[Effects of eye exercises on axial eye elongation in junior students].

Objective: To evaluate the association between the eye exercises and one-year axial eye elongation in grade 7 students in Beijing. Methods: Sampling was performed using a multistage random cluster approach, and 1 443 students of grade 7 were selected from 9 middle schools in 6 districts for the baseline survey. Data were collected by questionnaires and axial length measurement. Multiple linear regression analysis was used to evaluate the association between eye exercises and excessive axial eye elongation. Results: Among 1 197 (82.95%) students with complete information, the median (QR) age was 12.00 (1.00) years old, girls accounted for 44.28%, and the median (QR) axial eye elongation was 0.22 (0.18) mm. In the multiple linear regression analysis, the frequency of eye exercises was significantly correlated with excessive axial eye elongation in boys (ß=-0.135, 95%CI:-0.253--0.018) but not in girls (ß=-0.075, 95%CI:-0.207- 0.058) after adjusting for sex, age, body height, the number of myopic parents, time spent outdoors and time spent on reading and writing outside class; while the seriousness of eye exercises was not significantly associated with axial eye elongation in boys (ß=-0.028, 95%CI: -0.114-0.058) and girls (ß=-0.035, 95%CI: -0.134-0.064). Conclusion: The increased frequency of eye exercises is beneficial to control the axial eye elongation in boys in Beijing.

Drug-eluting bead bronchial arterial chemoembolization vs. chemotherapy in treating advanced non-small cell lung cancer: comparison of treatment efficacy, safety and quality of life.

OBJECTIVE: This present study aimed to compare the treatment response, survival profile, quality of life (QoL), and safety between drug-eluting bead bronchial arterial chemoembolization (DEB-BACE) and chemotherapy in the treatment of advanced non-small-cell lung cancer (NSCLC). PATIENTS AND METHODS: Totally, 44 advanced NSCLC patients were analyzed retrospectively and were divided into DEB-BACE group (n=23) and chemotherapy group (n=21). Treatment response, European Organization for Research and Treatment of Cancer QoL Questionnaire-Core 30 (EORTC QLQ-C30), progression-free survival (PFS), overall survival (OS), and adverse events were assessed during the follow-up. RESULTS: At month (M) 2, M4 and M6 post initial treatment, objective response rate (ORR) was elevated (all p <0.05), and disease control rate (DCR) tended to be higher (without statistical significance) in DEB-BACE group compared with chemotherapy group. Regarding the QLQ-C30 item scores, the scores of physical functioning, role functioning, emotional functioning, cognitive functioning, social functioning were increased, while the scores of nausea and vomiting, dyspnea, constipation were decreased in DEB-BACE group compared with chemotherapy group (all p <0.05). Based on survival profile, DEB-BACE group achieved better PFS and OS compared with chemotherapy group independent of TNM stage, which was also supported by further subgroup analysis and Cox's proportional hazard regression analysis (all p <0.05). Furthermore, two groups all exhibited mild and tolerable adverse events. CONCLUSIONS: DEB-BACE has the potential to be an additional treatment option with favorable therapeutic efficacy, improved QoL, and tolerable safety for advanced NSCLC patients.

Gender-specific SBNO2 and VPS13B as a potential driver of osteoporosis development in male ankylosing spondylitis.

To identify the critical genes and pathways that related to OP development in male AS patients, bioinformatic gene analysis and qRT-PCR validation were performed. SBNO2 and VPS13B were identified as the potential target for OP development, which may be valuable for the prevention of OP in male AS patients. INTRODUCTION: Osteoporosis (OP) is common in men with ankylosing spondylitis (AS). The specific pathogenesis of OP in AS, however, is still unclear. The present study attempted to identify potential genes associated with the development of OP in males with AS. METHODS: Gene expression profiles were downloaded from the GSE73754 and GSE35959 datasets from the Gene Expression Omnibus (GEO). Data from OsteoporosAtlas were downloaded as a supplement. Differentially expressed genes (DEGs) were determined with the limma package. The overlapping DEGs between male AS-related genes and OP-related genes were determined. The DEGs were validated by qRT-PCR in the blood samples of males with AS. Weighted gene co-expression network analysis (WGCNA) was utilized to establish a co-expression network to identify the hub genes. RESULTS: A total of 17 overlapping DEGs were identified; 6 genes in 17 overlapping DEGs were verified as the essential genes in the pathogenesis of OP in male AS by qRT-PCR analysis. After WGCNA, the modules of MEblue (> 0.6) and MEred (> 0.8) were screened out by the correlation analysis and were determined to function mainly in MAPK signaling pathway and osteoclast differentiation. Analysis of the two modules revealed VPS13B and SBNO2 as key genes due to the high degree of correlation. Both genes play an important role in bone metabolism regulation in male AS. Two hub genes MYD88 in MEblue and NCK1 in MEred with high degree of connectivity were selected. CONCLUSIONS: Gender-specific SBNO2 and VPS13B may be key genes involved in OP in male AS.

Delivery of an miR155 inhibitor by anti-CD20 single-chain antibody into B cells reduces the acetylcholine receptor-specific autoantibodies and ameliorates experimental autoimmune myasthenia gravis.

