurons. Roscovitine, Lenti-Cdk5-shRNA and expression of phospho-defect mutatant GFP-Drp1-S579A in neurons attenuated Aß1-42 induced mitochondrial fission, whereas expression of phospho-mimetic mutant GFP-Drp1-S579D alone resulted in mitochondiral fission similar to Aß1-42 stimulation. Moreover, Roscovitine and Lenti-Cdk5-shRNA suppressed the cleavage of caspase-3 and protected neurons against Aß1-42 induced neuronal apoptosis.Thus, our data indicate that Drp1 is a direct target of Cdk5, and Cdk5-mediated phosphorylation of Drp1 at Serine 579 regulates Aß1-42 induced mitochondrial fission and neuronal toxicity.

Fenofibrate ameliorates diabetic retinopathy by modulating Nrf2 signaling and NLRP3 inflammasome activation.

Oxidative stress and neuroinflammation contribute significantly to the development and progression of diabetic retinopathy. Fenofibrate has received great attention as it benefits diabetic patients by reducing retinal laser requirement. Nuclear factor erythroid-2-related factor 2 (Nrf2) is a master regulator of anti-oxidative defense. Activation of nucleotide binding domain, leucine-rich repeat-containing receptor (NLR), pyrin domain-containing 3 (NLRP3) inflammasome plays a pivotal role in neuroinflammation. The purpose of this study is to determine whether fenofibrate protects retinas from oxidative damage and neuroinflammation via modulating the Nrf2 pathway and blocking NLRP3 inflammasome activation during diabetes. Diabetes is induced by intraperitoneal injection of streptozotocin in mice. Fenofibrate was given to mice in rodent chow. Upregulation of Nrf2 and NLRP3 inflammasome, enhanced ROS formation, and increased leukostasis and vascular leakage were observed in diabetic mouse retinas. Notably, Nrf2 and Caspase-1 were mainly colocalized with glutamine synthetase, one of the Mȕller cell markers. Fenofibrate further increased the expression of Nrf2 and its target gene NQO-1 and HO-1 and reduced ROS formation in diabetic retinas. In addition, retinal expression of NLRP3, Caspase-1 p20, IL-1ß p17, and ICAM-1 were dramatically increased in vehicle-treated diabetic mice, which were abolished by fenofibrate intervention. Moreover, fenofibrate treatment also attenuated diabetes-induced retinal leukostasis and vascular leakage in mice. Taken together, fenofibrate attenuates oxidative stress and neuroinflammation in diabetic retinas, which is at least partially through modulating Nrf2 expression and NLRP3 inflammasome activation.

Ocular amphotericin B delivery by chitosan-modified nanostructured lipid carriers for fungal keratitis-targeted therapy.

CONTEXT: Fungal keratitis, a corneal fungal infection of the eye caused mainly by Candida species, has become the leading cause of blindness resulting from corneal disease in China. Present limitations in the management of ophthalmic fungal infections include the inability to provide long-term extraocular drug delivery without compromising intraocular structures and/or systemic drug exposure. OBJECTIVE: The aim of this study was to construct amphotericin B (AmB) loaded, chitosan-modified, nanostructured lipid carriers (AmB-CH-NLC) for prolonged ocular application and for the improvement of the targeted delivery of AmB to the ocular mucosa. MATERIALS AND METHODS: The AmB-CH-NLC was produced by the method of emulsion evaporation-solidification at low temperature. The particle size, zeta potential, and encapsulation efficiency, drug-release behavior, and corneal penetration ability were performed in vitro and in vivo. RESULTS AND DISCUSSION: The prepared AmB-CH-NLC nanoparticles exhibited a measured size of 185.4 nm, a zeta potential of 27.1 mV, and an entrapment efficiency of 90.9%. Sustained drug release behavior was observed in vitro. The in vivo ocular pharmacokinetic study indicated improved bioavailability of AmB-CH-NLC. The corneal penetration study showed that the AmB-CH-NLC could successfully penetrate into the cornea with no obvious irritation to the rabbits' eyes. CONCLUSION: The results support that this novel nanomedicine could be a promising system for effective ocular delivery of amphotericin B for fungal keratitis-targeted therapy.

The viral restriction factor tetherin prevents leucine-rich pentatricopeptide repeat-containing protein (LRPPRC) from association with beclin 1 and B-cell CLL/lymphoma 2 (Bcl-2) and enhances autophagy and mitophagy.

