Objective To predict the potential targets of apigenin by virtual screening .Methods The targets preliminarily forecast by PharmMapper ,were validated by associating data mining and Autodock Vina in PyRx 0 .8 .Subsequently ,receptor‐ligand interactions were analyzed by Discovery Studio 3 .5 .Results The virtual screening by PharmMapper indicated that apigenin coupled well with the disease‐related targets including insulin receptor ,estradiol 17‐beta‐dehydrogenase 1 ,and cathepsin K .According to the data mining ,insulin receptor was found in related experimental researches ,while the other two had few reports previously .And then ,the interactions between apigenin and the target proteins were analyzed by Autodock Vina and Discovery Studio Visualizer 3 .5 ,involving hydrogen bonds ,electrostatic forces ,van der Waals forces etc .Conclusion The most potential targets of apigenin were insulin receptor ,while 17‐beta‐dehydrogenase 1 and cathepsin K were also possible .

Objective:To explore grouping methods of subdividing adjacent diagnosis related groups(DRGs) by introducing patient clinical complexity level(PCCL) principle and provide references for exploring DRG grouping method in line with context in China.Methods:Clinical complexity level of each complication was assigned by clinicians.PCCL model was selected to calculate the scores of clinical complexity cases.Each adjacent DRG was subdivided into DRG groups by classification and regression trees(CART) model.The rank-sum test was applied to test the statistical significances of the grouping results.Results:9 surgical adjacent DRGs were subdivided into 18 DRG groups.There were statistical significances in the differences of hospitalization expenses and length of stay among different DRG groups in each adjacent group.Conclusion:PCCL model showed high performance in DRG subdivision.The unification of the quality of medical records and coding were the key factors to ensure the reasonable grouping results.

Objective:The regulatory mechanisms of LCRG1 gene expression is undear,this study was to investigate the transcription regulation of the promoter of human LCRG1 gene by transcription factors Sp1 and Egr-1.Methods:Analysis of putative binding sites of transcription factors in the promoter of human LCRG1 gene by online program MatInspector,Co-transfection with the expression plasmids of the known transcription factors such as Sp1、wtEgr-1、mtEgr-1with the LCRG1 reporter construct analyze potent transcription factor for enhancement of the promoter activity.Results:SP1 and Egr-1 transcription factor binding site sites were predicted in the region by bioinformatics analysis,mtEgr-1 can enhance the promoter activity.Conclusion:mtEgr-1 may be involved in the regulatory mechanisms of LCRG1 gene expression

Objective To compare clinical effect of MTA and Vitapex for young permanent teeth with periapical incomplete apical closuret . Method Teeth 90 were chosen from 80 patients at 7-25 years old young permanent teeth with periapical and randomly divided into MTA group and Vitapex group 45 in each group.Two groups were treated with MTA and Vitapex paste treatment respectively.6-month and 12-month after treatment followed up, observed clinical efficacy of two groups.Results The six-month recall, X-ray ( MTA group 93.33%, Vitapex group 88.89%) and clinical parameters (MTA group 95.56%, Vitapex group 86.67%) success rate of two group was no significant difference.When the 12-month followed up, X-ray examination of MTA group's success rate was 93.33%, significantly higher than 68.89%Vitapex group (P<0.05), clinical indicators of success rate of 95.56%MTA group,significantly higher than the 71.11%Vitapex group (P<0.05).Pain during root canal therapy (EIP) of the occurrence, MTA group than Vitapex group (P<0.05).Conclusion The effect of short-term treatment of MTA in treatment of young permanent teeth with periapical incomplete apical closure is definite,it is an ideal induce apical molding material.

[ABSTRACT]OBJECTIVETo investigate the cytomegalovirus infection in neonates, characteristics of gap junction protein Connexin26 gene mutation and the hearing follow-up results, and to analyze their correlations. METHODS60 CMV-DNA positive and 40 CMV-DNA negative neonatal newborn from The Second Affiliated Hospital of Wenzhou Medical University and The first people's Hospital of Yongkang were screened, the blood biochemistry was analyzed, and the umbilical cord blood was reserved to detect the Connexin26 gene expression of mRNA with RT-PCR.PCR results was sequenced to track the newborn hearing, and analyze the correlations between neonatal cytomegalovirus types, the mutation of Connexin26 gene and hearing test results.RESULTS 26 cases from 60 CMV-DNA positive newborns were found with blood biochemical abnormalities. In all of the newborns, a total of 41 cases had 235delC mutation, 11 cases in the mutations for the development of hearing impairment. The results of correlation analysis showed that there were correlations between cytomegalovirus infection, gene mutation and hearing impairment.CONCLUSION Cytomegalovirus infection in neonates can lead to mutations in the Connexin26 gene, and may further lead to hearing impairment, and the probability of the mutation of Connexin26 gene and sensorineural hearing loss were higher in symptomatic cytomegalovirus infection neonates.

