Table of Content

05 February 2015, Volume 35 Issue 2

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Notch signaling pathway regulates epithelial-mesenchymal transition and effects the invasiveness and drug resistance of bladder cancer

2015, 35(2):  145-151. 

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Objective To investigate the effect of notch signaling pathway on bladder cancer drug resistance and invasiveness. Methods We observed the changes of growth and morphological of bladder cancer T24, 5637 and J82 cells which treated for 48 hours using γ-secretase inhibitor by inverted microscope; We detected the mRNA and protein levels of the EMT molecular markers, including E-cadherin, N-cadherin, Vimentin and Alpha-smooth muscle actin, by RT-PCR and Western blot in bladder cancer cells; Detected the changes of drug resistance and invasion respectively by MTT and Transwell in bladder cancer cells. Results After completely blocking the Notch signaling pathway, the inverted microscope showed that bladder cancer cells became smaller and more disperse; RT-PCR and Western blot showed the mRNA and protein levels of E-cadherin were up-regulated (P < 0.05), contrast, N-cadherin, Vimentin and Alpha-smooth muscle actin were down-regulated (P< 0.05); The proliferation of bladder cancer cells was significantly inhibited by MTT test; The number of through microporous membrane cells was significantly decreased (P < 0.05) by Transwell test. Conclusion The Notch signaling pathway is completely blocked that could inhibit the proliferation and EMT of bladder cancer cells and reduce drug resistance and invasion in bladder cancer cells，it suggests that drug resistance and invasiveness of bladder cancer can be changed by EMT which is regulated by notch signaling pathway.

High concentrations of urea induces human brain microvascular endothelial cells to produce inflammatory cytokines

2015, 35(2):  152-156. 

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Objective To explore high concentrations of urea-induced human brain microvascular endothelial cells (HBMECs) to produce inflammatory cytokines and possible mechanism. Methods HBMECs were incubated in high concentrations of urea or mannitol(as osmotic control) for 3，6，12 and 24 hours. Expressions of TNF-a and iNOS were observed by Immunofluorescence. Western blot analysis was employed to assess the protein expressions of TNF-a, iNOS, COX-2, NF-κB/P65 and p-P65. NO concentration was determined by a commercial NO assay kit. Results Immunofluorescence showed high positive immunostaining of TNF-a and iNOS after high concentrations of urea stimulued compared with control group .The protein expressions of TNF-a, COX-2 and p-P65 were significantly increased at 3 and 6 hours after high urea treatment (p<0.01), and iNOS were continued to increase from 3 to 24 hours (p<0.01).Moreover, NO content was increased at 3 hours after high urea treatment (p<0.05). Conclusion High concentrations of urea can induce HBMECs to produce inflammatory cytokines.

The expression of CTCF in breast cancer and its impact on cell proliferation

2015, 35(2):  157-161. 

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Objective To observe the expression of CTCF in breast cancer cell lines, tumor tissue and serum of breast cancer patients, and explore preliminarily the effect of CTCF on proliferation of MCF7. Methods Western blot was used to detect CTCF expression in human breast cancer cell lines MCF7, SKBR3, MDA-MB-231 and normal breast cells MCF-10A. Real-time quantitative PCR and immunohistochemistry were applied to detect the mRNA and protein levels of CTCF in invasive ductal carcinoma (n=23), peritumoral tissue (n = 10) and fibroadenoma (n = 10). Enzyme-linked immunosorbent assay (ELISA) was used to detect the concentration of CTCF protein in serum. Furthermore, retroviral vector containing CTCF full length was constructed and retroviruses were packaged, then MCF7 cells were infected to screen clones stably expressing CTCF. Last, MTT assay was applied to detect cell proliferation. Results CTCF expression in MCF-10A was the highest, and decreased gradually in MCF7, SKBR3 and MDA-MB-231. CTCF expression in breast carcinoma tissue were significantly lower than that in peritumoral tissue and benign lesions (P <0.01). CTCF protein concentration in serum of breast cancer patients were also significantly lower than that of healthy control (P <0.01). In addition, CTCF overexpression could inhibit the proliferation of MCF7 cells. Conclusions CTCF expression were declined significantly in breast cancer cell lines, carcinoma tissues and serum of breast cancer patients, compared with the controls. CTCF could inhibit the proliferation of breast cancer cells.

