Frailty is a critical cause leading to elderly death. No drug is available to treat it, while prevention works. However, reliable blood screening and diagnostic methods for frailty are still lacking. Here, we show that the serum GCSF, in combination with the fatigue factor of the frailty scale, can improve the performance of serological screening for frailty.

BackgroundOsteoporosis is a foremost public health challenge, especially with the global aging population. Both frailty and osteoporosis share many risk factors, although the relationship between them remains partially explored. This study aims to explore the correlation between varying frailty statuses and osteoporosis incidence.MethodsParticipants from the 2017-2018 NHANES were classified into three groups: frailty, prefrailty, and robust, based on the frailty phenotype. The correlation between frailty and osteoporosis prevalence was assessed using weighted multivariate logistic regression models. Causal relationship was verified by Mendelian randomization using frailty data from the U.K. Biobank and osteoporosis data from the FinnGen database. Proteomic analysis including associated protein screening and functional enrichments was performed based on data from the Icelandic cohort.ResultsThe study group comprised 1814 participants. An increased incidence of osteoporosis was observed in older age and lower body mass index populations. A significant frailty-osteoporosis correlation (odds ratio [OR]: 1.37; 95% confidence interval [CI]: 1.14-1.64; p = 0.001) was indicated both in the crude model and after adjustments (OR: 1.23; 95% CI: 1.01-1.51; p = 0.039). The inverse variance weighting method observed a potential effect of frailty on osteoporosis risk (beta/SE, 0.209/0.099; OR: 1.233; 95% CI: 1.014-1.499; p = 0.036). Thirteen frailty-osteoporosis-associated proteins were found, and proteomic enrichment indicated oxidative stress-related pathways as a hypothesis-generating mechanism of frailty-mediated osteoporosis.ConclusionsOur findings suggest a potential causal association between frailty and osteoporosis, with risk exacerbating with the progression of frailty severity. Frailty potentially impacts the progression of osteoporosis through response to oxidative stress.

BackgroundFrailty is one of the most problematic expressions of population aging, but its underlying mechanism has not been fully elucidated. Circulating galectin-3 (Gal-3) is involved in the pathogenesis of many age-related diseases. This study aims to explore the influence of circulating Gal-3 on the regulation of frailty and aging and to identify the potential mechanism further.MethodsIn this cross-sectional analysis, the Fried frailty phenotype (FP) was assessed among 149 community elderly residents in Shanghai. Peripheral blood mononuclear cells (PBMCs) were isolated by the Ficoll-Paque density gradient method, and differentially expressed genes (DEGs) encoding transcription factors in frailty were detected by Illumina and bioinformatics analyzed with R software. Gene Ontology (GO) enrichment analyses and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to explore the functional roles of these DEGs and the target genes related to frailty phenotypes. The serum Gal-3 concentration was tested by enzyme-linked immunosorbent assay (ELISA). Mouse frailty phenotype was used to construct an in vivo model of frailty, after which the serum levels of circulating Gal-3 and its gene expression levels in mouse tissues were determined.ResultsParticipants’ mean age was 72.04 ± 7.05 years. In total, 21.48% were frail and 36.91% were pre-frail. The mean serum Gal-3 concentration was 46.34 ± 17.99 ng/mL in frail participants, 32.30 ± 8.14 ng/mL in pre-frail participants, and 26.00 ± 5.87 ng/mL in non-frail individuals (p < 0.001). Significant positive correlations between serum Gal-3 level and FP score, SARC-F score, C-reactive protein (CRP), interleukin-6, etc., were observed. In addition, the KEGG pathway and GO enrichment analyses showed that 265 DEGs in PBMCs of frail participants were mainly related to inflammatory response, translation, RNA binding, protein binding, ribosome, and primary immunodeficiency. LGALS3 was identified as the overlapping gene between frailty-related DEGs and aging-related DEGs. The elevated serum Gal-3 concentration in the in vivo model of frailty was consistent with the results in participants.ConclusionIn both community-dwelling older adults and aged mice, serum Gal-3 concentration was positively correlated with frailty. This circulating mediator may be a promising indicator of frailty.Clinical trial registrationChinese Clinical Trial Registry identifier, ChiCTR2000036399.

