Silibinin Prevents TGFß-Induced EMT of RPE in Proliferative Vitreoretinopathy by Inhibiting Stat3 and Smad3 Phosphorylation.

Purpose: The purpose of this study was to investigate the effects of silibinin on epithelial-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) and proliferative vitreoretinopathy (PVR) formation, as well as its underlying molecular mechanism. Methods: Cellular morphological change and EMT molecular markers were evaluated by using phase contrast imaging, qPCR, and Western blot (WB) to investigate the impact of silibinin on the EMT of ARPE-19 cells. Scratch assay and transwell assay were used to study the effect of silibinin on cell migration. An intravitreally injected RPE-induced rat PVR model was used to assess the effect of silibinin on PVR in vivo. RNA-seq was applied to study the molecular mechanism of silibinin-mediated PVR prevention. Results: Silibinin inhibited TGFß1-induced EMT and migration of RPE in a dose-dependent manner in vitro. Moreover, silibinin prevented proliferative membrane formation in an intravitreal injected RPE-induced rat PVR model. In line with these findings, RNA-seq revealed a global suppression of TGFß1-induced EMT and migration-related genes by silibinin in RPEs. Mechanistically, silibinin reduced TGFß1-induced phosphorylation levels of Smad3 and Stat3, and Smad3 nuclear translocation in RPE. Conclusions: Silibinin inhibits the EMT of RPE cells in vitro and prevents the formation of PVR membranes in vivo. Mechanistically, silibinin inhibits Smad3 phosphorylation and suppresses Smad3 nuclear translocation through the inhibition of Stat3 phosphorylation. These findings suggest that silibinin may serve as a potential treatment for PVR.

Expression of TXLNA in brain gliomas and its clinical significance: a bioinformatics analysis.

BACKGROUND: To analyze the expression of TXLNA in brain gliomas and its clinical significance. METHODS: Gene Expression Profiling Interactive Analysis（GEPIA）and Chinese Glioma Genome Atlas（CGGA）databases were retrieved as the methods. To assess the disparity between TXLNA expression in glioma and normal brain tissue. The Kaplan-Meier survival curve was employed to preliminarily evaluate the survival curves of the high and low expression groups, this was done for investigate the correlation between TXLNA expression level and the survival and prognosis of glioma. A Cox proportional regression risk model of multivariate nature was employed to evaluate the elements impacting the survival and prognosis of glioma. Gene pool enrichment analysis（GSEA）was used to investigate the related function of TXLNA in glioma. A Pearson correlation test and co-expression analysis were employed to identify the genes most associated with TXLNA expression. RESULT: The enrichment analysis results were observably enriched in signal pathways for instance the cell cycle and completion and coordination cascade pathways, and it is evident that high expression of TXLNA in gliomas is related to a poor survival and a bad patient prognosis, thus making it an independent prognostic factor for gliomas. Genes such as STK40 and R1MS1 are significantly correlated with TXLNA, playing a synergistic or antagonistic role. CONCLUSIONS: The prognosis of GBM patients is strongly linked to the high expression of TXLNA, which may be a viable therapeutic target for curbing cancer progression and creating new immunotherapies for GBM.

Covalent Organic Frameworks for Neuromorphic Devices.

Neuromorphic computing could enable the potential to break the inherent limitations of conventional von Neumann architectures, which has led to widespread research interest in developing novel neuromorphic memory devices, such as memristors and bioinspired artificial synaptic devices. Covalent organic frameworks (COFs), as crystalline porous polymers, have tailorable skeletons and pores, providing unique platforms for the interplay with photons, excitons, electrons, holes, ions, spins, and molecules. Such features encourage the rising research interest in COF materials in neuromorphic electronics. To develop high-performance COF-based neuromorphic memory devices, it is necessary to comprehensively understand materials, devices, and applications. Therefore, this Perspective focuses on discussing the use of COF materials for neuromorphic memory devices in terms of molecular design, thin-film processing, and neuromorphic applications. Finally, we provide an outlook for future directions and potential applications of COF-based neuromorphic electronics.

