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Objective To investigate the mechanism of chronic stress during pregnancy inducing depression in male offspring mice. Methods 8-week-old female C57 mice containing pure flox gene [flox/flox, corticotropin-releasing hormone receptor1(CRHR1) gene normal expression] and male C57 mice containing heterozygous flox gene and containing cre gene(flox/+, with cre; CRHR1 gene conditions Sex knockout) were put in cage together.The pregnant mice were randomly divided into the control group and the chronic stress group. After the mice were born,the male offspring mice were randomly divided into the control group( CON group),the control + CRHR1 gene knockout heterozygous mice group( CON + CKOH group),the control + CRHR1 gene knockout homozygous mice group( CON + CKOA group),the chronic unpredictable mild stress group( CUMS group),the chronic unpredictable mild stress + CRHR1 gene knockout heterozygous mice group( CUMS + CKOH group),the chronic unpredictable mild stress + CRHR1 gene knockout homozygous mice group( CUMS + CKOA group). The degree of depression in male offspring mice was observed by sucrose preference experiment,tail suspension experiment and forced swimming experiment. TUNEL staining was used to observe apoptosis in hippocampal CA3 area. Western blot was used to quantitatively detect the expression of m TOR and p-mTOR( Ser2448) in hippocampus. Results Chronic stress during pregnancy induced depression-like behavior,increased neuronal apoptosis index in hippocampal CA3 area,and attenuated the level of hippocampal m TOR and p-mTOR protein significantly in male offspring mice. Hippocampal CRHR1 gene conditional knockout could significantly improve depressive-like behavior,neuronal apoptosis in the hippocampus CA3 region and the levels of m TOR and p-mTOR proteins in the male offspring mice whose mother suffered from chronic stress during pregnancy. Conclusion Chronic stress during pregnancy can lead to depression-like behavior in male offspring mice through activating CRHR1 of hippocampus and attenuating m TOR protein expression in the hippocampus,which results in neuronal injury in the CA3 region of offspring hippocampus.

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Objective To establish SNHG9-knocked out U251 cells by combination of CRISPR/Cas9 and single cell sorting through flow cytometry, and test the effect of SNHG9 deletion on cell proliferation. And to explore the potential mechanism that SNHG9 involved by bioinformatic analysis. Methods Two targets were separately designed for Cas9 at the genomic sites upstream and downstream of SNHG9 gene, the two pairs of primers that guide the synthesis of sgRNA were annealed and cloned into px330-EGFP, and U251 cell were co-transfected with the two successfully constructed plasmids followed by single cell sorting into 96-well plates. Cell clones were raised and the genotypes were identified Gby PCR and sequencing, SNHG9-deleted clone cells were selected for subsequent experiments. Effect of SNHG9 deletion on cell proliferation was assessed by RTCA. Expression of lncRNA SNHG9, its co-expressed genes and their enrichment analysis were performed by online tools. Results Effective targets were designed and plasmid of SNHG9 knockout was successfully constructed. 8 clones survived after single cell sorting and culture, from which 1 clone with SNHG9 totally deleted was obtained. The proliferation capacity of U251 cells significantly decreased after SNHG9 knocking-out(P<0.05). SNHG9 was overexpressed glioblastoma multiforme(GBM) samples when compared with normal tissues, the co-expressed genes most significantly enriched in mitochondrion related functions. Conclusion The SNHG9-deleted U251 clone was successfully established; SNHG9 knocking-out suppressed the proliferation of U251 cells; bioinformatic analysis showed that SNHG9 might involve in the regulation of mitochondrial function.

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Objective To investigate the effect and mechanism of insulin-like growth factor binding protein 2(IGFBP2) on insulin-like growth factor-1(IGF-1) induced proliferation, migration and invasion of hepatocellular carcinoma(HCC)cell line of HepG2 cells. Methods 15.6, 31.2, 62.5, 125, 250 ng/ml IGFBP2 and 50 ng/ml IGF-1 were used to stimulate HepG2 cells. Cell proliferation was detected by CCK-8 method, and cell migration and invasion were detected by transwell method. Western blot was used to detect the activation and expression of intracellular signaling pathway-related proteins. Results The combination of IGFBP2 and IGF-1 could promote the proliferation, migration and invasion of HepG2 cells compared with the effect of IGF-1. The combination of IGFBP2 and IGF-1 increased phosphorylation levels of IGF1 R, Akt and ERK in HepG2 cells without significant changes in total expression, and the protein expression of early growth response gene 1(EGR1) also increased. Conclusion IGFBP2 enhances IGF-1 induced proliferation, migration and invasion of HepG2 cells by activating Akt and ERK signaling pathways.

