Table of Content

05 December 2016, Volume 36 Issue 12

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HGF/c-Met increases the migration ability of marrow EPCs in rats

2016, 36(12):  1611-1617. 

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Objective To investigate the effect of hepatocyte growth factor (HGF) and its receptor c-Met on the migration ability of rat bone marrow-derived endothelial progenitor cells (EPCs) and its mechanism. Methods The EPCs were separated, obtained and identified. The Ad-c-Met-EPCs were obtained by recombinant adenovirus vector mediates c-Met transfered EPCs. The expression of c-Met and proliferation capacity of each group cells were detected by real-time PCR, Western blot, and CCK8 respectively. The migration ability of Ad-c-Met-EPCs with different concentrations of HGF were checked by Transwell system. The each group cells were processed by proper concentration of HGF, while the PBS control group and phosphatidylinositol 3-kinase inhibitor group (add HGF and 10g/L LY294002) were also setted. The migration ability, Akt and P-Akt of the each group cells were detected by Transwell system and Western blot. Results 1)The results of QPCR and Western blot showed that c-Met gene and protein in Ad-c-Met-EPCs had high expression(P<0.05). 2)The c-Met gene did not have significant impact on the appreciation capacity of EPCs. 3)HGF could increased Ad-c-Met-EPCs migration with concentration increasing(0-50 ng/ml). 4)The migration capacity of HGF+Ad-c-Met-EPCs and P-Akt protein were significantly higher than other groups(P<0.05). Conclusion HGF/c-Met can remarkably increase the migration capacity of EPCs. Besides, HGF/c-Met may accelerate the migration of EPCs through PI3K/Akt signal path.

Identification of neural cell-type as source of IL-17A during cerebral ischemia/reperfusion injuries

2016, 36(12):  1618-1623. 

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Objective To identify the neural cell-type as source of IL-17A during cerebral ischemia/reperfusion injuries in vitro. Methods Primary cultured mouse cortical neurons, microglia and astrocytes were subjected to 1~4 h oxygen-glucose deprivation/24h reoxygenation (OGD/R) simulating cell ischemia/reperfusion injury model in vitro, and then the double immunofluorescence staining with IL-17A and their specific markers of NeuN, Iba-1 and GFAP, RT-qPCR and Western blot were performed to determine the neural cell-type of IL-17A production. Results The primary cultured microglia and astrocytes (but not NeuN+ neurons) could express IL-17A and respectively co-localized with their specific markers Iba-1 and GFAP after OGD/R treatment. The mRNA expression levels of IL-17A increased with OGD duration and reached the peak at 4h OGD [(2.74±2.48)，P<0.001, n=5 per group] in astrocytes after 1~6 h OGD/24 h R treatment. In addition, 4 h OGD/R treatment could promote IL-17A protein expression in primary cultured astrocytes [(3.17±0.91)，P<0.05，n=5 per group]. Conclusions These results suggested that astrocytes might be the main source of IL-17A production during cerebral ischemia/reperfusion injuries.

Wnt / β-catenin signaling pathway promotes cartilage differentiation of BMSCs

2016, 36(12):  1624-1629. 

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Objective Using Growth differentiation factor GDF-5 in combination with dexamethasone (Dex) to induce BMSCs into cartilage differentiation and to explore the role of Wnt/β-catenin signaling pathway in cartilage differentiation of rBMSCs.Methods BMSCs were collected from Sprague Dawley rats.The Morphology was observed under inverted microscope .rBMSCs at passage 3 were divided into 6 groups: BMSCs group，BMSCs+Dex group，BMSCs+GDF-5 group,BMSCs+ GDF-5+Dex group，BMSCs+ GDF-5+ Dex+SB216763 group,BMSCs+GDF-5+Dex+ XAV-939 group and induced for 14 days.Alcian blue stain was used to show the changes of proteoglycans ; RT-PCR was used to detecte the mRNA expression of Aggrecan,COL2,Sox9,COL1,Dvl1,Gsk3β and β-catenin.The protein expression levels of COL2 and β-catenin were detected by Western blot. Results Compared with the BMSCs group, BMSCs+GDF-5+Dex group showed deeper proteoglycan staining; Aggrecan, COL2, Sox9 and the protein expression levels of COL2 were significantly increased;β-catenin mRNA and protein expression levels also increased. Compared with the BMSCs + GDF-5 + Dex group,in adding SB216763 group proteoglycans, collagen type Ⅱ gene and protein expression were increased significantly (P <0.05); On the contrary,in adding XAV-939 group cartilage differentiation gene and protein expression were decreased (P <0.05).Conclusion GDF-5 in combination with dexamethasone (Dex) can induce differentiation of rat BMSCs into cartilage, Wnt/β-catenin signaling pathway may play a promoter role.