Protective effect of ginsenoside Rg1 on 661W cells exposed to oxygen-glucose deprivation/reperfusion via keap1/nrf2 pathway.

AIM: To construct an in vitro model of oxygen-glucose deprivation/reperfusion (OGD/R) induced injury to the optic nerve and to study the oxidative damage mechanism of ischemia-reperfusion (I/R) injury in 661W cells and the protective effect of ginsenoside Rg1. METHODS: The 661W cells were treated with different concentrations of Na2S2O4 to establish OGD/R model in vitro. Apoptosis, intracellular reactive oxygen species (ROS) levels and superoxide dismutase (SOD) levels were measured at different time points during the reperfusion injury process. The injury model was pretreated with graded concentrations of ginsenoside Rg1. Real-time polymerase chain reaction (PCR) was used to measure the expression levels of cytochrome C (cyt C)/B-cell lymphoma-2 (Bcl2)/Bcl2 associated protein X (Bax), heme oxygenase-1 (HO-1), caspase9, nuclear factor erythroid 2-related factor 2 (nrf2), kelch-like ECH-associated protein 1 (keap1) and other genes. Western blot was used to detect the expression of nrf2, phosphorylated nrf2 (pnrf2) and keap1 protein levels. RESULTS: Compared to the untreated group, the cell activity of 661W cells treated with Na2S2O4 for 6 and 8h decreased (P<0.01). Additionally, the ROS content increased and SOD levels decreased significantly (P<0.01). In contrast, treatment with ginsenoside Rg1 reversed the cell viability and SOD levels in comparison to the Na2S2O4 treated group (P<0.01). Moreover, Rg1 reduced the levels of caspase3, caspase9, and cytC, while increasing the Bcl2/Bax level. These differences were all statistically significant (P<0.05). Western blot analysis showed no significant difference in the protein expression levels of keap1 and nrf2 with Rg1 treatment, however, Rg1 significantly increased the ratio of pnrf2/nrf2 protein expression compared to the Na2S2O4 treated group (P<0.001). CONCLUSION: The OGD/R process is induced in 661W cells using Na2S2O4. Rg1 inhibits OGD/R-induced oxidative damage and alleviates the extent of apoptosis in 661W cells through the keap1/nrf2 pathway. These results suggest a potential protective effect of Rg1 against retinal I/R injury.

Clinical Features, Antibiotic Susceptibilities, and Outcomes of Endophthalmitis Caused by Streptococcal Infection: Children vs. Adults.

Streptococcus spp. are common causative organisms of endophthalmitis. Analysis of the clinical features, antibiotic susceptibilities, and outcomes of streptococcal endophthalmitis in children and adults may guide future management. Sixty-seven patients (67 eyes) with streptococcal endophthalmitis who were admitted to the Zhongshan Ophthalmic Center between January 2013 and December 2022 were retrospectively reviewed. The mean age was 20.7 ± 21.6 years, and 59.7% were children. Streptococcal infection accounted for 13.9% of culture-proven bacterial endophthalmitis cases; the proportion was higher in children than in adults (32.3% vs. 7.6%, p < 0.01) and increased from 8.1% in 2013-2017 to 20.1% in 2018-2022 (p < 0.01). Eye trauma was the most common etiology in both children and adults (82.5% and 66.7%, respectively). Viridans group streptococci were the most common isolates, followed by S. pneumoniae. The susceptibility rates of the streptococci to vancomycin, cefuroxime, and levofloxacin were 100%, 95.5%, and 93.0%, respectively. The overall mean best-corrected visual acuity increased from 2.74 ± 0.19 logMAR initially to 2.32 ± 0.75 logMAR at the last follow-up (p < 0.05). In conclusion, streptococcal infections have increased in cases of bacterial endophthalmitis in recent years and are more common in children. The commonly used antibiotics, vancomycin, cefuroxime, and fluoroquinolone, showed higher antibiotic susceptibility. After prompt treatment, visual outcomes improved.

