The aim of this study was to investigate the effect of femtosecond laser-assisted cataract surgery (FLACS) on tear film and ocular surface function. Patients with age-related cataract who underwent phacoemulsification (phaco) in Air Force Aviation Medicine Research Institute Affiliation Hospital from January 2016 to December 2016 were randomly divided into two groups. Patients in experimental group (n=123, 150 eyes) received FLACS, while patients in phaco group (n=110, 150 eyes) underwent conventional coaxial micro-incision phaco and were implanted with foldable intraocular lens (IOL). Our results showed that there were no statistically significant differences in general conditions between the two groups. Ocular surface disease index (OSDI) and corneal fluorescein staining (CFS) scores of patients in both groups after operation were significantly increased compared with those before operation, but breakup time (BUT) and Schirmer's I test scores decreased significantly at 1 week after operation compared with those before operation and basically returned to preoperative baseline levels at 3 months after operation. CFS scores and OSDI in the FLACS group at 1 day and 1 week after operation were increased more significantly than those in the phaco group, but there were no statistically significant differences at 3 months after operation. The above results showed that the effect on ocular surface function in the FLACS group after operation was greater than that in the phaco group, and the dry eye symptoms in the FLACS group were more obvious after operation. Both FLACS and conventional phaco have certain effects on the ocular surface function of patients, and there are statistically significant differences only in the early stage. FLACS has greater effects on CFS and dry eye symptoms.
Pre-eclampsia is a serious multisystem disorder and causes significant increase in both maternal and foetal morbidity and perinatal mortality globally. Due to the limited understanding of the molecular mechanism of pre-eclampsia, the current study conducted bioinformatic analyses to screen key regulators involved in pre-eclampsia. The gene expression profiling dataset GSE44711 containing 8 early-onset pre-eclampsia placentas and 8 gestational-age-matched control placentas was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were screened by limma software package, which were then subjected to Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis on the Database for Annotation, Visualization, and Integrated Discovery website. Finally, protein-protein interaction network was constructed using the Search Tool for the Retrieval of Interacting Genes database. In total, 192 DEGs including 106 upregulated and 86 downregulated genes were obtained. Proteoglycan 2 and podoplanin were the most significantly up- and downregulated genes, respectively. In addition, three potential pathways and their related DEGs: spermidine/spermine N1-acetyltransferase 1, amiloride-binding protein 1 and adenosylmethionine decarboxylase 1 were associated with arginine and proline metabolism. Vascular endothelial growth factor C; phosphatidylinositol-4, 5-bisphosphate 3-kinase, catalytic subunit beta; collagen, type I, alpha 1 (COL1A1); and fibronectin 1 (FN1) were associated with focal adhesion. COL6A1 as well as COL1A1 and FN1 were involved in extra-cellular matrix-receptor interaction. The current study identified several potential genes and three pathways which may be considered as candidate targets for diagnosis and therapy of pre-eclampsia.
Background: This study aimed to identify and evaluate potential molecular targets associated with the development of proliferative diabetic retinopathy (DR). Methods: The microarray dataset "GSE60436" generated from fibrovascular membranes (FVMs) associated with proliferative DR was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) from the active FVMs and control or inactive FVMs and control were evaluated and co-DEGs were identified using VEEN analysis. Functional enrichment analysis, and protein-protein interactions (PPI) network and module analyses were performed on the upregulated and downregulated coDEGs. Finally, several predictions regarding microRNAs (miRNAs) and transcription factors (TFs) were made to construct a putative TF-miRNA-target network. Results: A total of 1475 co-DEGs were screened in active/inactive FVM samples, including 461 upregulated and 1014 downregulated genes, which were enriched for angiogenesis [Hypoxia Inducible Factor 1 Subunit Alpha (HIF1A) and Placental Growth Factor (PGF)] and visual perception, respectively. In the case of the upregulated co-DEGs, Kinesin Family Member 11 (KIF11), and BUB1 Mitotic Checkpoint Serine/Threonine Kinase (BUB1) exhibited the highest values in both the PPI network and module analyses, as well as the genes related to mitosis. In the case of downregulated co-DEGs, several G protein subunits, including G Protein Subunit Beta 3 (GNB3), exhibited the highest values in both the PPI network and module analyses. The genes identified in the module analysis were found to be from the signal transduction-related pathways. In addition, we were able to identify four miRNAs and five TFs, including miR-136 and miR-374. Conclusions: In brief, HIF1A, PGF, KIF11, G protein subunits, and miR-136, miR-374 may all be involved in angiogenesis, retinal endothelial cell proliferation, and visual signal transduction in proliferative DR. This study provides a number of novel insights that may aid the development of future studies dedicated to discovering novel therapeutic targets in proliferative DR.
The purpose of the present study was to investigate the molecular mechanisms of myotonic dystrophy (DM) 1 and 2 cataracts using bioinformatics methods. A microarray dataset (E-MEXP-3365) downloaded from the Array Express database included lens epithelial samples of DM1 and DM2 cataract patients (n=3/group) and non-DM lens epithelial samples as a control (n=4). Differentially expressed genes (DEGs) were identified between DM1 and control samples, and between DM2 and control samples. Pathway enrichment analyses were performed for the DEGs. Potential micro (mi)RNAs regulating these DEGs were predicted. An miRNA-target gene network was constructed for DM1 and DM2. The study identified 223 DEGs in DM1, and 303 DEGs in DM2. DM1 and DM2 shared 172 DEGs. The DEGs in DM1 were enriched with calcium, Wnt and axon guidance signaling pathways. The DEGs in DM2 were linked by adherens junction signaling pathways. miRNA (miR)-197, miR-29b and miR-29c were included in the network modules of DM1. miR-197, miR-29c and miR-29a were involved in the network modules of DM2. It is therefore hypothesized that these signaling pathways and miRNAs underlie DM1 and DM2 cataracts, and may represent potential therapeutic targets for the treatment of this disorder.
Aims: The aim of this study was to identify potential candidates and explore the possible mechanism in congenital cataract induced by tudor domain-containing 7 (TDRD7) deficiency. Methods: The gene expression profile GSE25812 generated from 18 samples was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) between disease and normal groups were identified. Then, gene ontology and pathway enrichment analysis of DEGs were performed. The protein-protein interaction (PPI) network and transcription factor (TF) regulatory network were constructed. The modules in the PPI network were identified. Significant target genes were selected from the TF regulatory network. Results: A total of 329 DEGs were obtained, and downregulated DEGs were significantly enriched in biological processes including defense response and immune response. In the PPI network, high-degree genes of complement component 1, q subcomponent, A/B/C chain (C1QA/C1QB/C1QC), lymphocyte antigen 86 (LY86) and neuroblastoma RAS viral oncogene homolog (NRAS) were identified. From the TF regulatory network, the heat shock 27 kDa protein 1 (HSPB1) was the target of the estrogen receptor 1, and LY86 was the target of the v-myc avian myelocytomatosis viral oncogene homolog. Conclusion:HSPB1, NRAS, immune response, defense response and the related genes LY86, C1QA/C1QB/C1QC may play an important role in the development of congenital cataract induced by TDRD7 deficiency. However, further experiments are still needed.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.