Selenite induces apoptosis in colorectal cancer cell line SW480

2016, 36(12):  1630-1635. 

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Objective To investigate the signaling pathway involved in the colorectal cancer SW480 cell apoptosis induced by selenite. Methods SW480 cells were divided into three groups, respectively treated with selenite, MnTMPyP and their combinations. Monitoring the ROS content in SW480 cells by DCFH-DA fluorescence probes. The phosphorylation of JNK and ATF-2,and the expression of c-Myc,c-Jun,c-Fos,cyclin D1,cyclin A2,Bcl-2 and other related proteins were detected by Western blot. Cell apoptosis rate was detected by flow cytometry. Results Selenite can induce SW480 cells to produce ROS. Selenite can induced SW480 cell apoptosis by downregulating the phosphorylation of JNK and ATF-2,and the expression of c-Myc, c-Jun,c-Fos, cyclin D1, cyclin A2, Bcl-2(P<0.05). The ROS inhibitor MnTMPyP can reduced the effects caused by selenite(P<0.05). Conclusions Selenite can induce ROS generation,inhibit JNK and ATF-2 phosphorylation and the expression of c-Myc,c-Jun,c-Fos,cyclin D1,cyclin A2 and Bcl-2, thus promote apoptosis in SW480 cells.

Estrogen up-regulates the expression of p21 and cyclin E2 mRNA and enhances MCF-7cell invasion via activation of calpain

2016, 36(12):  1636-1640. 

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Objective To investigate the effect of 17β-estradiol(E2) on the gene expression and coincident enhanced invasion, and the role of ERK-calpain signaling in the E2 action, withthe purpose ofstudyingthe molecular mechanism for the E2 effect. Methods MCF-7 breast cancer cells were used as a model system，RT-PCR was employed to evaluate levels of mRNA of target genes. Transwell invasion assay was applied to access cell invasive ability. Western blot was used to analyze the proteolysis of target proteins, and siRNA was used to knockdown calpain2 gene expression and reduce the activity of calpain. Results Treatment of MCF-7 cells with E2induced significant up-regulation of both p21 and CCNE2 (P<0.01), as well as enhanced invasion. Calpain or MEK specific inhibitors, calpeptin (10μM) and PD98059(10μM), showed tremendous suppression of E2-stimulated expression of p21 /CCNE2 mRNA (P<0.01）. Knockdown of calpain2 blocked E2-stimulated calpain activation and cell invasion (P<0.01). ConclusionsE2 induces up-regulation of p21/CNNE2 mRNA and enhances invasion and this effect is mediated via calpain, indicating calpaincould be a potential target for the prevention of metastatic breast cancer.

Influence of PKM2 silencing on invasion and migration in tamoxifen-resistant breast cancer cell line MCF-7

2016, 36(12):  1641-1645. 

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Objective To investigate the effect of PKM2 down-regulation on invasion and migration in tamoxifen-resistant breast cancer MCF-7 cell line. Methods The tamoxifen-resistant breast cancer cell line (MCF-7R) was established by increasing tamoxifen concentration in a stepwise manner. CCK-8 was used to measure the proliferation of cells. The protein expression of PKM2 was determined by Western blot. shRNA for PKM2 gene lentiviral interference vectors were infected into MCF-7R cells, the effect of interference was determined by RT-qPCR and Western blot. Cell invasion and migration abilities were measured by transwell and wound-healing assays. Results The capability of tamoxifen resistance in MCF-7R cells was dramatically enhanced compared to that in MCF-7 cells (P<0.01). Protein level of PKM2 was markedly increased in MCF-7R cells (P<0.01). The mRNA and protein levels of PKM2 declined obviously in PKM2-silented MCF-7R cells (P<0.01). We also demonstrated that knockdown of PKM2 significantly inhibit the invasion and migration of MCF-7R cells (P<0.01). Conclusions The expression of PKM2 is apparently higher in MCF-7R than that in MCF-7 cells. Moreover, knockdown of PKM2 can inhibit the migration and invasion of MCF-7R cells.