Objective To investigate the effects of chitosan/pCDNA3.1 (+) CrmA on matrix metalloproteinase (MMP)-1 and tissue inhibitor of metalloproteinase (TIMP)-1 expression of chondrocytes induced by interleukin-1β (IL-1β) in mRNA and protein levels.Methods Rabbit chondrocytes were isolated and cultured.Chondrocytes were treated with PBS,10 μg/ml chitosan (CS) and chitosan/ pCDNA3.1 (+)CrmA respectively for 6 hours.Then 10 ng/ml IL-1β was added into the culture medium.After 48 hours,real time polymerase chain reaction (real time PCR) and Western blot assay were used to examine the changes of MMP1 and TIMP-1 in mRNA and protein levels.Results In CS/pCDNA3.1 (+)CrmA treated group (0.44±0.04),the messenger RNA expression of MMP-1 in chondrocytes was significantly suppressed compared with corresponding samples of PBS treated group (1.00±0.05) and CS treated group (0.76±0.07),There was significant difference between three groups (F=106.93,P＜0.01).The MMP-1 protein expression of chondrocytes in CS/pCDNA3.1 (+)CrmA treated group (0.28±0.03) was lower than that of PBS treated group (0.73±0.06) and CS treated group (0.46±0.05)(F=59.66,P＜0.01).No significant difference of TIMP-1 expression among the three groups was observed in mRNA and protein levels.Conclusion CS/pCDNA3.1(+) CrmA can significantly inhibit the mRNA and protein expressions of MMP-1 of chondrocytes induced by IL-1β,which leads to up-regulation the ratio of TIMPs to MMPs of IL-1β induced chondrocytes.It may be a part of the mechanisms of the therapeutic effects of CS/pCDNA3.1 (+)CrmA on osteoarthritis.

By sorting out 2005-2015's literature on the mechanism of acupuncture and moxibustuion treatment for lumbar intervertebral disc herniation, this article concludes that the studies focused mainly on six aspects: improvement in nail fold microcirculation, improvement in neural ultrastructure, regulation of bodily autoimmunity, improvement in hemorheological indicators, regulation of neuroelectrophysiology and regulation of chemical neuroinflamma- tory mediators. A summary is made from the six aspects.

OBJECTIVE To explore the effect of matrine induced proliferation, apoptosis and auto-phagy on human medulloblastoma cell line D341 in vitro. METHODS D341 cells in vitro were incubated with matrine 0, 0.5, 1.0, 1.5 and 2.0 g.L-1 for 24, 48 and 72 h, respectively. The proliferation of D341 cells was analyzed using Cell Counting Kit-8 assay. Apoptosis was detected by flow cytometry. The mor-phologic change of cells was observed under a transmission electron microscope. The expression of Bax, Bcl-2, caspase 3, microtubule associated protein 1 light chain 3 (LC3) and beclin1 was detected by Western blotting, and the expression of LC3 and beclin1 was detected by Western blotting with or without the autophagy inhibitor 3-methyladenine(3-MA). 3-MA was added 1 h before matrine and the final concentration of 3-MA was 5 mmol.L-1 . RESULTS Matrine significantly inhibited the proliferation of D341 cells. There was a concentration-effect relationship ( r24 h = 0.994, r48 h = 0.992, r72 h = 0.996, P<0.01). Matrine could induce the cell apoptosis (r24 h = 0.937, r48 h = 0.947, r72 h = 0.987, P<0.01). When the concentration of matrine was 2.0 g.L-1 , the inhibitory effect on D341 cell proliferation (r=0.999, P<0.01) and the induction of cell apoptosis (r=0.990, P<0.01) had a time-dependence. When the concen-tration of matrine was 2.0 g.L-1 , the ultrastructure of the D341 cells had obvious change. Cells with acoustic cavitation bubble structure, chromatin condensation, and marginalization were observed after matrine treatment for 24 h. After 48 h treatment with matrine, nuclear chromatin condensation and more vacuoles in the cytoplasm were observed. After 72 h treatment with matrine, cells exhibited apoptotic characteristics with obvious nuclear chromatin condensation, and nuclear fragmentation, significantly increased the larger cytoplasmic vacuoles. Western blotting analysis showed that matrine could increase the expression of Bax (r24 h =0.981, r48 h =0.967, r72 h =0.998, P<0.01), and decrease the expression of Bcl-2 (r24 h = -0.977, r48 h = -0.989, r72 h = -0.968, P<0.01). Matrine could increase the expression of caspase 3 when the effect time was 48 h (r48 h =0.995, P<0.01). Matrine also increased the expression of beclin1 (r24 h =0.989, r48 h =0.986, r72 h =0.966, P<0.01). The autophagy inhibitor 3-MA could reduce this effect ( P < 0.05). Matrine decreased the expression of LC3-Ⅰ but increased the expression of LC3-Ⅱ and thus the ratio of LC3-Ⅰ/ LC-Ⅱ was decreased (r24 h = -0.795, r48 h = -0.886, r72 h = -0.901, P<0.05). 3-MA could reduce the effects of matrine on LC3-Ⅰ and LC3-Ⅱ expression of D341 cells (P<0.05). CONCLUSION Matrine can inhibit proliferation, induce apoptosis and promote autophagy of D341 cells in vitro.

Objective:To explore the relationship of lymphocyte function-associated antigen 3 (LFA-3, CD58) expression in glioma with clinical features and its role in clinical prognosis. Methods:Clinical data and mRNA microarray data of 514 patients with glioma were obtained from The Cancer Genome Atlas and were used to study the expression of LFA-3 (CD58). Cox regression was used to analyze the relationship between CD58 expression and survival of patients with glioma. Multivariate analysis of variance was used to further analyze the relationship of CD58 with age, sex, and pathological grade of glioma. Results:The results of the stratified χ2 test of CD58 expression and tumor grading were shown, considering tumor type, gender and age of diagnosis (all P<0.05). CD58 expression was sig-nificantly correlated with overall survival (OS) and disease-free survival (DFS) of patients with glioma. Patients with high CD58 expres-sion presented short OS and DFS (P<0.0001). Conclusion:CD58 possibly promotes tumorigenesis in gliomas and thus can serve as a potential tumor diagnostic marker and individual therapeutic target.