Objective To investigate the radiobiological effects of VPA-BSANPs on C6 and U87 glioma cells in vitro.Methods C6 and U87 glioma cells were treated with different concentrations of VPA and VPA-BSANPs for 12 h and 24 h,and MTT assay was used to determine cell viability.C6 and U87 cells were treated with different concentrations of VPA and VPA-BSANPs conbined with X-ray irradiation (0,2,4,6,and 8 Gy),and colony formation assay was used to determine plating efficiency (PE).C6 and U87 glioma cells were treated with different concentrations of VPA and VPA-BSANPs for 12 h,followed by X-ray irradiation (0,4,and 8 Gy),and flow cytometry using Annexin V-FITC/PI staining was used to examine cell apoptosis.Western blot was used to evaluate the effects of VPA and VPA-BSANPs on radiation-induced apoptosis protein expression.One-way ANOVA was used for comparison of means with homogeneity of variance between multiple groups,and the t-test was used for comparison of means between two groups.Results Without irradiation,VPA and VPA-BSANPs had no significant inhibitory effects on the proliferation of C6 and U87 cells (P=0.328,0.920).The PE of cells treated with VPA-BSANPs combined with irradiation was significantly lower than that of cells treated with VPA combined with irradiation (P=0.000).In C6 and U87 cells,VPA-BSANPs combined with irradiation increased the expression of p53 and Bax (P =0.000,0.000 and P =0.010,0.002),but reduced the expression of Bcl-2 (P =0.008,0.000).Active caspase-3 fragments were only found in the cells treated with VPA-BSANPs combined with irradiation and VPA combined with irradiation,but were less in the former cells than in the latter cells (P=0.004).The active fragments of peroxisome proliferator-activated receptor were only found in the cells treated with VPA-BSANPs combined with irradiation.Conclusions VPA-BSANPs can increase the radiosensitivity of C6 and U87 glioma cells in vitro,possibly by promoting the apoptosis of tumor cells induced by radiation.

Objective To investigate proteolipid protein 1 (PLP1) mutations in six pedigrees with Pelizaeus-Merzbacher disease (PMD),and to provide prenatal consulting and prenatal diagnosis.Methods Subjects were six probands with PMD admitted in Department of Pediatrics,Peking University First Hospital from July 2006 to November 2011 and their family members.Genomic DNA sarnples were extracted from peripheral bloods of probands and their family members.Multiplex ligation-dependent probe amplification (MLPA) technique was used to detect PLP1 duplication mutation.Direct DNA sequencing was used to detect point mutation.Genetic diagnosis were based on PLP1 mutation genotype from probands.Prenatal diagnosis of nine fetuses were performed from seven PLP1 mutation female carriers by fetuses' DNA extracted from amniocytes or villus cells.Results PLP1 duplications were found in probands 1-4 (P1-4) whose mothers and the aunt of proband 1 (P1) were PLP1 duplications carriers.The two cases of point mutation,c.96C＞G(p.F32L) and c.623G＞T (p.G208V),were found in proband 5 (P5) and proband 6 (P6).Hcterozygous changes of the same mutations were found in P5' and P6' mothers with normal phenotypes.Seven female PLP1 mutation carriers were pregnant again.Prenatal diagnosis of PLP1 for nine fetuses presented one PLP1 duplication,one point mutation,one PLP1 duplication carrier,and six wildtypes.A segmental crossing over of X chromosome was detected in one male fetus of PLP1 wildtype.Conclusions PLP1 mutation analysis could help to diagnose PMD pedigree and to identify female PLP1 mutation carrier in the family.The following prenatal diagnosis and proper genetic counseling are very important to prevent PMD child from being delivered.

Primary liver cancer has various potential causes and insidious onset, and its progression is affected by many factors. Immunotherapy and targeted drug therapy have been used as non-radical treatment methods for primary liver cancer, but they cannot achieve a satisfactory effect and may lead to drug resistance. In recent years, the wide application of 16s high-throughput sequencing and the in-depth studies of microbiology have revealed the key role of microorganisms in the development and progression of liver cancer. The association of the liver with oral and intestinal flora is gradually clarified, and the regulation of oral and intestinal flora has brought new treatment methods for the disease. This article reviews the microbial theory of the oral-gut-liver axis and its application and development in the treatment of primary liver cancer.

Objective:To study the current status of longitudinal extrauterine growth restriction (EUGR) in extremely preterm infants (EPIs) and to develop a prediction model based on clinical data from multiple NICUs.Methods:From January 2017 to December 2018, EPIs admitted to 32 NICUs in North China were retrospectively studied. Their general conditions, nutritional support, complications during hospitalization and weight changes were reviewed. Weight loss between birth and discharge > 1SD was defined as longitudinal EUGR. The EPIs were assigned into longitudinal EUGR group and non-EUGR group and their nutritional support and weight changes were compared. The EPIs were randomly assigned into the training dataset and the validation dataset with a ratio of 7∶3. Univariate Cox regression analysis and multiple regression analysis were used in the training dataset to select the independent predictive factors. The best-fitting Nomogram model predicting longitudinal EUGR was established based on Akaike Information Criterion. The model was evaluated for discrimination efficacy, calibration and clinical decision curve analysis.Results:A total of 436 EPIs were included in this study, with a mean gestational age of (26.9±0.9) weeks and a birth weight of (989±171) g. The incidence of longitudinal EUGR was 82.3%(359/436). Seven variables (birth weight Z-score, weight loss, weight growth velocity, the proportion of breast milk ≥75% within 3 d before discharge, invasive mechanical ventilation ≥7 d, maternal antenatal corticosteroids use and bronchopulmonary dysplasia) were selected to establish the prediction model. The area under the receiver operating characteristic curve of the training dataset and the validation dataset were 0.870 (95% CI 0.820-0.920) and 0.879 (95% CI 0.815-0.942), suggesting good discrimination efficacy. The calibration curve indicated a good fit of the model ( P>0.05). The decision curve analysis showed positive net benefits at all thresholds. Conclusions:Currently, EPIs have a high incidence of longitudinal EUGR. The prediction model is helpful for early identification and intervention for EPIs with higher risks of longitudinal EUGR. It is necessary to expand the sample size and conduct prospective studies to optimize and validate the prediction model in the future.