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Objective To study the expression level changes of virulence genes ofhypervirulent Klebsiella pneumoniaeunder the action of antibiotics with subinhibitory concentration. Methods Disk diffusion method and ViteK2 instrument method were used to determine the susceptibility of the strains to common clinical antibiotics, and the MIC values of the strains to cefoxitin and amikacin were detected by broth dilution method.The serotypes of capsule(K1, K2, K5, K20, K54, K57) and virulence related genes(rmpA,aerobactin,kfu,alls,magA,wcaG,fimH,mrkD) were detected by polymerase chain reaction(PCR). According to the MIC value of the two drugs, the 1/2 MIC, 1/4 MIC and 1/8 MIC subantibiotic concentration gradient of antibiotics was prepared. qRT-PCR was used to detect the change of the relative expression of virulence genes in 1/2 MIC, 1/4 MIC, 1/8 MIC concentrations of cefoxitin and amikacin, and the difference was analyzed by SPSS software. The homology between the strains was detected by MALDI-TOF MS and ERIC-PCR. Results A total of 57 strains ofKlebsiella pneumoniaewere collected, which were sensitive to most of the commonly used antibiotics. PCR results showed that there were 17 strains of K1, 21 strains of K2, 2 strains of K20, 8 strains of K57, and 9 strains of unknown haemorrhagic type.RmpAandaerobactingenes were all positive.17, 21 and 16 strains ofwcaG,kfuandmagAgenes were detected respectively.FimHandmrkDwere all positive. Under the action of subinhibitory concentration of cefoxitin and amikacin, the two antibiotics of three concentrations(1/2 MIC, 1/4 MIC, 1/8 MIC) had obvious inhibitory effects on the two virulence genes(P<0.05), and the inhibition degree of cefoxitin was the highest. The inhibitory effect of 1/2 MIC was the strongest among the three concentrations. Conclusion Hypervirulent Klebsiella pneumoniaeis highly sensitive to commonly used antibiotics. Serotypes K1 and K2 are common serotypes ofhypervirulent Klebsiella pneumoniaethan other serotypes.The virulence gene expression ofrmpAandaerobactindecreased under the action of subinhibitory concentration of cefoxitin and amikacin.

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Objective To investigate the effect of tumor suppressor gene programmedcelldeath 4(PDCD4) expression level on inhibition of human gastric cancer xenograft growth in nude mice byCelastrus Orbiculatusextract(COE). Methods The exogenous recombinant eukaryotic plasmid pcDNA3.1-PDCD4 was transfected into human gastric cancer cell line SGC-7901, after screened by G418, a stable transfected cell line with high expression of PDCD4 was established. The subcutaneously transplant tumor model of human gastric cancer in nude mice was established and randomly divided into the control group, pcDNA3.1 group, pcDNA3.1-PDCD4 group, COE group, pcDNA3.1+COE group, and pcDNA3.1-PDCD4+COE group. The growth status and tumorigenic incubation period of xenograft were monitored, and protein expression level of PDCD4、E-cadherin、N-cdherin and Vimentin in xenograft was detected by immunohistochemistry assay. Results Compared with the control group, the tumor inhibition rates of pcDNA3.1-PDCD4 group, COE group, pcDNA3.1+COE group, pcDNA3.1-PDCD4+COE group were 59.29%, 57.52%, 58.41%, 71.68%, respectively. The protein expression level of PDCD4, E-cadherin was significantly up-regulated, while the protein expression level of N-cadherin, Vimentin significantly decreased. In pcDNA3.1-PDCD4+COE group, the tumor inhibition rate and the changes of PDCD4、E-cadherin、N-cdherin and Vimentin protein expression levels were significant higher than other groups(P<0.01). Conclusion The tumor suppressor gene PDCD4 may be involved in the inhibitory effect of COE on the growth of human gastric carcinoma xenograft tumor in nude mice, and its mechanism may be related to the influence of EMT process.

