To determine the effectiveness of different interventions to slow down the progression of myopia in children. We searched MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov from inception to August 2014. We selected randomized controlled trials (RCTs) involving interventions for controlling the progression of myopia in children with a treatment duration of at least 1 year for analysis. The primary outcomes were mean annual change in refraction (diopters/year) and mean annual change in axial length (millimeters/year). Thirty RCTs (involving 5422 eyes) were identified. Network meta-analysis showed that in comparison with placebo or single vision spectacle lenses, high-dose atropine (refraction change: 0.68 [0.52-0.84]; axial length change: -0.21 [-0.28 to -0.16]), moderate-dose atropine (refraction change: 0.53 [0.28-0.77]; axial length change: -0.21 [-0.32 to -0.12]), and low-dose atropine (refraction change: 0.53 [0.21-0.85]; axial length change: -0.15 [-0.25 to -0.05]) markedly slowed myopia progression. Pirenzepine (refraction change: 0.29 [0.05-0.52]; axial length change: -0.09 [-0.17 to -0.01]), orthokeratology (axial length change: -0.15 [-0.22 to -0.08]), and peripheral defocus modifying contact lenses (axial length change: -0.11 [-0.20 to -0.03]) showed moderate effects. Progressive addition spectacle lenses (refraction change: 0.14 [0.02-0.26]; axial length change: -0.04 [-0.09 to -0.01]) showed slight effects. This network analysis indicates that a range of interventions can significantly reduce myopia progression when compared with single vision spectacle lenses or placebo. In terms of refraction, atropine, pirenzepine, and progressive addition spectacle lenses were effective. In terms of axial length, atropine, orthokeratology, peripheral defocus modifying contact lenses, pirenzepine, and progressive addition spectacle lenses were effective. The most effective interventions were pharmacologic, that is, muscarinic antagonists such as atropine and pirenzepine. Certain specially designed contact lenses, including orthokeratology and peripheral defocus modifying contact lenses, had moderate effects, whereas specially designed spectacle lenses showed minimal effect.

Purpose: Cell membrane-camouflaged nanoparticles (NPs) are drawing increasing attention because their surfaces acquire some characteristics of the cell membranes, making them a unique class of biomimetic materials for diverse applications. Modification of cell membrane or combination of different types of membranes can enhance their functionality. Methods: We prepared platelet and tumor cell membrane camouflaged β-mangostin-loaded NPs, which were synthesized with platelet–C6 hybrid biomimetic coating, poly(lactic-co-glycolic acid), and β-mangostin (β-PCNPs). Then, we evaluated their targeting ability and anticancer activity against glioma in vitro and in vivo. Results: Biomimetic coating enhanced active drug targeting and immune escape properties of nanocarrier in C6 and THP-1 cells, respectively, which improved their cytotoxicity. β-PCNPs were characterized to study the inherent properties of both source cells. Compared with bare β-NPs, β-PCNPs exhibited high tumor-targeting capability and induced apoptosis of C6 cells in vitro. Similarly, intravenous administration of drug through β-PCNPs resulted in enhanced tumor-targeting and exhibited excellent rate of inhibition of glioma tumor growth in mice. Moreover, the blood circulation time of drug in mice in the β-PCNP group was markedly prolonged and these mice exhibited better outcome than those in the β-NP group. Conclusion: These results provide a new strategy of utilizing PCNPs as carriers for drug delivery, which improves the targeting efficiency and therapeutic efficacy of chemotherapeutic agents for glioma therapy.

Background: Brain tumors are one of the leading causes of epilepsy, and brain tumor‐related epilepsy (BTRE) is recognized as the major cause of intractable epilepsy, resulting in huge treatment cost and burden to patients, their families, and society. Although optimal treatment regimens are available, the majority of patients with BTRE show poor resolution of symptoms. BTRE has a very complex and multifactorial etiology, which includes several influencing factors such as genetic and molecular biomarkers. Advances in multi‐omics technologies have enabled to elucidate the pathophysiological mechanisms and related biomarkers of BTRE. Here, we reviewed multi‐omics technology‐based research studies on BTRE published in the last few decades and discussed the present status, development, opportunities, challenges, and prospects in treating BTRE.Methods: First, we provided a general review of epilepsy, BTRE, and multi‐omics techniques. Next, we described the specific multi‐omics (including genomics, transcriptomics, epigenomics, proteomics, and metabolomics) techniques and related molecular biomarkers for BTRE. We then presented the associated pathogenetic mechanisms of BTRE. Finally, we discussed the development and application of novel omics techniques for diagnosing and treating BTRE.Results: Genomics studies have shown that the BRAF gene plays a role in BTRE development. Furthermore, the BRAF V600E variant was found to induce epileptogenesis in the neuronal cell lineage and tumorigenesis in the glial cell lineage. Several genomics studies have linked IDH variants with glioma‐related epilepsy, and the overproduction of D2HG is considered to play a role in neuronal excitation that leads to seizure occurrence. The high expression level of Forkhead Box O4 (FOXO4) was associated with a reduced risk of epilepsy occurrence. In transcriptomics studies, VLGR1 was noted as a biomarker of epileptic onset in patients. Several miRNAs such as miR‐128 and miRNA‐196b participate in BTRE development. miR‐128 might be negatively associated with the possibility of tumor‐related epilepsy development. The lncRNA UBE2R2‐AS1 inhibits the growth and invasion of glioma cells and promotes apoptosis. Quantitative proteomics has been used to determine dynamic changes of protein acetylation in epileptic and non‐epileptic gliomas. In another proteomics study, a high expression of AQP‐4 was detected in the brain of GBM patients with seizures. By using quantitative RT‐PCR and immunohistochemistry assay, a study revealed that patients with astrocytomas and oligoastrocytomas showed high BCL2A1 expression and poor seizure control. By performing immunohistochemistry, several studies have reported the relationship between D2HG overproduction and seizure occurrence. Ki‐67 overexpression in WHO grade II gliomas was found to be associated with poor postoperative seizure control. According to metabolomics research, the PI3K/AKT/mTOR pathway is associated with the development of glioma‐related epileptogenesis. Another metabolomics study found that SV2A, P‐gb, and CAD65/67 have the potential to function as biomarkers for BTRE.Conclusions: Based on the synthesized information, this review provided new research perspectives and insights into the early diagnosis, etiological factors, and personalized treatment of BTRE.