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To examine whether vision impairment and eye diseases are independently associated with memory decline in older adults.

Cohort study.

We included 8,315 participants aged 50-94 years in China Health and Retirement Longitudinal Study (CHARLS) from China and 8,939 participants aged 50-95 years in Health and Retirement Study (HRS) from the United States in our analysis.

During 4.0 years' follow-up, the composite memory decreased by 0.16 points in CHARLS. During 3.9 years' follow-up, the composite memory decreased by 0.51 in HRS. Distance vision impairment was inversely associated with an annual change in composite memory (β [95% CI] -0.07 [-0.12, -0.01]) and immediate memory (-0.04 [-0.07, -0.02]) in CHARLS, and the corresponding values in HRS were -0.19 (-0.34, -0.05) and -0.07 (-0.13, -0.00), respectively. Selleckchem SMI-4a Near vision impairment was inversely associated with an annual change in delayed memory in CHARLS and composite memory, immediate memory, and delayed memory in HRS. In HRS, the association between distance vision impairment and memory decline was observed in individuals aged <65 years (β [95% CI] -0.54 [-0.78, -0.30]) but not in those aged ≥65 years (-0.01 [-0.20, 0.18]). Cataract surgery or glaucoma was not significantly associated with memory decline in either CHARLS or HRS.

Distance vision impairment was independently associated with an accelerated rate of memory decline in both China and the United States. Near vision impairment was predictive of decline in delayed memory in China and of decline in composite, immediate, and delayed memory in the United States.

Distance vision impairment was independently associated with an accelerated rate of memory decline in both China and the United States. Near vision impairment was predictive of decline in delayed memory in China and of decline in composite, immediate, and delayed memory in the United States.

The purpose of this study was to describe the clinical features of epivascular glia (EVG) using en face optical coherence tomography (OCT).

Retrospective cross-sectional study.

Single-institution en face OCT images were reviewed. Eyes displaying EVG were captured with manual internal limiting membrane (ILM) segmentation and analyzed with customized segmentation . A random age- and sex-matched control group was selected to determine relative epiretinal membrane (ERM) prevalence.

Characteristic hyper-reflective ILM plaques with dendrite-like radiations were identified using en face OCT and displayed vascular predilection. A total of 161 eyes with EVG (the EVG group) and 2,315 eyes without EVG (control group) were identified from a total cohort of 1,298 patients (or 2,476 eyes). The prevalence of EVG was 161 of 2,476 eyes (6.5%) and 119 of 1,298 patients (9.2%) in the cohort. Mean age was 79.3 ± 10.7 years old in the EVG group and 55.9 ± 24.6 years old in the control group (P <.001). An advanced postestudies.

To investigate the epidemiologic characteristics and risk of corneal surface damage in patients with aqueous-deficient dry eye disease (DED) in Taiwan.

Retrospective, population-based cohort study.

We used claims data in the Taiwan National Health Insurance Research Database from 1997 to 2013 of patients with DED, defined according to diagnoses, drug codes, and clinical follow-up. A comparison cohort without DED was selected through propensity score matching. The main outcome measures were corneal surface damage, including corneal erosion, corneal ulcers, or corneal scars.

Patients with DED had a significantly higher rate of corneal surface damage (hazard ratio [HR] 2.70; 95% confidence interval [CI] 2.38-3.06, P < .001), especially higher in patients aged <18 years (HR 6.66; 95% CI 3.58-12.41) than in older patients and in women (HR 2.98; 95% CI 2.57-3.46) than in men (HR 2.22; 95% CI 1.78-2.77), compared to those in the non-DED cohort. DED with diabetes mellitus (P=.002), rheumatoid arthritis (P=.029), or systemic lupus erythematosus (P=.005) was positively associated with corneal surface damage. The overall prevalence of DED was 7.85%, higher among women (10.49%) than men (4.92%), and increased with age (0.53%, 3.94%, 10.08%, and 20.72% for ages <18, 18-39, 40-64, and >65 years, respectively). The prevalence increased gradually during the study period.

The younger age group (<18 years) had the highest risk of corneal surface damage in aqueous-deficient DED. Other predisposing factors included female sex, diabetes, and autoimmune diseases. To improve clinical care, special attention is required for patients with DED with these risk factors.

The younger age group ( less then 18 years) had the highest risk of corneal surface damage in aqueous-deficient DED. Other predisposing factors included female sex, diabetes, and autoimmune diseases. To improve clinical care, special attention is required for patients with DED with these risk factors.Neurons in the subfornical organ (SFO) sense both neurotransmitters and circulating humoral factors such as angiotensin II (AII) and atrial natriuretic peptide (ANP), and regulate multiple physiological functions including drinking behavior. We recently reported that AII at nanomolar concentrations induced a persistent [Ca2+]i increase in acutely dissociated SFO neurons and that this effect of AII was reversibly inhibited by GABA. In the present study, we studied the inhibitory mechanism of GABA using Ca2+ imaging and patch-clamp electrophysiology. The AII-induced persistent [Ca2+]i increase was inhibited by GABA in more than 90% of AII-responsive neurons and by other two SFO inhibitory ligands, ANP and galanin, in about 60 and 30% of neurons respectively. The inhibition by GABA was mimicked by the GABAA and GABAB receptor agonists muscimol and baclofen. The involvement of both GABA receptor subtypes was confirmed by reversal of the GABA-mediated inhibition only when the GABAA and GABAB receptors antagonists bicuculline methiodide and CGP55845 were both present. The GABAB agonist baclofen rapidly and reversibly inhibited voltage-gated Ca2+ channel (VGCC) currents recorded in response to depolarizing pulses in voltage-clamp electrophysiology using Ba2+ as a charge carrier (IBa). Baclofen inhibition of IBa was antagonized by CGP55845, confirming GABAB receptor involvement; was reduced by N-ethylmaleimide, suggesting downstream Gi-mediated actions; and was partially removed by a large prepulse, indicating voltage-dependency. The magnitude of IBa inhibition by baclofen was reduced by the application of selective blockers for N-, P/Q-, and L-type VGCCs (ω-conotoxin GVIA, ω-agatoxin IVA, and nifedipine respectively). Overall, our study indicates that GABA inhibition of the AII-induced [Ca2+]i increase is mediated by both GABAA and GABAB receptors, and that GABAB receptors associated with Gi proteins suppress Ca2+ entry through VGCCs in SFO neurons.