Construction of eukaryotic expression vector of shRNA targeting CIP2A Gene and its inhibition effect on cell proliferation

2015, 35(2):  162-166. 

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Objective To construct eukaryotic vectors expressing short hairpin RNAs (shRNAs) targeting the CIP2A gene and explore its effects on gastric cell line BGC-823. Methods Four oligonucleotides targeting the CIP2A gene were synthesized and cloned into the eukaryotic expression plasmid pGPU6. The recombinant plasmids, pGPU6/GFP/Neo-CIP2A-shRNA-1, 2, 3 and 4, were introduced into BGC-823 cells by lipofectamine-mediated transfection and the infection rate were observed by fluorescence microscope. The gene silencing efficiency was measured by Real-time PCR and Western blot. The effects on proliferation of BGC-823 cells were detected by CCK-8. Results DNA sequencing and enzyme digestion analysis confirmed the identity of the four recombinant shRNA expression vectors. Immunofluorescsence demonstrated that transfection efficiency was above 70%. Transfection of shRNA-1, 2, 3 and 4, significantly knocked down the expression of CIP2A mRNA and protein at 24 h, 48 h and 72 h after transfection. Compared with the 2, 3 and 4, shRNA-1 had the more strong inhibitory effect on the expression of CIP2A mRNA and protein. The CCK-8 assay showed that the anti-proliferation effect on BGC-823 cells were significant (P < 0.05). Conclusion The recombinant vector could effectively inhibit the expression of CIP2A in BGC-823 cells and depress the proliferation of BGC-823 cells.

miR-34a-5p inhibits the erythroid differentiation of K562 cells

2015, 35(2):  167-173. 

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Objective To study the roles of microRNA-34a-5p in the erythroid differentiation of K562 cells.Methods K562 cells were transfected with the microRNA-34a-5p mimics and antisense inhibitors specifically targeting microRNA-34a-5p, respectively. The effects of over-expression or knocking-down of microRNA-34a-5p was examined by Quantitative RT-PCR. Flow Cytometry was performed to detect the levels of specific surface marker of erythroid cells. The benzidine staining assay was used to access the differentiation state of K562 cells. Western blot was performed to detect the level of miRNA targets. Results microRNA-34a-5p was down-regulated at the early stage of K562 erythroid differentiation. Over-expression of microRNA-34a-5p in K562 cells attenuates erythroid differentiation, in contrast, inhibition of microRNA-34a-5p accelerates erythroid pheotypes in K562 cells. c-MYB was the direct target of microRNA-34a-5p in erythroid cells.Conclusion microRNA-34a-5p regulates early erythroid differentiation of K562 cells via repressing c-MYB.

Quercetin-loaded PEG-PE micelles reverse drug resistance of MCF-7 ADRr human breast cancer cells

2015, 35(2):  174-177. 

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Objective To explore whether quercetin-loaded PEG-PE micelles(M-Q) will synergize the growth-inhibitory activity of adriamycin(ADR)by reversing the drug resistance of MCF-7 ADRr breast cancer cells in vitro. Methods M-Q were formed by adding saline to lipid film containing quercetin and PEG-PE. The size of M-Q was characterized by dynamic light scattering(DLS). The inhibition of MCF-7 ADRr cells was evaluated by MTS assay after incubation with M-Q and ADR. Results The incorporation efficiency of quercetin by the micelles was above 74%.The average size of M-Q was 11.11nm. Compared with the quercetin dissolved in ethanol, M-Q more effectively reversed the drug resistance of MCF-7 ADRr cells in vitro. Conclusions PEG-PE micelles may have potential for delivering quercetin to cancer cells for reversal of drug resistance.

CCK-8 Decreases the Expressions of CHOP/Caspase-11/Caspase-1 Induced by LPS in Mouse Monocyte RAW264. 7 cell

2015, 35(2):  178-182. 

