Children with autism spectrum disorders are often accompanied by abnormal eating behavior.The experiment also contains a variety of confounding factors.Due to unclear mechanism and various clinical manifestations.the treatment results of abnormal eating behavior are also different.We review the recent research progress research of abnormal eating behaviorin children with autism spectrum disorders.

Although the incidence of malignant solid tumors in children is not high,it is one of the major death causes in children.MYCN gene amplification is an independent poor prognosis factor of neuroblastoma.MYCN gene involves in neuroblastoma tumorgenesis and is the major evidence of treatment.MYCN gene amplification could be detected in other children's solid tumor.It is associated with unfavorable medulloblastoma pathology,poor outcome of Wilms' tumor and alveolar rhabdomyosarcomas.This review compares different MYCN gene detection methods,makes a summary about the clinical relationship between MYCN gene and children's solid tumor and investigates the possibility of increasing cure rate of malignant solid tumors through molecular specificity treatment.

Programmed cell death 5 ( PDCD5 ),formerly designated as TFAR19 ( TF-1 cell apoptosis-related gene 19),is an apoptosis-regulated gene cloned by Peking University Center for Human Disease Genomics.PDCD5 is expressed in many human tissues,with a high degree of homology,plays a regulatory role during cell apoptosis.Disorders of PDCD5 expression is correlated with tumorigenesis.This article reviews the structure,expression and functions of PDCD5,makes a summary of its relationship with kinds of tumors.Further studies about clinical application of PDCD5 are needed.

Objective To observe the effect of epidermal growth factor (EGF) on integrin α5 expression and its influence on human retinal pigment epithelium (RPE) cells. Methods Human RPE cells were treated in vitro with 0.1, 1.0, 10.0, 20.0 and 100.0 ng/ml of EGF, the mRNA and protein of integrin α5 was measured by reverse transcription polymerase chain reaction(RT-PCR)and flow cytometry. Human RPE cells were cultured under 4 conditions including DMEM/F12, DMEM/F12 + 10 ng/ml EGF, DMEM/F12 + 10 ng/ml EGF+ rabbit anti-human integrin α5 antibody (1: 100), DMEM/F12 + 10 ng/ml EGF+ rabbit anti-human vimentin antibody (1: 100), and their proliferation and migration were measured by methyl-thiazole tetrazolium(MTT)and Boyden chamber. Results The integrin α5 mRNA level of human RPE cells was not changed after 12 hours of EGF stimulation (F=0.618, P = 0. 687), however it was induced in a dose-dependent manner after 24 and 48 hours of EGF stimulation (F=465. 303, 212. 340; P= 0. 000, 0. 000). The protein level of integrinα5 was higher in 10 ng/ml EGF stimulation compared with the control group and 0. 1 ng/ml group (P<0. 01). MTT and Boyden chamber showed that the integrin α5 expression increased the proliferation and migration of human RPE cells. Conclusion EGF can induce integrin α5 expression, thus increase the proliferation and migration of human RPE cells.

Background Human retinal pigment epithelial(RPE) cells play a critical role in the pathogenesis of proliferative vitreoretinopathy(PVR) and other related ocular diseases.Research demonstrated that epidermal growth factor(EGF) stimulates activation of RPE cells and therefore causes PVR,and integrin α_5 mediates the adhesion of cells and EGF.Objective This study aims to investigate the role of mitogen-activated protein kinase(MAPK) in regulation of EGF on integrin α_5 expression in human RPE cells.MethodsHuman RPE cells strain(CRL2302) was cultured in DMEM/F12 with 10% calf serum and passaged in 0.25% trypsin.Cultured cells were divided into DMEM/F12control group,20μmol/L PD98059 +10 ng/mL EGF＋DMEM/F12(PD98059) group and 10 ng/mL EGF＋DMEM/F12(EGF) group.The expression of integrin α_5 protein in CRL2302 cells was detected by RT-PCR and calculated as α_5 mRNA/β-actin mRNA,and the expression of integrin α_5 mRNA in CRL2302 cells was detected evaluated by flow cytometry.The MAPK phosphorylation level in each group of human RPE cells was tested by Western blot.ResultsThe expression value of integrin α_5 mRNA was 0.93±0.06 in the control group,1.06±0.07 in PD98059 group and 1.97±0.09 in EGF group,showing a significant difference among the three groups(F=458.896,P<0.01).The fluorescence intensity of integrin α5 protein in CRL2302 cells after 24 hours was 1.94±0.22,4.56±0.25,2.39± 0.14 in three groups respectively with a significant difference(F=21.05,P<0.05).After 30 minutes of culture,Western blot result showed that the strongest phosphorylation levels of ERK1/2 activation in EGF group and the weakest phosphorylation levels of ERK1/2 activation in the control group;While that in PD98059 group was significantly stronger than control group and weaker than EGF group(F=143.14,P<0.01).ConclusionEGF stimulates activation of ERK1/2 pathway in human RPE cells and the expressions of integrin α_5 mRNA and protein in human RPE cells in vitro.

