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Objective: To evaluate the efficiency of photobiomodulation therapy (PBMT) or photodynamic therapy (PDT) in treating oral lichen planus (OLP) as well as identifiy the side effects when compared with steroid therapy. Background: Nowadays, PBMT and PDT are increasingly applied for treating OLP with minimal adverse effects. Methods: The electronic databases of PubMed, Cochrane Central Register of Controlled Trial, Web of Science, and Embase were searched until March 13, 2020. Randomized controlled trials (RCTs) with 1 month of followup period were selected. Two reviewers extracted data from selected studies independently. Cochrane collaboration's tool for assessing risk of bias was used for assessing the quality of the RCTs. The random-effects model was employed for meta-analysis. Results: One thousand fifteen studies were initially identified. Finally, nine RCTs were included for quality assessment and seven studies for meta-analysis. Four RCTs were of unclear risk of bias and five were assessed as high risk of bias. The comparison showed no significant differences for pain scores [visual analog scale (VAS)] [mean differences (MD) = 0.38, confidence interval (CI) = 95% -0.64 to 1.40] and severity scores (reticular-atrophic-erosive scores) (MD= 1.67, CI = 95% -1.13 to 4.46) between topical corticosteroid therapy and PBMT after 1 month. For PDT, no significant differences were observed for sign scores (Thongprasm sign scoring) (MD=-0.31, CI = 95% -1.52 to 0.91) and pain scores (VAS) (MD=-2.30, CI = 95% -5.88 to 1.28) of the lesions when compared with topical corticosteroid therapy after 1 month of follow-up period. One study reported the discomfort of the affected area in patients of the PDT group when probe tip was moved. Conclusions: PBMT and PDT could be reliable alternatives to topical corticosteroids for OLP with no or less severe complications in a short-term period. However, further well-designed RCTs with long-term period are recommended to consolidate the conclusions in this regard. [ABSTRACT FROM AUTHOR]

Background: FGFR2 encodes a fibroblast growth factor receptor whose mutations are responsible for the Crouzon syndrome, involving craniosynostosis and facial dysostosis with shallow orbits. However, few reports are available quantifying the orbital volume of Crouzon syndrome and there was little direct evidence to show FGFR2 mutation actually influencing orbital morphology. Methods: Ten Crouzon syndrome patients underwent a standard ophthalmologic assessment. Morphology study was carried out based on 3-dimensional computed tomography scan to calculate orbital volume. Genomic DNA was extracted from peripheral blood leukocytes of the patients and genomic screening of FGFR2. A threedimensional computer model was used to analyse the structural positioning of the mutation site that was predicted possible impact on functional of FGFR2 protein. Real-time PCR was performed to analyse the expression of bone maker gene. Results: We describe a FGFR2 mutation (p.G338R, c.1012G > C) in a Chinese family with Crouzon syndrome. Computational analysis showed the mutate protein obviously changes in the local spatial structure compared with wild-type FGFR2. The expression of osteocalcin and alkaline phosphatase two osteoblast specific genes significantly increased in orbital bone directly from patient compared to normal individual, which may lead to facial dysostosis. This is compatible with the shallow and round orbits in our Crouzon syndrome patient. Conclusions: Our study further identified G338R FGFR2 mutation (c1012G > C) lead to inherited Crouzon syndrome. Thus, early intervention, both medically and surgically, as well as disciplined by a multiple interdisciplinary teams are crucial to the management of this disorder. [ABSTRACT FROM AUTHOR]

Increasing evidence suggests that aberrant long non-coding RNAs (lncRNAs) are significantly correlated with the pathogenesis, development and metastasis of cancers. RHPN1 antisense RNA 1 (RHPN1-AS1) is a 2030-bp transcript originating from human chromosome 8q24. However, the role of RHPN1-AS1 in uveal melanoma (UM) remains to be clarified. In this study, we aimed to elucidate the molecular function of RHPN1-AS1 in UM. The RNA levels of RHPN1-AS1 in UM cell lines were examined using the quantitative real-time polymerase chain reaction (qRT-PCR). Short interfering RNAs (siRNAs) were designed to quench RHPN1-AS1 expression, and UM cells stably expressing short hairpin (sh) RHPN1-AS1 were established. Next, the cell proliferation and migration abilities were determined using a colony formation assay and a transwell migration/invasion assay. A tumor xenograft model in nude mice was established to confirm the function of RHPN1-AS1 in vivo. RHPN1-AS1 was significantly upregulated in a number of UM cell lines compared with the normal human retinal pigment epithelium (RPE) cell line. RHPN1-AS1 knockdown significantly inhibited UM cell proliferation and migration in vitro and in vivo. Our data suggest that RHPN1-AS1 could be an oncoRNA in UM, which may serve as a candidate prognostic biomarker and target for new therapies in malignant UM. [ABSTRACT FROM AUTHOR]