Influencing factors of low vision 2 years after vitrectomy for proliferative diabetic retinopathy: an observational study.

BACKGROUND: Proliferative diabetic retinopathy (PDR) can seriously affect the vision and quality of life of patients. The present study aimed to evaluate the clinical effect of vitrectomy for PDR by observing visual recovery and postoperative complications and to explore the factors influencing low vision. METHODS: This was a case series observational study. Consecutive eyes of patients with PDR who underwent 23G vitrectomy in our hospital within one year (2019.11-2020.11) were collected and followed up for more than 2 years. Patients' visual acuity, surgical complications and management were collected before the operation and during the follow-up. Decimal visual acuity was recorded and converted to the logarithm of the minimal angle of resolution (logMAR) for statistical analysis. Excel was used to establish a database, and SPSS 22.0 statistical software was used for data analysis. RESULTS: A total of 127 patients and 174 eyes were included in the study. The mean age was 57.8 years. The best corrected visual acuity (BCVA) was < 0.3 in 89.7% of eyes before surgery and ≥ 0.3 in 48.3% of eyes after surgery. Among 174 eyes, visual acuity improved in 83.3%. There was no change in 8.6% of eyes, while 8.1% of eyes had decreased visual acuity after surgery. The average logMAR visual acuity was 1.5 ± 0.7 before surgery and 0.7 ± 0.6 after surgery, indicating significant improvement (p < 0.05). Logistic regression analysis showed that intraoperative silicone oil filling and postoperative complication were significant risk factors for postoperative low vision, while preoperative pseudophakic lens and postoperative intra vitreal injection of anti-VEGF were protective factors for vision recovery (p < 0.05). The incidence of postoperative complications was 15.5%, top three of which were vitreous haemorrhage, neovascular glaucoma and traction retinal detachment. CONCLUSION: Vitrectomy is safe and effective in the treatment of PDR with few complication. Postoperative intra vitreal injection of anti-VEGF is a protective factor for vision recovery. TRIAL REGISTRATION: The trial registration number is ChiCRT2100051628, and the date of registration was September 28, 2021.

Antipsychotics-induced improvement of cool executive function in individuals living with schizophrenia.

Cool executive dysfunction is a crucial feature in people living with schizophrenia which is related to cognition impairment and the severity of the clinical symptoms. Based on electroencephalogram (EEG), our current study explored the change of brain network under the cool executive tasks in individuals living with schizophrenia before and after atypical antipsychotic treatment (before_TR vs. after_TR). 21 patients with schizophrenia and 24 healthy controls completed the cool executive tasks, involving the Tower of Hanoi Task (THT) and Trail-Marking Test A-B (TMT A-B). The results of this study uncovered that the reaction time of the after_TR group was much shorter than that of the before_TR group in the TMT-A and TMT-B. And the after_TR group showed fewer error numbers in the TMT-B than those of the before_TR group. Concerning the functional network, stronger DMN-like linkages were found in the before_TR group compared to the control group. Finally, we adopted a multiple linear regression model based on the change network properties to predict the patient's PANSS change ratio. Together, the findings deepened our understanding of cool executive function in individuals living with schizophrenia and might provide physiological information to reliably predict the clinical efficacy of schizophrenia after atypical antipsychotic treatment.

Inhibiting MiR-34α reduces retinal cell apoptosis and downstream NF-κB pathway in diabetic retinopathy rats through regulating HMGB1 expression.

BACKGROUND: This is a research aimed to study the effect of micro ribonucleic acid (miR)-34α on the retinal cell apoptosis in diabetic retinopathy (DR) rats and its key molecular mechanism. METHODS: Sprague-Dawley rats were randomly divided into healthy group (H group, N.=5), diabetes group (D group, N.=5), diabetes + negative control transfection group (N group, N.=5) and diabetes + miR-34α inhibitor transfection group (M group, N.=5). The rat model of diabetes was established via intraperitoneal injection of 2% streptozotocin solution (60 mg/kg). After 72 h, the urine glucose and blood glucose were detected, and the urine glucose above 3+ and the blood glucose concentration >16.7 mmol/L indicated the successful modeling. After the rats were normally fed for 4 months, the changes in expression of miR-34α in retinal tissues were detected via reverse transcription-polymerase chain reaction (RT-PCR), the pathological changes in retinal tissues were observed via hematoxylin-eosin (HE) staining, and the retinal cell apoptosis was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the changes in the number of cells containing active caspase-3 in retinal tissues were determined through immunohistochemistry, and the changes in expressions of caspase-3, high mobility group box 1 (HMGB1) and nuclear factor-κB (NF-κB) in retinal tissues were determined through Western blotting. RESULTS: Compared with those in H group, the cell density declined, and the cells were arranged disorderly with swelling in each retinal layer, the expression of miR-34α in retinal tissues was increased, the retinal cell apoptosis was enhanced, the number of cells containing active caspase-3 in retinal tissues rose, and the expressions of caspase-3, HMGB1 and NF-κB in retinal tissues were increased in D group, N group and M group (P<0.05). Compared with those in D group and N group, the cell density rose, and the cells were arranged less disorderly with milder swelling in each retinal layer, the expression of miR-34α in retinal tissues declined, the retinal cell apoptosis was weakened, the number of cells containing active caspase-3 in retinal tissues was decreased, and the expressions of caspase-3, HMGB1 and NF-κB in retinal tissues were reduced in M group (P<0.05). CONCLUSIONS: Inhibiting miR-34α reduces the retinal cell apoptosis in DR rats through regulating the HMGB1 expression and downstream NF-κB pathway.