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Objective To investigate the effect of CCK-8 on CHOP/caspase-11/caspase-1 expressions by LPS in RAW264. 7 cell. Methods RAW264. 7 cells were incubated with LPS and/or CCK-8 and/or CCK-8 1R blocking agent devazepide for indicated times. CHOP and caspase-11 protein expressions were determined by western blot, caspase-1 activity were analyzed by kit, IL-1β expression levels were analyzed by ELISA. Results Both CHOP and caspase-11 expression were upregulated in LPS-activated RAW264. 7 cell, which were inhibited by pre-treatment of CCK-8. Pre-treatment of devazepide inhibited the effects of CCK-8 significantly.The same results were seen in caspase-1 activity and IL-1β expression. Conclusion CCK-8 exerts an anti-inflammatory effect by inhibiting CHOP/caspase-11/caspase-1 expressions induced by LPS in RAW264. 7 cell. CCK 1R might be responsible for the anti- inflammatory effect of CCK-8.

HMGB1 RNAi inhibits TGF-β1 induced epithelial-mesenchymal transition in A549 cells

2015, 35(2):  183-186. 

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Objective To investigate the role of HMGB1 in epithelial-mesenchymal transition. Methods Specific siRNA of HMGB1 were designed and synthesized. Cultured typeⅡ alveolar epithelial cell line-A549 cells were divided into 4 groups: (1) control group, (2) model group induced by TGF-β1, (3) HMGB1 RNAi group, (4) RNAi negative control group. Cellular morphology changes were observed by phase-contrast microscope. HMGB1 and α-SMA expression in A549 cells was detected by RT-PCR and Western blotting respectively. Results mRNA and protein expression of HMGB1 and α-SMA in TGF-β1 group increased significantly than that in normal control group(P＜0.01). Both of HMGB1 and α-SMA mRNA and protein expression in siRNA-treated cells were decreased significantly compared with that in TGF-β1 group (P<0.01). Conclusions HMGB1 may participate in the TGF- β 1 induced EMT．

Intermedin1－53 inhibits collagen synthesis induced by angiotensinⅡin cadiac fibroblasts of rats

2015, 35(2):  187-190. 

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Objective To investigate collagen metabolism modulation of Intermedin1－53 (IMD1－53) on angiotensin Ⅱ (Ang Ⅱ)-induced rat cardiac fibroblasts. Metheds Cultured SD neonatal rat cardiac fibroblasts, and divided them into control group, AngⅡ + different concentrations IMD1－53 groups.Ⅰand Ⅲ collagen expression in cardiac fibroblasts were measured by Westem blot, IMD1－53 receptor - like receptor (calcitonin receptor-like receptor, CRLR) and transforming growth factor-β (TGF-β) mRNA expression by SYBR Green Ⅰ real-time PCR. Results IMD1-53 significantly inhibited AngII-induced collagen synthesis in cardiac fibroblasts, and this effect was more obvious with the increasment of IMD1－53( P < 0.01，P < 0.05). Similar phenomenon took place on TGF-β expression in cardiac fibroblasts( P < 0.05). Conclusion IMD1－53 inhibited collagen synthetic in cardiac fibrosis induced by AngⅡ, downed TGF-β expression. These might relate to IMD1－53 anti myocardial fibrosis.

Matrine suppresses IFNlammation and correctes Th1/Th2 imbalance in asthmatic rats via downregulating SOCS3

2015, 35(2):  191-195. 