IntroductionEndogenous glucocorticoids (GCs) played a pivotal role in the pathogenesis of skeletal muscle loss. However, to date, the underlying molecular mechanisms underlying are not yet fully understood. Galectin-3 (Gal-3) is a member of a beta-galactoside-binding animal lectins, consistently associated with inflammation and fibrosis in the pathogenesis of various disease states. The present study aimed to explore the role of Gal-3 in GC-induced skeletal muscle loss.Material and methodsMyogenic differentiation capacity was detected after in vitro Gal-3 knockdown (KD) or in vivo administration of Gal-3 inhibitor. The activation of transforming growth factor type beta 1 (TGFβ1) and Smad2/3 signaling pathways was determined by western blot, co-immunoprecipitation, and immunofluorescence.ResultsGal-3 was up-regulated during dexamethasone (Dex) administration in mice. In the established GC-induced muscle loss model, Gal-3 inhibition recovered grip strength and muscle mass. In vitro, Gal-3 KD promoted the myogenic differentiation capacity of C2C12 myoblasts, and prevented the reduction of fully differentiated myotubes. Gal-3 results in overexpression of TGFβ1 and TGFβR-I, which affects Smad2, 3 phosphorylation and subsequently mediates skeletal muscle reduction by activating the Smad2/3 signaling pathways.ConclusionsThe present study demonstrated that Dex elevated Gal-3 levels in skeletal muscle. Gal-3 facilitates the activation of TGFβ1-Smad2/3 signaling pathways in myoblasts, and contributes to myogenesis inhibition and skeletal muscle loss. This study raises awareness about the follow-up of patients receiving GC therapy. Further, inhibition of Gal-3 provides a possible therapeutic strategy for skeletal muscle loss.

Objective:To establish an in vitro capsular bag model and compare the inhibitory effects of different 360° square-edge intraocular lens (IOL) on lens epithelial cells (LECs) migration. Methods:In vitro capsular bag model with posterior capsule opacification (PCO) was established using Transwell compartment, cell climbing slices, human collagen type Ⅳ, and IOL.The models were divided into Plate-loop HydroSmart group, C-loop HydroSmart group, and C-compensation-loop Hydrophobic group according to the different square-edge IOL implanted.A blank control group was set using the Transwell compartment without IOL.The early PCO pathological manifestations in lens epithelial cell line SRA01/04 cultured in the Transwell compartment were observed with an inverted microscope.The cell morphology in different groups was observed by hematoxylin and eosin staining.The cell counting and cell migration inhibition rate of anterior capsule and posterior capsule were calculated by Transwell assay and cell-exclusion zone assay, respectively. Results:The early pathological characteristics of PCO, such as early Soemmering ring and small Elschnig pearl, could be found in cells in the in vitro capsular bag model after 48-hour culture.The migrating cells in model groups were fibrous.No changes mentioned above were found in blank control group.The number of migrating cells in the anterior capsule of Plate-loop HydroSmart group, C-loop HydroSmart group, C-compensation-loop Hydrophobic group was 18.80±5.53, 24.67±9.80, and 34.47±10.80, respectively, and the number of migrating cells in the optical area of the posterior capsule of the three groups was 56.43±9.00, 162.20±16.38, and 121.30±12.01, respectively.The cell migration inhibition rate in the anterior capsule of Plate-loop HydroSmart group, C-loop HydroSmart group, C-compensation-loop Hydrophobic group was (92.02±1.94)%, (89.76±3.10)%, (86.27±4.54)%, respectively, and the cell migration inhibition rate in optical area of the posterior capsule of the three groups was (91.60±3.65)%, (70.14±5.35)%, (78.43±3.48)%, respectively.The number of migrating cells in the anterior capsule was lower and the cell migration rate inhibition was higher in Plate-loop HydroSmart group than C-compensation-loop Hydrophobic group, with significant differences (both at P<0.05). The number of migrating cells in the optical area of the posterior capsule and the cell migration inhibition rate was greater than those of C-loop HydroSmart group and C-compensation-loop Hydrophobic group, showing statistically significant differences (all at P<0.001). Conclusions:The in vitro capsular bag model can be used in PCO research.Compared with C-loop HydroSmart IOL and C-compensation-loop Hydrophobic IOL, Plate-loop HydroSmart IOL can more effectively inhibit the migration of LECs to the optical area of the posterior capsule.

