Epithelial-mesenchymal transition( EMT) refers to the transdifferentiation from epithelial cells to mesenchymal cells. The initial understanding of EMT is originated from the research on embryonic develop-ment,followed by the discovery of EMT phenomenon in physiological and pathological process in multicellular organism. In recent years,the occurrence and development of infiltration and metastasis of tumor cells along with fibrotic diseases that related to EMT are becoming the hot researches nowadays.

From ethics angle analysis of the characteristics of the doctor -patient contradiction in the new peri-od, clear the hospital party committee in the political core position in the construction of a harmonious doctor -pa-tient relationship , and puts forward play the ethical function of the hospital party committee in building a harmoni -ous doctor-patient relationship , finally summarize the hospital party committee in rebuilding the harmonious doctor-patient relationship specific ethical measures , including: strengthening the ethical and moral education , in -depth professional moral education; Hospital ethics committee , and actively promote ethical operation system; To improve medical environment , mobilize the enthusiasm of the party branch;And improve the mechanism of doctor-patient communication , to protect patients′right to know and privacy;The treatment medicine , commercial brib-ery letter-inquiring-and-accusing work mechanism .

Delayed wound healing of diabetic cornea may be associated with the activation of MAPK signal pathway,impaired signal transduction of TGF-? signal pathway,abnormal expression of genes related to insulin signal pathway and reduced expression of insulin receptor.In addition,the activation of NF-?b and cytochrome C signal pathway also has harmful influence on delayed wound healing.This paper reviews research progress about signal pathway of delayed wound healing in diabetic cornea.

Objective To study the changes and clinical significance of serum matrix metalloproteinase-9(MMP-9) ,tissue inhibi-tor of metalloproteinase-1(TIMP-1) and vascular endothelial growth factor (VEGF) in infants with early wheezing .Methods Ser-um levels of MMP-9 ,TIMP-1 and VEGF in 116 infants with early wheezing(wheeling group)and 36 healthy infant (control group) were detected by using ELISA .Results Serum levels of MMP-9 ,TIMP-1 and VEGF in wheeling group were significantly higher than those in control group(P<0 .05);In wheeling group ,there was a linear relationship between the level of MMP-9 and VEGF ;the ratio of MMP-9/TIMP-1 was significantly lower in wheeling groups than in control group(P<0 .05) .Conclusion The infants with early wheezing have the dangerous of airway remodeling .Detection of serum levels of MMP-9 ,TIMP-1 and VEGF is of a cer-tain significance for intervention therapy to wheezing infants as early as possible .

Objective To investigate the current formaldehyde pollution levels in the decoration materials in Beijing. Methods Some of the detecting samples were collectted selectively by sampling and some were provided by the manufacturers voluntarily. The contents of formaldehyde in the samples were determined according to the National Standard Detecting Method for the threshold of harmful substances in decoration materials. Results The emission levels of formaldehyde in 15 of 27 man-made board samples were higher than 1.5 mg/L and the rate exceeding the national standard was 56%. The formaldehyde emission level from 1 of the 4 wall-dope samples was higher than the national standard. In 7 gooey samples,the content of formaldehyde in 1 sample was higher than the national standard. The detecting results of 3 wallpaper samples were all accorded with the national hygienic standard. Conclusion The results of this investigation indicated that some problems did exist in the current decoration materials made in our country. The relatively serious problem among them was that the emission level of formaldehyde from the man-made boards and its related products was much higher than the national standard.

Objective To observe inhibition rate of mouse mammary adenocarcinoma(EMT6) and inhibition effect on tumor angiogenesis of Panax notoginseng F.H. Chen and Cordyecps sinensis Sacc. powder. Methods BALB/C mice as bearing cancer animals with subcultured mouse-transplantable EMT6 cell train had accepted intervention treatment by Panax notoginseng F.H. Chen and Cordyceps sinensis Sacc. powder. In this way,inhibition rate of the mouse-transplanted EMT6 by the powder was recorded and the expression of microvessel density(MVD),vascular endothelial growth factor(VEGF) and tissue inhibitor of metalloproteinase-2(TIMP-2) in the tumor tissue after paraffin imbedding and section were detected through immunohistochemistry technique. Results The tumor inhibition rates of two designed dose groups were separately 48.95% and 37.64%. MVD and VEGF expressions of tumor tissue in the two group were significantly suppressed while the TIMP-2 expression increased. Conclusions Panax notoginseng F.H.Chen and Cordyceps sinensis Sacc. powder can restrain the growth of EMT6,and the pathway of this function is likely related to inhibiting tumor angiogenesis.