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Objective To investigate the inhibitory effect of matrine on IFNlammation by regulating Th1/Th2 balance in asthmatic rats and underlying mechanism related to SOCS3. Methods Rats, ovalbumin-sensitized to establish asthma model, SD rats were randomly divided into four groups, as follows: control (without any treatment), model group(using ovalbumin-sensitized method to establish asthma mode), treatment group A (low-dose matrine treated asthma rats) and treatment group B (high-dose matrine treated asthma rats). The eosinophil count, goblet cells percentage, IFNlammatory cell IFNiltration in rat lung were analyzed and scored by morphological examination. IL-4 and IFN-γ level in BALF were determined by ELISA and IFN-γ/IL-4 ratio was further calculated. Furthermore, the expression of SOCS3 in mRNA and protein level was detected by qRT-PCR and Western blot, respectively. Results Eosinophil count and percentage, goblet cell percentage and IFNlammatory cell IFNiltration score were significantly lower in treatment group A and B, compare to model group (P<0.05). Compared to control group, group A exhibited a lower IFN-γ level and a higher IL-4 level (P<0.05). IFN-γ level in treatment group A and B were higher while IL-4 level were lower, compare to model group. Meanwhile, SOCS3 mRNA level in rat lung tissue was elevated in model group, compare to control group. Matrine treatment decreased SOCS3 expression in treatment group A and B. Similar trend was found in SOCS3 protein level. Conclusion matrine may exhibit its anti-IFNlammatory effect by inhibiting SOCS3 expression and maintaining Th1/Th2 balance in asthmatic rats.

Effects of microRNA-1 and microRNA-133a on L-type calcium channel Cavβ2 and ?1C subunit during rat cardiomyocyte hypertrophy

2015, 35(2):  196-202. 

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Objective To investigate the regulation of miR-1 and miR-133a on L-type calcium channel β2 subunit(Cavβ2) and ??1C subunit during rat cardiomyocyte hypertrophy. Methods Cardiomyocyte hypertrophy was induced by isoproterenol (ISO, 10 ?mol/L). The targets of miR-1 and miR-133a were predicted by online database microCosm and Targetscan, respectively. The 3' untranslated region sequence of Cavβ2 and ?1C were respectively cloned into reporter vector and then transiently transfected into HEK293 cells. The luciferase activities of samples were measured to verify the expression of luciferase reporter vector. The protein expression of Cavβ2 and ?1C were evaluated by Western blot. The expression level of Cavβ2 and ?1C were inhibited by RNAi to determine the effects of Cavβ2 and ?1C on cardiomyocyte hypertrophy. Results 1) Cavβ2 was the one of potential targets of miR-1, ?1C was the one of potential targets of miR-133a. 2) The luciferase activities of HEK293 cells with the plasmid containing widetype Cavβ2 3'UTR sequence or ?1C were significantly decreased when compared with that of control group(P＜0.05, P＜0.01). 3) Upregulation of the miR-1 and miR-133a level by miR-1 mimic and miR-133a mimic transfection could suppress the protein expression of Cavβ2 and ?1C, respectively(P＜0.01, P＜0.05). 4) Downregulation of Cavβ2 and ?1C by RNAi could markedly inhibit the increase of cell surface area(P＜0.01), the mRNA expression of ANP and ?-MHC(P＜0.05). Conclusion Cavβ2 is the target of miR-1, ?1C is the target of miR-133a. MiR-1 and miR-133a can negatively regulate the expression of L-type calcium channel Cavβ2 and ?1C subunit, resulting in the attenuation of cardiomyocyte hypertrophy.

Epigallocatechin-3-gallate（EGCG）in reducing the LPS induces injury of rat primary cultured glial cells

2015, 35(2):  203-207. 

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Objective To determine the effects of EGCG on lipopolysaccharide (LPS) -induced neuroinflammation and further investigate the role of neuroprotection mediated by EGCG. Method Primary cultures of rat gliacyte were used as an in vitro model to examine the effects of EGCG on LPS-induced neuronal damage. The intracellular Glu and γ-GABA were quantified via HPLC.Then the protein levels of TNF-α,IL-1βand IL-8 were determined by ELISA and western blot assay. Result Compared with the control group, LPS apparently induced the production of intracellular ROS (P<0.05) and released the TNF-α, IL-1β and IL-8 in the primary cultures supernatant (P<0.05). Compared with the LPS group,EGCG significantly attenuated the release of TNF-α, IL-1β and IL-8(P<0.05) and the level of iNOS protein(P<0.05). Result Compared with the control group, LPS apparently induced the production of intracellular ROS(P<0.05) and released the TNF-α,IL-1β and IL-8 in the primary cultures supernatant (P<0.05).Compared with the LPS group, EGCG significantly attenuated the release of TNF-α, IL-1β and IL-8 (P<0.05) and the level of iNOS protein(P<0.05),and rugulated the concentration of Glu/γ-GABA (P<0.05).Conclusion EGCG is effective in protecting against LPS-induced neuroinflammation by anti-inflammatory effects and regulating extracellular Amino acid levels.