Progressive Changes in Brain Regional Homogeneity Induced by Electroconvulsive Therapy Among Patients With Schizophrenia.

OBJECTIVES: Electroconvulsive therapy (ECT) has significant effects on improving psychotic symptoms in schizophrenia (SZ), but the changes of brain function induced by it are unclear. The purpose of the study was to explore progressive ECT-induced changes in regional homogeneity (ReHo) at multiple time points before, during, and after a course of ECT. METHODS: The 27 in-patients with SZ (SZ group) who met the recruitment criteria accepted clinical evaluations and resting-state functional magnetic resonance imaging scans before the first ECT (pre-ECT), after the first ECT (ECT1), and after the eighth ECT (ECT8), all conducted within 10 to 12 hours. Forty-three healthy controls (HCs; HC group) who matched well with the patients for age, sex, and years of education were recruited. For Positive and Negative Syndrome Scale (PANSS) and ReHo, progressive changes were examined. RESULTS: Pair-wise comparisons of patient pre-ECT, ECT1, and ECT8 ReHo values with HC ReHo values revealed that ECT normalized the ReHo values in bilateral superior occipital gyrus (SOG), right lingual gyrus (LG), left medial prefrontal cortex. Furthermore, improved ReHo in bilateral SOG and right LG appeared after the first ECT application. The ReHo values in right middle occipital gyrus, right middle temporal gyrus, and right inferior parietal lobule were not significantly altered by ECT. The total PANSS score was lower even after the first ECT application (mean ΔPANSSECT1, 11.7%; range, 2%-32.8%) and markedly reduced after the eighth application (mean ΔPANSSECT8, 86.3%; range, 72.5%-97.9%). CONCLUSIONS: The antipsychotic effects of ECT may be achieved through regulating synchronization of some regions such as bilateral SOG, right LG, and left medial prefrontal cortex. Furthermore, the enhanced synchronizations also take place in other regions.

LINC00028 regulates the development of TGFß1-treated human tenon capsule fibroblasts by targeting miR-204-5p.

Glaucoma is a leading cause of blindness worldwide with complex pathogenesis. The excessive proliferation and fibrosis of human tenon capsule fibroblasts (HTFs) trigger the scar formation after glaucoma filtration surgery. The purpose was to investigate the role of long intergenic non-protein coding RNA 28 (LINC00028) and mechanism in transforming growth factor ß1 (TGFß1)-treated HTFs. The detection of LINC00028 and miR-204-5p expression was conducted using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was assessed by cell counting kit-8 (CCK-8) assay. Cell migration and invasion were monitored by transwell assay. The expression of Epithelial-mesenchymal transition (EMT)-related markers, including E-cadherin, α-Smooth muscle actin (α-SMA), fibronectin and ß-catenin, and autophagy-related markers, including Beclin 1 and light chain 3 (LC3-II and LC3-I) at the protein level was quantified using western blot. The prediction of the relationship between LINC00028 and miR-204-5p was performed by the online tool miRcode, and the verification of the relationship between them was conducted using dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay. The expression of LINC00028 was elevated in glaucoma tissues and TGFß1-treated HTFs. LINC00028 downregulation blocked proliferation, migration, invasion, EMT, fibrosis and autophagy of TGFß1-treated HTFs. MiR-204-5p was a target of LINC00028, and its reintroduction exerted a similar role of LINC00028 downregulation. The inhibition of miR-204-5p reversed the effects of LINC00028 downregulation in TGFß1-treated HTFs. LINC00028 regulated proliferation, migration, invasion, EMT, fibrosis and autophagy to induce the development of HTFs by competitively targeting miR-204-5p, and LINC00028 was regarded as a promising biomarker for glaucoma filtration treatment.

TGF-ß2 induces proliferation and inhibits apoptosis of human Tenon capsule fibroblast by miR-26 and its targeting of CTGF.

AIM: The aim of this study was to research the effect of TGF-ß2 on human enon capsule fibroblasts proliferation and apoptosis and its potential mechanism. METHODS: Human eyeball fascia tissues (n = 45) were derived from ocular fascia tissues of patients who were underwent glaucoma filtration surgery, and Tenon capsule fibroblasts were obtained from these tissues. Liposome-mediated transfection, CCK8 assay, Hoechst33258 staining, qRT-PCR detection, western blot, and luciferase reporter assay were performed. RESULTS: TGF-ß2 promoted proliferation and inhibited apoptosis of human Tenon capsule fibroblasts in a dose-dependent manner. TGF-ß2 induced down-regulation of miR-26 and up-regulation of CTGF in a dose-dependent manner. CTGF was the target gene of miR-26 and miR-26 had a negative regulatory effect on CTGF expression. miR-26 up-regulation could significantly decrease proliferation and increase apoptosis of human Tenon capsule fibroblasts after induced by TGF-ß2 (P < 0.05). Down-regulation of CTGF could markly decrease proliferation and increase apoptosis of human Tenon capsule fibroblasts after induced by TGF-ß2 (P < 0.05). CONCLUSION: miR-26 could inhibit proliferation and promote apoptosis of human Tenon capsule fibroblasts after they were induced by TGF-ß2 through suppressing CTGF expression.