Characterization of tangeretin as an activator of nuclear factor erythroid 2-related factor 2/antioxidant response element pathway in HEK293T cells.

Numerous studies have reported that tangeretin is a polymethoxylated flavone with a variety of biological activates, but little research has been done on the antioxidant mechanism of tangeretin. Hence, we investigated the effect of tangeretin on the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway and its potential molecular mechanisms by in vitro and in silico research. The results of molecular docking suggested that tangeretin bound at the top of the central pore of Kelch-like ECH-associated protein 1 (Keap1) Kelch domain, and the hydrophobic and hydrogen bond interactions contributed to their stable binding. Herein, the regulation of Nrf2-ARE pathway by tangeretin was explored in the human embryonic kidney cell line HEK293T, which is relatively easy to be transfected. Upon binding to tangeretin, Nrf2 translocated to the nucleus of HEK293T cells, which in turn activated the Nrf2-ARE pathway. Luciferase reporter gene analysis showed that tangeretin significantly induced ARE-mediated transcriptional activation. Real-time PCR and Western blot assays showed that tangeretin induced the gene and protein expressions of Nrf2-mediated targets, including heme oxygenase 1 (HO-1), nicotinamide adenine dinucleotide phosphate (NADPH) quinone dehydrogenase 1 (NQO1), and glutamate-cysteine ligase (GCLM). In addition, tangeretin could effectively scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radicals. In summary, tangeretin may be a potential antioxidant via activating the Nrf2-ARE pathway.

Increased GABAergic projections in the paraventricular nucleus regulate colonic hypersensitivity via oxytocin in a rat model of irritable bowel syndrome.

Irritable bowel syndrome (IBS) is characterized by gastrointestinal dysmotility and visceral hyperalgesia, and the impaired brain-gut axis is accepted as a crucial cause for the onset of IBS. The objective of this study is to investigate the effects of the adaptive changes in the central neural system induced by stress on IBS-like syndromes in rats. Long-term water avoidance stress (WAS) was used to prepare IBS animals. The changes in neuronal excitation and GABA expression were shown by immunohistochemistry. The mRNA and protein expressions of neurotransmitters were detected with Quantitative reverse-transcription PCR (qRT-PCR) and Enzyme-linked immunosorbent assay (ELISA). The intestinal transit time, fecal moisture content, and abdominal withdrawal reflex scores of rats were recorded to monitor intestinal motility and visceral hyperalgesia. In the WAS-treated rats with enhanced intestinal motility and visceral hypersensitivity, more GABAergic projections were found in the paraventricular nucleus (PVN) of the hypothalamus, which inhibited the firing rate of neurons and decreased the expression of oxytocin. Exogenous oxytocin improved gut motility and decreased AWR scores. The inhibition of oxytocin by the adaptive GABAergic projection in the PVN might be an important mediator of IBS, which indicates a potential novel therapeutic target.

Th17 Activation and Th17/Treg Imbalance in Prolonged Anterior Intraocular Inflammation after Ocular Alkali Burn.

Ocular alkali burn (OAB) is a sight-threatening disease with refractory ocular inflammation causing various blinding complications. Th17 lymphocytes account for the pathogeneses of the autoimmune disease and chronic inflammation, but their role in prolonged anterior intraocular inflammation after OAB is still unknown. A rat OAB model was established for this purpose. Anterior intraocular inflammation was observed in both the acute and late phases of OAB, and histological examination confirmed the presence of inflammatory cell infiltration and fibrin exudation in the anterior segment. Luminex xMAP technology and qPCR were used to evaluate the intraocular levels of cytokines. The levels of IL-1ß, IL-6, and TNF-α were significantly elevated during the acute phase. The expression of IL-17A gradually increased from day 7 onwards and remained at a relatively high level. Immunofluorescence was performed to identify Th17 cells. CD4 and IL-17A double positive cells were detected in the anterior chamber from days 7 to 28. Flow cytometry showed that the frequency of Th17 cells increased in both lymph nodes and spleen, while the frequency of Treg cells remained unchanged, resulting in an elevated Th17/Treg ratio. The present study suggests that Th17 activation and Th17/Treg imbalance account for prolonged anterior intraocular inflammation after OAB.