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Objective To investigate the effect of baicalein on breast cancer cell mcf-7 and xenograft tumor in nude mice and its possible molecular mechanism. Methods CCK-8 was used to detect the effect of different concentrations(0, 20, 50, 100 μmol/L) of baicalein on the proliferation of breast cancer cells; flow cytometry was used to detect the cycle distribution and apoptosis rate of breast cancer cells. Transcriptome sequencing was used to analyze the possible signaling pathways affected by baicalein. Western blot was used to detect the effects of baicalein on related proteins; in addition,in vivoexperiments with nude mice xenograft model were used to explore the effects of baicalein on nude mice Impact. Results Compared with the control group, baicalein could inhibit the proliferation of breast cancer cells in a time-and concentration-dependent manner, induce breast cancer cell cycle arrest, and significantly induce its apoptosis; meanwhile, after baicalein treated mcf-7 cells 48 h, the expression level of PCNA, a marker of proliferation, significantly reduced. The expression level of Cleaved-Caspase3 protein gradually increased, and the expression level of Caspase3 protein gradually reduced. In addition, baicalein could also regulate the PTEN/PI3 K/AKT signaling pathway. The expression level of tumor suppressor protein PTEN gradually increased with concentration increasing, and the expression levels of p-PI3 K and p-AKT protein decreased significantly with concentration increasing; meanwhile,in vivoexperiments showed that baicalein could inhibit mcf-7 xenograft tumor growth. Conclusion Baicalein has an inhibitory effect on the proliferation of breast cancer cell line mcf-7 and induces apoptosis. The mechanism may be related to the regulation of PTEN/PI3 K/AKT signal axis, providing a new antitumor activity for baicalein basis.

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Objective To investigated the effects of gene-interfering long-chain non-coding RNA(lncRNA) SPRY4-IT1 on stem cell-like characteristics and mitochondrial membrane potential changes in gallbladder cancer cell line GBC-SD. Methods shRNA-SPRY4-IT1 shRNA was designed and synthesized. shRNA-SPRY4-IT1 was transfected into GBC-SD cells,and the expression level of SPRY4-IT1 was detected by RT-PCR. BrdU staining was used to detect cell proliferation. Cell apoptosis was detected by flow cytometry. Tumor cell pelleting assay was used to detect the characteristics of tumor stem cells. The changes of mitochondrial membrane potential were detected by flow cytometry. Western blot was used to detect the protein expression of dry tumor characteristic markers and mitochondrial damage markers. Results sh RNA-SPRY4-IT1 was transfected into GBC-SD cells,the expression level of SPRY4-IT1 decreased. Interference with SPRY4-IT1 inhibited proliferation of GBC-SD cells,improved mitochondrial membrane potential and promoted apoptosis of GBC-SD cells,reduced stem cell-like properties of gallbladder cancer,inhibited the expression of SOX2,OCT4,CD44,c-Myc,Bcl-2 and promoted the expression of cleaved Caspase-3,cleaved Caspase-9,Bax. Conclusion Gene interference with lncRNA SPRY4-IT1 can reduce the characteristics of GBC-SD cancer stem cells in gallbladder cancer cells,increase mitochondrial membrane potential,and promote apoptosis of gallbladder cancer cell line GBC-SD.

