Table of Content

05 September 2016, Volume 36 Issue 9

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Relationship between histone acetylation and DNA methylation in GATA4 promoter region during Islet-1 induced differentiation of C3H10T1/2 cells specifically into cardiomyocytes

2016, 36(9):  1179-1186. 

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Objective To research the interaction between early myocardial developmental gene GATA4 histone acetylation and its DNA methylation of promoter during Islet-1 inducing the mesenchymal stem cells of C3H10T1/2 cells to differentiate specifically into cardiomyocytes.Method Constructing the model of Islet-1 over-expression cells,in the process of GATA4 gene expression by using chromatin immunoprecipitation(CHIP)to detecte histone H3K9 acetylation sequential changes of its promoter region and using the methylation-specific PCR(MSP)to detect methylation sequential changes in CpG island of its promoter region,to elucidate the interaction between the both.Result With prolongation of time during Islet-1 inducing C3H10T1/2 to differentiate specifically into cardiomyocytes,the expression of the GATA4 gene increased(P<0.05),the level of histone H3K9 acetylation raised(P<0.05),while the DNA methylation level decreased in the second CpG site of its promoter(P<0.05).Conclusion During the Islet-1 promotes cells into cardiac-specific differentiation process,it is indicated that histone acetylation and DNA methylation exist mutual antagonism in regulation of the process of early myocardial specific transcription factor GATA4 expression,which promoted its sequential expression.

TRPV1 inhibits apoptosis mediated by PI3K/Akt signaling pathway in myocardial ischemia /reperfusion mouse heart

2016, 36(9):  1187-1192. 

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Objective To investigate the effects of TRPV1 on myocardial apoptosis and PI3K/Akt expressions during ischemia/reperfusion injury in mice. Methods 54 wild type (WT) mice and 54 TRPV1-null mutant (TRPV1-/-) mice were randomly divided into six groups: WT + Sham group, TRPV1-/- + Sham group, WT + I/R group, TRPV1-/- + I/R group, WT + LY group and TRPV1-/- + LY group. The mice hearts were perfused with a Langendorff apparatus and the indexes of cardiac mechanical function were measured. Cardiomyocyte apoptosis was detected by TUNEL. Expression of Bcl-2, Bax, Akt and P-Akt was measured by Western blot. Infarct size was measured by TTC staining. Results Compared with the WT + I/R group, the LVEDP significantly increased, and LVDP significantly decreased in the TRPV1-/- + I/R group (P < 0.001). The expression of Bcl-2/Bax and P-Akt in the myocardium of the TRPV1-/- + I/R group was significantly lower than that of the WT + I/R group (P < 0.001), while the proportion of apoptotic cardiomyocytes and infarct size increased significantly in the TRPV1-/- + I/R group as compared with the WT + I/R group (P < 0.01). Compared with I/R group, blockade of the PI3K with LY294002 significantly increased the apoptosis index (P < 0.01), infarct size (P < 0.001) and diminished expression of Bcl-2/Bax and P-Akt in WT + LY group (P < 0.001). Conclusion TRPV1 could attenuate I/R-induced apoptosis in the isolated heart probably through PI3K/Akt signaling pathway.

Se Ganoderma lucidum polysaccharides ameliorate the symptome of high fat diet induced non-alcoholic fatty liver in disease rats

2016, 36(9):  1193-1198. 

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Objective To investigate the expression of ACCα and SREBP-1c of selenium-enriched Ganoderma lucidum polysaccharides on fatty liver rats model. Methods 120 SD rats were randomly divided into control, high-fat diet, polyene phosphatidylcholine, Se G. lucidum polysaccharides low, medium and high group, after 4 and 8 weeks of treatment the rats were sacrificed, measuring the AST, ALT, CHOL and TG in blood serum, detect SREBP-1c, ACCα mRNA and protein expression by Western Blot and PCR respectively. Results With the increase of treatment dose and treatment time of Se G. lucidum polysaccharides, fatty infiltration of the liver was significantly reduced, fat particles significantly reduced; liver function and blood lipids significantly improved; SREBP-1c, ACCα mRNA and protein expression was significantly decreased. Conclusion Se G. lucidum polysaccharides can relieve the symptoms of non- alcoholic fatty liver disease in rats.

Exogenous H2S restores ischemic postconditioning-induced protection against I/R injury in heart of aging rats

2016, 36(9):  1199-1205. 