Lateral rectus muscle differentiation potential in paralytic esotropia patients.

PURPOSE AND BACKGROUND: Recently, we found that maximal medial rectus recession and lateral rectus resection in patients with complete lateral rectus paralysis resulted in a partial restoration of abduction. In an attempt to understand some of the mechanisms involved with this effect we examined gene expression profiles of lateral recti from these patients, with our focus being directed to genes related to myogenesis. MATERIALS AND METHODS: Lateral recti resected from patients with complete lateral rectus paralysis and those from concomitant esotropia (controls) were collected. Differences in gene expression profiles between these two groups were examined using microarray analysis and quantitative Reverse-transcription PCR (qRT-PCR). RESULTS: A total of 3056 differentially expressed genes (DEGs) were identified between these two groups. Within the paralytic esotropia group, 2081 genes were up-regulated and 975 down-regulated. The results of RT-PCR revealed that PAX7, MYOG, PITX1, SIX1 and SIX4 showed higher levels of expression, while that of MYOD a lower level of expression within the paralytic esotropia group as compared with that in the control group (p < 0.05). CONCLUSION: The decreased expression of MYOD in the paralytic esotropia group suggested that extraocular muscle satellite cell (EOMSCs) differentiation processes were inhibited. Whereas the high expression levels of PAX7, SIX1/4 and MYOG, suggested that the EOMSCs were showing an effective potential for differentiation. The stimulation resulting from muscle surgery may induce EOMSCs to differentiate and thus restore abduction function.

Surface engineering induced superstructure Ta2O5-x mesocrystals for enhanced visible light photocatalytic antibiotic degradation.

Mesocrystals are types of fascinating multifunctional materials in fabricating rapid charge transport pathways, and surface engineering could be considered as a significant influencing factor in boosting charge separation for efficient photocatalytic application. In this work, surface engineered Ta2O5-x mesocrystals were synthesized by facile alkali treatment strategy for enhanced visible light photocatalytic tetracycline degradation. The highly enhanced photocatalytic activity could be attributed to the highly increased surface areas and surface hydroxyl groups to compare with those of commercial Ta2O5 and pristine Ta2O5-x mesocrystals, which could provide more surface reactive sites and high electron density center for trapping photo-generated holes. Besides, possible tetracycline transformation pathways over surface engineered Ta2O5-x mesocrystals and visible light photocatalytic mechanism were also proposed in this work. Current work also provides a facile strategy for regulating surface property of ultrawide bandgaps semiconductors for enhanced visible light photocatalytic performance.

Lidocaine Inhibits Myoblast Cell Migration and Myogenic Differentiation Through Activation of the Notch Pathway.

PURPOSE: To assess the cellular and molecular effects of lidocaine on muscles/myoblasts. METHODS: Cultured myogenic precursor (C2C12) cells were treated with varying concentrations of lidocaine. RESULTS: Cell viability of C2C12 cells was inhibited by lidocaine in a concentration-dependent manner, with concentrations ≥0.08%, producing a dramatic reduction in cell viability. These ≥0.08% concentrations of lidocaine arrested cell cycles of C2C12 cells in the G0/G1 phase. Moreover, lidocaine inhibited cell migration and myogenic processes in C2C12 cells at low concentrations. Results from QRT-PCR assays revealed that following treatment with lidocaine, Notch1, Notch2, Hes1, Csl and Dll4 all showed higher levels of expression, while no changes were observed in Mmal1, Hey1, Dll1 and Jag1. CONCLUSION: This work provides the first description of the effects of lidocaine upon the regeneration of muscles and maintenance of satellite cells at the cellular and molecular levels. In specific, we found that the Dll4-Notch-Csl-Hes1 axis was up-regulated suggesting that the Notch signaling pathway was involved in producing these effects of lidocaine. These findings provide a new and important foundation for future investigations into the effects of drug therapies in muscle diseases.