Silencing CHOP gene reduces apoptosis of hepatocellular carcinoma Hepa 1-6 cells of mice induced by tunicamycin

2016, 36(12):  1646-1651. 

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Objective We construct an effective eukaryotic expression vector of short hairpin RNAagainstmouse C/EBPhomologous protein, and study the effect on apoptosis of Heap 1-6 cells when silencing of CHOP. Methods We designed and synthesized shRNA target sequence and non-homology shRNA sequence as negative control, which were recombinantd into pLKO.1-TRC vector after annealing. Then products of transformation and amplificationwere indentified by rapid double enzyme digestion.Heap 1-6 cells were transfected with viral supernatant from 293T cells transfected with the lentiviral packaging method. A stable strain was obtained from 10 days of continuous screening with a culture medium containing adenine. We detected the protein expressions of caspase9 and c-PARP by western blot and analysed cell cycles by flow cytometry. Results The results showed that shRNA lentiviral vectors were constructed successfully. Compared with the negative group, the shCHOP group could significantly inhibit the expression of CHOP protein and reduced the apoptosis induced by tunicamycin (p<0.05). Conclusion CHOP gene silencing could down-regulated the apoptosis of Heap 1-6 cells induced by endoplasmic reticulum stress.

Expression and localization of endogenous neuroprotective protein Iduna in neonatal rat brain

2016, 36(12):  1652-1657. 

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Objective To clear the expression of endogenous neuroprotective protein Iduna in brain tissues of neonatal rats and the localization. Methods Take the organ tissues and different brain regions of SD neonatal rats, evaluate the tissue specificity of Iduna protein expression using Western blot. Make the brain paraffin and frozen section of SD neonatal rats. Observe the expression of Iduna and the localization through IHC, then determine the positioning of Iduna in nerve cell and astrocyte through IF. Culture the primary neurons and astrocyte, and detect the expression of Iduna mRNA through the real-time PCR. Verify the cellular localization of Iduna through the IF double-stained NeuN and GFAP. Results Iduna had a rich expression in the brain of neonatal rats, especially in hippocampus and cortex. Iduna was mainly expressed in the cytoplasm of neuron (79.85%), which was also proved by primary neurons IF triple-staining (80.6%). The expressive abundance of Iduna mRNA in neurons was far higher than that in astrocytes (P<0.001). Conclusions Iduna is mainly distributed in the neuron plasma in hippocampus and cortex of brain , indicating that the function may be closely related to neuron's activity.

Prognostic value of leptin receptor in early breast cancer

2016, 36(12):  1658-1663. 

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Objective To investigate the prognostic value of leptin receptor in early breast cancer, and its correlation with clinicopathlogical parameters. Methods We searched Pubmed, Embase and Cochrane Central Register of Controlled Trials databases in relevant studies for evaluating leptin receptor expression and breast cancer survival. Fixed- and random-effect meta-analyses were conducted based on heterogeneity of included studies. Publication bias was evaluated by funnel plot and Egger’s test. Results There are seven studies with 1990 patients included in this meta-analysis. Leptin receptor expression has no correlation with menopausal status, body mass index, hormone receptor status, Her2 status, ipsilateral lymph node metastases, p53 and leptin expression level. Leptin receptor has no significant impact on disease-free survival or overall survival. Within the subgroup using immunohistochemical staining as assessment assay, leptin receptor positivity is contributed to prolonged disease-free survival (HR 0.63, 95% CI 0.40~0.99, p<0.05). Conclusions: Early breast cancer patients with leptin receptor positivity have low risk for disease recurrence.

Influence of migration, invasion and cell cycle of human hepatocellular carcinoma cell line HepG2 by silencing EMS1/cortactin

2016, 36(12):  1664-1669. 

