Table of Content

    05 November 2016, Volume 36 Issue 11
    The action and mechanism of blueberry anthocyanins on apoptosis and proliferation in human colon cancer cells LS174T
    2016, 36(11):  1467-1471. 
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    Objective: We observed actions and effects of anthocyanins on antiproliferation and proapoptosis in human colon cancer cells LS174T, making further investigation of anti-cancer mechanism of blueberry anthocyanin, accordingly, those provide the experimental basis for the prevention and therapy of colon cancer in clinic. Methods: Colon cancer cells ls174t were cultured in vitro,treating LS174T cells with blueberry anthocyanins (25、50、100 and 200μg/mL).We tested the effects of blueberry anthocyanins on proliferation and apoptosis by CCK and Hoechst 33258 chromatin staining dye; We analyzed mRNA expression of apoptosis-related genes(including p53、ccnd3、p73、sfn、caspase8 and fam200a) by real-time PCR. In addition, protein levels of caspase8 and p73 were also analyzed using western blot. Results: The blueberry anthocyanins suppressed the proliferation and induced the apoptosis of LS174T cells respectively in a dose-dependent and time-dependent manners; the expression of ccnd3、p73 and sfn mRNA were up-regulated while the expression of caspase8、fam200a and p53 mRNA were down-regulated; the expression of protein levels of caspase8 and p73 were down-regulated and up-regulated respectively. Conclusion: Blueberry anthocyanins induce cell cycle arrest and apoptosis of colon cancer LS174T cells, which were associated with an up-regulation of the expression of tumor suppressor p73 and a down-regulation of the expression of caspase8.
    miR-146a regulates platelet immune activation
    2016, 36(11):  1472-1477. 
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    Objective To investigate the potential roles of miR-146a in effecting on platelet immune activation. Methods Using flow cytometry to detect PAC-1 and CD62-P expression level of whole blood and q-PCR and light transmittance aggre-gometry to test miR-146a expression level and platelet aggregation rate of plasma in Coronary Artery Disease (CAD) patients (n = 31) compared with controls (n = 35). In addition, an in vitro megakaryocytic maturation and platelet formation model, as measured by CD41 and CD61 through flow cytometry, has been established by using K562 cells treated with PMA induction. The mimics, inhibitor, mimics NC and inhibitor NC of miR-146a were used to study the biological function of it. Results In CAD patients the miR-146a, PAC-1 and CD62-P positive expression rate and platelet aggregation rate were increased (P<0.05) compared with controls. In addition, miR-146a leaded to enhance TLR-4, PAC-1 and CD62-P expression level (P<0.05) when challenged with miR-146a mimics. Conclusion This study has demonstrated that miR-146a can affects the platelet immune activation via TLR-s signal pathway, which imply that miR-146a might be able to act as novel tools for regulation of platelet activation.
    Screening gene expression profiles of both aortic aneurysm and normal aorta by microarray
    2016, 36(11):  1478-1482. 
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    Objective To investigate the difference of gene expression profile in aortic aneurysm and normal aorta. Methods The total RNA of 5 cases of aortic aneurysm and 4 normal aorta were isolated and cDNA was synthesized, then aRNA labeled by biotin were synthesized by in vitro transcription. The mixed probes were hybridized with Affymetrix GeneChip? Human Genome U133 Plus 2.0 Array .The fluorescent signal was scanned by Affymetrix GeneChip? Scanner 3000 .The acquired image was analyzed by GCOSvL.4 software. 6 different expression genes from profiles were validated by RT-qPCR. Results Totally 270 genes had more than two fold changed expression in aortic aneurysm, which included 211 upregulated and 59 downregulated genes. Different expressed genes were mainly involved in signal transduction, immune system process, and inflammatory response and so on. 6 genes associated with the formation of aortic aneurysms were selected for quantitative analysis, and the results of RT-qPCR were completely consistent with the results of gene microarray. Conclusions Gene differentially expressed in aortic aneurysms identified by microarray may be provide the molecular basis for the study of the pathogenesis of aortic aneurysm.
    Effect of BRAP on mucous hypersecretion induced by LPS in human airway epithelial cells
    2016, 36(11):  1483-1487. 
