HSV-1 infection in the cornea could lead to blindness. The infected cell polypeptide 4 (ICP4) of herpes simplex virus 1 (HSV-1) is a regulator of viral transcription that is required for productive infection. It has been previously demonstrated that miR-H6 encoded from HSV-1 genome targets ICP4 to help maintain latency. In this study, synthesized miR-H6 mimics were transfected into HSV-1-infected human cornea epithelial (HCE) cells. The inhibition of HSV-1 replication and viral ICP4 expression in miR-H6-transfected HCE was confirmed by plaque assay, immunofluorescence, and Western blot. Compared to nontransfection or mock, miR-H6 produced a low-titer HSV-1 and weak ICP4 expression. In addition, miR-H6 can decrease the interleukin 6 released into the medium, which was determined by ELISA. Taken together, the data suggests that miR-H6 targeting of ICP4 inhibits HSV-1 productive infection and decreases interleukin 6 production in HCE, and this may provide an approach to prevent HSV-1 lytic infection and inhibit corneal inflammation.

This study aimed to identify the microbial etiology of infectious endophthalmitis and to determine the antibacterial susceptibilities of bacterial isolates at an eye hospital in South China. A retrospective analysis was carried out on 330 patients with clinically diagnosed infectious endophthalmitis who underwent microbiological evaluation from January 2010 to December 2014. Of the 330 patients, 193 patients (58.5%) had posttraumatic endophthalmitis, 67 patients (20.3%) had postoperative endophthalmitis, 61 patients (18.5%) had endogenous endophthalmitis, and 9 patients (2.7%) had postcorneal infective endophthalmitis. Of the 105 cases (31.8%) of culture-positive endophthalmitis, 79 cases (75.2%) had bacterial growth and 26 cases (24.8%) had fungal growth. In posttraumatic endophthalmitis, Gram-positive bacteria were the predominant species, followed by Gram-negative bacteria and fungi. In endogenous endophthalmitis, Gram-negative bacteria were the predominant species, followed by fungi and Gram-positive bacteria. In postsurgical endophthalmitis, all infections were bacterial. However, in postcorneal infective endophthalmitis, all infections were fungal. Overall, levofloxacin showed the highest activity against bacterial isolates. There was a significant difference in the susceptibility to tobramycin between the isolates from posttraumatic and postoperative endophthalmitis (p < 0.05). The results of this study identify the microbial spectrum of infectious endophthalmitis in this clinical setting.

Background and Aims Bone is the second most frequent site of metastasis for HCC, which leads to an extremely poor prognosis. HCC bone metastasis is typically osteolytic, involving the activation of osteoclasts. Long noncoding RNA H19 plays an important role in the pathogenesis of human cancers. Nonetheless, the mechanism underlying the participation of H19 in HCC bone metastasis remains unclear. Approach and Results The current study established a mouse HCC bone metastasis model by using serial intracardiac injection and cell isolation to obtain cells with distinct bone metastasis ability. H19 was highly expressed in these cells and in clinical HCC bone metastasis specimens. Both osteoclastogenesis in vitro and HCC bone metastasis in vivo were promoted by H19 overexpression, whereas these processes were suppressed by H19 knockdown. H19 overexpression attenuated p38 phosphorylation and further down‐regulated the expression of osteoprotegerin (OPG), also known as osteoclastogenesis inhibitory factor. However, up‐regulated OPG expression as well as suppressed osteoclastogenesis caused by H19 knockdown were recovered by p38 interference, indicating that p38 mitogen‐activated protein kinase (MAPK)–OPG contributed to H19‐promoted HCC bone metastasis. Furthermore, we demonstrated that H19 inhibited the expression of OPG by binding with protein phosphatase 1 catalytic subunit alpha (PPP1CA), which dephosphorylates p38. SB‐203580‐mediated inactivation of p38MAPK reversed the down‐regulation of HCC bone metastasis caused by H19 knockdown in vivo. Additionally, H19 enhanced cell migration and invasion by up‐regulating zinc finger E‐box binding homeobox 1 through the sequestration of microRNA (miR) 200b‐3p. Conclusions H19 plays a critical role in HCC bone metastasis by reducing OPG expression, which is mediated by the PPP1CA‐induced inactivation of the p38MAPK pathway; and H19 also functions as a sponge for miR‐200b‐3p.

Circular RNAs (circRNAs), which act as initiators and promoters of various diseases, were thought to be mostly noncoding RNAs (ncRNAs) in eukaryotes, until recent studies confirmed that some circRNAs have the function of encoding proteins. Accumulating research findings have proved that dysregulation of circRNAs is associated with the developmental process of multiple cancers. circHIPK3, an example of circRNA, is frequently expressed in many diseases, such as diabetes, age-related cataract, idiopathic pulmonary fibrosis, preeclampsia, osteoblasts, and retinal vascular dysfunction, leading to disease development and progression. In addition, circHIPK3 may also serve as a potential biomarker, to help us know more about the rules of occurrence and development of cancers. In recent studies, many circHIPK3-related cancers have been identified, including nasopharyngeal carcinoma, gallbladder cancer, lung cancer, hepatocellular carcinoma, osteosarcoma, glioma, colorectal cancer, ovarian cancer, bladder cancer, prostate cancer, gastric cancer, oral squamous cell carcinoma, and chronic myeloid leukemia. This review summarizes recent studies on the biological mechanisms of circHIPK3 and expounds the molecular mechanisms of circHIPK3 in these malignant tumors.

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Background: Hepatocellular carcinoma (HCC) is one of the most prevalent common cancer worldwide with high mortality. Transforming growth factor-β (TGF-β) signaling pathway was reported dysregulated during liver cancer formation and progression. As a key component of TGF-β signaling, the role of SMAD2 and its regulatory mechanisms in HCC remain unclear. Methods: SMAD2 expression in paired HCC specimens were determined by western blot and immunohistochemistry (IHC). quantitative real-time PCR (qRT-PCR) was used to measure mRNA and microRNA (miRNA) expression level. Cell migration, invasion and proliferation ability were evaluated by transwell, CCK8 and EdU assay. In silico websites were used to manifest overall survival rates of HCC patients or to predict miRNAs targeting SMAD2. Dual luciferase reporter assay and anti-Ago2 immunoprecipitation assay were performed to confirm the binding between SMAD2 mRNA and miRNA-148a-3p (miR-148a). Tumorigenesis and lung metastasis mouse model were used to explore the role of miR-148a in vivo. In situ hybridization (ISH) was conducted to determine the expression of miR-148a in liver tissues.

Purpose To investigate the incidence and risk factors of intraocular foreign body- (IOFB-) related endophthalmitis. Methods A total of 1701 patients diagnosed with IOFB between January 1, 2005 and June 30, 2015 were included. Two groups of patients were defined according to the presence or absence of endophthalmitis, and a comparison of personal information, IOFB characteristics, and wound location were performed. Results In total, 279 patients (16.4%) developed endophthalmitis, older age (P=0.01) was a risk factor. IOFBs retained in the crystal lens or wall of the eyeball conferred lower risks (P=0.01 and 0.04, respectively) compared to the vitreous chamber. The coexistence of different IOFB types and plant IOFBs conferred higher risks (P=0.02 and 0.03, respectively), while glass/plastic IOFBs conferred a lower risk (P=0.03) compared to metallic IOFBs. Conclusions Age, IOFB locations, and types were related to development of endophthalmitis, while IOFB number, size, or timing of primary repairs was not related.

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