Corneal dystrophy is a common type of hereditary corneal diseases. It includes many types, which have varied pathology, histology and clinical manifestations. Recently, the examination techniques of ophthalmology and gene sequencing advance greatly, which do benefit to our understanding of these diseases. However, many aspects remain still unknown. And due to the poor knowledge of these diseases, the results of the treatments are not satisfoctory. The purpose of this review was to summarize the clinical, histological and genetic characteristics of different types of corneal dystrophies.

Purpose. To identify the potential key genes and molecular pathways associated with keratoconus and allergic disease. Methods. The pubmed2ensembl database was used to identify the text mining genes (TMGs) collectively involved in keratoconus and allergic disease. The GeneCodis program was used to perform the Gene Ontology (GO) biological process and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of TMGs. The protein‐protein interaction (PPI) network of the TMGs was established by STRING; the significant gene modules and hub genes of PPI were further performed using the Cytoscape software. The DAVID database was used to perform the GO and KEGG analyses of the significant module. Results. In total, 98 TMGs collectively involved in keratoconus and allergic disease were identified. 19 enriched biological processes including 71 genes and 25 enriched KEGG pathways including 59 genes were obtained. A TMG PPI network was constructed, and 51 genes/nodes were identified with 110 edges; 3 most significant modules and 12 hub genes were chosen from the PPIs. GO enrichment analysis showed that the TMGs were primarily associated with collagen catabolic process, extracellular matrix organization and disassembly, cell adhesion and migration, collagen‐containing extracellular matrix, extracellular matrix, and structure organization. KEGG pathway analysis showed that these DEGs were mainly involved in the IL‐17 signaling pathway, inflammatory bowel disease, rheumatoid arthritis, allograft rejection, T cell receptor signaling pathway, cytokine‐cytokine receptor interaction, and TNF signaling pathway. Conclusions. The results revealed that IL10, IL6, MMP9, MMP1, HGF, VEGFA, MMP3, MMP2, TGFB1, IL4, IL2, and IFNG were potential key genes involved in keratoconus. IL‐17 signaling pathway was the potential pathways accounting for pathogenesis and development of keratoconus.

To identify the 100 most cited papers in cataract surgery, we performed a comprehensive bibliometric analysis basing on the literature search on the Thomson Reuters Web of Knowledge. The number of citations, including the total citations, latest 5y citations and average citation number per year (ACY), authorship, year of publication, major topics, journal of publication, country and institution of origin of each paper were recorded and then analyzed. Pearson's correlation analysis was conducted to evaluate the correlation between the published year and the number of citations. The correlation between journal's impact factor (IF) and number of citations was assessed as well. The most cited paper was the classic paper done by the European Society of Cataract & Refractive Surgeons (ESCRS) group. This paper focused on the topic of endophthalmitis. Not only the most cited papers originated from the USA, but also some American institutions like Johns Hopkins University, Harvard Medical School, etc. had the most citations. Pearson's correlation analysis indicated that the latest 5y citations and ACY were significantly related with the published year (5y citations: r=0.615, P<0.001; ACY: r=0.657, P<0.001), whereas no association between the total number of citations and published year was found (r=0.045). Moreover, the IFs of journals were found to have no significant effect on the number of total citations. To our knowledge, this is the first study on the most influential papers in cataract surgery after a comprehensive research of relevant literatures. The present work may provide us concise information concerning the development history of cataract surgery over the past 66y.

In this work, we aim to evaluate the association of the genetically proxied effect of metformin on blood pressure (BP) and hypertension through a drug target-based Mendelian randomization (MR) analysis. Thirty-two instrumental variables for five metformin targets (i.e., AMP-activated protein kinase (AMPK), growth differentiation factor 15 (GDF15), mitochondrial glycerol 3 (MG3), mitochondrial complex I (MCI), and glucagon (GCG)) were introduced to the MR analysis on the datasets of hypertension, systolic and diastolic blood pressure (SBP and DBP). The MR analyses demonstrated that the MCI- and MG3-specific metformin’s use would significantly reduce SBP, DBP, and hypertension risk. The meta-analyses showed that the genetically proxied metformin’s use equivalent to a 6.75 mmol/mol reduction on HbA1c could decrease both the SBP (beta = − 1.05, P < 0.001) and DBP (beta = − 0.51, P = 0.096). Furthermore, metformin’s use was also implied to reduce the hypertension risk. The MG3- and MCI-dependent metformin’s effect may play key roles in the anti-hypertension function. Graphical Abstract

Blood-based B-cell activating factor (BAFF), growth differentiation factor-15 (GDF-15) and osteopontin (OPN) have been identified to be promising biomarkers for the metastases of uveal melanoma (UM). This study intended to assess their kinetics and to evaluate their significance as a three-marker panel. A group of 36 UM patients with and 137 patients without metastases were included in the study. Their plasma OPN levels were measured by ELISA; serum BAFF and GDF-15 levels were determined with a Luminex MAGPIX system. Receiver operating characteristic (ROC) analysis was performed to calculate the cutoff values of the three markers for identifying the patients with metastases. The ability to identify patients with metastases was compared between the single markers and the combination as a three-marker panel. By using the Student’s t-test, we also investigated the kinetic changes of the levels of BAFF, GDF-15 and OPN across six periods (i.e., 0–6 months, 6–12 months, 12–18 months, 18–24 months, >24 months and post-metastasis) before the imaging diagnosis of metastases. By maximizing the Youden’s index, the serum GDF-15 level of 1209 pg/mL and the plasma OPN level of 92 ng/mL were identified to have the best performance for distinguishing the metastatic patients from non-metastatic patients. The three-marker panel offered a better performance in distinguishing patients with metastases, with an area under the curve of 0.802, than any single biomarker. Increasing trends of the levels of three biomarkers were observed in the two-year period before the imaging diagnosis of metastases. The combined panel of BAFF, GDF-15 and OPN might be a utilizable implementation for the detection of UM metastases. In the bioinformatics study with two external datasets, the high expression of gene BAFF and GDF-15 in primary UM tissues was identified to be associated with poor overall survival rates. As the current work is a single-center retrospective study, more well-designed prospective investigations employing larger cohorts are urgently needed to validate our findings.