The effect of shRNA interfering PLCε1 gene on proliferation and cell cycles of human esophageal carcinoma Eca109 cells

2015, 35(2):  208-212. 

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Objective To explore the impact of silencing PLCε1 gene on proliferation and cell cycles of esophageal carcinoma Eca109 cells. Methods Three plasmid expression vectors (PLCε11, PLCε12 and PLCε13) were constructed to silence PLCε1 gene. A negative control plasmid expression vector (HK) was constructed at the same time to serve as control. The plasmid expression vectors were transfected into esophageal carcinoma Eca109 cells by cations liposome. The plasmid expression vector with the best interference effect (PLCε12) was chosen. The study included Eca109 group, HK group and PLCε12 group. Cell viability of Eca109 cells were evaluated by MTT assay. The cell cycles were detected by FCM. The mRNA expression of P16 and CyclinD1 gene were measured by RT-PCR. Results The cell viability of Eca109 cells in PLCε12 group were 80.73% and 75.88% at 48h and 72h after transfection, which were significantly lower than that of Eca109 cells in HK group (P<0.001). The percentage of S phase Eca109 cells in PLCε12 group was lower than that of Eca109 cells in HK group (P<0.01), the cell cycle of PLCε12 group Eca109 cells was arrested in G0/G1 phase. The P16 gene mRNA expression of PLCε12 group Eca109 cells was higher than that of HK group Eca109 cells (P<0.01). Conclusions Silencing PLCε1 gene might up-regulate P16 gene mRNA expression, arrest the cell cycle in G0/G1 phase and inhibit the proliferation of Eca109 cells.

miR-141 suppresses cell proliferation by targeting EphA2 in human oral squamous cell carcinoma

2015, 35(2):  213-217. 

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Objective To assess the effect of miR-141 on proliferation of human oral squamous cell carcinoma and target relationship between miR-141 and EphA2. Methods pcDNATM6.2-GW-pre-miR-141 was constructed and identified by qRT-PCR. EphA2-WT and EphA2-MT sequences were respectively cloned into pmirGLO plasmid. The potential proliferation function of miR-141 on CAL27 cells was analyzed by MTT. The target relationship between miR-141 and EphA2 was identified by Dual-Luciferase Assay System, qRT-PCR and Western blot. Results We constructed successfully the recombinant plasmids, including pcDNATM6.2-GW-pre-miR-141, pmirGLO-EphA2-WT and pmirGLO-EphA2-MT, and the transfection efficiency of pre-miR-141 was increased in CAL27 cells compared to control group(P＜0.001). miR-141 could suppress the proliferation of CAL27 cells(P＜0.05). Furthermore, a significant reduction of luciferase activities of CAL27 cells co-transfected with pre-miR-141 and EphA2-WT(P＜0.001). The mRNA(P＜0.001) and protein expression levels of EphA2 were decreased in CAL 27 cells transfected with pre-miR-141. Conclusion Overexpression of miR-141 could suppress cell proliferation by targeting EphA2 in CAL27 cells.

Establishment and identification of HUVEC cell strains with over-expression and low expression of RACK1

2015, 35(2):  218-223. 