Tetherin has been characterized as a key factor that restricts viral particles such as HIV and hepatitis C virus on plasma membranes, acts as a ligand of the immunoglobulin-like transcript 7 (ILT7) receptor in tumor cells, and suppresses antiviral innate immune responses mediated by human plasmacytoid dendritic cells. However, the normal cellular function of Tetherin without viral infection is unknown. Here we show that Tetherin not only serves as a substrate of autophagy but itself regulates the initiation of autophagy. Tetherin interacts with the autophagy/mitophagy suppressor LRPPRC and prevents LRPPRC from forming a ternary complex with Beclin 1 and Bcl-2 so that Beclin 1 is released to bind with PI3KCIII (class III PI3K) to activate the initiation of autophagy. Suppression of Tetherin leads to impairment of autophagy, whereas overexpression of Tetherin causes activation of autophagy. Under mitophagic stress, Tetherin is concentrated on mitochondria engulfed in autophagosomes. Tetherin plays a general role in the degradation of autophagosomes containing not only the symbiotic mitochondria but also, possibly, the infected virus. Therefore, Tetherin may enhance autophagy and mitophagy to suppress tumorigenesis, enhance innate immune responses, or prevent T cell apoptosis or pyroptosis.

Bhlhb5 is required for the subtype development of retinal amacrine and bipolar cells in mice.

BACKGROUND: BHLHB5, an OLIG-related basic helix-loop-helix transcription factor, is required for the development of a subset of gamma-amino butyric acid-releasing (GABAergic) amacrine cells and OFF-cone bipolar (CB) cells in mouse retinas. In order to determine BHLHB5's functional mechanism in retinogenesis, we used the Cre-loxP recombination system to genetically trace the lineage of BHLHB5+ cells in normal and Bhlhb5-null retinas. The Bhlhb5-Cre knock-in allele was used to activate the constitutive expression of a GFP reporter in the Bhlhb5-expressing cells, and the cell fates of Bhlhb5-lineage cells were identified by using specific cell markers and were compared between normal and Bhlhb5-null retinas. RESULTS: In addition to GABAergic amacrine and OFF-CB cells, Bhlhb5 lineage cells give rise to ganglion, glycinergic amacrine, rod bipolar, ON-bipolar, and rod photoreceptor cells during normal retinal development. Targeted deletion of Bhlhb5 resulted in the loss of GABAergic amacrine, glycinergic amacrine, dopaminergic amacrine, and Type 2 OFF-CB cells. Furthermore, in the absence of BHLHB5, a portion of Bhlhb5 lineage cells switch their fate and differentiate into cholinergic amacrine cells. CONCLUSIONS: Our data reveal a broad expression pattern of Bhlhb5 throughout retinogenesis and demonstrate the cell-autonomous as well as non-cell-autonomous role of Bhlhb5 in the specification of amacrine and bipolar subtypes.

Mitochondrion-associated protein LRPPRC suppresses the initiation of basal levels of autophagy via enhancing Bcl-2 stability.

The mitochondrion-associated protein LRPPRC (leucine-rich pentatricopeptide repeat-containing) interacts with one of the microtubule-associated protein family members MAP1S (microtubule-associated protein 1 small form), originally named C19ORF5 (chromosome 19 open reading frame 5), to form a complex. MAP1S interacts with LC3 (light chain 3), the mammalian homologue of yeast autophagy marker ATG8 and one of the most important autophagy markers in mammalian cells, and helps the attachment of autophagosomes with microtubules for trafficking and recruitment of substrate mitochondria into autophagosomes for degradation. MAP1S activates autophagosomal biogenesis and degradation to remove misfolded/aggregated proteins and dysfunctional organelles such as mitochondria and suppress oxidative stress-induced genomic instability and tumorigenesis. Previously, various studies have attributed LRPPRC nucleic acid-associated functions. Instead, in the present study, we show that LRPPRC associates with mitochondria, interacts with Beclin 1 and Bcl-2 and forms a ternary complex to maintain the stability of Bcl-2. Suppression of LRPPRC leads to reduction in mitochondrial potential and reduction in Bcl-2. Lower levels of Bcl-2 lead to release of more Beclin 1 to form the Beclin 1-PI3KCIII (class III phosphoinositide 3-kinase) complex to activate autophagy and accelerate the turnover of dysfunctional mitochondria through the PI3K (phosphoinositide 3-kinase)/Akt/mTOR (mammalian target of rapamycin) pathway. The activation of autophagy induced by LRPPRC suppression occurs upstream of the ATG5-ATG12 conjugate-mediated conversion of LC3-I into LC3-II and has been confirmed in multiple mammalian cell lines with multiple autophagy markers including the size of GFP-LC3 punctate foci, the intensity of LC3-II and p62 protein and the size of the vacuolar structure. The activated autophagy enhances the removal of mitochondria through lysosomes. LRPPRC therefore acts to suppress the initiation of basal levels of autophagy to clean up dysfunctional mitochondria and other cellular debris during the normal cell cycle.