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    Objective To investigate the effect of bombesin receptor activated protein(BRAP) on lipopolysaccharide(LPS)-induced mucous hypersecretion in airway and mechamism. Methods After cultivating HBE16 cells in vitro , the constructed p-EGFP-N1-BRAP eukaryotic vector was transfected into the cells,with empty plasmid as a vector control. At the same time in order to LPS as a stimulus to extracellular signal-regulated protein kinase(ERK) specific inhibitor U0126,P38 inhibitor SB203580 and c-jun N-terminal kinase (JNK) inhibitor SP600125 for the intervention factors. The content of ROS, the expression of MUC5AC mRNA and protein, the NF-ΚB activity and cell vitality were detected. Results After transfected pEGFP-N1-BRAP, ROS production was decreased (P < 0.01). The MUC5AC protein production and mRNA level of the group transfected pEGFP-N1-BRAP were significantly decreased as compared with LPS group(P < 0.01), the NF-ΚB activity showed the same trend(P < 0.05). In U0126 group, the expression of MUC5AC was significantly decreased as compared with transfected recombination plasmid group(P < 0.01), the NF-ΚB activity was also significantly decreased(P < 0.05). Conclusions BRAP prevents NF-ΚB activation via ROS/ERK/MAPK signaling pathway,thus reducing LPS-induced mucin5AC production.
    Effect of iron overload on c-MYC protein express in human breast cancer cell
    2016, 36(11):  1488-1492. 
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    Objective To investigate the effects of iron overload induced oxidative stress on the expression of c-MYC protein in human breast cancer cells. Methods The human breast cancer MCF-7 cells were treated by 0, 50 and 500 μmol/L ferrous sulfate respectively. After 24 hours, immunocytochemistry stain and western blot methods were used to investigate the changes of reactive oxygen species and the expression of IRP1、IRP2、c-MYC、P-ERK、GSK、PP2A protein. The changes of ROS activity and c-MYC protein were further examed by blocking NADPH oxidase pathway using Diphenyliodonium iodide (DPI). Result With the increase of ferrous sulfate, both ROS activity of and IRP2 protein expression of MCF-7 cell were increased significantly (P<0.05), but IRP1 was not. Iron overload also increased c-MYC protein expression, and enhanced the levels of phosphorylation of ERK1/2 and reduced the expressions of GSK and PP2A proteins (P<0.05). NADPH oxidase inhibitor (DPI) could significantly inhibit the enhancement of ROS activity and the expression of c-MYC protein (P<0.05). Conclusion Iron overload may enhance the expression of c-MYC protein by upregulated ROS activity.
    Effects of HSP27 and ADSC transplantation on expression of caspase3 after acellular nerve allograft in mice
    2016, 36(11):  1493-1498. 
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    Objective To study the effect of Heat shock protein 27 (Hsp27) and adipose-derived stem cell (ADSC) transplantation on expression of caspase3 and function recovery after acellular nerve allograft repair of the sciatic nerve gap in mice. Methods A total of 30 healthy C57BL/6 mice were randomly divided into ANA group, ADSC group and Hsp27+ADSC group. The sciatic functions index (SFI), electrophysiology and the rate of tibialis anterior muscle wet weight were used to evaluate nerve regeneration and functional recovery. Observe the protein expression of ChAT and the fluorescence signal of ADSC labeled with PKH-26 in the nerve graft by using immunofluorescence. Results Compared with ANA group, the expression of HSP27 protein, the number of ChAT labeled motor axon and PKH-26 labeled ADSC in Hsp27+ADSC group were increased, however, the expression of caspase protein was decreased (P<0.05). Compared with ANA group, SFI, nerve conduction velocity ,wave amplitude, rate of tibialis anterior wet muscle weight were significantly increased in ADSC group and Hsp27+ADSC group (P<0.05), however, incubation period were significantly decreased in two treatment group (P<0.05), moreover, the effect of Hsp27+ADSC group was more powerful than ADSC group (P<0.05). Conclusion The combined Hsp27 and ADSC transplantation treatment promoted motor axon regeneration and function recovery significantly more than ADSC treatments, which may be related with HSP27 inhabited caspase3 apoptotic signaling pathway, and promoted the survival of the transplanted ADSC.