Sarcopenia is the age-related decrease in skeletal muscle mass, and current therapies for this disease are ineffective. We previously showed that ileal farnesoid X receptor (FXR)-fibroblast growth factor 15/19 (FGF15/19) signaling acts as a regulator of gut microbiota to mediate host skeletal muscle. However, the therapeutic potential of this pathway for sarcopenia is unknown. This study showed that ileal FXR-FGF15/19 signaling was downregulated in older men and aged male mice due to changes in the gut microbiota and microbial bile acid metabolism during aging. In addition, the intestine-specific FXR agonist fexaramine increased skeletal muscle mass and improve muscle performance in aged mice. Ileal FXR activation increased skeletal muscle protein synthesis in a FGF15/19-dependent way, indicating that ileal FXR-FGF15/19 signaling is a potential therapeutic target for sarcopenia.

Background: Mobile phone-based digital interventions have been shown to be a promising strategy for HIV prevention among men who have sex with men (MSM). Objective: This study aimed to evaluate the cost-effectiveness of a mobile phone-based digital intervention for HIV prevention among MSM in China from the perspective of a public health provider. Methods: The cost-effectiveness of the mobile phone-based digital intervention was estimated for a hypothetical cohort of 10,000 HIV-negative MSM who were followed for 1 year. A model was developed with China-specific data to project the clinical impact and cost-effectiveness of two mobile phone-based digital strategies for HIV prevention among MSM. The intervention group received an integrated behavioral intervention that included 1) individualized HIV infection risk assessment, 2) recommendation of centers testing for HIV and other STIs, 3) free online order of condoms and HIV and syphilis self-test kits and 4) educational materials about HIV/AIDS. The control group was only given educational materials about HIV/AIDS. Outcomes of interest were the number of HIV infections among MSM averted by the intervention, intervention costs, cost per HIV infection averted by the mobile phone-based digital intervention, and quality-adjusted life-years (QALYs). Univariate and multivariate sensitivity analyses were also conducted to examine the robustness of the results. Results: It is estimated that the intervention can prevent 48 MSM from becoming infected with HIV and can save 480 QALYs. The cost of preventing 1 case of HIV infection was US $2599.87, and the cost-utility ratio was less than 0. Sensitivity analysis showed that the cost-effectiveness of the mobile phone-based digital intervention was mainly impacted by the average number of sexual behaviors with each sexual partner. Additionally, the higher the HIV prevalence among MSM, the greater the benefit of the intervention. Conclusions: Mobile phone-based digital interventions are a cost-effective HIV-prevention strategy for MSM and could be considered for promotion and application among high-risk MSM subgroups.

Background: Recent evidence indicates that host-gut microbiota crosstalk has nonnegligible effects on host skeletal muscle, yet gut microbiota-regulating mechanisms remain obscure.Methods: C57BL/6 mice were treated with a cocktail of antibiotics (Abx) to depress gut microbiota for 4 weeks. The profiles of gut microbiota and microbial bile acids were measured by 16S rRNA sequencing and ultra-performance liquid chromatography (UPLC), respectively. We performed qPCR, western blot and ELISA assays in different tissue samples to evaluate FXR-FGF15/19 signaling.Results: Abx treatment induced skeletal muscle atrophy in mice. These effects were associated with microbial dysbiosis and aberrant bile acid (BA) metabolism in intestine. Ileal farnesoid X receptor (FXR)-fibroblast growth factor 15 (FGF15) signaling was inhibited in response to microbial BA disturbance. Mechanistically, circulating FGF15 was decreased, which downregulated skeletal muscle protein synthesis through the extracellular-signal-regulated protein kinase 1/2 (ERK1/2) signaling pathway. Treating Abx mice with FGF19 (human FGF15 ortholog) partly reversed skeletal muscle loss.Conclusions: These findings indicate that the BA-FXR-FGF15/19 axis acts as a regulator of gut microbiota to mediate host skeletal muscle.