[Effects of basic fibroblast growth factor composite sponge treated collagen on vascularization of orbital implants: a histopathologic analysis].

OBJECTIVE: To evaluate the effect of basic fibroblast growth factor (bFGF) treated collagen composite sponge on vascularization of HA orbital implants. METHODS: New Zealand rabbits received three different orbital implants:naked implants, implants wrapped with collagen composite sponge and implants wrapped with bFGF treated collagen composite sponge.Implants were harvested 2, 4, 6, 8 and 12 weeks after surgery. The vascularization of implants was then assessed by light and electron microscopy. RESULTS: At post-surgery weeks of 2, 4 and 6, bFGF treated collagen composite sponge induced the highest degree of vascularization of orbital implants. Collagen composite sponge alone resulted in higher extent of vascularization than naked implants. Complete vascularization of implants was observed at post-surgery 6 weeks by bFGF treated collagen composite sponge, which was not observed in the other two groups until post-surgery 8 weeks. There were significant differences in the average length of fibrovasculature and in the degree of vascularization among each group at post-surgery 2, 4 and 6 weeks (P<0.05), while no statistical difference was observed at post-surgery 8 and 12 weeks (P>0.05). CONCLUSIONS: bFGF treated collagen composite sponge facilitates fibrovascularization of orbital implants, and shortens the time required for complete vascularization. Collagen composite sponge alone promotes early-stage fibrovascularization, but fails to facilitate complete vascularization of orbital implants.

[Distal axonopathy in glaucomatous optic neuropathy].

Glaucoma is a complex class of degenerative optic neuropathy. Multiple mechanisms were involved in glaucomatous optic nerve damage. In recent years, research progression has been made in the relationship between axonal degeneration and glaucoma with more attention and effort dedicated to explicate the pathogenesis of progressive optic nerve injury. Series of studies indicate that the interplay between distal axonal degeneration and axon neuron damage may play an important role in the progression of the disease. Distal axonal lesions may contribute to glaucoma, the pathological basis may be the retrograde degeneration of the optic nerve in visual pathways. In this article, we review the latest findings in the distal axonal degeneration and glaucomatous optic neuropathy.

Efficacy and Safety of Biosimilar QL1207 vs. the Reference Aflibercept for Patients with Neovascular Age-Related Macular Degeneration: A Randomized Phase 3 Trial.

INTRODUCTION: This trial aimed to compare the efficacy and safety between biosimilar QL1207 and the reference aflibercept for the treatment of neovascular age-related macular degeneration (nAMD). METHODS: This randomized, double-blind, phase 3 trial was conducted at 35 centers in China. Patients aged ≥ 50 years old with untreated subfoveal choroidal neovascularization secondary to nAMD and best-corrected visual acuity (BCVA) letter score of 73-34 were eligible. Patients were randomly assigned to receive intravitreous injections of QL1207 or aflibercept 2 mg (0.05 ml) in the study eye every 4 weeks for the first 3 months, followed by 2 mg every 8 weeks until week 48, stratified by baseline BCVA ≥ or < 45 letters. The primary endpoint was BCVA change from baseline at week 12. The equivalence margin was ± 5 letters. The safety, immunogenicity, pharmacokinetics (PK), and plasma vascular endothelial growth factor (VEGF) concentration were also evaluated. RESULTS: A total of 366 patients were enrolled (QL1207 group, n = 185; aflibercept group, n = 181) from Aug 2019 to Jan 2022 with comparable baseline characteristics. The least-squares mean difference in BCVA changes was - 1.1 letters (95% confidence interval - 3.0 to 0.7; P = 0.2275) between the two groups, within the equivalence margin. The incidences of treatment-emergent adverse events (TEAE; QL1207: 71.4% [132/185] vs. aflibercept: 71.8% [130/181]) and serious TEAE (QL1207: 14.1% [26] vs. aflibercept: 12.7% [23]) appeared comparable between treatment groups, and no new safety signal was found. Anti-drug antibody, PK profiles, and VEGF concentration were similar between the two groups. CONCLUSIONS: QL1207 has equivalent efficacy to aflibercept for nAMD with similar safety profiles. It could be used as an alternative anti-VEGF agent for clinical practice. TRIAL REGISTRATION: ClinicalTrials.gov: NCT05345236 (retrospectively registered on April 25, 2022); National Medical Products Administration of China: CTR20190937 (May 20, 2019).