αB-Crystallin Alleviates Endotoxin-Induced Retinal Inflammation and Inhibits Microglial Activation and Autophagy.

αB-Crystallin, a member of the small heat shock protein (sHSP) family, plays an immunomodulatory and neuroprotective role by inhibiting microglial activation in several diseases. However, its effect on endotoxin-induced uveitis (EIU) is unclear. Autophagy may be associated with microglial activation, and αB-crystallin is involved in the regulation of autophagy in some cells. The role of αB-crystallin in microglial autophagy is unknown. This study aimed to explore the role of αB-crystallin on retinal microglial autophagy, microglial activation, and neuroinflammation in both cultured BV2 cells and the EIU mouse model. Our results show that αB-crystallin reduced the release of typical proinflammatory cytokines at both the mRNA and protein level, inhibited microglial activation in morphology, and suppressed the expression of autophagy-related molecules and the number of autophagolysosomes in vitro. In the EIU mouse model, αB-crystallin treatment alleviated the release of ocular inflammatory cytokines and the representative signs of inflammation, reduced the apoptosis of ganglion cells, and rescued retinal inflammatory structural and functional damage, as evaluated by optical coherence tomographic and electroretinography. Taken together, these results indicate that αB-crystallin inhibits the activation of microglia and supresses microglial autophagy, ultimately reducing endotoxin-induced neuroinflammation. In conclusion, αB-crystallin provides a novel and promising option for affecting microglial autophagy and alleviating symptoms of ocular inflammatory diseases.

METTL3 attenuates proliferative vitreoretinopathy and epithelial-mesenchymal transition of retinal pigment epithelial cells via wnt/ß-catenin pathway.

Proliferative vitreoretinopathy (PVR) is a refractory vitreoretinal fibrosis disease, and epithelial-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells is the key pathological mechanism of PVR. However, few studies focused on the role of METTL3, the dominating methyltransferase for m6A RNA modification in PVR pathogenesis. Immunofluorescence staining and qRT-PCR were used to determine the expression of METTL3 in human tissues. Lentiviral transfection was used to stably overexpress and knockdown METTL3 in ARPE-19 cells. MTT assay was employed to study the effects of METTL3 on cell proliferation. The impact of METTL3 on the EMT of ARPE-19 cells was assessed by migratory assay, morphological observation and expression of EMT markers. Intravitreal injection of cells overexpressing METTL3 was used to assess the impact of METTL3 on the establishment of the PVR model. We found that METTL3 expression was less in human PVR membranes than in the normal RPE layers. In ARPE-19 cells, total m6A abundance and the METTL3 expression were down-regulated after EMT. Additionally, METTL3 overexpression inhibited cell proliferation through inducing cell cycle arrest at G0/G1 phase. Furthermore, METTL3 overexpression weakened the capacity of TGFß1 to trigger EMT by regulating wnt/ß -catenin pathway. Oppositely, knockdown of METTL3 facilitated proliferation and EMT of ARPE-19 cells. In vivo, intravitreal injection of METTL3-overexpressing cells delayed the development of PVR compared with injection of control cells. In summary, this study suggested that METTL3 is involved in the PVR process, and METTL3 overexpression inhibits the EMT of ARPE-19 cells in vitro and suppresses the PVR process in vivo.

High-Performance Perovskite Solar Cells Based on NaCsWO3@ NaYF4@NaYF4:Yb,Er Upconversion Nanoparticles.

