Influence of super-hydrophobic silicone rubber substrate on the growth and differentiation of human lens epithelial cells.

Materials with low cell adhesion are advantageous for production of replacement intraocular lens (IOL) to prevent posterior capsular opacification (PCO). We evaluated the feasibility of compression molding for manufacture of silicone rubber with super-hydrophobic surface and low cell infiltrative characteristics compared to ordinary hydrophobic silicone rubber. Silicone specimens with complex surface topology (super-hydrophobic) or smooth surfaces (hydrophobic) were manufactured by vacuum deforming and molding. Contact angle, microscopic surface structure, and transparency were evaluated. Super-hydrophobic and smooth samples were compared for effects on proliferation, adhesion, and morphology of human lens epithelial cells (hLECs). Epithelial-mesenchymal transition (EMT) was examined by immunofluorescence expression of fibronectin (Fn), Alpha-smooth muscle actin (α-SMA), and vimentin. The surface contact angle of super-hydrophobic silicone was greater than that of smooth silicone (153.8° vs. 116°). The super-hydrophobic surface exhibited a micron-scale palisade structure under scanning electron microscopy (unit length, width, and height of 80, 25, and 25 µm, respectively). However, cell number per 50 × microscopic field on super-hydrophobic surfaces was markedly reduced 24 and 72 h post-seeding compared to smooth surfaces (p < 0.01). Cells were cuboidal or spherical after 72h on super-hydrophobic surfaces, and exhibited numerous surface microvilli with fluff-base polarity, while cells on smooth surfaces exhibited morphological characteristics of EMT. Expression levels of the α-SMA and vimentin were reduced on super-hydrophobic surfaces compared to smooth surfaces. Super-hydrophobic silicon inhibits proliferation, adhesion, and EMT of hLECs, properties that may prevent fibrosis following cataract surgery.

Clipping versus Coiling for Ruptured Intracranial Aneurysms: A Meta-Analysis of Randomized Controlled Trials.

BACKGROUND: The treatment strategies of ruptured intracranial aneurysms (RIAs) include surgical clipping and endovascular coiling, and the efficacy and safety of clipping versus coiling are yet controversial. OBJECTIVE: To summarize the available randomized controlled trials to determine the optimal treatment method for patients with RIA. METHODS: PubMed, Embase, and the Cochrane Library were systematically searched for randomized controlled trials published up to September 5, 2017. The summary analysis was performed using a random-effects model. The primary outcomes included poor outcome, mortality, and rebleeding, whereas the secondary outcomes included complete occlusion, incomplete occlusion, severe disability, and vegetative state. RESULTS: We identified 5 trials with data collected from 2883 patients. The summary results indicated that surgical clipping in patients was associated with a high incidence of poor outcome (relative risk [RR], 1.34; 95% confidence interval [CI], 1.18-1.51; P < 0.001), whereas no significant effect was observed on mortality (RR, 1.09; 95% CI, 0.79-1.49; P = 0.608) and rebleeding (RR, 0.65; 95% CI, 0.20-2.06; P = 0.460) compared with endovascular coiling. Furthermore, we noted that surgical clipping significantly increased the incidence of complete occlusion compared with endovascular coiling (RR, 1.30; 95% CI, 1.09 1.55; P = 0.004). Conversely, surgical clipping was associated with a low incidence of incomplete occlusion (RR, 0.67; 95% CI, 0.45-0.99; P = 0.044). No significant differences were noted between surgical clipping and endovascular coiling with respect to the outcomes of severe disability (RR, 1.39; 95% CI, 0.90-2.16; P = 0.140) and vegetative state (RR, 1.35; 95% CI, 0.84-2.17; P = 0.213). CONCLUSIONS: This meta-analysis provides moderate evidence that surgical clipping has few benefits than endovascular coiling for the treatment of RIA.

Erratum: LOXL1 regulates cell apoptosis and migration in human neuroglioma U87 and U251 cells via Wnt/ß-catenin signaling.

[This corrects the article on p. 2032 in vol. 11, PMID: 31938310.].

Carnosic Acid Mitigates Early Brain Injury After Subarachnoid Hemorrhage: Possible Involvement of the SIRT1/p66shc Signaling Pathway.

Carnosic acid (CA) has been reported to exhibit a variety of bioactivities including antioxidation, neuroprotection, and anti-inflammation; however, the impact of CA on subarachnoid hemorrhage (SAH) has never been elucidated. The current study was undertaken to explore the role of CA in early brain injury (EBI) secondary to SAH and the underlying mechanisms. Adult male Sprague-Dawley rats were perforated to mimic a clinical aneurysm with SAH. CA or vehicle was administered intravenously immediately after the SAH occurred. Mortality, SAH grade, neurologic function scores, brain water content, Evans blue extravasation, and the levels of reactive oxygen species (ROS) levels in the ipsilateral cortex were determined 24 h after the SAH occurred. Western blot, immunofluorescence, Fluoro-Jade C (FJC) and TUNEL staining were also performed. Our results showed that CA decreased ROS levels, alleviated brain edema and blood-brain barrier permeability, reduced neuronal cell death, and promoted neurologic function improvement. To probe into the potential mechanisms. We showed that CA increased SIRT1, MnSOD, and Bcl-2 expression, as well as decreased p66shc, Bax, and cleaved caspase-3 expression. Interestingly, sirtinol, a selective inhibitor of SIRT1, abolished the anti-apoptotic effects of CA. Taken together, these data revealed that CA has a neuroprotective role in EBI secondary to SAH. The potential mechanism may involve suppression of neuronal apoptosis through the SIRT1/p66shc signaling pathway. CA may provide a promising therapeutic regimen for management of SAH.

