Improvement of UCVA, BCVA, and Intraocular Pressure after Phakic Posterior Chamber Intraocular Lens Implantation for Myopia.

Objective: The purpose of this study is to explore the artificial lens planting of the back room shape of the crystal eye eyes and The clinical effect of ICL in patients with myopia. Methods: A Retrospective Study Spanning from 2021 to 2023 within Huai'an First People's Hospital. This study involves the comparative analysis of 100 eyes subjected to 'Crystalline Lens Extraction + IOL' and 100 eyes undergoing 'ICL' treatment. We evaluate various postoperative parameters, including near and distant visual acuity, Visual Acuity (CVA), Best-Corrected Visual Acuity (BCVA), refractive outcomes, endothelial cell count, glare sensitivity, and the incidence of macular edema. The control group underwent Crystalline Lens Extraction + IOL, and the observation group underwent 'ICL' treatment. Visual acuity recovery, intraocular pressure, endothelial cell count, adverse reactions, and therapeutic effect were compared between the two groups. Results: The CVA before treatment and the IOP and endothelial cell count before and after treatment in the observation group were similar to those in the control group, and the differences were not statistically significant (P > .05). The CVA, BCVA, and refraction after treatment in the observation group were all higher than those in the control group, and the differences were statistically significant (P < .05). The number of people with significant and effective treatment effects in the observation group (total effective rate 98.00%) was higher than that in the control group (82.00%), and the difference was statistically significant (P < .05). Conclusions: The implantation of 'ICL' treatment in cases of myopia demonstrates favorable surgical outcomes in clinical practice. It effectively enhances postoperative visual function recovery while minimizing the risk of adverse reactions. The ICL implantation procedure is irreplaceable in the treatment of myopia.

Reduced graphene oxide-wrapped ZnS-SnS2 heterojunction bimetallic hollow cubic boxes as high-magnification and long lifespan supercapacitor anode materials.

Metal sulfides have attracted extensive attention due to their excellent electrochemical performance. However, issues such as poor conductivity and severe volume expansion during charge and discharge processes affect the applications of sulfides as electrode materials. Here, a combination of coprecipitation and high-temperature sulfidation methods are employed to synthesize a ZnS-SnS2 composite with a hollow cubic structure, which is further composited with reduced graphene oxide (RGO) to form ZnS-SnS2 hollow cubic boxes encapsulated in a conductive framework of reduced graphene oxide (RGO) (denoted as ZnS-SnS2@RGO) for electrode materials. The hollow structure effectively alleviates the pulverization of ZnS-SnS2@RGO caused by volume expansion during charge and discharge processes. The heterogeneous structure formed by ZnS and SnS2 effectively reduces the electron transfer resistance of the material. The use of RGO wrapping enhances the conductivity of the ZnS-SnS2 hollow cubic boxes, and RGO's dispersion effect on the ZnS-SnS2 cubes improves particle agglomeration, further mitigating volume expansion of the material. These results indicate the outstanding electrochemical performance of heterostructural ZnS-SnS2 hollow cubic electrodes encapsulated with reduced graphene oxide as a conductive framework. The fabrication process provides a novel approach for addressing volume expansion and poor conductivity issues in other pseudocapacitive materials.

Analysis of the Macular Region Following Panretinal Photocoagulation for the Treatment of Diabetic Retinopathy Using Optical Coherence Tomography.

Background: Diabetic retinopathy (DR) is the most prevalent microvascular complication of diabetes. Panretinal photocoagulation (PRP) is the established treatment for mitigating severe visual impairment resulting from proliferative DR. Objective: This study aims to investigate the impact of PRP on the macular region in patients with DR, utilizing optical coherence tomography (OCT) for assessment. Design: An experimental study was meticulously designed, implementing PRP as the primary intervention. Setting: The investigation was conducted within the Department of Ophthalmology at the Affiliated Huaian No.1 People's Hospital, Huai'an, Jiangsu, China. Participants: A total of 120 participants diagnosed with DR and undergoing treatment at our hospital were enrolled in the study. Interventions: The participants were randomly assigned to either the control group (CG, n = 60) or the study group (SG, n = 60). The CG received conventional drug treatment involving oral iodized lecithin, while the SG received PRP. OCT was employed to monitor changes in macular fovea volume and macular retinal thickness. Primary Outcome Measures: Evaluation criteria encompassed clinical efficacy, macular fovea volume, macular retinal thickness, IL-6 and VEGF levels, incidence of adverse reactions, and quality of life in both groups. Results: The study resulted in a higher total effective rate in the SG (96.67%) compared to the CG (80.00%) (χ2 = 8.09, P < .05). Post-treatment, reductions were observed in macular fovea volume and macular retinal thickness, with significantly lower SG values than CG values (P < .05). Both serum IL-6 and VEGF levels exhibited reductions in both groups after treatment, with the SG displaying a more significant decrease compared to the CG (P < .05). The occurrence of adverse reactions significantly decreased in the SG relative to the CG (P < .05). Quality of life scores for the SG was notably elevated compared to the CG (P < .05). Conclusions: PRP emerges as a highly valuable approach in the management of DR. It contributes to retinal thickness improvement within the macular region and inflammation reduction, and also enhances therapeutic outcomes, minimizes adverse reactions, and optimizes patients' quality of life. These findings warrant further clinical adoption and widespread promotion.