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Objective To explore the myocardial protective effects and possible mechanisms of hydrogen sulfide (H2S) on the recovery of ischemic post-conditioning (PC) in the aging rats. Methods Wistar young and aging rats were randomly divided into control group, ischemia/reperfusion (I/R) group, ischemic post-conditioning (PC) group. In addition, aging rats were treated with NaHS (PC+NaHS). The model of myocardial I/R injury and PC in isolated rats hearts was induced with Langendorff system; LDH, CK activities of coronary effluent and SOD activity and MDA content as well as H2S production rate of myocardial tissue homogenate were measured by colorimetric method; Myocardial ultrastructure was detected by transmission electron microscope; The myocardial infarct size was measured by TTC staining; Myocardial cell apoptosis was detected by TUNEL staining; The expression of Bcl-2, caspase-3 and caspase-9 was detected by Western blot. Results Compared with the control group, I/R decreased H2S production rate, SOD activity and CSE expression, increased LDH and CK activity, MDA content, myocardial injury, apoptosis, myocardial infarct size, caspase-3 and caspase-9 and Bcl-2 expression(P<0.01); Compared with the I/R group, PC reduced I/R injury and apoptosis in the young hearts (P<0.01), however, PC lost myocardial protective effect in the aging hearts; Exogenous H2S restored the PC-induced cardioprotection in aging hearts. Conclusion Our results suggest that exogenous H2S restores the myocardial protective effect of PC via anti-oxidation, scavenging free radical and inhibiting apoptosis.

UHRF2 promoting H3K9 acetylation and cell proliferation in DNA damage response induced by hydroxyurea

2016, 36(9):  1206-1210. 

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Objective To investigate the effect of UHRF2 on H3K9 acetylation and cell proliferation in DNA damage response induced by Hydroxyurea. Methods HEK293 cells cultured in vitro treated with Hydroxyurea for different time to construct cell models of DNA damage; HEK293 cells were transfected with pCMV-3×FLAG-UHRF2.We evaluated transfection efficiency of pCMV-3×FLAG-UHRF2 and H3 K9 acetylation in DNA damage response with Western blot. CCK8 assay was used to detect cell proliferation. Results HEK293 cells treated with 2.5mmol/L Hydroxyurea 12h later, obvious DNA damage was detected. After pCMV-3×FLAG-UHRF2 was transfected into the cells, The expression of UHRF2 was increased (P<0.01). The acetylation level of H3 K9 significantly increased (P<0.05). The cell proliferation was decreased By CCK8 (P<0.05). Conclusion UHRF2 can promote H3 K9 acetylation and cell proliferation in DNA damage response induced by Hydroxyurea.

Notch1 activation attenuates myocardial reperfusion injury in diabetic mice

2016, 36(9):  1211-1215. 

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Objective: To test whether Notch1 attenuates myocardial ischemia/reperfusion (MI/R) injury after diabetes, and clarify the role of TNF-α inhibitor in it. Methods: A mice model of type 2 diabetes mellitus was induced by STZ intraperitoneal injection along with a high fat diet. And Notch1 specific small interfering RNA (siRNA, 20 μg) was delivered through intramyocardial injection to knockdown cardiac Notch1 levels. After 48 hours, myocardial ischemia/reperfusion (30 minutes) mice model was prepared. Then, etanercept (8 mg/kg) was administrated by intraperitoneal injection 10 minute before reperfusion. Mice were subjected to 30 minutes of myocardial ischemia followed by 3 hours (for TNF-α contents determined by ELISA, Notch1 activation and LDH release measured by western blot and cell apoptosis detected by caspase-3 activity assay) or 24 hours (for myocardial infarct size assessed by Evans blue/ (TTC) doubles staining and cardiac function determined by ultrasound) reperfusion. Results: TNF-α level of plasma and the myocardial tissue in diabetes mice was increased, while cardiac Notch1 was significantly suppressed (P<0.05). Etanercept apparently mitigated MI/R injury in mice subjected to diabetic, evidenced by decreased release of LDH, improved cardiac function, lessened myocardial infarct size and reduced myocardial apoptosis (P<0.01). In addition, etanercept obviously reduced the contents of TNF-α in both plasma and myocardium, in contrast, enhanced the expression of Notch1 intracellular domain (Notch1 ICD) in cardiac tissues (P<0.05). The disturbance of Notch1 pathway partly reversed etanercept's cardioprotection. Conclusion: TNF-α inhibitor attenuates myocardial ischemia/reperfusion injury via activating Notch1 in diabetic mice.