A common observation in metabolic disorders and aging is the elevation of free fatty acids (FFAs), which can form ectopic fat deposition and result in lipotoxicity. Ectopic fat deposition of skeletal muscle has been recognized as an important component of aging, frailty, and sarcopenia. Previous studies have suggested that lipotoxicity caused by FFAs mainly stemmed from saturated fatty acids and decreased unsaturated/saturated fatty acid ratio in serum are also observed among metabolic disorder patients. However, the different effects of saturated fatty acids and unsaturated fatty acids on skeletal muscle are not fully elucidated. In this study, we verified that palmitate (PA), a saturated fatty acid, could lead to impaired differentiative capacity of C2C12 myoblasts by affecting Pax7, MyoD, and myogenin (MyoG), which are master regulators of lineage specification and the myogenic program. Then, oleate (OA), a monounsaturated fatty acid, were added to culture medium together with PA. Results showed that OA could ameliorate the impairment of differentiative capacity in C2C12 myoblast cells. In addition, we found PI3K/Akt signaling pathway played an important role during the process by RNA sequencing and bioinformatics analysis. The positive effect of OA on myoblast differentiative capacity disappeared if PI3K inhibitor LY294002 was added. In conclusion, our study showed that PA could destroy differentiative capacity of C2C12 myoblasts by affecting the expression of Pax7, MyoD, and MyoG, and OA could improve this impairment through PI3K/Akt signaling pathway.

Objective To assess the association of socioeconomic status with the burden of cataract blindness in terms of year lived with disability (YLD) rates and to determine whether ultraviolet radiation (UVR) levels modify the effect of socioeconomic status on this health burden. Methods National and subnational age-standardized YLD rates associated with cataract-related blindness were derived from the Global Burden of Disease (GBD) study 2017. The human development index (HDI) from the Human Development Report was used as a measure of socioeconomic status. Estimated ground-level UVR exposure was obtained from the Ozone Monitoring Instrument (OMI) dataset of the National Aeronautics and Space Administration (NASA). Results Across 185 countries, socioeconomic status was inversely associated with the burden of cataract blindness. Countries with a very high HDI had an 84% lower age-standardized YLD rate [95% confidence interval (CI): 60%-93%, P < 0.001] than countries with a low HDI; for high-HDI countries, the proportion was 76% (95% CI: 53%-88%, P < 0.001), and for medium-HDI countries, the proportion was 48% (95% CI: 15%-68%, P = 0.010; P for trend < 0.001). The interaction analysis showed that UVR exposure played an interactive role in the association between socioeconomic status and cataract blindness burden (P value for interaction = 0.047). Conclusion Long-term high-UVR exposure amplifies the association of poor socioeconomic status with the burden of cataract-related blindness. The findings emphasize the need for strengthening UVR exposure protection interventions in developing countries with high-UVR exposure.

Galectin-3 (Gal3) is an essential regulator of a number of metabolic disorders. Previous studies have established that Gal3 is a positive regulator of inflammation, fibrosis, and insulin resistance. However, its function in the early pathogenesis of hepatic lipid accumulation in non-alcoholic fatty liver disease (NAFLD) remains unresolved. Here, we demonstrate the presence of significantly upregulated extracellular concentrations of Gal3 in the fatty livers of high-fat diet (HFD)-induced mice. Systemic inhibition of Gal3 by injection of TD139 reduced the accumulation of lipid in the livers of HFD-fed mice, accompanied by the decreased expression of CD36 and peroxisome proliferator-activated receptor-gamma (PPARγ). Treatment with Gal3 protein elicited the opposite response in palmitic acid (PA)-induced HepG2 hepatocytes. It was additionally discovered that Gal3 positively regulates CD36 transcription by increased activation of PPARγ, thereby increasing fatty acid uptake, resulting in hepatic steatosis. In conclusion, the present study confirmed the roles of Gal3 in hepatic lipid metabolism in both in vitro and in vivo studies and revealed that Gal3 is a secretory protein that promotes hepatic steatosis through the PPARγ-CD36-dependent pathway, suggesting that targeting Gal3 may represent a potential therapeutic approach for the treatment of NAFLD and related metabolic disorders.