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Objective To explore expression and function of EMS1/cortactin in HCC cell line HepG2. Methods RT-qQPCR was used to detect expression of EMS1. Location of cortactin (protein encoded by EMS1 gene) was detected with immunofluorescence assay. L02 (normal liver cell) was used as control. Then a short-hairpin-RNA -expression plasmid against EMS1 (pS-EMS1) was constructed and transfected into HepG2. The downregulation of EMS1 and cortactin were tested by RT-qPCR and Western blot analysis. The proliferation, division capacity, migration and invasion of HepG2 were tested through CCK8 assay, flow cytometry assay, wound healing and transwell invasion assays, respectively. Results As compared with L02， the level of EMS1 gene in HepG2 was 10.5 (relative fold units). Confocal microscopy showed that cortactin in HepG2 accumulated to a high extent in the cell-substratum contact sites while it diffusely distributed in the cytoplasm in LO2. As compared with untreated group, RNAi-mediated suppression of EMS1/ cortactin in HepG2 cells was 68.00% in mRNA level, and 52.80% in protein level. In CCK8 assay, the inhibiting rate was 9.50% while in flow cytometry assay，reduction in the S phase was 37.89%.Inhibiting rates of migration and invasion were 45.40% and 64.91% (P<0.05, respectively). Conclusions EMS1/ cortactin plays a more important role in cellular invasive potential of HCC cell line HepG2.

Mechanism of damage induced by cisplatin in esophageal cancer cell line ECA109

2016, 36(12):  1670-1674. 

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Objective To investigate the mechanism of cisplatin-induced damage in the esophageal cancer cell line ECA109. Methods The proliferation with different time and concentrations of cisplatin was determined by MTT assay in ECA109 cells, the cell growth curve was drawn, and the low concentration drug，which be used in subsequent experiments，was selectd。The cisplatin induced nuclear foci (IF) average number changes of r-H2AX, P-STAT1 and CHK2-T68 at 24 h in 50 ECA109 cells were detected by immunofluorescence. The cisplatin induced nucleus foci (IF) average number changes of r-H2AX, P-STAT1 and CHK2-T68 at 24 h in 50 ECA109 cells were determined by immunofluorescence before and after silence H2AX gene or STAT1 respectively. Results The inhibition of proliferation induced by cisplatin in ECA109 cells were time and dose-dependent. Cisplatin can induce ECA109 cells to produce r-H2AX, P-STAT1 and CHK2-T68 nucleus foci (P<0.05). Cisplatin-induced r-H2AX, P-STAT1 and CHK2-T68 nucleus foci were reduced through silence H2AX gene, P<0.05. Cisplatin-induced P-STAT1 within CHK2-T68 nuclear foci were reduced by silence STAT1 gene (P<0.05). Conclusions Cisplatin can induce esophageal cancer cell injury, resulting in a variety of nuclear foci. In this damage response, H2AX is at the top regulating STAT1 and CHK2; STAT1 located downstream of H2AX and upstream of CHK2, adjusting CHK2.

miRNA-146a targets AUF1 and regulates cytokine expression in THP-1 cell line

2016, 36(12):  1675-1680. 

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Objective To investigate the role of miR-146a in regulating cytokine expression and the possible underlying mechanisms involved. Methods miR-146a mimics or inhibitor were transfected into human acute monocytic leukemia cell line (THP-1 cell line) by lentiviral vectors, and THP-1 cell in normal culture were used as control group. The expression levels of AUF1 in THP-1 cell lines were dectected by real-time PCR and Western blot. The levels of interleukin-8(IL-8) and interleukin-35(IL-35) in the culture supernatant were dectected by ELISA. Results miR-146a mimics decreased, while miR-146a inhibitor did not affect the expression of AUF1 in IL-1β-induced THP-1 cell lines. In addition, miR-146a mimics decreased（P<0.01; P<0.05）, while miR-146a inhibitor increased（P < 0.01；P < 0.01）, the expression of inflammatory cytokine IL-8 and anti-flammatory cytokine IL-35. Conclusions AUF1 is one of targets of miR-146a. miR-146a regulates the pro-inflammatory cytokine IL-8 secretion, which is accompanied by anti-flammatory cytokine IL-35.

siRNA silencing EGFR expression alleviates brain injury after intracerebral hemorrhage in rats

2016, 36(12):  1681-1686. 