Objective To observe the influence of down-regulation of HtrA1 expression by small interfering RNA on light-injured human retinal pigment epithelium (RPE) cells.Methods Cultured human RPE cells(8th-12th generations)were exposed to the blue light at the intensity of (2000 ± 500) Lux for 6 hours to establish the light injured model.Light injured cells were divided into HtrA1 siRNA group,negative control group and blank control group.HtrA1 siRNA group and negative control group were transfected with HtrA1 siRNA and control siRNA respectively.The proliferation of cells was assayed by CCK-8 method.Transwell test was used to detect the invasion ability of these three groups.Flow cytometry was used to detect the cell cycle and apoptosis.The expression of HtrA1 and vascular endothelial growth factor (VEGF)-A was detected by real time-polymerase chain reaction and Western blot respectively.Results The mRNA and protein level of HtrA1 in the light injured cells increased significantly compared to that in normal RPE cells (t=17.62,15.09;P＜0.05).Compared with negative control group and blank control group,the knockdown of HtrA1 in HtrA1 siRNA group was associated with reduced cellular proliferation (t=6.37,4.52),migration (t =9.56,12.13),apoptosis (t =23.37,29.08) and decreased mRNA (t=17.36,11.32,7.29,4.05) and protein levels (t=12.02,15.28,4.98,6.24) of HtrA1 and VEGF-A.Cells of HtrA1 siRNA group mainly remained in G0/G1 phase,the difference was statistically significant (t=6.24,4.93;P ＜0.05).Conclusion Knockdown of HtrA1 gene may reduce the proliferation,migration capability and apoptosis of light-injured RPE cells,and decrease the expression of VEGF-A.

Objective To compare the efficacy and safety of vitrectomy combined with internal limiting membrane flap and vitrectomy combined with internal limiting membrane peeling for the treatment of idiopathic macular hole with different sizes.Methods A total of 127 consective patients (127 eyes)were divided into two groups according to the size of the hole diameter of the smallest split points by less than or equal to 500 μm (small diameter macular hole group) and more than 500 μm (huge diameter macular hole group).According to different surgical methods the patients were divided into non ILM flap coverage group (peeling 1 group and peeling 2 group) and ILM flap cover group (covering 1 group and covering 2 group).All the patients underwent vitrectomy combined with internal limiting membrane peeling or vitrectomy combined with limiting membrane flap.Preoperative and postoperative best correct visual acuity,closure ratio of macular hole and postoperative major complications were observed and followed up.Results The postoperative best correct visual acuity improved in all the groups,there was no significance difference between small diameter macular hole group and huge diameter macuiar hole group (t =0.112 2,0.750 8;all P ＞0.05).The closure ratio of peeling 1 group and covering 2 group at postoperative 6 months were all 100％,there was no statistical difference (P ＞ 0.05),which in peeling 2 group and covering 2 group were 84.85％ and 100.00％,there was statistical difference (x2 =13.292,P ＜ 0.05).There was no statistical difference in preoperative defect diameter of the inner and outer junction between peeling 2 group and covering 2 groups (P ＞0.05),there was also no statistical difference between peeling 2 group and covering 2 groups at postoperative 1 months (P ＞ 0.05),but there were statistical differences at postoperative 3 months,6 months and 12 months (all P ＜ 0.05),the covering 2 group were less than the peeling 2 group.Conclusion ILM flap coverage helps to heal macular holes greater than 500 μm diameter,and has no extra effect on healing of diameter less than 500 μm.

The credibility of the third-party mediation agencies in medical disputes lies in their own advantages of efficiency,neutrality,professionalism and objectivity.However,because of the differences of actual operation,the credibility of the third-party mediation agencies often is questioned by both doctors and patients and the public.Aiming at these,this paper would study the status and the pushing approach of the third-party mediation agencies credibility from the perspective of professionalism and neutrality,legislation,fundraising channels and supervision.

0.05). But the amplitudes of the PhNR were significantly reduced in group of primary optic nerve atrophy (P

This study investigated the effect of etoposide, an anticancer chemotherapy drug, on B7-H1 expression in retinoblastoma (Rb) cells and the role of miR-513a-5p in the process. Rb cells were divided into control and etoposide groups. In the etoposide group, cells were treated with etoposide at different concentrations (2.5, 5, 10, 20 and 40 μg/mL) for 24 h. Those given no treatment of etopside served as controls. Reverse transcription polymerase chain reaction (RT-PCR), fluorescence quantitative PCR and flow cytometry were performed to measure the mRNA and protein expression of B7-H1 in Rb cells. The mRNA expression of miR-513a-5p in Rb cells before and after etoposide treatment was also detected by fluorescence quantitative PCR. The miR-513a-5p mimics and the miR-513a-5p inhibitor were transfected into Rb cells separately, and fluorescence quantitative PCR and flow cytometry were used to detect the effect of the miR-513a-5p mimics or inhibitor on B7-H1 expression. TargetScan5.2 was employed to predict the miR-513a-5p binding sites in the 3'-untranslated region of B7-H1 mRNA. Luciferase reporter plasmids carrying this site were prepared and transfected into Rb cells and luciferase activity analyzed. The results showed that etoposide stimulated the mRNA and protein expression of B7-H1 in Rb cells, which reached a maximal level after treatment with 5 μg/mL etoposide (P<0.05). However, miR-513a-5p expression was decreased in Rb cells after etoposide treatment. When the miR-513a-5p inhibitor was added, B7-H1 expression was increased with the concentration of the miR-513a-5p inhibitor (P<0.05). Moreover, B7-H1 expression was decreased gradually with the concentration of the miR-513a-5p mimics increased (P<0.01). Additionally, the miR-513a-5p mimics were found to inhibit the luciferase activity. It was concluded that etoposide can promote B7-H1 expression in Rb cells, which may be associated with chemoresistance. The promoting effect of etoposide on B7-H1 expression can be reversed by miR-513a-5p mimics. MiR-513a-5p inhibits the mRNA and protein expression of B7-H1 via binding to the 3'-UTR of B7-H1 mRNA.