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Long noncoding RNAs (lncRNAs) have been reported to play vital roles in various human cancers. The aim of this study was to explore the critical role of lncRNA HOXA11-AS in uveal melanoma (UM) progression. Briefly, we found that HOXA11-AS is overexpressed in UM tissues and cells; HOXA11-AS could regulate UM cell growth, invasion, and apoptosis. Mechanistically, RNA immunoprecipitation demonstrated that HOXA11-AS could simultaneously interact with enhancer of zeste homolog 2 (EZH2) to suppress its target p21 protein expression. In addition, we demonstrated that HOXA11-AS functioned as a molecular sponge for miR-124, and overexpression of miR-124 attenuated the proliferation and invasion-promoting effect of HOXA11-AS. Collectively, our findings reveal an oncogenic role for HOXA11-AS in UM tumorigenesis.

The body changes markedly during pregnancy; each system behaves differently from a nonpregnant state. As the eyes are the only windows to see directly what is going on in the internal environment, more and more researches have been done to explain the association between ocular changes and the physiological and pathological changes during pregnancy. The choroid is one of the critical parts of the eye, providing nutrition. And abnormal choroid may result in ocular dysfunction and visual problems. As the optical coherence tomography develops, a rapid, direct, noninvasive, and nontoxic way is available to obtain the choroid situation of pregnant women, which may explain the mechanism of pregnancy-related eye diseases. This review would summarize relevant original articles published from January 1, 2008 to December 1, 2016 to assess the changes of choroidal thickness (CT) with enhanced depth imaging optical coherence tomography (EDI-OCT) during pregnancy. And the relationship between choroidal thickness changes and pregnancy remains uncertain. To our knowledge, this is the first review of EDI-OCT in assessing the choroidal thickness of the pregnant women.

We conducted a meta-analysis of analytic and observational studies to evaluate the association between smoking and epiretinal membrane (ERM). The pertinent studies were identified via a literature search using three databases (MEDLINE, Cochrane Library, Embase) and the reference lists of retrieved studies. Cohort, case-control and cross-sectional studies meeting the predefined criteria were included. We extracted the odds ratios (OR) and 95% confidence intervals (CI) from each study. Overall risk estimates were pooled using random-effects models. Subgroup analyses based on several stratified factors were also performed. Two cohort studies and six cross-sectional studies involving 46,837 subjects were included. The pooled effect of all eight studies showed an unexpected significant decreased association between smoking and the occurrence of ERM (OR, 0.72; 95% CI 0.61–0.84; p = 0.29, I2 = 17.9%). Subgroup analyses supported this finding, except for the age-unadjusted group (OR, 0.87; 95% CI 0.63–1.22), the ERM classification group (cellophane macular reflex (CMR) OR, 0.93; 95% CI 0.68–1.28; preretinal macular fibrosis (PMF) OR, 0.74; 95% CI 0.41–1.32), the Asian group (OR, 0.75; 95% CI 0.52–1.09) and the past smoker group (OR, 1.02; 95% CI 0.85–1.22). The pooled effects from the current literature suggested a declining association between smoking and ERM, which requires further studies to confirm.

Purpose: To investigate the association of interleukin (IL)-6 with proliferative diabetic retinopathy (PDR) of type 2 diabetes (T2D) in a Chinese population. Methods: Two subtypes of the IL-6 promoter (-174 and -572 G/C) were genotyped in 215 T2D patients with PDR and 207 T2D patients with a normal retinal function (controls) using the PCR-RFLP method. The mRNA and protein expression of IL-6 was examined by real-time PCR. Results: T2D patients with PDR had a significantly higher frequency of IL-6 -174 GC (OR 0.58; 95% CI 0.34-0.99; p = 0.011) and IL-6 -572 GG (OR 0.53; 95% CI 0.24-1.14; p = 0.016) than T2D controls. The mRNA expressions of the rs1800795 GC and rs1800796 GG genotype were significantly increased compared to other cases (Fsig = 0.002, p = 0.001, respectively), followed by a relative increase in IL-6 in protein. Conclusions: IL-6 genotypes of rs1800795 GC and rs1800796 GG might point to a relatively high risk for T2D patients suffering from PDR in a Chinese population and they were associated with elevation of IL-6 expression in both mRNA and protein.