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Objective To explore the effects of siRNA for epidermal growth factor receptor (EGFR) on rat brain injury after intracerebral hemorrhage and its related mechanisms. Methods The intracerebral hemorrhage model was established by injecting of VII collagenase into the caudate nucleus in rats. Rats were then treated with injection of 10 μL empty viral vector or EGFR siRNA lentivirus expression vector into lateral ventricles. The neurological function score was evaluated, and HE staining was used to observe the pathological changes of cerebral tissues. Brain water content was examined by the dried and wet weight method. EGFR expression was measured using immunohistostaining. Glial fibrillary acidic protein (GFAP) mRNA levels were analyzed through fluorescence real-time quantitative PCR. Western blot was used to detect EGFR, GFAP, signal transducers and activators of transcription 3 (STAT3) and phosphorylated STAT3 (p-STAT3). Results With the extension of intracerebral hemorrhage time, ERGF expression in cerebral tissues around hemotomas was gradually upregulated, and reached the peak on day 7 (P<0.01). In comparison with model group, EGFR siRNA relieved pathological impairment of cerebral tissues, reduced neurological function score and brain water content, and decreased the expression levels of EGFR, GFAP and p-STAT3 in cerebral tissues around hemotomas (P<0.01). Conclusions Gene silence of EGFR inhibits the activation of astrocytes through blockade of STAT3 phosphorylation, leading to reduced brain injury after intracerebral hemorrhage in rats.

Metalloproteinase inhibitor-1 reduced retinal injury in diabetic mice

2016, 36(12):  1687-1692. 

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Objective To investigate the protective effect and mechanism of matrix metalloproteinase inhibitor-1 (TIMP-1) against diabetic retinopathy in mice. Methods A total of 96 of 6-8 weeks old C57bl mice were randomly divided into 3 groups: control group, diabetic group and TIMP-1 group (mice were intravitreously injected with TIMP-1 5μl (1μg/ml) in the first and second months respectively after diabetes-induced). Retinal vascular leakages were investigated by retinal perfusion of evans blue after 5 months. The mRNA and protein expression levels of metalloproteinase 9 (MMP-9), vascular endothelial growth factor (VEGF), tumor necrosis factor alpha (TNF-α) and epoxy synthase -2 (COX-2) were also analyzed by RT-qPCR and Western blot. And the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activity and malondialdehyde (MDA) content in the retina tissue were also detected with bio-chemical method. Results There was no retinal leakage in control group, but diabetic group was significantly higher than TIMP-1 group (p＜0.01). The mRNA and protein expression levels of MMP-9, VEGF, TNF-α, COX-2 and the MDA content in diabetic group were significantly higher than control group (p＜0.01), while in TIMP-1 group they decreased (p＜0.01) and also higher than control group (p＜0.01). The SOD and GSH-Px activity in diabetic group were significantly lower than control group（p＜0.01),while in TIMP-1group they increased (p＜0.01) and also lower than control group (p＜0.01). Conclusions TIMP-1 can protect the retina of diabetic mice by reducing the oxidative stress and the expression of VEGF.

RNA interfering histone deacetylase 4 induces apoptosis of osteosarcoma cells

2016, 36(12):  1693-1698. 

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Objective:To explore the functions of HDAC4 gene on the biological behaviorsof HOS and U2OS osteosarcoma cells lines whichinhibit HDAC4 gene expression using a small interfering RNA.Methods: The HOS and U2OS cells were transfected with a chemical synthesized small interfering RNA targeting HDAC4; The real time-PCR and Western blot assays were performed to detect the mRNA and protein expression levels of HDAC4 and its downstream genes HIF-1α, respectively; The CCK-8, flow cytometry (FCM), invasion assays were used to identifythe cell proliferation, apoptosis and invasion abilities after the transfection with si-HDAC4, respectively.Results:The q-PCR analysis showed that HDAC4 mRNA expression was down-regulated in HOS and U2OS cellsafter transfected with si-HDAC4 (P<0.01); in addition, the cell proliferation was inhibited and cell apoptosis was induced after suppression of HDAC4. (P<0.05); The cells of HOS and U2OS migrating through themembrane insi-con group and si-HDAC4 group were (146±34), (45±20)and (207±35)、(121±23), (P<0.05), respectively.Western blot showed that the expression of HDAC4 and HIF-1α was significantly reduced. Conclusion:HDAC4si-RNA can inhibit cell proliferation, invasion and induce cell apoptosis in human HOS and U2OSosteosarcoma cells.