Extending photoelectric response to the near-infrared (NIR) region using upconversion luminescent (UCL) materials is one promising approach to obtain high-efficiency perovskite solar cells (PSCs). However, challenges remain due to the shortage of highly efficient UCL materials and device structure. NaCsWO3 nanocrystals exhibit near-infrared absorption arising from the local surface plasmon resonance (LSPR) effect, which can be used to boost the UCL of rare-earth-doped upconversion nanoparticles (UCNPs). In this study, using NaCsWO3 as the LSPR center, NaCsWO3@NaYF4@NaYF4:Yb,Er nanoparticles were synthesized and the UCL intensity could be enhanced by more than 124 times when the amount of NaCsWO3 was 2.8 mmol %. Then, such efficient UCNPs were not only doped into the hole transport layer but also used to modify the perovskite film in PSCs, resulting in the highest power conversion efficiency (PCE) reaching 18.89% (that of the control device was 16.01% and the PCE improvement was 17.99%). Possible factors for the improvement of PSCs were studied and analyzed. It is found that UCNPs can broaden the response range of PSCs to the NIR region due to the LSPR-enhanced UCL and increase the visible light reabsorption of PSCs due to the scattering and reflection effect, which generate more photocurrent in PSCs. In addition, UCNPs modify the perovskite film by effectively filling the holes and gaps at the grain boundary and eliminating the perovskite surface defects, which lead to less carrier recombination and then effectively improve the performance of PSC devices.

Flavonoids Sophoranone Promotes Differentiation of C2C12 and Extraocular Muscle Satellite Cells.

INTRODUCTION: Paralytic strabismus involves a functional loss of extraocular muscles resulting from muscular or neuronal disorders. Currently, only a limited number of drugs are available for functional repair of extraocular muscles. Here, we investigated the effects of a novel drug, flavonoids sophoranone, on the differentiation of extraocular muscles as assessed in bothin vivo and in vitro models. MATERIALS AND METHODS: The effect of flavonoids sophoranone on C2C12 cells was examinedin vitro as evaluated with use of apoptosis, reactive oxygen species (ROS), and cell viability assays. Then, both in vivo and in vitro effects of this drug were examined on the differentiation of C2C12 and satellite cells within extraocular muscles in rabbits. For these latter experiments, RT-PCR and Western blot assays were used to determine expression levels of markers for myogenic differentiation. RESULTS: With use of flavonoids sophoranone concentrations ranging from 0 to 10 µM, no effects were observed upon cell apoptosis, ROS, and cell cycle in C2C12 cells. Based on MTT assay results, flavonoids sophoranone was shown to increase C2C12 cell proliferation. Moreover, flavonoids sophoranone promoted the differentiation of C2C12 and satellite cells within extraocular muscles in rabbits, which were verified as based on cell morphology and expression levels of mRNA and protein markers of myogenic differentiation. Finally, flavonoids sophoranone treatment also increased gene expressions of Myh3, Myog, and MCK. CONCLUSION: The capacity for flavonoids sophoranone to upgrade the differentiation of both C2C12 and satellite cells within extraocular muscles in rabbits at concentrations producing no adverse effects suggest that this drug may provide a safe and effective means to promote repair of damaged extraocular muscles.

m6A methyltransferase METTL3 promotes retinoblastoma progression via PI3K/AKT/mTOR pathway.

Retinoblastoma (RB) is a common intraocular malignancy in children. Due to the poor prognosis of RB, it is crucial to search for efficient diagnostic and therapeutic strategies. Studies have shown that methyltransferase-like 3 (METTL3), a major RNA N (6)-adenosine methyltransferase, is closely related to the initiation and development of cancers. Nevertheless, whether METTL3 is associated with RB remains unexplored. Therefore, we investigated the function and mechanisms of METTL3 in the regulation of RB progression. We manipulated METTL3 expression in RB cells. Then, cell proliferation, apoptosis, migration and invasion were analysed. We also analysed the expression of PI3K/AKT/mTOR pathway members. Finally, we incorporated subcutaneous xenograft mouse models into our studies. The results showed that METTL3 is highly expressed in RB patients and RB cells. We found that METTL3 knockdown decreases cell proliferation, migration and invasion of RB cells, while METTL3 overexpression promotes RB progression in vitro and in vivo. Moreover, two downstream members of the PI3K/AKT/mTOR pathway, P70S6K and 4EBP1, were affected by METTL3. Our study revealed that METTL3 promotes the progression of RB through PI3K/AKT/mTOR pathways in vitro and in vivo. Targeting the METTL3/PI3K/AKT/mTOR signalling axis could be a promising therapeutic strategy for the treatment of RB.