[Prevalence of blindness and moderate and severe visual impairment among adults aged 50 years or above in Ji'an county of Jiangxi province:the China Nine-Province Survey].

OBJECTIVE: To investigate the prevalence of blindness and moderate and severe visual impairment among adults aged 50 years or above in Ji'an county of Jiangxi province, China. METHODS: It was a population-based cross-section study. Geographically defined cluster sampling was used in 5402 randomly selected individuals aged ≥ 50 years in 28 clusters in Ji'an from September to November 2006. The survey was preceded by a pilot study where operational methods were refined and quality assurance evaluation was carried out. All participants were enumerated through village registers followed door-to-door visits. Eligible individuals were invited to receive visual acuity measurement and eye examination. Statistical analyses were performed using Stata/SE Statistical Software, release 9.0. Chi-square test was used to investigate the association of age, gender and education with presenting and best corrected visual acuity. RESULTS: Five thousands four hundreds and two individuals were enumerated and 5010 persons were examined, the response rate was 92.74%. Based on the criteria of World Health Organization visual impairment classification in 1973, 78 persons were diagnosed as blindness, 265 persons were diagnosed as moderate and severe visual impairment defined as best corrected visual acuity, the prevalence of blindness and moderate and severe visual impairment were 1.56% and 5.29% respectively. Ninety-four persons were diagnosed as blindness, 726 persons were diagnosed as moderate and severe visual impairment defined as presenting visual acuity, the prevalence of blindness and moderate and severe visual impairment defined as presenting visual acuity was 1.88% and 14.50% respectively. The prevalence of blindness and moderate and severe visual impairment was higher in aged (trend χ(2) = 970.15, P = 0.000), female (χ(2) = 89.81, P = 0.000), and illiterate persons (trend χ(2) = 241.85, P = 0.000). Cataract was still the first leading cause of blindness and visual impairment, the retinal diseases was the second. Un-corrected refractive error also was the main cause of visual impairment. CONCLUSIONS: The prevalence of blindness and moderate and severe visual impairment was higher than other district in China. The first leading cause of blindness and visual impairment is still cataract.

[Prevalence of blindness and low vision among adults aged 50 years or above in Ji'an county of Jiangxi province: the China nine-province survey].

OBJECTIVE: To estimate the prevalence of cataract, the outcomes of cataract surgery, cataract surgical coverage rate, cataract blindness social burden rate in Ji'an county of Jiangxi province, China. METHODS: Cluster sampling was used in randomly selected 5010 individuals aged ≥ 50 years in Ji'an county of Jiangxi province. All individuals were received visual acuity and eye examination, including the evaluation of lens status and cataract surgical status by slit lamp biomicroscopy. Data bank was established by Epi-info Software. Statistical analyses were performed using Stata/SE Statistical Software, release 9.0 (Stata Corp, College Station, TX). Confidence intervals and P values (considered significance at the P < 0.05 level) for prevalence of cataract, cataract surgical coverage rate, cataract blindness social burden rate and outcomes of surgery were calculated with adjustment for clustering effects and stratification associated with the sampling design. RESULTS: In 5010 individuals, 1158 cases of cataract were found, the prevalence of cataract was 23.11% among adults aged 50 or above. The prevalence of cataract was higher in the aged, female (P < 0.01). In 99 eyes with cataract surgery, 50.51% and 5.05% of eyes were performed by the modern extra-capsular surgery and phacoemulsification respectively. The rate of intraocular lens implantation was 55.56%. Post-operative presenting and best corrected visual acuity equal to or more than 0.7 was 10.1% and 45.5% of operated eyes respectively. The main causes of the post-operated eyes with worse visual acuity were post-capsular opacity and refractive error. The cataract surgical coverage rate was 32.29%, and the cataract blindness social burden rate was 3.83%. The cataract surgical rate was lower and cataract blindness social burden rate was higher in the aged persons (P < 0.01). CONCLUSIONS: Cataract is the most common eye disease that may lead into blindness and severe visual impairment among older adults aged equal or more than 50 years. The cataract surgical coverage rate is not high but the cataract blindness social burden rate is heavy in Ji'an county. The rate of intraocular lens implantation need increase and the visual outcomes of the surgery should be further improved in the future.