BACKGROUND:The incidence and mortality rates of hepatocellular carcinoma are among the highest of all cancers all over the world. However the survival rates are relatively low due to lack of effective treatments. Efforts to elucidate the mechanisms of HCC and to find novel prognostic markers and therapeutic targets are ongoing. Here we tried to identify prognostic genes of HCC through co-expression network analysis.METHODS:We conducted weighted gene co-expression network analysis with a microarray dataset GSE14520 of HCC from Gene Expression Omnibus database and identified a hub module associated with HCC prognosis. Function enrichment analysis of the hub module was performed. Clinical information was analyzed to select candidate hub genes. The expression profiles and survival analysis of the selected genes were performed using additional datasets (GSE45267 and TCGA-LIHC) and the hub gene was identified. GSEA and in vitro experiments were conducted to further verify the function of the hub gene.RESULTS:Genes in the hub module were mostly involved in the metabolism pathway. Four genes (SLC27A5, SLC10A1, PCK2 and FMO4) from the module were identified as candidate hub genes according to correlation analysis with prognostic indicators. All these genes were significantly down-regulated in tumor tissues compared with non-tumor tissues in additional datasets. After survival analysis and network construction, SLC27A5 was selected as a prognostic marker. GSEA analysis and in vitro assays suggested that SLC27A5 downregulation promoted tumor cell migration via enhancing epithelial-mesenchymal transition.CONCLUSION:SLC27A5 is a potential biomarker of HCC and SLC27A5 downregulation promoted HCC progression by enhancing EMT.

Objectives: Fine particulate matter (PM2.5) is the principal air pollutant and poses a serious threat to public health. This study explored the effects of PM2.5 on the action spectrum of ultraviolet radiation for vitamin D production (UVvitD) received by manikin surfaces. Methods: Multi-inclination angle ultraviolet radiation monitoring was conducted with different concentrations of PM2.5. Combining monitoring data with the PM2.5 concentration, solar elevation angle (SEA), and inclination angle, a UVvitD exposure model for human body multi-inclined surfaces was constructed through a multiple linear regression analysis. A 3D manikin model was used to examine the PM2.5 effects on UVvitD received by the manikin surface. Results: When PM2.5 concentrations ranged from 35 μg/m3 to 100 μg/m3 (average concentration of PM2.5 in this range: 62 μg/m3), the UVvitD received by the whole body was reduced by approximately 8.45% to 19.82% compared with the UVvitD received when PM2.5 concentrations ranged from 6 μg/m3 to 35 μg/m3 (average concentration of PM2.5 in this range: 17 μg/m3) with SEAs between 30° and 50°. Moreover, the UVvitD dose was reduced by 11.82% in the above comparisons. When further comparing PM2.5 concentrations from 100 μg/m3 to 161 μg/m3 (average concentration of PM2.5 in this range: 132 μg/m3) with those from 6 μg/m3 to 35 μg/m3 (average concentration of PM2.5 in this range: 17 μg/m3), the UVvitD received by the whole body was reduced by approximately 21.6% to 50.64% at SEAs between 30° and 50°. The UVvitD dose was reduced by 30.2%. Conclusions: The occurrence of PM2.5 obviously reduced the UVvitD received by the manikin surface.

目的 调查社区老年人衰弱的患病率及危险因素,探讨躯体衰弱与肌少症的相关性.方法 随机选取1 349例60岁及以上社区老人为研究对象,现场采集一般人口学资料、肌少症筛检问卷(SARC-F)、微型营养评估量表(MNA);测定骨骼肌肌量、握力及步速.采用Fried衰弱表型(FP)进行衰弱评估,将受试者分为衰弱或衰弱前期组和非衰弱组.结果 社区老年人中衰弱或衰弱前期患病率为39.88％.衰弱或衰弱前期组和非衰弱组性别、年龄、受教育程度、腰围、臀围、步速、握力、SARC-F、ADL、MNA差异均有统计学意义(P＜0.001).年龄(r=0.36,P＜0.001)和握力下降(r=0.39,P＜0.001)与衰弱呈正相关.多因素回归分析显示年龄、步速下降、握力下降、肌少症、ADL及MNA是躯体衰弱的危险因素,而性别是衰弱的保护因素.肌少症患者中,年龄、握力下降、ADL和MNA是衰弱的危险因素,而性别和臀围是衰弱的保护因素.结论 社区老年人衰弱患病率不低,衰弱和肌少症密切相关,高龄、营养不良的肌少症患者更易发生躯体衰弱.