Tanshinone ⅡA inhibits the apoptosis of HUVECs induced by aristolochic acid and its mechanism

2016, 36(9):  1216-1221. 

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Objective To observe the protective effect of tanshinone ⅡA(TSN) on the apoptosis of human umbilical vein endothelial cells(HUVECs) stimulated by aristolochic acid(AA) and its possible mechanism. Methods Cultivated HUVECs were divided into four groups: control group, AA group(the final concentration of AA was 10 mg/L), TSN treatment group(HUVECs was added with AA after incubation with 0.2, 0.4 and 0.8 mg/L of TSN for one hour) and LY294002 pretreatment group(HUVECs was pretreated with 20 μmol/L of PI3K antagonist LY294002 for 30 min before TSN was added). After 24 hours, cell viabilities were evaluated by the MTT assays. The morphological changes of apoptotic cells were observed by Hoechst 33258 fluorescence staining. The proportions of apoptotic cells were assessed by flow cytometry. Western blot was used to determine the expressions of Bcl-2, Bax and phophorylated Akt. Meanwhile, the caspase-3 activity was detected by colorimetric method. Results Compared with control group, AA increased the proportions of apoptotic cells(P < 0.05), inhibited the expressions of Bcl-2 and phosphorylated Akt(P < 0.05), and promoted the expression of Bax(P < 0.05). After intervention with TSN, the above-mentioned parameter changes were reversed(P < 0.05). The protective effects of TSN were partially inhibited by PI3K antagonist LY294002(P < 0.05). Conclusion TSN can inhibit the apoptosis of HUVECs stimulated by aristolochic acid.

Genotyping analysis of G6PD deficiency in Chengmai area of Hainan province

2016, 36(9):  1222-1226. 

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Objective To analyze the prevalence and the genotypic mutant characteristics of G6PD deficiency in Chengmai area of Hainan province. Methods The G6PD enzyme activity of a total of 1299 subjects consisting of 650 males and 649 females were determined by Zinkham method. All the positive samples were subjected to genotype by a melting curve analysis-based PCR assay for 16 known common mutations in Chinese population. Those samples with no detectable mutantions were sequenced in exons. Results The prevalence of G6PD deficiency in Chengmai area was 5.54% (72/1299). Of 650 males and 649 females tested, 6.62% (43/650) and 4.47% (29/649) were found to have G6PD deficiency, respectively. Of the 72 G6PD deficient subjects genotyped, 61 subjects had mutation. 6 kinds of mutation were indentified including 24 cases of 1376 G>T (33.33%), 19 cases of 1388 G>A (26.39%), 4 cases of 95 A>G (5.56%), 6 cases of 1024 C>T (8.33%), 4 cases of 392 G>T (5.56%), 3 cases of 871 G>A (4.17%), 1 case of 1376 G>T combined with 1388 G>A (1.39%). No any new mutations could detected in the 11 cases of unknown mutations(15.28%). Conclusions The incidence of G6PD deficiency is high in Chengmai area. 1376 G>T and 1388 G>A are the most common variants in this area.

Down-regulation of microRNA-210 enhances radiosensitivity in radiation-resistant nasopharyngeal carcinoma cells

2016, 36(9):  1227-1231. 

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Objective To explore the effect of miRNA-210 down-regulation on radiosensitivity of radiation-resistant nasopharyngeal carcinoma cells. Methods The radiation-resistant nasopharyngeal carcinoma cells(CNE-2R) were established by dose gradient method. The miRNA microarray was used for detecting miRNA expression profiles of the CNE-2 cells and CNE-2R cells, and miR-210 was verified by qPCR. After LV-hsa-miR-210-inhibition were infected CNE-2R cells, the miR-210 in 210-inhibition cells were verified by qPCR. Apoptosis and cell cycle of 210-inhibition and CNE-2R cells were detected by flow cytometry, the survival fraction of cells were detected by clone formation assay. Results There were 93 miRNAs expression remarkable changed over>2 fold in CNE-2R cell lines which we established, compared with CNE-2. 210-inhibition, which expressing a low level of miR-210 had a higher apoptosis rate than CNE-2R cells(P<0.05). The proportion of 210-inhibition cells in the G2/M phase were more than in the CNE-2R cells(P<0.05), and the S phase of they were less than in the CNE-2R cells(P<0.05). The survival fractions of 210-inhibition cells significantly reduced, compared with CNE-2R cells. Conclusions Down-regulation of microRNA-210 can enhance radiosensitivity in radiation-resistant nasopharyngeal carcinoma cells, which may be used as a new target for the treatment of radiation resistance.