Superficial Retinal Vessel Density and Foveal Avascular Zone in Myopic Anisometropia: An OCTA-Based Study in Young Chinese Children.

This retrospective study investigated superficial retinal vessel density (SRVLD) and foveal avascular zone (FAZ) area using optical coherence tomography angiography (OCTA) in children with myopic anisometropia. We included 84 eyes of 42 individuals with myopic anisometropia and no posterior segment abnormalities. All eyes underwent OCTA. Individual SRVLD and FAZ area were measured on OCTA. Using a paired t-test, we compared the interocular difference between the fellow eyes for all the measurements. SRVLD was significantly higher in the relatively more myopic eyes than in the fellow eyes in the whole population and in patients with an interocular difference of >1.5 D (p = 003 and 0.01, respectively). In patients with an interocular difference of ≤1.5 D in spherical equivalent refraction, only the nasal sector showed higher SRVLD in the less myopic eyes. SRVLD in the whole image and parafoveal sector was significantly lower in the dominant eye (paired t-test, p = 003 and 0.03, respectively), while other locations showed no difference. The area, perimeter, and circularity index in FAZ parameters showed no difference. SRVLD showed no significant differences between the two types of eyes, with an interocular difference of ≤1.5 D but increased in the relatively more myopic eyes than in the fellow eyes in children with myopic anisometropia, with an interocular difference of >1.5 D. Increasing SRVLD may show a compensatory increase to maintain retinal function and thus maintain normal visual function in the relatively more myopic fellow eyes. As the study to use patients as self-control with OCTA analysis in both eyes, this study provides some reference value for further interpretation of the pathogenesis of anisometropia.

[The morphology and thickness of cornea in patients with Marfan syndrome].

OBJECTIVE: To search for the characteristics of MFS in corneal morphology and thickness. METHODS: Twenty-four patients (48 eyes) with MFS and 24 healthy age- and gender-matched volunteers (48 eyes) were recruited in this clinical prospective, and comparative series study. Firstly, biomicroscopic examination and Type-A ultrasonometry was conducted to search for ectopia lentis and axis length. Secondly, the corneal morphologic parameter [including the height of anterior and posterior surface, the centre corneal curvature, the mean astigmatism in the 3.0-mm central zone (Mean A), the mean simulated astigmatism (Sim A), the mean keratometry in the 3.0-mm central zone (Mean K), the mean simulated keratometry (Sim K), the 3.0-mm zone irregularity (3.0ZI), the 5.0-mm zone irregularity (5.0ZI), corneal thickness index (CTI)] and thickness (at the central location and at eight midperipheral locations) were obtained by the the autorefractometer and the Orbscan II Z corneal topography. Last, the statistics method including Crosstabs, One-way ANOVA, student-t test and discriminant analysis were applied and the correlations were established. RESULTS: There is no statistically significance between MFS group and control group in ages (38 ± 7) and (37 ± 8) years, gender (8/16) and (9/15), and axis length (23.12 ± 1.06) mm and (24.26 ± 2.96) mm (age χ(2) = 0.091, P = 0.763;gender t = 0.324, axis length t = 1.976, P > 0.05). Flat cornea ratio (66.7% and 12.5%) and topography of the oval (25.0% and 16.7%), irregular bow-shaped (41.7% and 37.5%) and irregular-shaped (12.5% and 8.3%) were increased significantly in patients with MFS. The corneal topography (MFS/control) showed that there are statistically significance in the thinnest thickness of cornea (489.8 ± 42.9)µm and (544.8 ± 25.7)µm, Mean K (40.60 ± 1.30) D and (42.80 ± 1.40) D, Sim K (40.50 ± 1.30) D and (42.80 ± 1.20) D, Sim A (1.08 ± 0.86)D and (0.91 ± 0.46) D, CTI 1.57 ± 0.24 and 1.21 ± 0.14, 3.0ZI (1.76 ± 0.96) D and (1.54 ± 0.82) D, and 5.0ZI (1.91 ± 1.26) D and (0.92 ± 0.68) D (thinnest thickness t = 6.996, Mean K t = 2.554, Sim K t = 3.326, Sim A t = 2.324, CTI t = 3.116, 3.0ZI t = 2.686, 5.0ZI t = 3.768, P < 0.05), while no statistically significance in the Mean A between the MFS (1.11 ± 0.89) D and control group (0.99 ± 0.49) D (Mean A t = 1.898, P = 0.08); except for temple inferior, the significant decrease of pachymetry (including the center and the seven midperipheral locations) appeared in the MFS group compared with the control group. CONCLUSION: The characteristic of MFS in corneal topography is that corneal axial refractive power descends and corneal thickness decreases.