目的 探讨氧化应激情况下miR-24对晶状体细胞凋亡的调控.方法 采用实时定量PCR检测40例白内障患者晶状体上皮组织及临近晶状体上皮组织中miR-24的表达水平,并在氧化应激情况下检测miR-24的表达变化.通过miR-24 mimics、miR-24 inhibitor转染晶状体上皮细胞SAR01/04以过表达和敲低miR-24,利用pcDNA3.1-SIRT1转染SAR01/04以过表达SIRT1,FITC/PI流式细胞术检测晶状体细胞凋亡情况,Western blot检测凋亡相关蛋白Bcl-2、Bax表达情况,CCK-8检测细胞活性状态.结果 miR-24在白内障晶状体上皮组织中的表达高于临近组织,氧化应激情况下促进miR-24表达增高,差异有统计学意义(P＜0.05);氧化应激情况下,敲低miR-24抑制晶状体上皮细胞的凋亡;过表达或敲低miR-24可以分别降低或促进SIRT1的表达;过表达miR-24和过表达SIRT1后抑制了晶状体细胞的凋亡.结论 氧化应激促进晶状体上皮细胞miR-24表达上调,miR-24通过下调SIRT1促进晶状体上皮细胞的凋亡,为白内障的靶向治疗提供一定的策略.

目的 探讨上海市社区55岁及以上人群衰弱的分布特点及其与共病之间的相关性.方法 对上海市某社区55岁及以上人群1 671例进行横断面调查研究.采用Fried衰弱表型量表进行衰弱评估,根据评估结果将研究对象分为衰弱或衰弱前期组及非衰弱组;采用查尔森合并症指数(CCI)进行共病严重程度评估.收集比较人群的临床资料,分析衰弱的分布特点.结果 1 671例研究对象中,衰弱601例(35.97％),其中男性多于女性,差异有统计学意义(42.25％vs 32.56％,P＜0.001).衰弱或衰弱前期组与非衰弱组CCI、高血压、冠状动脉粥样硬化性心脏病、中重度肾脏疾病、退行性骨关节炎和肿瘤患病率差异有统计学意义(均P＜ 0.05).性别、年龄、CCI和高血压是衰弱的危险因素,退行性骨关节炎是衰弱的保护因素.结论 性别、年龄、教育程度和共病严重程度是衰弱的影响因素,衰弱和共病存在一定相关性.

目的 探讨不同瞳孔直径下的角膜球差情况,比较OPD波前像差分析仪和Pentacam三维眼前节分析仪在测量角膜球差时的一致性,并探讨不同年龄段人群的角膜球差特征.方法 回顾性选取2017年1月至11月在我院入院做过OPD波前像差分析仪或Pentacam三维眼前节分析仪检查的20 ～ 89岁调查对象各350人,分别记作OPD组及Pentaeam组.记录瞳孔直径为3 mm、4 mm、5 mm、6 mm、7 mm、8 mm、9 mm时的角膜球差值;分析6 mm瞳孔直径下的角膜球差频数分布情况及不同年龄段人群的角膜球差特征.结果 两组比较发现,瞳孔直径在3 mm、4 mm、5 mm、7 mm时,差异均有统计学意义(均为P＜0.05).瞳孔直径为6 mm、8 mm、9 mm时,两组差异均无统计学意义(均为P＞0.05).大瞳孔直径下,两种检查的一致性较好.6 mm瞳孔直径时OPD组和Pentacam组角膜球差值分别为(0.271±0.069) μm、(0.310±0.158) μm,两组角膜球差均具有明显的瞳孔依赖性,并随着瞳孔直径的增大而增高.6 mm瞳孔直径时,OPD组和Pentacam组角膜球差分布于0.10～0.40 μm的比例分别为97.71％和66.28％.Pentacam三维眼前节分析仪测得的角膜球差随着年龄的增长而增大,而OPD波前像差分析仪测得的角膜球差与年龄无明显关系.结论 角膜球差随着瞳孔直径的增大而增高.瞳孔较大时,OPD波前像差分析仪和Penta-cam三维眼前节分析仪测得的角膜球差的一致性较好.不同设备测量的角膜球差值随年龄的增长有一定的变化规律.