Changing Trends in Firework-Related Eye Injuries in Southern China: A 5-Year Retrospective Study of 468 Cases.

Firework-related eye injury is a horrible medical problem and creates huge health and social burdens. Herein, we explored the changing trends and demographic and clinical features of firework-related eye injury, in an effort to inform strategies to prevent this injury. We reviewed the data of 468 hospitalized patients who underwent surgery for firework-related eye injury at the Zhongshan Ophthalmic Center between January 2013 and December 2017. During this period, the trend in firework-related eye injuries was stable (mean, 93 ± 14 cases per year), and fireworks were the major cause of explosive eye injury. The average age of the patients was 24 ± 18 years and 87% of the patients were male, with boys under 10 years of age comprising the largest group (27% of patients). There were an average of 24 ± 7 cases per year from urban areas and 70 ± 8 cases from rural areas (P < 0.05). Furthermore, 21 ± 5% of cases occurred during Spring Festival. After treatment, the best corrected visual acuity was increased compared to that before treatment, and the intraocular pressure tended to become normal by the final visit (P < 0.05). The top three diagnoses were cataract (39%), retinal detachment (18%), and choroidal detachment (14%). Additionally, the most common surgery was cataract extraction (25%), followed by pars plana vitrectomy (19%) and pars plana vitrectomy plus pars plana lensectomy (10%). Over the five-year study period, day surgery hospitalization increased from 1% to 32%. This was associated with a corresponding decrease in the length of hospitalization, without adverse events, demonstrating that day surgery is feasible in firework-related eye injury cases. The present study results suggest that greater attention should be paid to firework-related eye injury, and a variety of measures should be taken to prevent this kind of ocular tragedy.

Curcumin Inhibits Proliferation and Epithelial-Mesenchymal Transition in Lens Epithelial Cells through Multiple Pathways.

BACKGROUND: Posterior capsule opacification (PCO), a complication of extracapsular lens extraction surgery that causes visual impairment, is characterized by aberrant proliferation and epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). Curcumin, exerting inhibitive effects on cell proliferation and EMT in cancer, serves as a possible antidote towards PCO. METHODS: Cellular proliferation of LECs after treatment of curcumin was measured with MTT assay and flow cytometry. The transcriptional and expressional levels of proteins related to proliferation and EMT of LECs were quantified by western blotting and real-time PCR. RESULTS: Curcumin was found to suppress the proliferation of LECs by inducing G2/M arrest via possible inhibition of cell cycle-related proteins including CDK1, cyclin B1, and CDC25C. It had also inactivated proliferation pathways involving ERK1/2 and Akt pathways in LECs. On the other hand, curcumin downregulated the EMT of LECs through blocking the TGF-ß/Smad pathway and interfering Notch pathway which play important roles in PCO. CONCLUSIONS: This study shows that curcumin could suppress the proliferation and EMT in LECs, and it might be a potential therapeutic protection against visual loss induced by PCO.

Visible light photocatalysis of amorphous Cl-Ta2O5-x microspheres for stabilized hydrogen generation.

Harvesting broad spectral absorption and visible light photocatalysis of ultrawide bandgap semiconductors are one of most significative topics in the solar energy conversion and utilization fields. In this work, amorphous Cl-Ta2O5-x microspheres were prepared by facile solvothermal method for stabilized visible light photocatalytic hydrogen generation. The acetone absorbed on the interfaces of Ta2O5 nanoparticles induced the formation of oxygen vacancies, enhanced visible light absorption, and formation of Ta2O5-x microspheres with preferred orientations as well as Cl doping. The Cl-Ta2O5-x microspheres showed typical amorphous characteristics and obvious visible light absorption in comparison to those of commercial Ta2O5. More importantly, the prepared Cl-Ta2O5-x microspheres also showed stabilized visible light photocatalytic hydrogen generation performance in the spectral regions of 400 nm ≤ λ ≤ 600 nm mainly because of the introduction of oxygen vacancy defects and Cl doping, which might significantly expand the application of tantalum oxide semiconductors in the broad spectral photocatalytic water splitting.