Induction of dihydroartemisinin on prostate cancer PC-3 apoptosis

2016, 36(9):  1232-1236. 

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Objective To investigate the induction of dihydroartemisinin(DHA) on prostate cancer PC-3 apoptosis and it possible mechanisms. Methods PC-3 were treated with different concentrations (0, 25, 50, and 100 μmol/L) of DHA for 48 h. The apoptosis was deteleted by flow cytometry. HSP70 mRNA expression levels were determined by RT-qPCR.HSP70,Apaf-1 and Caspase-3 protein expressions were determined by western blot. Two more groups were added in RT-qPCR and western blot, the 100 μmol/L HSP70 inhibitor group and the DMSO group. Results DHA can significantly induced the apoptosis of PC-3 cells (P<0.05). Compared with control group, the expressions of HSP70 mRNA and protein were significantly decreased (P<0.05), while the expressions of Apaf-1 and Caspase-3 proteins were increased (P<0.05). Conclusion DHA significantly inhibit the apoptosis of PC-3 cells in vitro. These mechanisms may be due to the reduced expression HSP70 and the induced expression of Apaf-1 and Caspase-3 by DHA.

Effects of estrogen on estrogen receptors gene expression of condylar cartilage of ovariectomized rats

2016, 36(9):  1237-1241. 

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Objective This study investigated the role of estrogen receptors in the metabolism of temporomandibular cartilage by applying different concentration of 17β-estradiol (17β-E2) to ovariectomized (OVX) rats.Methods 1.The female SD rats were randomly assigned to the control group,sham group,OVX group and hormone replacement therapy group . Different concentration of 17β-E2 were injected timely and delayed. 2. The change of estrogen level was verified by testing the shape and mature index of vaginal epithelium exfoliated cells, then the ERα and ERβ in rat condylar cartilage were tested by using Western-blot and Real-time PCR analysis subsequently. Results 1)The maure index of vaginal epithelium exfoliated cells of OVX rats was 180/12/8, indicating low levels of estrogen in vivo(P＜0.05). 2) ER mRNA could maintain at the normal level when 5×102μg/kg of 17β-E2 were supplemented immediately. Yet this was not the case when 17β-E2 were given delayed. 3. Both 50μg/kg and 5×103μg/kg of 17β-E2 administration can suppress the expression of ER, either in protein or mRNA level, and this inhibitory effect is more obvious in 5×103μg/kg group(P＜0.05).Conclusion The biological effects of OVX rats of ER depend on normal physiological concentration and accurate period of estrogen secretion.

Emodin inhibits pancreatic cancer cells by upregulating the expression of Smad4

2016, 36(9):  1242-1245. 

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Objective Treat the Jab1 as targets to investigate the effects and possible mechanisms that the emodin effects on the pancreatic cancer cells. Methods Determine the protein expression of Jab1 and Smad4 in the PANC-1 and AsPC-1 cell lines with Western Blot method. The 293T cells were randomly divided into control group (no treatment), emodin group (20μmol / L emodin), Jab1 group (transfected with HA-Jab1 plasmid)；Determine the binding between the β-TrCP1 and Smad4 with the IP method in the 293T cells. Determine the level of Smad4 protein expression between control group and emodin group using Western Blot method .Results Jab1 was highly expressed and Smad4 protein expression was low in pancreatic cancer cell lines, both of which were negatively correlated（P＜0.05）. Jab1 can induce the binding of Smad4 and β-TrCP1 and promote Smad4 protein degradation in the 293T cells; emodin increase the level of Smad4 by inhibiting the binding betweenβ-TrCP1 and Smad4（P＜0.05）. Conclusion Contract to Jab1, emodin play an anti-tumor role by inhibiting the degradation of Smad4,which is probably by inhibiting ubiquitin pathway enzymes.

Associations of the 4P14 and CTLA-4 gene polymorphisms with graves’ disease

2016, 36(9):  1246-1251. 