LOXL1 regulates cell apoptosis and migration in human neuroglioma U87 and U251 cells via Wnt/ß-catenin signaling.

The role of extracellular matrix proteins in glioma progression is largely unknown. In the current study, we screened different published GSE datasets and found that an extracellular matrix protein Lysyl Oxidase-Like 1 (LOXL1) is highly expressed in different cohorts of glioma patients. To confirm the results from datasets, we examined the level of LOXL1 in 30 matched glioma tissues and we found that LOXL1 is highly expressed in glioma malignant tissues. We further investigated the biological functions of LOXL1 in glioma cells with both loss- and gain-function assays. These show that highly expressed LOXL1 promotes glioma cell proliferation and growth through regulating Wnt/ß-catenin signaling. In conclusion, we report that thesecretory protein LOXL1 is highly expressed in malignantglioma tissues and promotes glioma cell proliferation through Wnt/ß-catenin signaling.

Inhibition of microRNA-299-5p sensitizes glioblastoma cells to temozolomide via the MAPK/ERK signaling pathway.

Glioblastomas (GBMs) are a lethal class of brain cancer, with a median survival <15 months in spite of therapeutic advances. The poor prognosis of GBM is largely attributed to acquired chemotherapy resistance, and new strategies are urgently needed to target resistant glioma cells. Here we report a role for miR-299-5p in GBM. The level of miR-299-5p expression was detected in glioma specimens and cell lines by qRT-PCR. Luciferase reporter assays and Western blots were performed to verify GOLPH3 as a direct target of miR-299-5p. In vitro cell proliferation, invasion, cell cycle distribution, and apoptosis were assessed to determine whether or not miR-299-5p knockdown sensitized GBM cells to temozolomide (TMZ). We demonstrated that miR-299-5p levels were up-regulated in the GBM groups compared with the normal control group. The highest expression of miR-129-5p occurred in the highest GBM stage. miR-299-5p knockdown significantly inhibited the MAPK/extracellular signal-regulated kinase (ERK) signaling pathway. We also showed that miR-299-5p knockdown enhanced sensitivity of GBM cells to TMZ both in vitro and in vivo by inhibiting cell proliferation and invasion and promoting apoptosis. In addition, we demonstrated that GOLPH3 is a novel functional target of miR-299-5p GOLPH3 regulates the MAPK/ERK axis under miR-299-5p regulation. In conclusion, we identified a link between miR-299-5p expression and the GOLPH3/MAPK/ERK axis, thus illustrating a novel role for miR-299-5p in GBM.

Rapid fabrication of bio-inspired nanostructure with hydrophobicity and antireflectivity on polystyrene surface replicating from cicada wings.

The fine nanostructure on the cicada wing of Cryptotympana atrata fabricius, which exhibits hydrophobicity and antireflectivity, is carefully examined. A promising strategy is proposed for facilely and successively replicating the natural functional nanostructure of the cicada wing onto polystyrene (PS) surfaces. First, a nickel replica with tapered nanopores is fabricated by combining electroless plating and subsequent electroplating with the natural cicada wing as an original template. Then, using microinjection compression molding, with the nickel replica as a template, the tapered nanopores are transcribed onto the PS surface, resulting in orderly and densely arranged nanopillars with a mean diameter of about 156 nm and a mean pitch of about 180 nm. The natural cicada wing and fabricated nickel replica are reusable. Interestingly, the PS replica surface exhibits a water contact angle of 143° ± 2° and a reflectance of about 4% in the wavelength range of 400-1000 nm. These results mean that the bionic PS replica not only inherits the nanostructure of the natural wing, but also its hydrophobic and antireflective properties. The mechanisms for the hydrophobic and antireflective properties are revealed via composite wetting interface and effective medium layer on the replica surface, respectively. The proposed fast and efficient replication strategy can be an excellent candidate for mimicking bio-inspired functional micro/nanostructures without complicated procedures and expensive materials.

Circular RNA hsa_circ_0021001 in peripheral blood: a potential novel biomarker in the screening of intracranial aneurysm.

Circular RNAs (circRNAs) in the peripheral blood have been reported to be associated with cancer. However, there are few studies about circRNAs in intracranial aneurysms (IA). The purpose of the current study was to investigate the characteristic expression of circular RNA hsa_circ_0021001 in the peripheral blood of patients with intracranial aneurysms and its potential as a diagnostic biomarker for IA. In this study, a cohort of 223 cases of IA patients who were admitted in the department of neurosurgery in the First People's Hospital of Wenling from January 2009 to July 2012 were collected as the experimental group, and 131 healthy volunteers over the same period served as the control group. Peripheral blood of each subject in both groups was collected on an empty stomach. The expression of hsa_circ_0021001 in peripheral blood was detected by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and the difference was analyzed by paired t-test. The effectiveness of hsa_circ_0021001 in the diagnosis of IA was assessed by ROC curve. Multivariate Cox proportional hazards regression analysis was used to analyze the prognosis. Hsa_circ_0021001 level in the peripheral blood of IA patients was relatively lower than that in the control group (P=0.002). The area under ROC (AUC) was 0.87, indicating that hsa_circ_0021001 was highly effective in the diagnosis of IA. In addition, hsa_circ_0021001 expression was correlated with aneurysm rupture, Hunt, Hess level, and timing of surgery (P= 0.041, 0.013, and 0.001, respectively). Patients with high expression of hsa_circ_0021001 had longer disease-free survival (DFS) and overall survival (OS) (P < 0.05). We found for the first time that hsa_circ_0021001 decreased significantly in the peripheral blood of IA patients, which suggested that hsa_circ_0021001 might be used as a potential novel marker for the diagnosis of IA.