Purpose To evaluate the correlation between lens opacity degrees and phacoemulsification cumulated dissipated energy (CDE) values in patients with age-related cataract by applying 25-MHz panoramic ultrasound biomicroscopy (UBM). Methods This observational study was conducted in 227 patients (294 eyes) with age-related cataract. Patient ages ranged from 45 to 91 years. According to the lens images acquired by 25-MHz UBM, the objective indexes of lens opacity degrees were determined by using the ImageJ software. The correlation between lens opacity degrees (pixel units) and CDE values of phacoemulsification were mainly analyzed. Results The means of measurements were as follows: preoperative LogMAR corrected distance visual acuity, anterior chamber depth, and central lens thickness was 1.10 ± 0.61, 2.52 ± 0.51, and 4.34 ± 0.60 mm, respectively. The mean 25-MHz UBM-measured lens opacity degree was 101.30 ± 19.70 pixel units, and the mean CDE value was 9.74 ± 9.10. There was a linear correlation between pixel units and the CDE value, as well as LogMAR corrected distance visual acuity (r = 0.38 and 0.50, respectively; both P < 0.05). Age correlated with anterior chamber depth and lens thickness (r = −0.18 and 0.16, respectively; both P < 0.05) but not with pixel units (r = −0.08, P > 0.05). Conclusion The 25-MHz UBM has significant advantages in displaying the opacity feature of age-related cataract. The 25-MHz UBM combined with ImageJ software can be used to evaluate the opacity degree of age-related cataract quantitatively and may help predict the phacoemulsification parameters in cataract surgery. Translational Relevance Combination of the lens ultrasonic image and image analysis software enables researchers to evaluate lens opacity degree quantitatively and predict the parameters of phacoemulsification surgery.

PurposeTo assess the effects of posterior sclera reinforcement (PSR) in refractive outcomes, choroidal thickness (CT), and retinal thickness (RT) during a 3-year follow-up in eyes with pathological myopia.MethodsThirty-eight eyes of 26 adults with pathological myopia who underwent PSR (the PSR group) and 30 eyes of 18 adults with matched age and myopia who did not receive PSR treatment (the control group) were followed up with measurements of axial length (AL), spherical equivalent (SE), best corrected visual acuity (BCVA), CT, and RT at baseline, 1 and 3months, and 1, 2, and 3years postoperatively. Data were analyzed by repeated measures analysis of variance and independent-samples t test.ResultsIn the PSR group, AL, SE, BCVA, and CT were tending to be relatively stable and no statistically significant changes were found during the follow-up (all P>0.05). In contrast, in the control group, compared with the measurements taken at baseline, AL, SE, BCVA, and CT altered gradually from 1month onward to 3years postoperatively. At 2-year and 3-year follow-ups, significant differences in AL, SE, BCVA, and CT were noted between the PSR group and the control group (all P<0.05). RTs of the center subfield and the inner ring were equal to the baseline in the control group; however, RTs of the center subfield at 1year, 2years, and 3years postoperatively significantly slightly reduced compared with those at the baseline in the PSR group (all P<0.05).ConclusionsThe effects of PSR in restraining eyeball elongation, stabilizing vision, and strengthening the structure of posterior pole are more prominent 2years or more postoperatively compared with the natural progression of pathological myopia.

Objective To analyze the correlation between Dysfunctional Lens Index (DLI) and other functional indexes.Methods From October 2016 to May 2017,patients with early cataract who were treated in Ophthalmology Clinic of our hospital,the best corrected visual acuity was ≥ 0.6,slit lamp,i-Trace,OQAS,C-Quant and OPD-Scan Ⅲ and Pentacam and measured DLI,OSI,Log (S),total high order aberrations of the lens and lens coma,trefoil aberration,spherical aberration,lens density and other indexes.Pearson correlation analysis was used to compare DLI values with other indexes.Results The lens dysfunction index and subjective and objective visual quality included objective scattering index (r=-0.321,P=0.004),intraocular light scattering (r=-0.329,P=0.003),higher order aberrations (r=-0.272,P=0.015),lens coma aberration (r=-0.259,P=-0.021),trefoil aberration (r=-0.322,P=0.004),spherical aberration (r=-0.349,P=0.001).There was a negative correlation between the lens dysfunction index and the average density of lens (r=-0.312,P=0.005),which had statistical significance.Conclusions The lens dysfunction index combined visual quality evaluation indicators can be used to evaluate the visual function of patients with early lens crystalline,which can provide better evidence for refractive cataract surgery.