Eotaxin-1 is related to proliferation of clear cell renal cell carcinoma

2016, 36(12):  1699-1702. 

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Objective To investigate the expression of Eotaxin-1 in clear cell renal cell carcinoma(ccRCC) and its relationship with tumor proliferation. Methods The Eotaxin-1 and PCNA expression from 58 tissues of ccRCC and para carcinoma were analysised by immunohistochemistry or western blot. Results Eotaxin-1 were mainly expressed in the cytoplasm while PCNA were expressed in the cell nucleus, positive rate of Eotaxin-1 and PCNA in ccRCC tissues was significantly higher than that in para carcinoma tissues(P＜0.05), positive rate of Eotaxin-1 and PCNA in pathologic stageⅡ/Ⅲ was significantly higher than that in pathologic stageⅠ(P＜0.01). The positive rate of Eotaxin-1 and PCNA in clinical stage Ⅲ/Ⅳ was significantly higher than that in clinical stageⅠ/Ⅱ(P＜0.05). The protein level of Eotaxin-1 and PCNA in ccRCC were significantly higher than that in para-carcinoma tissues(P＜0.01，P＜0.05), Eotaxin-1 was positively related to PCNA in ccRCC tissues(P＜0.05). Conclusion Eotaxin-1 was related to proliferation in ccRCC and was expected to be a clinical indicator for ccRCC.

ICAM-1 and VCAM-1 are involved in the invasibility of glioma

2016, 36(12):  1703-1707. 

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Objects To explore the relationship between ICAM-1, VCAM-1 and invasibility of glioma. Methods The peripheral, central part of glioma and the normal brain tissue were obtained from 44 specimens with glioma. The expression of ICAM-1 and VCAM-1 in these specimens was detected by immunohistochemistry (IHC), RT-PCR and Western blot. Results The difference between peripheral, central part of glioma and normal brain tissue is statistically significant(p<0.05). And the difference between two of these three groups was statistically significant(p<0.01) when the pairwise comparison of these three groups was done. The expression in tumor peripheral tissue is the highest, followed by the tumor central tissue, and the expression in normal brain tissue is the lowest. The result is the same as above when these specimens were grouped by pathological grade. Conclusions ICAM-1 and VCAM-1 have significant relation to invasibility of glioma.

Astragaloside suppresses the decrease of connexin43 expression and junctional intercellular communication hypofunction in TM3 cells

2016, 36(12):  1708-1712. 

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Objective To investigate the protective effect of astragaloside(As) against cadmium(Cd) toxicity on the expression of connexin43 (Cx43) and the changes of connexin43-mediated gap junctional intercellular communication(GJIC) in TM3 cells . Method The TM3 cells were cultured, and four groups were designed : control, As(20㎎/L), Cd(10μmol/L) and Cd +As. The expression of connexin 43(Cx43) was detected by immunohistochemistry. The real-time quantitative PCR was used to detect the expression levels of Cx43 mRNA, and the Western blot was used to detect the expression levels of Cx43 protein. Furthermore, the GJIC was estimated by scrape-loading and dye transfer (SLDT). Results Compared with the control group, the average optical density ( AOD) of the positive product of Cx43 in Cd group was obviously decreased ( P＜0.01) , the expression levels of Cx43 mRNA and protein in Cd group was decreased ( P＜0.01), and the GJIC of TM3 cells was also decreased（P＜0.01）. On further analysis, the positive productives of Cx43, the expression levels of Cx43 mRNA and protein and GJIC of TM3 cells in Cd +As group were significantly higher than those in Cd group, though lower than of the control group. Conclusions As can inhibit the down-regulation of the expression levels of Cx43 and damage of GJIC of TM3 cells induced by Cd, which results in protective effects on TM3 cells function.

Variants identification of PKD1/PKD2 genes in an autosomal dominant polycystic kidney disease family

2016, 36(12):  1713-1715. 

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Changes of integrin β4 expression in rats with age

2016, 36(12):  1716-1717. 

