Diabetic retinopathy (DR) is the common and important cause for visual impairment and blindness in working-aged people. Microangiopathy and inflammatory reactions are the key components of DR. Recently, long non-coding RNA myocardial infarction-associated transcript (MIAT) has emerged as a vital player in regulation for inflammatory processes and microvascular dysfunction. Additionally, cell-based therapy provides a potential option for the treatment of DR. The antiinflammatory effects and repair therapy of mesenchymal stem cells (MSCs) have been paid more attention. This study investigated the effects of human umbilical-cord mesenchymal stem cells (HUMSCs) injection on diabetic rat model. The results show that the level of MIAT is significantly decreased in the diabetic retina after the injection of HUMSCs. Moreover, HUMSCs can significantly decrease the expression of IL-1β and IL-6 mRNA; alleviate microvascular permeability, and upregulate Occludin expression. Studies have shown that MIAT knockdown could alleviate diabetes-induced inflammation responses and vascular leakage. Furthermore, our findings also showed that the expression of MIAT was positively correlated with the expression of IL-1β and IL-6. These results suggest that MIAT might play important regulatory roles in alleviating inflammatory reactions and microangiopathy inducing by DR after transplantation of HUMSCs.

Purpose The correlations between the axial length-to-corneal radius (AL/CR) ratio and corneal astigmatism (CA) were studied by prospectively analyzing and comparing survey data from school children in the Beijing urban area from 2014 to 2015. Methods In this longitudinal study, a total of 2,970 students were enrolled in 2014, and 2,179 students were enrolled in 2015. The students were in grades 1 and 4 of primary schools located in the Yangfangdian district of Beijing. The students were examined using the standard logarithmic visual acuity chart for uncorrected visual acuity (UCVA) and IOLMaster for ocular components. Results From 2014 to 2015, the students from grades 1 and 4 had significantly worse UCVA results, longer axial lengths (AL), and greater AL/CRs (p < 0.001). The boys had a longer AL and corneal radius (CR) than the girls (p < 0.001). A significantly higher rate of increased CA was observed for the students with increased AL/CR than for those with decreased or unchanged ratios (AL/CR for grade 1, X2 = 12.304, p=0.001; for grade 4, X2 = 29.044, p < 0.001). In addition, with increased AL/CR over one year, the CA value of the students in grades 1 and 4 became significantly larger (grade 1, p=0.001; grade 4, p < 0.001); moreover, the UCVA became worse (p < 0.001). Conclusions We found that UCVA and AL growth were affected by aging. An increase in the AL/CR ratio is a risk factor for the progression of corneal astigmatism for school children.

The lncRNA small nucleolar RNA host gene 1 (SNHG1) is a cerebral infarctionassociated gene, its biological role and mechanism in diabetic retinopathy remain to be illuminated. The present study was designed to investigate the role of SNHG1 in high glucose induced human retinal pigment epithelial cells (ARPE-19). Methods: ARPE-19 cells were cultured and exposed to 60 mM high glucose for 48h, and 5.5mM glucose-exposed ARPE-19 cells were used as the control. The levels of the epithelial-mesenchymal transition (EMT) markers E-cadherin, ZO-1, vimentin and α-SMA were measured, and the Cell inflammatory response was evaluated by detecting IL-6 and IL-1β levels. Then, cell migration, proliferation and apoptosis were detected. The expression of the lncRNA SNHG1 in ARPE-19 cells was detected by quantitative real-time PCR. SNHG1 was knocked down by small interfering RNA (siRNA) transfection. The effects of SNHG1 inhibition on inflammation, EMT, migration, proliferation and apoptosis were observed. Results: The results showed that the expression of SNHG1 was significantly increased in ARPE-19 cells exposed to high glucose. Silencing SNHG1 reduced the expression of vimentin, α-SMA, and the expression of inflammatory chemokines IL-6 and IL-1β, inhibited migration and proliferation, elevated the expression of E-cadherin and ZO-1, and promoted apoptosis in ARPE-19 cells. Conclusion:The lncRNA SNHG1 is involved in hyperglycemia-induced EMT and the inflammatory response of ARPE-19 cells and provides a new understanding of the pathogenesis of DR.

In addition to the improvement in BCVA and the reduction in CFT, IVR improved macular retinal function, as assessed by mf-ERG, in diabetic eyes. The combination of OCT and mf-ERG for macular evaluation may better assess DME.

Dictamnine (4-methoxyfuro[2,3-b]quinolone, DIC), a common furoquinoline alkaloid in the family of Rutaceae, showed diverse biological activities. To investigate the in vivo metabolic pathways of DIC, metabolism of DIC in mice was studied using a high-performance liquid chromatography coupled to electrospray ionization of hybrid linear trap quadrupole orbitrap (HPLC-LTQ-Orbitrap) mass spectrometer. Nine metabolites were identified in the DIC-treated mouse urine, plasma, and fecal samples, of which two were identified as new metabolites. The major metabolic pathways of DIC in animal and human liver microsomes were confirmed in the present study, including o-demethylation, monohydroxylation, N-oxidation, and 2,3-olefinic epoxidation pathways. For the first time, a mono-acetylcysteine conjugate of DIC (M9) was detected from DIC-treated mouse urine and plasma samples, and 4-methoxy-2-oxo-1,2-dihydroquinoline-3-carboxylic acid (M10) and 2-(2,8-dihydroxy-4-methoxyquinolin-3-yl)acetaldehyde (M11) were identified as new metabolites of DIC; furthermore, using an in vitro human fecal incubation model, furo[2,3-b]quinolin-4-ol (M1) was verified to be a microbial demethylated metabolite of DIC. Collectively, the present study provided new information on the in vivo metabolic fate of DIC.