Circ_0047835 Combines with miR-144-3p to Promote the Proliferation, Invasion, Migration, and Fibrosis of TGF-ß1-Treated Human Tenon's Capsule Fibroblasts by Upregulating SP1.

PURPOSE: Glaucoma is the leading cause of blindness worldwide with complex pathogenesis. Circular RNAs (circRNAs) play critical roles in various diseases, including glaucoma. The purpose of this study was to investigate the role of circ_0047835 and underlying mechanisms in the development of fibrosis after glaucoma filtration surgery. METHODS: Human Tenon's capsule fibroblasts (HTFs) were stimulated using transforming growth factor-ß1 (TGF-ß1) to mimic a cellular model of glaucoma in vitro. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) assay and 5-ethynyl-2'-deoxyuridine (EdU) assay. Cell invasion and migration were detected by transwell assay and wound healing assay, respectively. Western blot assay was used to measure protein levels. The expression levels of circ_0047835, microRNA-144-3p (miR-144-3p) and specific protein 1 (SP1) mRNA were determined by real-time quantitative polymerase chain reaction (RT-qPCR). The interaction between miR-144-3p and circ_0047835 or SP1 was confirmed by dual-luciferase reporter assay and RNA Immunoprecipitation (RIP) assay. RESULTS: Circ_0047835 expression was elevated in glaucoma tissues and TGF-ß1-treated HTFs. Circ_0047835 or SP1 knockdown suppressed the proliferation, migration, invasion, and fibrosis of TGF-ß1-treated HTFs. MiR-144-3p was a target of circ_0047835, and miR-144-3p inhibition reversed the effects of circ_0047835 knockdown in TGF-ß1-treated HTFs. Moreover, SP1 was identified as a target of miR-144-3p, and miR-144-3p overexpression weakened TGF-ß1-induced proliferation, migration, invasion, and fibrosis by targeting SP1 in HTFs. Furthermore, circ_0047835 combined with miR-144-3p to regulate SP1 expression. CONCLUSION: Circ_0047835 might contribute to fibrosis progression after glaucoma surgery by regulating the miR-144-3p/SP1 axis.

Down-Regulation of circCOL1A2 Suppresses the Dysfunction of Diabetes-Related Retinal Microvascular Endothelial Cells via miR-646/FGF7 Axis.

PURPOSE: Diabetic retinopathy (DR), the major complication of diabetes, is the leading cause of vision loss and blindness globally. Altered circular RNAs (circRNAs) expression has been found to be involved in DR process. Hence, this work aimed to explore the role and mechanism of circCOL1A2 in DR. METHODS: Human retinal microvascular endothelial cells (RMECs) treated with high glucose (HG) were used for functional analysis. Levels of genes and proteins were detected using quantitative real-time polymerase chain reaction and western blotting. In vitro experiments were conducted by transwell, tube formation, CCK-8 assays and ELISA, respectively. The binding interaction between miR-646 and circCOL1A2 or FGF7 (Fibroblast Growth Factor 7) was confirmed using dual-luciferase reporter and RNA immunoprecipitation assays. RESULTS: CircCOL1A2 was highly expressed in retinal tissues of DR patients and HG-induced RMECs. Then RMECs were exposed to HG treatment to mimic the diabetic conditions in vitro. Functionally, circCOL1A2 knockdown attenuated HG-evoked RMEC migration, proliferation, angiogenesis, blood-retina barrier (BRB) injury and inflammation. Mechanistically, circCOL1A2 functioned as a sponge for miR-646, and miR-646 directly targeted FGF7. Further rescue experiments showed that miR-646 inhibition abated the protective effects of circCOL1A2 knockdown on RMEC function under HG treatment. Besides that, miR-646 was decreased in HG-induced RMECs, re-expression of miR-646 reversed HG-evoked RMEC dysfunction, which was rescued by FGF7 overexpression. CONCLUSION: CircCOL1A2 silencing can suppress HG-induced migration, proliferation, angiogenesis, BRB injury and inflammation in RMECs through miR-646/FGF7 axis, suggesting the potential involvement of circCOL1A2 in DR process.