MicroRNA-155 (miR155) is required for antibody production after vaccination with attenuated Salmonella. miR155-deficient B cells generated reduced germinal centre responses and failed to produce high-affinity immunoglobulin (Ig)G1 antibodies. In this study, we observed up-regulation of miR155 in the peripheral blood mononuclear cells (PBMCs) of patients with myasthenia gravis (MG), and miR155 was also up-regulated in torpedo acetylcholine receptor (T-AChR)-stimulated B cells. We used an inhibitor of miR155 conjugated to anti-CD20 single-chain antibody to treat both the cultured B cells and the experimental autoimmune MG (EAMG) mice. Our results demonstrated that silencing of miR155 by its inhibitor impaired the B cell-activating factor (BAFF)-R-related signalling pathway and reduced the translocation of nuclear factor (NF)-κB into the nucleus. Additionally, AChR-specific autoantibodies were reduced, which may be related to the altered amounts of marginal zone B cells and memory B cells in the spleens of EAMG mice. Our study suggests that miR155 may be a promising target for the clinical therapy of MG.

Nrf2-mediated protection against UVA radiation in human skin keratinocytes.

Ultraviolet A (UVA, 320-400 nm) radiation is an oxidizing agent that causes significant damage to cellular components and that leads to photoaging and cancer. It strongly induces NF-E2-related factor 2 (Nrf2) expressions in cultured FEK4 human skin fibroblasts but weakly induces it in transformed HaCaT skin keratinocytes. Nrf2 silencing increases cell damage at a moderate dose of UVA irradiation (250 kJ•m(-2)) in FEK4 fibroblasts, but whether a decrease in Nrf2 sensitizes HaCaT keratinocytes to a moderate to high dose (250-500 kJ•m(-2)) of UVA irradiation (i.e., 400 kJ•m(-2), peak emission 365 nm) is currently unknown. A moderate to high dose of UVA irradiation only slightly increased Nrf2 expression in HaCaT skin keratinocytes. Knockdown of Nrf2 by specific silencing of Nrf2 (siNrf2) strongly increased cell damage as gauged by membrane damage (LDH) and cell viability (MTT assay) following this dose of UVA irradiation. These results suggest that decreased Nrf2 significantly increased UVA irradiation-induced cell damage in skin keratinocytes. Nrf2 may play a role in protecting human skin keratinocytes from UVA radiation-induced damage.

Edaravone neuroprotection effected by suppressing the gene expression of the Fas signal pathway following transient focal ischemia in rats.

Preclinical and clinical studies have demonstrated that a free radical scavenger edaravone has neuroprotective effects on ischemic stroke but the underlying mechanism is not fully understood. The aim of this research is to explore the effect of edaravone on the apoptotic process involving the Fas/FasL signaling pathway. Transient focal ischemia in rats was induced for 2 hours by middle cerebral artery occlusion (MCAO). After reperfusion rats were treated i.v. with either edaravone or physiological saline. The expression of Fas-associated death domain protein (FADD), death-associated protein (Daxx) and caspase-8 was examined by immunohistochemistry. The mRNA levels for FADD and Daxx by reverse-transcriptase PCR (RT-PCR) and apoptosis was assessed by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL). Neurological scores and infarction volumes were also evaluated. Edaravone significantly improved the neurological outcome (p<0.05) and reduced the total infarct volumes (p<0.05), compared with saline control. In addition, edaravone-treatment significantly reduced the number of TUNEL-positive cells (p<0.01), reduced expression levels of FADD, Daxx and caspase-8 immunoreactivity (p <0.05 approximately 0.01), and decreased mRNA levels of FADD and Daxx (p<0.05 approximately 0.01) within the peri-infarct area. We conclude that edaravone may protect ischemic neurons from apoptosis via suppressing the gene expression of the Fas/FasL signaling pathway.

[Kindling model of SD rats induced by injection of PTX intraperitoneally].

OBJECTIVE: To observe the kindling model of Sprague-Dawley (SD) rats induced by injection of different doses of picrotoxin (PTX) intraperitoneally, and to evaluate the effect of the drug on the model. METHODS: SD rats were devided randomly into four groups: control group, epilepsy Group I (PTX, 1.5 mg.kg-1.d-1), epilepsy Group II (PTX, 2 mg.kg-1.d-1) and the phenobarbital group. The kindling model of rats was induced by daily injection of PTX intraperitoneally. The seizures in the rats were observed, and the results of electroencephalography (EEG) were recorded. RESULTS: On the 20th day after injection of PTX, 71% SD rats were kindled in epilepsy Group I; 4 rats were dead, 2 rats were at stage IV of convulsions, and 2 rats were at stage V of convulsions in epilepsy Group II; 17% rats were kindled in the phenobarbital group. The EEG demonstrated spike discharges in the kindled rats. CONCLUSIONS: In this models, the better dose of PTX is 1.5 mg.kg-1.d-1, and phenobarbital sodium can protect SD rats injected PTX intraperitoneally from seizure.