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Objective To investigate the antioxidant and neuroprotective effects of morroniside on hypoxic ischemic brain injury(HIBI) model rats and its possible mechanism. Methods Rice method was used to establish HIBI rat model. Rats were randomly divided into 6 groups: Control group, model group, Morroniside(25, 50, 100 mg/kg) group and Nimodipine group. The first two groups were given normal saline by gavage, and the last four groups were given corresponding doses of Morroniside and nimodipine, once every day for 28 consecutive days.The cerebral nerve function of rats was scored and the cerebral water volume was measured.HE staining was used to observe the histopathological changes of rat brain tissue. The levels of malondialdehyde(MDA), lactate dehydrogenase(LDH) and superoxide dismutase(SOD) in rat brain tissue were measured by ELISA. The protein expression levels of B cell lymphoma-2(Bcl-2),Bcl-2 associated X protein(Bax), Caspase-3, Caspase-9, brain-derived neurotrophic factor(BDNF), basic fibroblast growth factor(bFGF), synaptophysin(SYP), postsynaptic density-95(PSD95), transcription factor nuclear factor erythroid 2(NF-E2)-related factor 2(Nrf2) and heme oxygenase 1(HO-1)in brain tissue were detected by Western blot. Results Compared with the model group, the neurological function score and hydrocephalus volume of rats in Monoside treatment group decreased(P<0.01), the pathological damage degree of brain tissue improved, Bcl-2 increased, Bax, Caspase-3 and Caspase-9 decreased(P<0.01), and SOD activity increased(P<0.01), LDH and MDA content decreased(P<0.01). In addition, the expressions of bFGF, BDNF, PSD95, SYP and antioxidant pathway proteins Nrf2 and HO-1 were up-regulated(P<0.01). Conclusion Monoside has antioxidant and neuroprotective effects on hypoxic-ischemic brain injury model rats, and its function may be related to the mediating Nrf2 signaling pathway.

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Objective To investigate the effect of ultrashort wave intervention on the articular function, joint capsule morphology, expression of transforming growth factor β1(TGF-β1) and connective tissue growth factor(CTGF) of rabbit knee extension contracture, and to explore the process of knee joint contracture. The changes of joint capsule fibrosis and the mechanism of ultrashort wave therapy were preliminary discussed. Methods New Zealand rabbits were randomly divided into 4 groups and treated with different interventions: a blank control group(O group) without any treatment, a simple fixed group(P group) killed immediately after 8 weeks of fixation, and removed after 8 weeks of fixation, the natural recovery group(group N) with 4 weeks of free movement of gypsum, and the ultrashort wave treatment group(group M) with 4 weeks of ultrashort wave treatment after removing the plaster for 8 weeks. Immediately after the rabbit was sacrificed, the knee mobility was recorded using a joint mobility measuring instrument after myotomy. The posterior joint capsule was selected from the group, Masson staining was used to detect the expression level of collagen in the posterior joint capsule of each group, semi-quantitative RT-PCR was used to detect the mRNA expression of TGF-β1 and CTGF in the joint capsule; Western blot was used to detect the joint capsule in the posterior knee joint TGF-β1 and CTGF protein expression levels. Results Compared with group O, the movement of knee joint in group P decreased after myotomy(P<0.05), the percentage of collagen in the joint capsule behind the knee joint, and the protein and mRNA expression levels of TGF-β1 and CTGF increased(P<0.05). Compared with group P, there was no significant difference in knee joint mobility and CTGF protein expression level after myotomy in group N, and CTGF mRNA expression level increased(P<0.05). The percentage of collagen in the joint capsule and the expression of TGF-β1 protein and mRNA in the posterior knee joint decreased(P<0.05). Compared with group P, the activity of the knee joint increased after myotomy in group M(P<0.05), the percentage of collagen in the joint capsule behind the knee joint, the protein and mRNA expression of TGF-β1 and CTGF decreased(P<0.05). Compared with the N group, the knee joint activity after the myotomy in the M group increased(P<0.05), the percentage of collagen in the joint capsule behind the knee joint, the protein and mRNA expression levels of TGF-β1 and CTGF became lower(P<0.05). Conclusion Ultrashort wave may reduce the expression of TGF-β1 and CTGF in the joint capsule, reduce the fibrosis of the posterior joint capsule of the knee joint, and then effectively improve the progress of straight knee contracture.