O-GlcNAcylation is the addition of a single N-acetylglucosamine(GlcNAc)moiety to the hydroxyl groups of serine or threonine residues of nuclear and cytoplasmic proteins. The transcription factors, kinases of the metabolic pathways and some cytoplasmic enzymes can be O-GlcNAcylated to affect cell transcription, signal transduction, cell metabolism and other biological functions. Abnormal glucose metabolism of tumors has been a hotspot in the research field of tumor pathogenesis and therapeutic targets recently. O-GlcNAclation regulates the glucose metabolism of tumor by affecting the activity of kinases in the metabolic pathway, which is closely associated with the abnormal glucose metabolism of tumor. The abnormal O-GlcNAcylation is one of the potential reasons of cancer. In this review, in order to provide a theoretical reference for developing anti-tumor targets and drugs targeting O-GlcNAc modification, we briefly summarized how O-GlcNAcylation regulated glucose metabolism on glucose metabolism, glucose uptake, glycolysis, pentose phosphate pathway and tricarboxylic acid cycle in cancer cell.

Objective To investigate the effects of leptin on proliferation of the breast carcinoma MCF-7 cells in terms of protein and nRNA of Rab-25 and C-myc.Methods MCF-7 cells were treated with leptin and normal saline (NS) as control.The 490 nm OD values of cells were read by MTT and the protein and mRNA expressions of Rab-25 and C-myc were measured by western blot and RT-PCR methods in two groups.Results Compared with control group,leptin can promote the proliferation of MCF-7 cells in a dose and time dependent manner within certain limit and up-regulate the protein expressions of Rab-25 and C-myc in the breast carcinoma MCF-7 cells (P ＜ 0.05).However,leptin also can up-regulate the mRNA expressions of Rab-25 but without significance (P =0.05).On the contrary,leptin can also up-regulate the mRNA expressions of C-myc (P ＜ 0.05).Conclusion Leptin promotes breast cancer cells proliferation,which may be related to up-regulate the protein and mRNA expressions of Rab-25 and C-myc.It could provide theoretical foundation and new target of gene therapy in the clinical treatment of breast cancer.

Objective: To investigate the effect of alendronate on serum total alkaline phosphatase (AKP) and bone specific alkaline phosphatase (BAP) in the elderly female patients with postmenopausal osteoporosis and explore their correlations.Methods: A retrospective study was performed.Totally 286 elderly female patients with postmenopausal osteoporosis were divided into two groups(according to AKP levels before the treatment of alendronate): the normal AKP group (n=245) and the elevated AKP group (n=41).Raised AKP of all the patients in the elevated AKP group was not associated with hepatobiliary problems.The changes of AKP and BAP levels were analyzed after the treatment of alendronate.The correlations between BAP and AKP levels before and after the treatment of alendronate were analyzed, as well as between the changes in AKP (ΔAKP) and BAP (ΔBAP) levels.Results: AKP and BAP tended to be higher in elderly patients.BAP levels in the normal AKP group were higher than those in the elevated AKP group (P＜0.05).BAP was signicantly correlated with AKP both before and after the treatment (P＜0.05), as well as the correlation between ΔAKP and ΔBAP (P＜0.05).Conclusion: AKP and BAP both tend to increase with age.In elderly female patients with postmenopausal osteoporosis and elevated AKP associated with non-hepatobiliary problems, alendronate treatment can lower AKP levels, and the decrease is strongly correlated with the decrease in BAP.

AIM:To explore the regulatory effect of microRNA-3666 (miR-3666) on the expression of its tar-get gene phosphatase and tensin homologue deleted on chromosome ten (PTEN) in leukemic cells.METHODS: miR-3666 expression levels in normal peripheral blood mononuclear cells and leukemic cells were determined by quantitative real-time PCR.miR-3666 targeting PTEN 3'-untranslated region (3'UTR) was predicted by TargetScan software .3'UTR of PTEN was inserted in the dual luciferase reporter vector psiCHECK 2.The reporter activity was evaluated by the Dual-Lu-ciferase Reporter Assay System after the luciferase promoter vector and miRNA were co -transfected into HEK293T cell line. K562 cells were transfected with synthetic miR-3666 inhibitor ( anti-miR-3666) or a synthetic control miRNA ( anti-miR-C) .The expression of PTEN protein in the above transfected K 562 cells was determined by Western blotting .RESULTS:miR-3666 was up-regulated in the human leukemic cell lines and primary leukemic cells compared to normal peripheral blood mononuclear cells .The results of dual luciferase assays validated PTEN as a specific target gene of miR-3666.Inhi-bition of miR-3666 resulted in an up-regulation of PTEN protein expression in the K 562 cells.CONCLUSION:miR-3666 is over-expressed in leukemic cells .The abnormal over-expression of miR-3666 may play a key role in leukemia due to the down-regulation of PTEN .