    Tyrosine kinase 2 facilitates site-specific tyrosine phosphorylation of androgen receptor at Tyr-267 in prostate cancer cell lines
    2016, 36(11):  1499-1504. 
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    Objective To investigate the effect of the JAK family member Tyk2 on androgen receptor (AR) phosphorylation and the proliferation of prostate cancer cells. Methods LNCaP and LAPC-4 cell lines as subjects, without androgen settings, after epidermal growth factor (EGF) stimulation, giving AIM-100/Baricitinib (INCB 028050) management, immunoprecipitation and/or western blot was used to observe AR phosphorylation. RNA interference targeted silence Tyk2 gene was transfected into LNCaP and LAPC-4 cell lines. Western blot was used to observe the effect on AR phosphorylation. CCK-8 was used to measure cell proliferation. Results EGF can induce AR phosphorylation at Tyr-267 and proliferation of prostate cancer cells (P <0.05). AIM-100 inhibited the proliferation of prostate cancer cells (P <0.05), and AR Tyr-267 phosphorylation mediated by Ack1 and Tyk2. However, INCB inhibited Tyk2 phosphorylation and AR Tyr-267 phosphorylation, as well as the proliferation of prostate cancer cells (P <0.05). Conclusions The JAK family member Tyk2 played a critical role in facilitating EGF-induced AR site-specific phosphorylation at Tyr-267 and in promoting prostate cancer cell proliferation.
    Effect of Vimentin expression by Regulated Nampt in glomerular cells in diabetic nephropathy
    2016, 36(11):  1505-1510. 
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    Objective To study the function of endogenous Nampt on vimentin expression in glomerular cells. Methods With C57/BL6 diabetic mice experiment, the renal pathological tissue bebing embedded, fixated and sliced, endogenous Nampt and vimentin expression and location are analysized by appling confocal microscope technique. After 5 days in cultured with 200 mmol/L high concentration glucose (hyperglucose), HBZY-1 cells intervened with 10 μmol/L FK866 and 1 mmol/L NMN, Nampt, NF-κB, Sirt1 and vimentin are measured by immunofluorescence and Western blot assay respectively. HBZY-1 cells were divided into groups (24 h,48 h,72 h,96 h,120 h and 144 h) after cultured with hyperglucose, The time-effect course on expression of endogenous Nampt, NF-κB and Sirt1are measured by Western blot assay. Results 1) With glomerular atrophy, excess vimentin expression clearly increased along with Nampt high expression in DN glomerular cells, as compared with the control group (P﹤0.01). 2) After the cells treated with FK866, vimentin expression decreased significantly following Nampt expression inhibited (P﹤0.01). With NMN intervention, vimentin expression is very lower than that of control group (P﹤0.01). 3) With the extension of incubation time of the in the HBZY-1 cells in high concentrations glucose, the expression of Nampt and NF-κB obviously increased (P﹤0.01), while the SIRT1 expression decreased significantly, as compared with control groups (p﹤0.01). Conclusion In DN glomerular fibrosis, Nampt can control vimentin expression by enhenced NF-κB and inhibited SIRT1signaling pathway.
    ITGB1 induces epithelial-mesenchymal transition and cell migration in breast epithelial cellline MCF10A
    2016, 36(11):  1511-1516. 