Analysis of Improvement Time and Influencing Factors of Diplopia after Intermittent Exotropia in Children.

Objective: To observe and analyze the occurrence rate, improvement time, and influencing factors of diplopia after intermittent exotropia in children. Methods: A total of 135 children with intermittent exotropia treated in our hospital from February 2019 to April 2021 were recruited. A reasonable surgical plan was exerted according to the preoperative examination of the children, the children were divided into groups according to their age, degree of strabismus, visual acuity, and binocular visual function, and the postoperative diplopia occurrence rate and improvement time of diplopia in different groups were observed and compared. Results: Postoperative diplopia occurred in 74 of 135 children with intermittent exotropia, and the postoperative incidence of diplopia was 54.81%. All diplopia occurred on the first day after the operation. There were 62 cases of contradictory diplopia (83.78%) and 12 cases of fusion of powerless diplopia (16.22%). Except for 1 case of amalgamated powerless diplopia, diplopia was not significantly improved after 6 months, which seriously affected the life of the children after the second operation, and all the others were significantly improved within 90 days. The improvement time of diplopia was 3-90 days, and the average improvement time of diplopia was 13.25 ± 3.16 days. According to their age, the children were divided into the 3-6 years old group (n = 69), the 7-10 years old group (n = 47), and the 11-14 years old group (n = 19). Postoperative diplopia occurred in 25 cases (36.23%) in the 3-6 years old group, 34 cases (72.34%) in the 7-10 years old group, and 16 cases (84.21%) in the 11-14 years old group. There was a significant difference in the incidence of postoperative diplopia among the three groups (P < 0.05). There was a significant difference in the improvement time of diplopia among the three groups (P < 0.05). According to the degree of strabismus before the operation, the children were divided into the <50△ group (n = 74) and the ≥50△ group (n = 61). Postoperative diplopia occurred in 32 cases (43.24%) in the <50△ group and 43 cases (70.49%) in the ≥50△ group. There was a significant difference in the incidence of postoperative diplopia between the two groups (P < 0.05). There was a significant difference in the improvement time of diplopia among the three groups (P < 0.05). According to the results of the visual acuity examination, the patients were divided into the ≥0.8 (naked eye) group (n = 21), the ≥0.8 (ametropia) group (n = 32), and the <0.8 (amblyopia) group (n = 32). Among them, diplopia occurred in 10 cases (47.62%) in the ≥0.8 (naked eye) group, 40 cases (48.78%) in the ≥0.8 (ametropia) group, and 24 cases (75.00%) in the <0.8 (amblyopia) group. The incidence of diplopia in the <0.8 (amblyopia) group was significantly higher than that in the ≥0.8 (naked eye) group and the ≥0.8 (ametropia) group, and the difference was statistically significant (P < 0.05). The postoperative diplopia improvement time in the <0.8 (amblyopia) group was significantly higher than that in the ≥0.8 (naked eye) group and the ≥0.8 (ametropia) group, and the difference was statistically significant (P < 0.05). There was no significant difference in diplopia occurrence rate and diplopia improvement time between the ≥0.8 (naked eye) group and the ≥0.8 (ametropia) group (P > 0.05). According to the results of binocular visual function examination, 92 cases had a primary function, 45 cases (48.91%) had diplopia after the operation, the average recovery time of diplopia was 12.58 ± 3.16, 43 cases had no primary function, and 30 cases (69.77%) had diplopia after the operation. The average recovery time of diplopia was 13.02 ± 3.84. There was a significant difference in the incidence of diplopia between the two groups (χ 2 = 5.162). There was no significant difference in the recovery time of diplopia between the two groups (χ 2 = 0.570, P < 0.05). In 80 cases with secondary function, diplopia occurred in 36 cases (45.00%), and the average recovery time of diplopia was 10.14 ± 2.88; in 55 cases without secondary function, diplopia occurred in 39 cases (70.91%), and the average recovery time of diplopia was 14.86 ± 3.73. There was a significant difference in the incidence of diplopia between the two groups (χ 2 = 8.861, P < 0.002). There was a significant difference in the recovery time of diplopia between the two groups (χ 2 = 6.469, P < 0.001). In 77 cases with tertiary function, diplopia occurred in 32 cases (41.56%), and the average recovery time of diplopia was 9.61 ± 2.39; in 58 cases without tertiary function, diplopia occurred in 43 cases (74.14%), and the average recovery time of diplopia was 13.11 ± 3.05. There was a significant difference in the incidence of diplopia between the two groups (χ 2 = 14.221 P < 0.001). There was a significant difference in the recovery time of diplopia between the two groups (χ 2 = 5.355, P < 0.001). Conclusions: The age, degree of strabismus, visual acuity, and binocular visual function of children with intermittent exotropia are significant factors affecting the occurrence rate and recovery time of diplopia after the operation. The younger the age, the smaller the degree of strabismus, the better the vision and the second or third grade of visual function, the smaller the occurrence rate of diplopia, and the shorter the recovery time of diplopia. Thus, the above influencing factors have a certain guiding significance in predicting the improvement of postoperative diplopia and the time of diplopia disappearance. The purpose of intermittent exotropia surgery in children is not only to correct eye position and improve appearance but also to establish normal retinal correspondence in order to obtain binocular monocular function. Furthermore, postoperative diplopia in children with concomitant exotropia is very common; therefore, careful examination, comprehensive analysis, and surgical plan should be designed according to the above factors. Stereoscopic vision training as early as possible after the operation is beneficial to the establishment of normal retinal correspondence and the elimination of diplopia.