[A study on visual development among preschool children].

OBJECTIVE: To evaluate the visual development and prevalence of amblyopia, strabismus among preschool children. METHODS: A random sample survey was performed in 4 610 preschool children from both urban and rural, aged 3 to 6 years. Participants underwent eye examination including visual acuity, refractive status, eye position, strabismus and amblyopia. RESULTS: Percentage of visual acuity above 1.0 was 28.4%, 39.3%, 46.2% and 76.5% in children of 3, 4, 5 and 6-year-old group, respectively. The mean visual acuity of each group was 0.63 ± 0.19 in 3-years old, 0.69 ± 0.16 in 4-year-old, 0.71 ± 0.22 in 5-year-old, 0.79 ± 0.29 in 6-year-old. Rural children have better vision acuity compared with those from urban. Hypermetropic was frequent refractive errors. Manifeststrabismus was found in 2.21%, with exotropia being more prevalence than esotropia; detection rate of recessive strabismus was 33.52%, mainly being exophoria; Based on current diagnostic criteria, the prevalence of amblyopia were 2.93% in 6 year-old group, 4.81% in 5-year-old group, 16.21% in 4-year-old group, 33.33% in 3-year-old group. CONCLUSION: Vision acuity is increasing with age in preschool population. A diagnosis standard of amblyopia suitable for each age group should be established to substitute the current one which has a high visual standard for amblyopia. Refractive error, strabismus and amblyopia are the leading causes of visual impairment among preschool-aged children, which represent the focus of prevention of blindness in preschool children.

A comparison of visual acuity measured by ETDRS chart and Standard Logarithmic Visual Acuity chart among outpatients.

AIM: To compare the results of visual acuity (VA) measured by Early Treatment Diabetic Retinopathy Study (ETDRS) chart, 5 m Standard Logarithm Visual Acuity (5SL) chart, and 2.5 m Standard Logarithm Visual Acuity (2.5SL) chart in outpatients of age 12-80y. METHODS: Each patient (totally 2000 outpatients) had both eyes tested with ETDRS chart at 4 m, 5SL chart at 5 m, and 2.5SL chart at 2.5 m in random order. The VA values of outpatients were categorized by ages. VA values were expressed by logMAR recording method. RESULTS: The mean VA results of ETDRS charts, 5SL, and 2.5SL chart were 0.52±0.28, 0.50±0.30, and 0.46±0.28 logMAR, respectively. There was a statistically significant difference in the three eye charts in the whole group (P<0.001). For all subjects, the correlation of VA tested with three charts was statistically significant (Spearman correlation coefficient=0.944, 0.937, 0.946, all P<0.001). Bland-Altman analysis shows the 95% limits of agreement between the 5SL and 2.5SL chart were -0.182 to 0.210, -0.139 to 0.251, and -0.151 to 0.235 logMAR, respectively). CONCLUSION: The agreement between the three eye charts is not high. The VA measured by 5SL chart is slightly better than that by ETDRS chart and 5SL chart would be a suitable alternative when ETDRS chart are not available in the clinical situation. The VA measured by 2.5SL chart is about 0.5 line better than VA tested with ETDRS chart, which may overestimate VA.

The Prevalence of Glaucoma and Its Related Factors in Rural Residents: A Cross-Sectional Study in Jiangxi, China.

BACKGROUND: This study aims to investigate the prevalence of glaucoma and its related factors among residents aged 40 and over in Jiangxi Province, China, and provide a scientific basis for the prevention and control of glaucoma. METHODS: The cluster sampling method was used to randomly select six townships. Similarly, eight villages were randomly selected from each sample township. A total of 5385 rural residents from 48 villages were collected for a questionnaire survey. A logistic regression model was used to explore the personal behavioral factors related to glaucoma. RESULTS: Among the 5385 participants, the prevalence rate of glaucoma was 1.4%. The logistic regression model found that alcohol consumption, vegetable consumption, physical exercise, daily reading time, and frequent reading environment were related to glaucoma. CONCLUSION: To prevent the occurrence of glaucoma, it is important for rural residents to reduce the frequency of alcohol consumption, increase the frequency of vegetable consumption and physical exercise, control the length of daily reading, and read in a moderately lit environment.