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    Objective To investigate the effect of overexpressed-integrin beta 1 (ITGB1)gene on epithelial-mesenchymal transition (EMT) and cell migration in breast epithelial cell lineMCF10A. Methods Recombinant plasmid pBABE-puro-myc-ITGB1 was constructed and retrovirus was packaged in HEK293T cells. MCF10A cells were transfected with the retrovirus carrying ITGB1 gene or the controls. Blank group(MCF10A), negative control group(MCF10A-vector), ITGB1overexpression group(MCF10A-ITGB1)were set up. After treatment with puromycin 3days, the expression of ITGB1in MCF10A cells was determined by quantitative real-time PCR and Western blot assays. The ability of migration and invasion were analyzed by Transwell assays. The expression of epithelial-mesenchymal transition (EMT) marker proteins (E-cadherin,vimentin,fibronectin and N-cadherin) and ITGB1 downstream proteins (ILK, p-FAK and FAK) in MCF10A cells were detected by Western blotting. Results ITGB1 gene was successfully delivered into MCF10A cells, resulting in the stable expression of ITGB1 mRNA and protein.Compared with MCF10A and MCF10A-vector cells, the ability of migration and invasion were enhanced notably in MCF10A-ITGB1 cells (p<0.05). The expression of the epithelial marker E-cadherin protein was down regulated (p<0.01), the mesenchymal marker proteins (vimentin,fibronectin and N-cadherin) and ITGB1 downstream proteins(ILK and p-FAK)were upregulated in MCF10A-ITGB1 cells (p<0.01). Conclusions ITGB1 induces EMT and promotes cell migration and invasion in breast epithelial cell line MCF10A.
    Effect of botulinum toxin type A on substance P and inflammation of rats with chronic neurogenic pain
    2016, 36(11):  1517-1524. 
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    Objective To explore the influence and mechanism of botulinum toxin A on chronic neurogenic pain.Methods Wistar rats were randomly divided into control group, sham group,pain model group (the left L5 and L6 nerves of rats were ligated,after 3 daythe left was injected with normal saline from ipsilateral plantar subcutaneous.) and botulinum toxin treatment group (the left L5 and L6 nerves of rats were ligated, after 3 day the left was injected with 30U/kg BoNT-A from ipsilateral plantar subcutaneous). The botulinum toxin treatment group was further divided into 1d, 3d and 1w group according to the execution time. The cell morphology changes were observed by HE staining.The protein and mRNA expression levels of substance P (SP),interleukin6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected by immunohistochemical method,in-situ hybridization and real-time quantitative PCR.Results HE staining showed spinal cord inflammatory cells infiltration after SNL rats. Inflammatory infiltration degree was aggravated in the spinal cord as the extension of the ligation time.Protein and mRNA expression levels of SP, IL-6 and TNF-α were significantly higher in pain model 1d,3d and 1w group than that incontrol group (P<0.05).But those were lower in botulinum toxin treatment group at 1d,3d and 1w than that inpain model group (P<0.05) as determined by immunohistochemistry,in-situ hybridization and real-time quantitative PCR.Conclusions Neurotransmitter SP and inflammatory mediators IL-6 and TNF-α were involved in the analgesic effect of BoNT-A on chronic neurogenic pain.
    siRNA down-regulating 14-3-3ζ expression inhibits proliferation and induces apoptosis in SGC-7901cell line in vitro
    2016, 36(11):  1525-1530. 
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    Objective To investigate the effects of siRNA targeting 14-3-3ζ gene on the proliferation and apoptosis in human gastric adenocarcinoma cell line SGC-7901 and the latent mechanisms. Methods Three groups were devided as blank, siRNA-control and siRNA-14-3-3ζ groups. The 14-3-3ζ-siRNA was transfected into SGC-7901 cells by LipofectamineTM 2000. The gene silencing effect of siRNA targeting 14-3-3ζ was determined by quantity real-time PCR (RT-qPCR) and western blot at mRNA and protein levels respectively. Cell proliferation was detected by CCK8 assay. The cell cycle and apoptosis were detected by flow cytometry (FCM). The protein levels of p53, cylinD1, PUMA, Bax and Bcl-2 were analyzed by western blot. Results After transfection of 14-3-3ζsiRNA into SGC-7901 cells, the mRNA and protein levels of 14-3-3ζ were both significantly reduced. Compared with the control groups, the down-regulation of 14-3-3ζ in SGC-7901 cells resulted in significant decrease of cell proliferation (P<0.05). FCM showed significant increase G0/G1 phase of cell cycle and apoptotic rate in siRNA-14-3-3ζ cells (P<0.05). Besides, down-regulation of 14-3-3ζ cells also increased the expression of p53, PUMA and Bax protein, reduced the expression of cyclinD1 and Bcl-2 protein (P<0.05). Conclusion Down-regulation of 14-3-3ζ in SGC-7901 cells can inhibit proliferation and induce apoptosis via p53 pathway by down-regulating CcyclinD1 and Bcl-2 proteins and up-regulating PUMA and Bax proteins.