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Objective To establish several human umbilical vein endothelial cell(HUVEC) strains with over-expression or low expression of Receptor for Activated C Kinase 1 (RACK1), which will provide effective means for future studying the function of RACK1 in arrhythmia. Methods The full-length cDNA sequence of RACK1 gene was amplified and inserted into pIRES2-EGFP. At the same time, designed and synthesised complementary DNA sequences of 3 pairs of short hairpin structure and a pair of negative control sequence, then subcloned into the plasmid pGenesil-1. The HUVEC cells were transfected with these plasmids and screened by using G418. And the expression of RACK1 mRNA and protein in the cells were assayed by qRT-PCR and Western blot, respectively. Results RACK1 eukaryotic expression vector and siRNA expression vectors of RACK1 were constructed successfully. After a 48 h transfection of HUVEC cells with the recombinant vectors and G418 selection, the positive cell clones were obtained. qRT-PCR and Western blot showed that over-expression vector and interference vectors could effectively enhance and knock-down RACK1 expression in HUVEC strains. Conclusion HUVEC cell strains with over-expression and low expression of RACK1 have been established successfully.

Strategy application of invasive-noninvasive mechanical ventilation in COPD patients wich weaning difficulty

2015, 35(2):  224-227. 

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Objective To study the strategy of sequential invasive-noninvasive mechanical ventilation in chronic obstructive pulmonary disease (COPD) specially explore the role of mechanical ventilation in patients with weaning difficulty. Method: Forty-five cases withe weaning difficulty during January 2009 ~December 2013 from Huludao central hospital emergency section guardianship room were recruited. Compare the rate of re-tracheal intubation rate and withdrawal machine success rate in two groups（intervention group, n=21, control group, n=24,）. Result: In the intervention group after weaning the 24h pH, PaCO2, significantly better than that of the control group (p <0.01),in the endotracheal intubation intervention group ，48h re-tracheal intubation rate was 9.5%, less than the control group ( 41.7%) (P<0.05), The intervention group relative risk of re-intubation was 0.147 (95%CI, 0.028~0.781). Intervention weaning success rate significantly higher than that of the control group (85.7% vs 50.0%,P<0.05) Conclusions Sequential invasive-noninvasive mechanical ventilation strategy helps reduce 48h intubation rate and improve the success rate of weaning.

β-NGF reduces the injury of H2O2 to HUEVCs

2015, 35(2):  228-230. 

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The alterations of eNOS phosphorylation in mesenteric arteries of metabolic syndrome rats

2015, 35(2):  231-233. 

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Estrogen deficiency up-regulates the expression of renin and angiotensin-converting enzyme in kidney of rats

2015, 35(2):  234-236. 

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Nuclear translocation of AQP5 and lipid raft in rat parotid acinar cells induced by M3-mAChR agonist

2015, 35(2):  237-239. 

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Progress on diabetic cognitive dysfunction

2015, 35(2):  240-243. 

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Diabetic cognitive dysfunction is one of the important complications of diabetes mellitus. Insulin plays an important protective role in cognitive function through MAPK and PI3-K/Akt signaling pathway. Insulin resistance may give rise to excessive tau protein phosphorylation, formation of neurofibrillary tangles; competitively inhibit insulin degrading enzyme, reduce the degradation of amyloid β; enhance oxidative stress, further damage the integrity of the neuronal structure and function, eventually lead to cognitive dysfunction.

Progress on the Molecular Pathways of Radiation-Induced Cognitive Impairment

2015, 35(2):  244-247. 

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Radiation-induced cognitive impairment is hypothesized to occur because of dynamic interactions between multiple cell types, including astrocytes, endothelial cells, microglia, neurons, and oligodendrocytes. The precent studies indicate that radiation-induced changes include the decrease in hippocampus neurogenesis, alterations of neuronal functions, particularly synaptic plasticity, as well as the elevation of neuroinflammatory cytokines.

Advance of microenvironment and the pathogenesis of Hepatocellular carcinoma (HCC)

2015, 35(2):  248-252. 

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Hepatocellular carcinoma (HCC) is a prevalent primary liver cancer that is driven by cumulative changes in the hepatocyte genome which were influenced by the liver microenvironment. The tumor microenvironment is a dynamic system, including cancer cells, stroma, the extracellular matrix. tissue hypoxia, diet, gastrointestinal tract (GIT) microflora and circulating microvesicles, etc, The liver microenvironment plays a pivotal role in HCC tumerigenesis, progression and therapeutic efficienry. The study of the HCC microenvironment will provide new insights into the mechanism of tumourigenesis and potential novel targets in the treatment of HCC.