Three-dimensional graphene encapsulated hollow CoSe2-SnSe2nanoboxes for high performance asymmetric supercapacitors.

Construction of metal selenides with a large specific surface area and a hollow structure is one of the effective methods to improve the electrochemical performance of supercapacitors. However, the nano-material easily agglomerates due to the lack of support, resulting in the loss of electrochemical performance. Herein, we successfully design a three-dimensional graphene (3DG) encapsulation-protected hollow nanoboxes (CoSe2-SnSe2) composite aerogel (3DG/CoSe2-SnSe2) via a co-precipitation method coupled with self-assembly route, followed by a high temperature selenidation strategy. The obtained aerogel possesses porous 3DG conductive network, large specific surface area and plenty of reactive active sites. It could be used as a flexible and binder-free electrode after a facile mechanical compression process, which provided a high specific capacitance of 460 F g-1at 0.5 A g-1, good rate capability of 212.7 F g-1at 10 A g-1The capacitance retention rate is 80% at 2 A g-1after 5000 cycles due to the fast electron/ion transfer and electrolyte diffusion. With the as-prepared 3DG/CoSe2-SnSe2as positive electrodes and the AC (activated carbon) as negative electrodes, an asymmetric supercapacitor (3DG/CoSe2-SnSe2//AC) was fabricated, which delivered a high specific capacity of 38 F g-1at 1 A g-1and an energy density of 11.89 Wh kg-1at 749.9 W kg-1, as well as excellent cycle stability. This work provides a new method for preparing electrode material.

Design, synthesis and biological evaluation of a novel spiro oxazolidinedione as potent p300/CBP HAT inhibitor for the treatment of ovarian cancer.

Histone acetylation is one of the most essential parts of epigenetic modification, mediating a variety of complex biological functions. In these procedure, p300/CBP could catalyze the acetylation of lysine 27 on histone 3 (H3K27ac), and had been reported to mediate tumorigenesis and development in a variety of tumors by enhancing chromatin transcription activity. Ovarian cancer, as an extremely malignant tumor, has also been observed to undergo abnormal acetylation of histones. However, whether the treatment of ovarian cancer could be achieved by inhibiting the acetylation activity of p300/CBP on H3K27 has not been well investigated. In this article, we modified the structure of p300/CBP HAT domain inhibitor A-485 and obtained a highly active small molecule known as 13f, which has an IC50 value of 0.49 nM for inhibiting the in vitro enzyme activity of p300, as well as the anti-proliferation IC50 value on ovarian cancer cell line OVCAR-3 was 153 nM. In addition, 13f had strong acetylase family selectivity, good metabolic stability and promising in vivo anti-tumor activity in OVCAR-3 xenograft model. The discovery of 13f revealed a more active chemical entity of the HATs domain of p300/CBP and provided a novel idea for the application of epigenetic inhibitors in the treatment of ovarian cancer.