    Significance of apoptotic and proliferative indices and stat3 expression in colorectal carcinoma
    2016, 36(11):  1531-1536. 
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    Objective To investigate the relationship between apoptosis and cell proliferation and the expression of stat3 as well as their prognostic significance in colorectal carcinoma(CRC). Methods Samples from 129 patients with CRC and adjacent normal mucosa were analyzad for stat3 and CyclinD1 expression with immunohistochemistry, and the apoptotic index with TUNEL method. The association of stat3 expression with clinicopathological parameters, prognosis, apoptotic and proliferative activities was subsequently analyzed. Results The expression of stat3 and CyclinD1 showed significant difference (P<0.05) between CRC tissues and adjacent non-cancerous tissues. The level of AI in CRC tissues was statistically lower than that in adjacent non-cancerous tissues (P<0.05).The expression of stat3 was correlated with Dukes staging, lymph node metastasis and tumor location of CRC (P<0.05).Stat3 expression was positively correlated with CyclinD1 (P<0.05).Kaplan-Meier univariate analysis revealed stat3 positive expression, Dukes staging, lymph node metastasis and AI had significance for survival time(P<0.05). Cox model analysis revealed Dukes staging was a dangerous factor for independent prognosis of CRC. Conclusions Stat3 might participate in the development and progression of colorectal cancer. Stat3 protein can be acted as index to judge lymph node metastases and prognosis assessment of colorectal carcinoma.
    Expression of miR -31 and its target gene LATS2 in rat hypertrophic cardiomyocytes
    2016, 36(11):  1537-1541. 
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    ObjectiveTo observe the expression of miR-31 and its target gene LATS2 in the hypertrophy process of rat cardiomyocytes.MethodsTargeting regulation of miR-31 on LATS2 was identified by a dual luciferase gene reporter system. Rat primary cardiomyocytes were isolated and cultured in vitro, and hypertrophic model of cardiomyocytes was constructed by administering 10-6mol/L AngII. MiR-31,LATS2 and hypertrophy genes ANP,β-MHCwere detected by RT-qPCR.Morphology of the cardiomyocyteswas observed by fluorescence staining to F-actin.LATS2 protein was further detected by western blot.ResultsMiR-3l could specifically bind to 3'UTR of LATS2,which made the luciferase activity decrease significantly.Hypertrophy genes ANP and β-MHCwere up-regulated at 48 hour and the area of cardiomyocytes was increased significantly at 96 hour after administration of 10-6mol/LAngII. Accompanied with the hypertrophic changes of cardiomyocytes, miR-31 was significantly up-regulated, while LATS2 in gene and protein levels were reduced obviously.ConclusionsAccompanied with the hypertrophic changes of rat cardiomyocytes, miR-31 was significantly up-regulated, while LATS2 in gene and protein levels were reduced obviously.
    Imperatorin ameliorates estrogen deficiency induced-osteoporosis through elevation of autophagy in rats
    2016, 36(11):  1542-1547. 
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    Objective To determine the therapeutic effect and mechanism of imperatorin on estrogen deficiency induced-osteoporosis. Methods Rats were randomly distributed into group control, OVX and OVX+Imp. Ten days after modeling, rats in group OVX+Imp,control and OVX were intravenously administrated with Imperatorin, 75 mg/kg or chloroform, twice per week, 10 weeks.Trabecular morphologyand indexes of distal femurs were analysed by μCT and HE staining. Mechanics strength of femurs and lumbars was analyzed by mechanical testing.Mineral deposition was labeling by calcein. Serum PINP and B-ALP were detected by ELISA. Ossification of BMMSCs was tested by ALP staining. mRNAs and proteins were tested by real-time PCR or Western blot respectively. New bone formation in subcutaneous implants was tested by HE staining. Results 1)Bone volume, trabecular indexes, mechanics strength of femurs and lumbars, mineral deposition, serum PINP and B-ALP of OVX were lower than control and OVX+Imp(P<0.05).2)ALP activity, osteogenic genes and ectopic osteogenesis of endogenous BMMSCs from OVX were lower than control andO VX+Imp(P<0.05).3) Autophagy of OVX was lower than control and OVX+Imp(P<0.05).4) Autophagy BMMSCs+3-MA was lower than BMMSCs, and the osteogenesis correspondly decreased(P<0.05);autophagy BMMSCs+3-MA+Imp was higher than BMMSCs+3-MA, and the osteogenesisc orrespondly increased(P<0.05).Conclusions Imperatorin ameliorated estrogen deficiency induced-osteoporosis through osteogenesis promotion caused by elevation of autophagy.
