Efficacy of Vectored Thermal Pulsation and Warm Compress Treatments in Meibomian Gland Dysfunction: A Meta-Analysis of Randomized Controlled Trials.

PURPOSE: Meibomian gland dysfunction is the main cause of dry eye disease (DED) and is traditionally managed using warm compress treatment (WCT). Vectored thermal pulsation treatment (VTPT) is a novel method for treating DED. METHODS: We conducted a systematic review and meta-analysis of randomized controlled trials that compared the efficacy of VTPT and WCT in treating DED. The primary outcome was the gland function. The secondary outcomes were the tear breakup time, Schirmer test, tear osmolarity, lipid layer thickness, Standard Patient Evaluation for Eye Dryness, and the improvement of subjective symptoms as assessed by using the Ocular Surface Disease Index. PubMed, Embase, Cochrane Library, and ClinicalTrials.gov registries were searched for studies published before July 2018. RESULTS: This study consisted of 4 trials with 385 patients. Significantly greater improvement was observed in meibomian gland function [mean difference (MD): 2.19 (95% confidence interval (CI), 0.95, 3.43)], tear breakup time [MD: 1.08 (95% CI, 0.06, 2.10)], and Standard Patient Evaluation for Eye Dryness [MD: -2.76 (95% CI, -4.22, -1.30)] at 2 to 4 weeks in the VTPT group than in the WCT group. A significantly greater decrease in Ocular Surface Disease Index was observed at 2 to 4 weeks [MD: -8.61 (95% CI, -13.62, -3.61)] and 3 months [MD: -6.92 (95% CI, -11.95, -1.89)] in the VTPT group than in the WCT group. CONCLUSIONS: A single 12-minute VTPT was more efficacious than traditional WCT in treating DED either in objective or subjective measurements. We recommended choosing an appropriate treatment after shared decision-making.

Diabetic polyneuropathy and the risk of developing diabetic retinopathy: a nationwide, population-based study.

PURPOSE: To assess the relationship between diabetic polyneuropathy (DPN) and the risk of diabetic retinopathy (DR). METHODS: From 1997 to 2010, we identified 5031 newly diagnosed DPN patients and 20 124 controls matched for sex, age, and index year. Cox proportional hazards regression analyses were used to estimate the adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) of DR between the DPN patients and the non-DPN group. The adjusted hazard ratio was calculated and adjusted for age, sex, duration of diabetes and comorbidities of hypertension, cardiovascular disease and diabetic nephropathy. RESULTS: The incidence rate of DR was 5.87-fold higher in the DPN patients than in the non-DPN group (44.0 vs. 7.22 per 1000 person-years), with an adjusted HR of 5.41(95% CI = 4.92-5.94). The DPN-to-non-DPN DR incidence rate ratio decreased with age (adjusted HR = 6.63 for subgroup younger than 65 years and adjusted HR = 3.91 for subgroup aged 65 years or older). Compared with the non-DPN group, the DPN patients had a 5.63-fold risk of non-proliferative DR (adjusted HR = 5.63, 95% CI = 5.11-6.21) and a 3.67-fold risk of proliferative DR (adjusted HR = 3.67, 95% CI = 2.57-5.23). CONCLUSION: The patients with DPN had an increased risk of developing DR and advanced DR compared with the non-DPN group, particularly among the subgroup aged younger than 65 years.

Effects of size and surface of zinc oxide and aluminum-doped zinc oxide nanoparticles on cell viability inferred by proteomic analyses.

Although the health effects of zinc oxide nanoparticles (ZnONPs) on the respiratory system have been reported, the fate, potential toxicity, and mechanisms in biological cells of these particles, as related to particle size and surface characteristics, have not been well elucidated. To determine the physicochemical properties of ZnONPs that govern cytotoxicity, we investigated the effects of size, electronic properties, zinc concentration, and pH on cell viability using human alveolar-basal epithelial A549 cells as a model. We observed that a 2-hour or longer exposure to ZnONPs induced changes in cell viability. The alteration in cell viability was associated with the zeta potentials and pH values of the ZnONPs. Proteomic profiling of A549 exposed to ZnONPs for 2 and 4 hours was used to determine the biological mechanisms of ZnONP toxicity. p53-pathway activation was the core mechanism regulating cell viability in response to particle size. Activation of the Wnt and TGFß signaling pathways was also important in the cellular response to ZnONPs of different sizes. The cadherin and Wnt signaling pathways were important cellular mechanisms triggered by surface differences. These results suggested that the size and surface characteristics of ZnONPs might play an important role in their observed cytotoxicity. This approach facilitates the design of more comprehensive systems for the evaluation of nanoparticles.