5'-Epi-SPA-6952A, a new insecticidal 24-membered macrolide produced by Streptomyces diastatochromogenes SSPRC-11339.

A new 24-membered macrolide, 5'-epi-SPA-6952A (1), was isolated from the cultured broth of Streptomyces diastatochromogenes. The structure was elucidated by means of spectroscopic methods and comparing with literature data of the known 24-membered macrolide SPA-6952A. Compound 1 was found to show significant insecticidal activity against oriental armyworm(Mythimna separata Walker) with LC50 value of 10.26 mg/L.

PF-06409577 activates AMPK signaling to protect retinal pigment epithelium cells from UV radiation.

Ultra-violet (UV) radiation (UVR) to human retinas induces oxidative injury to the resident retinal pigment epithelium (RPE) cells. PF-06409577 a novel, potent and direct AMP-activated protein kinase (AMPK) activator. In ARPE-19 cells and primary murine RPE cells, PF-06409577 significantly inhibited UVR-induced viability reduction, cell death and apoptosis. PF-06409577 activated AMPK signaling in RPE cells by increasing AMPKα1-acetyl-CoA carboxylase phosphorylation and AMPK activity. AMPK inhibition, by AMPKα1-shRNA, -CRISPR/Cas9 knockout or -T172A dominant negative mutation, almost abolished PF-06409577-induced RPE cytoprotection against UVR. PF-06409577 enhanced nicotinamide adenine dinucleotide phosphate (NADPH) activity and expression levels of Nrf2-dependent genes in RPE cells. Furthermore, UVR-induced reactive oxygen species (ROS) production, lipid peroxidation and DNA damage were largely inhibited by the AMPK activator. In summary, PF-06409577 inhibits UVR-induced oxidative stress and RPE cell death by activating AMPK signaling.

Cytotoxic effects of Avermectin on human HepG2 cells in vitro bioassays.

Avermectin (AVM) has been widely used in agriculture and animal husbandry based on its broad spectrum of effective anthelmintic activity and specificity targets. However, AVM induction of cytotoxicity in human liver is largely unknown. In this study, we investigate the cytotoxic effects of AVM on HepG2 cells in vitro. The results revealed that AVM inhibited the viability of HepG2 cells and enhanced apoptosis. Established assays of cytotoxicity were performed to characterize the mechanism of AVM toxicity on HepG2 cells. Typical apoptosis morphological changes were shown in AVM-treatment cells including chromatin condensation and DNA fragmentation. We demonstrated that AVM-induced apoptosis of HepG2 cells were mediated by generated ROS. Moreover, a decrease in mitochondrial membrane potential (MMP) and up-regulating the Bax/Bcl-2 ratio, resulted in a release of cytochrome-c as well as activation of caspase-9/-3. In conclusion, our experimental results show that AVM has a potential threat to human health which may be induce apoptosis of human hepatocyte cells via caspase-dependent mitochondrial pathways.

Tebufenozide induces G1/S cell cycle arrest and apoptosis in human cells.

Tebufenozide is a non-steroidal insect growth regulator and is extensively used to control pests, although it is considered to be safe for mammals and environmentally friendly. However, previous studies have found that tebufenozide is cytotoxic to man, although the exact mechanism remains elusive. This study will investigate the apoptotic molecular mechanisms which result from tebufenozide-induced DNA damage in HeLa cells. Our results demonstrate that tebufenozide could trigger arrest in G1/S phase related to a downregulation of cyclin E and cyclin-dependent kinase (CDK) 2 protein. In addition, Western blotting showed apoptosis was associated with the upregulation of p53, Bax and cleaved-PARP, as well as downregulation of Bcl-2 and PARP. Tebufenozide also regulated changes in mitochondrial permeability and reduced mitochondrial number and intracellular ATP production. Briefly, these results suggest that tebufenozide- induces cell cycle arrest and apoptosis through activating p53 protein in a Bax- and Bcl-2-triggered mitochondrial pathway. This work provides some scientific context for the safe use of tebufenozide in agriculture.