    Expression and functional analysis of WTAP gene in gastric cancer
    2016, 36(11):  1548-1553. 
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    Objective To investigate the expression change of WTAP gene in clinical gastric cancer samples and its functional significance in gastric carcinogenesis. Methods The WTAP mRNA was detected by qRT-PCR in 45 cases of gastric cancer samples and their paired adjacent normal control tissues. The expression of WTAP mRNA was subjected to analysis combined with patients’ clinical pathological data. The effects of WTAP knock-down on cell proliferation, cell migration and invasion were detected by CCK-8, wounding heal and trans-well assays, respectively. Results The expression of WTAP mRNA in gastric tumor tissues was significantly lower than the adjacent tissues (p<0.05), and was closely related with gastric cancer clinical stage (p<0.05). Furthermore, knock-down of WTAP in MGC-803 cells could promote cell proliferation, cell migration and invasion. Conclusions WTAP was down-regulated in gastric cancers, and it might sever as a tumor suppressor gene in gastric carcinogenesis.
    Analyse of clinic distribution and antibiotic resistance of 2 499 isolates of Klebsiella pneumoniae
    2016, 36(11):  1554-1557. 
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    Objective To investigate the trend of the clinic distribution and antibiotic resistance of Klebsiella pneumoniae,and to provide the reasonable clinical application scheme of antibiotics. Methods To analyse the antibiotic resistance of 2,499 isolates of klbsiella pneumoniae from clinical samples collected in our hospital during the period of 2013-2015.Results The Klebsiella pneumonia-positive specimens were mostly derived from sputum(52.7%), urine(12.28%), and blood(10.04%). The rates of resistance for cephalosporins and penicillins were above 80%. As for carbapenems,clinical isolates of Klebsiella pneumoniae have still displayed high degrees sensitivity for tigecycline and ertapenem, while the resistance rate for imipenem was incresing,The rates of multidrug resistance in 2,499 strains isolated in 2013- 2015 were 24.45% which was higher than before.Conclusion: Accordding to the changing of drug resistance of Klebsiella pneumoniae, for effectively to control the production of resistant bacteria and reduce the rate of drug resistance,we take augnt to the early warning guidance of antimicrobial agents in time and using of antibiotics rationally.
    Vaspin improves insulin resistance in type 2 diabetic rats
    2016, 36(11):  1560-1562. 
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    Research advances on regulation of SDF-1/CXCR4 in neurogenesis after ischemic stroke
    2016, 36(11):  1563-1566. 
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    Expression ofstromal cell-derived factor 1(SDF-1) and C-X-C chemokine receptor 4(CXCR4) increased after cerebral ischemia, and this up-regulated expression could regulate proliferation, differentiation and migration of endogenous neural stem cells.
    Research advances in antitumor mechanism of IL24
    2016, 36(11):  1567-1572. 
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    Melanoma differentiation-associated gene-7 (MDA-7)/interleukin 24(IL24) is a member of the IL-10 family of cytokines, mainly expressed in human spleen, thymus, peripheral blood leukocytes and normal melanocytes. Recently, several studies have shown that IL24 is a unique inhibitor of tumor cells, significantly inhibiting tumor cell growth and proliferation, invasion, metastasis and angiogenesis, and inducing apoptosis in tumor cells. Moreover, increasing evidence implies thatIL24 mayalso enhance chemotherapy sensitivity and kill a variety of tumor cells without harming the normal cells. However, the molecular mechanism behind these effects is still not fully understood yet.