Choroideremia is a bilateral and progressive X-linked inherited disease characterized by widespread chorioretinal atrophy with relative sparing of the macular region. It is caused by mutations in the ubiquitously expressed CHM gene, which lead to the absence of the Rab escort protein 1 (REP-1), resulting in prenylation deficiency. Typical fundus appearances for choroideremia were found in 3 probands from three unrelated Chinese families in our study. We firstly used the targeted exome sequencing (TES) technology to detect mutations in CHM gene. Based on an established filtering strategy of data analyses, along with confirmation by co-segregation, a previously reported mutation (c.1584_1587del TGTT, p.V529Hfs*7) was identified in one family, while two novel mutations (c.227_232delinsTGTCATTTCA, p.Q76Lfs*7; c.710dupA, p.Y237_S238delinsX) were identified in the other two families. These findings not only expands the currently limited spectrum of Chinese disease-causing variants in CHM gene, but also increases our understanding of the phenotypic and genotypic correlations of choroideremia, and may potentially lead to improved genetic counseling and specific treatment for families with choroideremia as well.

Objectives: To provide anatomical data to help identify and locate the anterior ethmoidal artery (AEA) precisely during endoscopic procedures. Method: We dissected 15 adult cadaver heads, which provided 30 specimens, to study morphological characteristics, courses, and several types of variations. Results: We found the average diameter of the AEA to be 0.80 ± 0.24 mm. In 85.7% of the cases, the artery was seen between the second and third lamella. Other locations were over the roof of the frontal recess cells (10.7%) and the roof of the posterior ethmoid sinus (3.6%). The AEA ran parallel to the ethmoid roof and formed a slight curve. When viewed from the superior side, the angle formed by the long axis of the artery and the lamina papyracea was 60.5 degrees ± 16.4 degrees. In 83.3% of the cases, the anterior ethmoidal canal (AEC) was identified as a separate canal, and in 16.7% the canal was embedded in the ethmoid roof. In 10 of the 30 cases (33.3%), the AEC presented some degree of dehiscence. Conclusion: As a result of these dissections, we found that the AEA's course in the ethmoid roof varies. The morphological characteristics—that the AEA runs parallel to the ethmoid roof, forming a slight posterolateral to anteromedial curve as it passes from the orbit to the cribriform plate—are the most reliable factors used to identify the artery during surgery.

Retinitis pigmentosa (RP) is an inherited retinopathy, which affects the photoreceptors in the retina. Lysophosphatidylcholine acyltransferase (LPCAT) is a critical phospholipid biosynthesis enzyme, which promotes the conversion of lysophosphatidylcholine into phosphatidylcholine in the remodeling pathway of PC biosynthesis. A previous study reported a homozygous insertion in the LPCAT1 gene in mice exhibiting retinal degeneration (rd11). However, whether genetic mutations in LPCAT1 predispose individuals to RP remains to be elucidated. Therefore, the aim of the present study was to investigate whether LPCAT1 mutations exist in patients with RP. A total of 50 unrelated patients diagnosed with either a sporadic or recessive inheritance pattern of RP were recruited in the present study. All of the patients were comprehensively screened for genes associated with the predisposition of RP, and no pathogenic mutations were identified. Reverse transcription-polymerase chain reaction and Sanger sequencing were performed to investigate the coding regions and exon‑intron boundaries of the LPCAT1 gene in the recruited patients. In total, three genetic variations in the coding regions, which lead to amino acid changes, were identified. Although two of these mutations were predicted to be pathogenic, co‑segregation analysis in the pedigrees excluded these as disease‑causing mutations. In addition, the LPCAT1 gene was screen in a panel of RP patients who exhibited no identifiable mutations in any of the known RP‑associated genes. No disease‑causing mutations in the LPCAT1 gene were identified, indicating that LPCAT1 either does not confer a genetic predisposition to RP, or that the incidence of mutations in LPCAT1 is particularly rare in patients with RP.