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Subcellular localization of tumor-inhibiting factor PTEN in ischemia-anoxia brain damage

2016, 36(12):  1718-1722. 

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Phosphatase and tensin homologue deleted on chromosome 10（PTEN）is a protein contains lipid and protein phosphatase activity. The activation of PTEN and increased mitochondria or nuclear translocation after ischemia-anoxia in brain may determin the fate of neurons. Therefore, elucidation the molecular mechanisms of subcellular localization of PTEN after ischemia-anoxia would provide new insights in the target therapy of a large number of acute/chronic neurodegenerative disorders and drug design.

Research progress of QD-based multiplexed imaging technique for tumor biomarker detection

2016, 36(12):  1723-1727. 

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Tumor markers plays an important role in clinical diagnosis and treatment of malignant tumor. New fluorescent semiconductor nanocrystalquantum dots with high fluorescence intensity, good stability and excellent optical physics properties such as emission spectrum adjustable, combined with tumor markers, applied to the simultaneous detection of multiple tumor marker.

Recent advances of spermatogonial stem cell conversion and transdifferentiation in vitro

2016, 36(12):  1728-1732. 

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Under the testicular seminiferous tubule microenvironment control, spermatogonial stem cells (SSC) can only differentiate into sperms. Recent studies have shown that SSC may reprogram into pluripotent stem cells, or even directly reprogramming transdifferentiation into functional terminally differentiated cells under certain conditions in vitro. This potential of SSC makes it promise in the regenerative medicine and precise medicine application.

Progress in epigenetic regulation of endotoxin tolerance

2016, 36(12):  1733-1737. 

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Endotoxin tolerance is a protective mechanism of excessive inflammatory response. TLR4 signaling pathway plays critical roles in endotoxin tolerance. Epigenetics is a phenomenon that alters gene expression pattern without DNA sequence;it could modulates the process of endotoxin tolerance through microRNA, long non-coding RNA regulation and histone modification.

Research progress of breast cancer related Long non-coding RNAs

Hong-Chao TANG

2016, 36(12):  1738-1742. 

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The breast cancer’s incidence is higher than any other malignant tumors in women. In recent studies, lncRNAs play a role in breast cancer’s development, metastasis and prognosis. LncRNAs could make a significant sense to breast cancer’s therapeutic effect and prognosis by interacting with miRNA, mRNA or protein to regulating gene expression.

Progress in basic research,diagnosis and management of tophaceous gout

2016, 36(12):  1743-1746. 

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The tophus is the characteristic feature of advanced gout，which usually causes functional and psychological deficiency，and it always takes a long time for the drug therapy to take effect. Neutrophil extracellular traps（NETs） may lead to the formation of tophus and can limit acute inflammation by degrading cytokines and chemokines.Recently，the improvement of early diagnosis，new drugs and surgical methods can contribute to the prevent of the further destruction of tophaceous gout.

Development and present situation of the application of human face recognition technology in medical diagnosis

2016, 36(12):  1747-1750. 

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Some diseases or congenital abnormalities cause a certain pattern of facial changes, which are important for disease screening and diagnosis. Duringlast ten years, face recognition technology has been applied in the diagnosis of endocrine diseases such as acromegaly, Cushing's syndrome, and genetic syndromes such as Down syndrome and Cornelia de Lange syndrome.The detection rates of face recognition technology are not less than, in some cases even higher than,those of clinical workers.More importantly, this technology has more value in identifying patients with endocrine disease in the early stage. The technology is expected to be applied to the screening of endocrine diseases and genetic syndromes, to shorten the delay period before diagnosis and to help the staging of endocrine diseases.

Exploration of teaching physiology in English to foreign students of MBBS

2016, 36(12):  1751-1754. 

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Medical education of foreign students to China is the important part of higher medical education. Improving the quality of teaching for foreign students is the difficult problem for many medical colleges. The authors accumulated some experience in teaching physiology in English to foreign students of MBBS. Those experiences include the characters of foreign students, the policies of the university, the condition of teachers, the teaching method, choosing and compiling the textbooks, and so on. The authors hope that the experiences summarized in this article could provide communication and reference for other teachers, so as to cultivate more high level medical foreign students who adapting to the international competition，and contribute more for the international society.