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Objective In order to solve the baculovirus as a gene delivery vector transient expression defect, this study intends to construct a sleeping beauty(SB) transposon-mediated baculovirus expression vector, using green fluorescent protein gene EGFP as the target gene, to evaluate the system expression efficiency in mammals.Methods Using the p FastBac DUAL plasmid as the skeleton,the pPh promoter was replaced with the CMVSB100 X-SV40 PA expression element along with the IR/DR-CMV-EGFP-SV40 PA-IR/DR sequence,and the obtained plasmid was named pBacSB-CE. Meanwhile,as a control,pBac-CE was constructed by inserting the CMVEGFP expression element downstream of p Ph promoter. The constructed recombinant plasmids were transformed into DH10 Bac competent cells,and the recombinant bacmids were obtained by blue-white screening. Then the recombinant bacmids were transfected into Sf-9 insect cells by liposome,resulting in recombinant baculovirus BacSB-CE and Bac-CE. U87 cells were transduced with recombinant virus,the cell proliferation and the expression efficiency of EGFP were detected by MTT,inverted fluorescence microscopy and flow cytometry. The subcutaneous glioma tumor model of nude mice was established and the transduction efficiency of recombinant virus in vivo was further observed by immunofluorescence. Results The results showed that the recombinant viruses BacSB-CE and Bac-CE were successfully obtained by PCR identification. MTT results showed that the recombinant virus had no side effect on the proliferation of U87 cells. The results of inverted fluorescence microscopy and flow cytometry showed that EGFP could be expressed for at least 60 d in BacSB-CE transduced U87 cells and 109a. u. total fluorescence intensity could still be detected after 15 d of transduction,while in Bac-CE transduced cells,no fluorescence cells and fluorescence signal could be detected after 15 d. Conclusion In this study,the SB transposon-mediated baculovirus gene delivery system was successfully constructed. The recombinant virus has a good biosafety and can be sustained and stable expressed in vitro and in vivo of mammals.

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Objective To analyze the expression of Lnczc3 h7 a in colorectal cancer cells and its effect on the proliferation and migration of colorectal cancer cells, and explore its potential mechanism. Methods Six colorectal cancer cell lines including SW620、SW480、HCT116、DLD-1、Caco-2、HT-29 and normal colorectal epithelial cell FHC were selected. The expression of Lnczc3 h7 a in colorectal cancer cell lines and normal colorectal epithelial cells was detected by RT-PCR. Lnczc3 h7 a mimics and Lnczc3 h7 a inhibitor were used to transfect colorectal cancer cells SW620 respectively and named as Lnczc3 h7 a mimics group and Lnczc3 h7 a inhibitor group respectively, and the untransfected cells were used as the control group.CCK-8 method and cell scratch test were used to detect the difference of cell proliferation and migration ability among the three groups, and Western blot method was used to detect the effect of Lnczc3 h7 a on the expression of CTHRC6 protein in colorectal cancer cells. Results The results of RT-PCR showed that the relative expression levels of Lnczc3 h7 a in the six colon cancer cell lines were significantly lower than those of normal colorectal epithelial cells FHC, and all were statistically significant(P<0.05). CCK-8 test results showed that the cell proliferation ability of the Lnczc3 h7 a mimics group was significantly lower than that of the Lnczc3 h7 a inhibitor group and the control group(P<0.05), and the cell proliferation ability of the Lnczc3 h7 a inhibitor group was significantly higher than that of the control group after 4 and 5 days of transfection. The scratch test results showed that the difference of wound healing rate among the three groups was statistically significant(F= 395.524, 480.165,P<0.05); compared with the control group, the cell migration ability of the Lnczc3 h7 a mimics group significantly reduced(P<0.05), and the cell migration ability of the Lnczc3 h7 a inhibitor group significantly increased(P<0.05). Western blot results showed that compared with the control group, the expression of CTHRC6 protein in the Lnczc3 h7 a inhibitor group significantly increased(P<0.05), and the expression of CTHRC6 protein in the Lnczc3 h7 a mimics group significantly reduced(P<0.05). Conclusion Lnczc3 h7 a may inhibit the proliferation and migration of colorectal cancer cells by targeting CTHRC6.