    Research progress of the mucus high-secretion mechanisms in airway
    Yu-Mei CHEN Jin TONG
    2016, 36(11):  1573-1577. 
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    High airway mucus secretion is mainly characterized by the changes of airway mucus in the physicochemical property, including the changes of mucus components which are mainly changed with MUC5AC and mucous secretory cells which are mainly changed from mucus cells to goblet cells. The harmful inhalation substance mainly in cigarette smoke and bacterial infection are the main irritants to induce the high airway mucus secretion. Besides, heat shock protein, signal transduction pathway and the increase of MUC5AC expression are the major mechanisms of high airway mucus secretion .
    Polyamine anabolism and oncotherapy
    2016, 36(11):  1578-1581. 
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    Ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (AdoMetDC) are the key enzymes in the pathway of polyamine anabolism, they are closely related to the occurrence and metastasis of tumor. The effects of existing inhibitors are toxic or have poor effect in clinic trails, the inhibitor and other drugs combined together or development of small molecule inhibitors by coupling computational and experimental tools are expected to provide new ideas for tumor treatment.
    Pharmacological mechanism and clinical progress of puerarin in the treatment of type 2 diabetes
    2016, 36(11):  1582-1585. 
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    Puerarin has been shown to act as a hypoglycemic, lipid-lowering, improvement of insulin resistance, anti-inflammatory, anti-oxidative stress compound in recent years. Puerarin may partly ameliorated the development of diabetes and its complications such as retina, kidney, cardiovascular and neurological diseases, and thus can be an effective approach for the intervention in clinical diabetes.
    Progress on miR-200b regulating chronic angiogenesis of diabetes
    2016, 36(11):  1586-1590. 
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    microRNA,the regulator which has main effects at transcription level, plays a privotal role on angiogenesis, and the negative regulation of miR-200b on angiogenesis in chronic wound of diabetes is deeply studied. Targets presently known of miR-200b cover Ets-1, VEGF, VEGFR1, VEGFR2,GATA proteins and so on.
    Progress on microRNA identified as early diagnostic biomarkers of sepsis
    2016, 36(11):  1591-1595. 
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    microRNAs are endogenous non-coding RNA molecules of about 22 nucleotides that play a key role in posttranslational gene silencing.Circulation miRNA, such as miR-146a, miR-223, miR-150, miR-15 and miR-16, play important roles in the evaluation of septic patients' status. In this article, we summarize the recent progress on the circulating miRNAas biomarkers for the diagnosis of sepsis and how miRNAs regulate the inflammatory responses in sepsis.
    PI3K/Akt signal pathway in pathogenesis of polycystic ovary syndrome
    2016, 36(11):  1596-1602. 
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    Polycystic ovary syndrome (PCOS) is a common endocrine disease, with reproductive functional disturbance and metabolic disorders. However, its etiology and pathogenesis are not clear yet. Inside the cell, phosphatidylinositol 3-kinase/Protein Kinase B (PI3K-Akt) is one of the important signal pathway, and the change of PI3K-Akt signal pathway is related to processes of PCOS, such as insulin resistance, adipocyte differentiation, cell proliferation, treatment and prognosis.
    Explorationof onlineautonomous learning theory framework
    2016, 36(11):  1603-1607. 
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    It is a significant change from classic teaching to online learning. Self-regulated online learningis a further step based on online learning, which includes personalized learning, active learning and scientific learning . In the framework of onlineself-regulated learning system, PDCA cycle as a learning strategy is the key process. Management, technical and interface factorsplay three differentroles,which have various influence to this PDCA cycle. Peking Union Medical College Hospital merges traditional teaching model into a self-regulated on linelearning in clinical training and thus developed a new type clinical education theory as well as practicing technology.
    The role of WeChat public platform in autonomic learning of medical students
    2016, 36(11):  1608-1610. 
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    WeChat public platform is a new way to broadcasting and interaction. Assisting the autonomic learning of medical students is feasible as it is instant, convenient and intelligent. The WeChat public platform PUMC08 investigates how WeChat public platform could influence autonomic learning of medical students. Models base on interest, cooperation and introspection are applied and favorable effects are achieved.