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Objective To investigate the associations of the rs6832151 within chromosomal band 4P14 and four single-nucleotide polymorphisms (SNPs) in CTLA-4 gene with Graves’disease（GD）in a Chinese Han population from Bengbu city, Anhui province , as well as gene - gene interaction on Graves’disease .Methods A total of five SNPs were genotyped in a cohort of 611 GD patients and 644 healthy controls,by using the TaqMan SNP Genotyping Assay.The relation of these SNPs sites with GD were analyzed with Plink v1.07 and Haploview 4.0.Results An association was observed when the rs6832151 was directly analyzed or analyzed under three genetic models between GD and controls( P<0.05). The frequencies of genotypes under dominant model of SNPs in CTLA-4(rs231804, rs231726) were significantly different between GD and controls.Gene-gene interactions among Graves’ disease were significant (P=0.001) . Significant epistasis was found between rs1024161 and rs10197319 (P<0.05). Conclusion Polymorphism of the rs6832151（4P14）、rs231804 and rs231726(CTLA-4) were susceptible gene to Graves’ disease for a Chinese Han population from Bengbu city.A gene-gene interaction on Graves’ disease was identified among rs10197319、rs231726、rs231804、rs1024161(CTLA-4) and rs6832151(4P14).Epistatic interaction was observed between rs1024161 and rs10197319 in GD.

Expression of RON in bladder cancer tissues and its effect on proliferation in T24 cell line

2016, 36(9):  1252-1256. 

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Objective This study aimed to investigate effects of RON on proliferation and migration in T24 cell line. Methods First, RT-PCR was used to detect expression of RON mRNA in bladder cancer tissues. Second, Knockdown of RON expression in T24 cell line was conducted by transfection of a chemical synthesized small interfering RNA specifically targeted to RON. Efficacy of RON-silenced was determined ?by real time -PCR and western blot, The CCK-8, Transwell migration and invasion assays were performed to measure the proliferation, migration and invasion abilities, respectively. Flow cytometry was adopted to detect cell apoptosis. Results The results showed that the RON mRNA relative expression level was positive correlation with TNM stage; in RON-siRNA group, cell proliferation and migration abilities were degraded (P<0.05), and cell apoptosis was increased (P<0.05), compared with other groups. Conclusion RON gene promoted proliferation and migration of bladder cancer cells, maybe become a new target for the treatment of bladder cancer.

Effects of ursolicacid on HMGB1 expression and NF-кB activity of THP-1 monocytes

2016, 36(9):  1257-1261. 

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Objective To investigate the effects of ursolic acid on the expression of HMGB1 and activity of NF-κB in THP-1 cells. Methods After being stimulated by different concentrations UA (0,0.1,1,5 and 10μmol/L), the cells were detected correspondingly.⑴The cell proliferation were checked by MTT. ⑵The HMGB1 and p65 destination genes were amplificated with PCR.⑶HMGB1 and p65 protein was detected by Western blot. ⑷Transfecting of Plasmid pGl3-NF-кB-luciferase report gene:Plasmid pGl3-NF-кB-luciferase report gene was transient transfected into THP-1 cells.After transfecting for 40 hours, 1 μmol/L UA were added. Luciferase activity detection was performed when transfecting for 48 hours. Results ⑴UA can obviously inhibit THP-1 cell proliferation with the concentration increasing.⑵The influence of UA on THP-1 cell HMGB1 mRNA and protein exhibits a certain bidirectional and the influence of 1 μmol/L UA is the strongest.⑶UA can influence the expression of p65 mRNA and protein andaffect the NF-кBactivity.Conclusion UA can influence the HMGB1 expression and NF-кB activity of THP-1 cell.

Permanent atrial fibrillation related transcriptome profiling and the establishment of miRNA regulatory network

2016, 36(9):  1262-1267. 