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Objective To study the effects of GDF-associated serum protein-1(GASP-1) gene interference on malignant invasion, epithelial-mesenchymal transition(EMT) and microtubule formation in non-small cell lung carcinoma(NSCLC) cells. Methods Lung cancer A549 cells were used as a model. The shRNA1 screened in the previous experiment was transfected into lung cancer A549 cells with Lipofectamine 2000. Grouping: control group, shRNA group and GASP-1-shRNA1 group. Transwell test was used to detect cell invasion ability, scratch test was used to detect cell migration ability; microscopic observation was used to observe EMT; microtubule formation test was used to detect the number of microtubule nodules; Western blot was used to detect EMT markers E-cadherin, N-Expression of cadherin, Fibronectin and VEGF protein. Results Compared with the control group, the number of cell invasions per field in the GASP-1-shRNA1 group significantly reduced, and the rate of scratch healing significantly reduced, indicating that interference with the GASP-1 gene could significantly inhibit the invasion and migration of A549 cells. Compared with the control group, the EMT in the GASP-1-shRNA1 group was significantly inhibited. In the microtubule formation experiment, compared with the control group, the number of microtubule nodules in the GASP-1-shRNA1 group significantly reduced, and the expression level of vascular endothelial growth factor(VEGF) protein significantly reduced. Conclusion GASP-1 gene interference can significantly inhibit the malignant invasion, EMT and microtubule formation of NSCLC cells.

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Objective To investigate the effects of renal denervation(RDN) on ventricular arrhythmia after acute myocardial infarction(AMI) and its mechanism. Methods Using a rat myocardial infarction model, 24 Sprague-Dawley(SD) rats were divided into four groups: the control group(Control), the AMI group, the RDN-1 d+AMI group and the RDN-2 w+AMI group. The SD rats were subjected to RDN intervention, and the AMI model was established after feeding for different times. PowerLab multi-channel ECG monitor was continuously recorded after surgery to monitor the inhibitory effect of RDN on the occurrence of ventricular arrhythmia. After 1 h of observation,the heart tissue was collected,and TH staining was used to detect cardiac sympathetic nerve activity. Western blot was used to detect the expression of various ion channel proteins in the myocardial infarction area. Renal sympathetic nerve activity was detected by Power Lab/8 SP biological information acquisition instrument. Results Compared with the AMI group,the frequency of ventricular tachycardia in the RDN-1 d + AMI group and RDN-2 w +AMI group reduced,the difference was statistically significant( P<0. 01),and the decrease in the RDN-1 d group was more obvious. Compared with the sympathetic nerve discharge in the Control group,the RDN-1 d group and the RDN-2 w group decreased,the difference was statistically significant( P<0. 01),and the RDN-1 d group was more effective. TH staining suggested that RDN could inhibit local sympathetic nerve activity after AMI. Compared with the control group,the protein expressions of Nav1. 5,Cav1. 2 and Kir2. 1 in the AMI group were down-regulated,while compared with the AMI group,the RDN-2 w + AMI group could inhibit the down-regulation of Nav1. 5,Cav1. 2 and Kir2. 1 protein expression,while the RDN-1 d + AMI group could not inhibit the down-regulation of protein expression. Conclusion RDN can effectively reduce the occurrence of ventricular arrhythmias after AMI.In the early stage,it mainly inhibits renal sympathetic nerve discharge,and later inhibits renal sympathetic discharge and ion channel protein upregulation.

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Objective To explore the mechanism of PVT1 aggravating the malignant biological behavior of cervical cancer cells. Methods shRNA was designed to interfere with PVT1, and then SiHa cells were transfected with sh-PVT1 either alone or with miR-484 inhibitor. The expression levels of PVT1 and mir-484 were detected by fluorescence quantification. The luciferase reporter assay confirmed the targeting relationship between PVT1 and miR-484. The effect of PVT1 on cell growth was detected by BrdU staining. The invasion and migration abilities were detected by Transwell and wound healing assay. The expression of proliferation, invasion and migration related proteins and phosphorylation of p38 MAPK were detected by Western blot. The translocation of p38 to nuclei was imaged by immunofluorescence. Results sh-PVT1 significantly decreased the expression of PVT1 in cervical cancer cells(P<0.05) and promoted the expression of miR-484(P<0.05). The luciferase reporter assay indicated that there was miR-484 binding site on PVT1. Interference with PVT1 significantly inhibited the proliferation of cervical cancer cells and the protein expression levels of Ki67 and proliferating cell nuclear antigen(PCNA)(P<0.05). Meanwhile, sh-PVT1 significantly inhibited the invasion and migration of cervical cancer cells and the protein expression of vascular endothelial growth factor(VEGF), matrix metalloproteinase-9(MMP-9) and E-cadherin, and significantly enhanced the expression of N-cadherin protein(P<0.05). In addition, inhibition of miR-484 expression significantly attenuated the inhibitory effect of sh-PVT1 on invasion, migration and epithelial-mesenchymal transition(EMT) of cervical cancer cells(P<0.05). Conclusion PVT1 can promote the growth, movement and EMT of cervical cancer cells by interfering with miR-484, and induce the activation of p38 MAPK pathway, thereby aggravating the malignant biological behavior of cervical cancer cells.