Metabotropic glutamate receptor 5 and related clinical diseases

2015, 35(2):  253-256. 

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mGlu5 ( Metabotropic glutamate receptor 5 ) does not only exist in nervous system, but also in many peripheric organs and tissues. The vital role that mGlu5 plays in both nervous and non-nervous system diseases, which will be beneficial for further studying the pathogenesis of diseases. Moreover, it can provide us with new ideas and methods for precaution and cure of illness with mGluRs.

The research progress of miR - 126 and blood vessels

2015, 35(2):  257-261. 

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MicroRNAs (MiRNAs) is one kind of highly conservative endogenous non-coding single-stranded RNAs with small molecule, it is able to regulate gene expression at the translation level by non-specific identification of target genes’ mRNA, and it can regulate various biological functions of cells. Up to now a variety of microRNAs have been found, in which MiR-126 mainly exists in vascular endothelial cells and platelets, and is closely related to the generation, development and repairing of blood vessels. Therefore, MiR-126 will become a very good breach to study coronary heart disease and other vascular diseases.

Role of TNF-α in retinal neural degeneration diseases

2015, 35(2):  262-265. 

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Retinal neural degeneration diseases is one of the main causes of vision loss, TNF-α as an inflammatory cytokine with pleiotropic biological activity, after binding to its receptor by a variety of signaling pathways, may have play critical role in pathogenesis of retinal neural degeneration diseases, which is including glaucoma, ischemic retinopathy, age-related macular degeneration and retinitis pigmentosa.

Progress of Wnt signaling pathway and non-small cell lung cancer

2015, 35(2):  266-269. 

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Wnt signaling pathway alterations are prominent in human malignancies.Wnt signaling is important in non-small cell lung cancer cell lines, and Wnt inhibition reduces proliferation. Wnt signaling substantially impacts NSCLC tumorigenesis, prognosis,and resistance to therapy. Wnt pathway as a therapeutic option in advanced NSCLC.

Issue analysis and coping strategy study of non-profit hospital management system

2015, 35(2):  270-272. 

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Due to the deep-rooted structural problems of political and sanitary structures,most methods and measures of cure for public hospital are low efficient or none effective. Analysed the hospital background such as institution,marketing and culture,we should hold the tendency that hospital reforming didn’t fit in with our country’s situation,it is important that the reforming become more systemcial and harmonized. Therefore ,we have to strengthen the governmental responsibility of public sanitation,introduce a competitive mechanism ,promote the reform of property right, Drawing lessons and experiences from state-owned enterprise reform, we should explore a kind of standard modern management system which is suitable to non-profit hospitals in China.

The role of stem cells and inducing technology in breeding adult cells, screening drugs and the basic research and transplantation

2015, 35(2):  273-277. 

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Stem cells and inducing technology for adult cells is the basic of stem cell research and clinical transplanation test to potential treatment of human diseases. In addition, stem cells and induce technology can play a positive role in drug screening.

As an opportunity to the international certification in medical education and explore establishment the whole system of quality assessment about biochemistry

2015, 35(2):  278-280. 

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With the increasing international exchange of medical education, frequent exchanges increasingly of medical personnel through the cross-border and trans-regional. It caused widespread concern about the quality of the standardization of the countries of medical education. This focus on quality performance on the certification requirements of the standard of medical education. We take it as an opportunity to assess international medical education accreditation, and promote the reform of teaching and examination reforms actively. We explore and establish the full quality assessment system on biochemistry.

The application of CBL teaching method on neuroanatomy teaching in evening undergraduate

2015, 35(2):  281-283. 

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To introduce the application of CBL teaching method on neuroanatomy teaching in evening undergraduate. Cases selection and reconstruction, designing problems, organization and implementation and standardized teaching were analyzed by combining the concrete cases. Finally, we discuss the advantages and disadvantages of CBL teaching method.

Recurrent epistaxis for 10 years，abdominal pain for 6 months and edema for 1 month

2015, 35(2):  284-288. 

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