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Objectives: To screen for the atrial fibrillation related miRNAs and their target gene. to research the pathogenesis of permanent AF. Methods: Left atrium miRNA and mRNA profiling in patients with permanent AF (n=7) were compared with healthy heart donors in sinus rhythm (n=4) using microarrays. By predicting potential miRNA targets and making negative correlation analysis with differentially expressed mRNA, miRNA-target gene regulatory network was established. and key miRNA their target genes related with permanent AF were found, and qRT-PCR analysis were used to validated the expression of key miRNAs and gene in the network in another cohort. Bioinformatics analyses were performed to understanding the global regulating roles of miRNAs-gene network. Results: 610 mRNAs (fold change>2, P<0.05) were shown to be significantly changed in permanent AF patients compared with healthy controls. The target prediction and negative correlations analyses with the mRNA array have identified 20 dysregulated miRNAs and their 107 target genes. The corresponding miRNA-gene regulatory network were established. The miRNAs including miR-144, miR-1284, miR-1827, miR-1, miR-3613-3p and miR-101 and target genes containing CACNB2, EFNB1, PTEN, TAOK1, RUNX1 and TPM3 were found to be in the central part of the network.Some of their expression were further verified by qRT-PCR analysis on another cohort. Conclusions: Through the analysis of gene expression profile chip and miRNAs chip joint small sample of pAF left atrial tissue samples, establishing the miRNA-gene network, found that the pathogenesis of pAF important micrornas - target gene regulation and function, the result is more accurate.

Effects of erythropoietin on endoplasmic reticulum stress-related proteins in the rat rhabdomyolysis induced acute kidney injury

LI Jian-dong

2016, 36(9):  1268-1273. 

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OBJECTIVE: To investigate whether erythropoietin (EPO) attenuates rhabdomyolysis-induced acute kidney injury by regulating endoplasmic reticulum stress associated proteins. METHODS: Healthy male SD rats were randomly divided into four group: control group (n=6), acute kidney injury group (AKI，n=18)，AKI+EPO group (n=18), CN+EPO group (n=18), AKI group, AKI+EPO group and CN+EPO group based oninjection time is divided into three subgroups, 1, 6 and 24h groups of six rats. All animals were sacrificed on thire each time. Blood samples and kidney tissues were collected to evaluate blood urea nitrogen (BUN) , serum creatinine （SCr）and plasma Mb. The expression of GRP78 and CHOP was detected by immunohistochemistry and fluorescence quantitative RT-PCR. RESULTS: Compared with control group, significant increases in the levels of SCr, BUN and Mb were observed in AKI group and AKI+EPO group（P<0.05）. The over-expression of AKI-induced GRP78 and CHOP was suppressed by EPO（P<0.05）. CONCLUSION: AKI activates UPR in renal tubular epithelial cells. EPO has a protective effect on the kidneys with rhabdomyolysis-induced acute kidney injury, which may be related to the regulation of UPR-induced apoptosis.

Curcumin inhibits proliferation of human hepatoma cells via down-regulation of PI3K/AKT/mTOR signaling pathway

2016, 36(9):  1274-1279. 

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Objective: The effect of curcumin over human hepatoma cell line HL-7702 proliferation and the inhibitory mechanism were investigated.Methods: HL-7702 cultured in vitro was treated with a gradient concentration of curcumin（0，10，20，40,80μmol/L）for 48h or subjected to combinational treatment of PI3K/AKT inhibitor LY294002 with curcumin. Then MTT was applied to detect cell proliferation and Western blot was used to detect PI3K，AKT，mTOR，Bax,Bcl-2 protein level and caspase-3 activation status.Results: Curcumin inhibited HL-7702 proliferation in a dose-dependent manner via upregulating phosphorylation of PI3K, AKT and mTOR. Curcumin induced apoptosis of HL-7702 cells with increased Bax and caspase3 activation as well as decreased Bcl-2. In addition, LY294002 attenuated the effect of curcumin over cell proliferation and apoptosis. Conclusion: Curcumin inhibited proliferation and triggered apoptosis of human hepatoma cell HL-7702, which may be caused by downregulating PI3K/AKT/mTOR signaling pathway.

Reducing the expression of inflammatory cytokines expression at acute myocardial ischemia injury in rat by H2S

2016, 36(9):  1280-1281. 

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Establishment of Tunicamycin-induced L02 cells endoplasmic reticulum stress model

2016, 36(9):  1282-1284. 

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Research progress on phenotype transition and efferocytosis of macrophages in chronic skin ulcer

2016, 36(9):  1285-1289. 

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Macrophages play a central role in all stages of wound healing and orchestrate the wound healing process. Efferocytosis and phenotype transition are not two independent biological processes, but have the connection and necessary relationship. The phagocytosis of neutrophils influences macrophage phenotype, causing the chronic inflammation.

Roles of necroptosis in neurological diseases

2016, 36(9):  1290-1294. 