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Objective To study the effect of miR101 on glucose absorption in placental trophoblast by regulating EZH2 protein, and the possible mechanism of miRNA101 in gestational diabetes mellitus(GDM). Methods The toatal of 30 pregnant women with GDM and 30 normal pregnant women were selected as the observation group and the control group respectively. The expression of miR101 and EZH2 mRNA in placental tissue was detected by qRT-PCR, and the expression of EZH2 protein in placental tissue was detected by Western blot. Human chorionic trophoblast cells were transfected with mir101 mimic, mir101 mimic control sequence, mir101 inhibitor and mir101 inhibitor control sequence as M group, M-NC group, I group and I-NC group respectively. Blank control group B was set up with 6 parallel multiple pores in each group. qRT-PCR was used to detect miR101 and EZH2 mRNA expression. Western blot was used to detect EZH2 protein expression, and glucose detection kit was used to detect glucose uptake. Results The expression level of miR101 in the observation group was significantly higher than that in the control group(t=5.433,P<0.05), and the expression level of EZH2 in the observation group was lower than that in the control group(t=2.178,P<0.05). After cell transfer:(1) The expression level of miR101 in group M was significantly higher than that in group B and M-NC(t=2.133,2.167,P<0.05). The expression level of miR101 in group M was significantly lower than that in group B and I-NC(t=2.918, 2.331,P<0.05).(2) The expression of EZH2 in group M was significantly lower than that in group B and M-NC(t=2.018, 2.257,P<0.05). The expression level of EZH2 in group M was significantly lower than that in group B and I-NC(t=3.271, 3.167,P<0.05).(3) Glucose consumption in group M was lower than that in group B and M-NC(t=3.106, 2.115,P<0.05). Glucose consumption in group M was higher than that in group B and I-NC(t=2.002, 2.158,P<0.05). Conclusion The expression of miR101 in patients with GDM placental trophoblast abnormally increase. MiR101 could regulate the expression of EZH2 and decrease the absorption of glucose by placental trophoblasts, which was involved in the pathological mechanism of GDM.

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Objective To investigate the effect and potential mechanism of nicotinamide on proliferation, apoptosis and migration of nasopharyngeal carcinoma(NPC) CNE-1 cells. Methods NPC CNE-1 cells were divided into blank control group and the experimental groups, which were treated with 10, 20, 40 and 80 μmol/L of nicotinamide respectively, while the blank control was treated without nicotinamide. The proliferation rate of CNE-1 cells was detected by CCK-8 after 48 h and 72 h treatment with the concentrations mentioned above, the apoptosis rates and the cell cycle retardation of CNE-1 cells treated with 40 μmol/L nicotinamide for 48 h were detected by Annexin V-FITC/PI double staining flow cytometry. Cell migration and invasion were evaluated by transwell assay.Real-time fluorescent quantitative PCR and Western blot were used to detect the mRNA level and the expression of p53 and matrix metalloproteinases 9(MMP-9) proteins in CNE-1 cells. Results Compared with the blank control group, the data of CCK-8 assay showed that nicotinamide had an effective inhibition on the proliferation activity of CNE-1 cells(P<0.01), and the effect was in time-dose dependence manner. Flow cytometry results showed that the nicotinamide could promote apoptosis of CNE-1 cells treated with 40μmol/L nicotinamide for 48 h(P<0.01), with the number of cells increased in G2/M and decreased in G0/G1phase(P<0.05). And the migration and invasion were inhibited. Compared with the control group, the level of p53 protein was upregulated, while the level of MMP-9 protein decreasedwith 40 μmol/L nicotinamide treatment for 48 h. Conclusion Nicotinamide can inhibit the proliferation and promote the apoptosis of human nasopharyngeal carcinoma CNE-1 cells by up-regulating the expression of p53 protein and restoring the cell cycle, and also affect the expression of MMP-9 protein, thus reducing the migration and invasion ability of CNE-1 cells.