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Necroptosis plays crucial roles in the genesis and development of many diseases involved in different organisms and systems. Neuronal damage is common in all kinds of neurological diseases. According to recent reports, necroptosis is an important pattern of neuronal death. Inhibition of neuronal necroptosis shows protective roles in neurological diseases. Therefore, studies on neuronal necroptosis will be the focus of prevention and treatment of neurological diseases in the future.

Research progress of the relationship between circular RNA and diseases

2016, 36(9):  1295-1300. 

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Circular RNA is a recently discovered endogenous non-coding RNA, which is generated by the model of intron-pairing-driven circularization and is regulated by the relevant regulatory factors. One of the important biological functions of circular RNA is as a miRNA sponge, which makes the level of miRNA changed significantly in a short time. The circular RNA is closely related to the disease, which is a potential molecular of diagnosis and treatment. This paper deals with the three aspects of the biosynthesis and regulation of circular RNA, the biological function of circular RNA and the relationship between circular RNA and diseases.

Heat shock protein 70 and hepatocellular carcinoma

2016, 36(9):  1301-1305. 

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Heat shock protein 70(HSP70)exists in cells widely, and is highly expressed in responsing to stress,it also plays an important role in composing and repairing the protein. The function of HSP70 in hepatocellular immunotherapy is becoming more and more important:Because of the specificity, immunogenicity and being molecular chaperone, HSP70can induces the immune responses. But it also has many questions which are needed to research for. In a word,HSP70 has a good prospect in the therapy of hepatocellular carcinoma.

Advance of lncRNA in infectious diseases

Ying-Hua LI

2016, 36(9):  1306-1309. 

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Researches in lncRNAs have been booming for the past few years, but only a few studies about lncRNAs in infectious diseases have been reported. After pathogen infected a host, on the one hand, changes of its own lncRNAs may lead to a host of pathogenic; on the other hand, the pathogen may cause adaptive changes in host lncRNAs, which may play a role in immune defense.

Progress on the clinicalappl application of low-dose aspirin and ventricular remodeling of myocardial hypertrophty

2016, 36(9):  1310-1312. 

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The effect of aspirin is extensive, which can treat many diseases such as stroke.But curative effect of different doses of aspirin is not completely the same。In recent decades of research，we found that low-dose aspirin can irreversiblly inhibit the activity of epoxidase (COX-1), blocking the formation of thromboxane A2, inhibiting platelet aggregation, preventing thrombosis, thus it plays a role of delaying the progress of the ventricular remodeling of myocardial hypertrophy.

Research on the management andpractice of residents traininginformationization

2016, 36(9):  1313-1318. 

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Residents training gets more and more emphasis, therefore residents training informationization related works get great development in China. Based on the review of residents training informationization research, the paper presents primary principles of establishing residents training IT system, which includes optimizing management rules, realizing multi-roles system, realizing overall assessments and strengthening tutor management. The paper analyzes residents training informationizationpractices of Peking Union Medical College Hospital, and proposes several directions of residents training informationization in the future.

Comparison of two methods of transesophageal echocardiography simulation training

2016, 36(9):  1319-1322. 

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Objective To assess the impact of transthoracic echocardiography（TTE） skills training in Transesophageal endocardiography（TEE）trainees; Methods In this prospective randomized study, 84 anesthesiologists (novice in echocardiography) were randomized to either TTE+TEE group (n=41) or TEE group(n=43). A standardized pretest was administered before the training. The trainees in TTE+TEE group firstly learned TTE skills followed by simulation-based TEE training. And the trainees in TEE group only had simulation-based TEE training session. Comprehension in both groups was then assessed using a written posttest immediately after training and 4 weeks later; Results Pretest scores revealed similar knowledge among the trainees. The TTE group scored higher on echocardiography anatomy after the training session (71.5%±18.3% vs 48.8%±18.3%，p＜0.01；TTE+TEE group versus TEE group, respectively)，but scored lower in clinical applications(38.4%±8.7% vs 45.2%±14.2%，p＜0.01). The two groups showed no difference in patient safety，probe manipulation and pathology scores. In 4-weeks later test, TTE+TEE group scored higher on both view identification and structure identification questions. Conclusion This prospective randomized study demonstrated that，after TTE training, the trainees could know better in echocardiography anatomy，and the memory of TEE views and structures lasted longer.