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Objective To investigate the effect of miR-21 on STAT3 signaling pathway on the proliferation and migration of nephroblastoma cells. Methods The expression of miR-21 was detected by RT-PCR in human nephroblastoma and paracancerous tissues. Human nephroblastoma cells were divided into three groups: Blank group, si-miR-21 group(transfected with si-miR-21) and si-miR-21 NC group(transfected with si-miR-21 NC). The expressions of related proteins and apoptosis related proteins in STAT3 signaling pathway were detected by Western blot.The cell proliferation activity was detected by MTS. The cell apoptosis was detected by flow cytometry, and the cell migration ability was detected by Transwell. Results The relative expression of miR-21 in human nephroblastoma was significantly higher than that in adjacent tissues(P<0.05). After transfection, there were significant differences in the relative expression of p-STAT3, Bcl-2, Bcl-xl, A490 absorbance value and cell migration number among the three groups(P<0.001). Compared with the Blank group, si-miR-21 group increased(P<0.05), si-miR-21 NC group decreased(P<0.05). There were significant differences in cell apoptosis among the three groups(P<0.001).Compared with the Blank group, si-miR-21 group decreased(P<0.05), si-miR-21 NC group increased(P<0.05). miR-21 was positively correlated with p-STAT3, Bcl-2 and Bcl-xl(r=0.824, 0.778, 0.837;P<0.001). Conclusion Over expression of miR-21 can promote the proliferation and migration of nephroblastoma cells, which may be due to the up regulation of STAT3 signaling pathway.

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Objective To study the effect of long non-coding RNA prostate cancer-associated transcript 1(lncRNA PCAT-1) on the proliferation and apoptosis of pancreatic cancer cells, and to explore its mechanism. Methods The expression level of lncRNA PCAT-1 in pancreatic cancer cell lines Capan-1,Capan-2, PANC-1,SW1990 and normal pancreatic cell hTERT-HPNE was detected by qRT-PCR. The highest lncRNA PCAT-1 expressing pancreatic cancer cell line was divided into sh-NC group and sh-PCAT-1 group. NC interfering with lentivirus(shRNA) and PCAT-1 shRNA infection were performed, qRT-PCR was used to detect the expression level of lncRNA PCAT-1 in each group of cells. [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2 H-tetrazolium, MTS] test was used to detect the effect of silenced lncRNA PCAT-1 expression on cell proliferation, flow cytometry was used to detect the effect of silenced lncRNA PCAT-1 on cell cycle and apoptosis, subcutaneous transplantation tumor test was used to detect the effects of silenced lncRNA PCAT-1 expression on pancreatic cell growthin vivo. Western blot was used to detect the effects of lncRNA PCAT-1 on the expression of cell cycle-related proteins, apoptosis-related proteins and key proteins of the PI3 K/AKT signaling pathway. Results qRT-PCR results showed that the expression level of lncRNA PCAT-1 in pancreatic cancer cell lines was higher than that in normal pancreatic cells hTERT-HPNE(P<0.05). Compared with Capan-1, Capan-2 and SW1990 cells, the expression of lncRNA PCAT-1 was the highest in PANC-1 cells, and the highest expression of lncRNA PCAT-1 was in PANC-1 cells. PANC-1 cells were infected with PCAT-1 shRNA, and qRT-PCR results showed that compared with the sh-NC group, the expression of lncRNA PCAT-1 in the cells of the sh-PCAT-1 group reduced(P<0.05); after silenced the lncRNA PCAT-1 expression in PANC-1 cells, cell proliferation ability reduced, cell cycle was arrested at G0/G1 phase, the apoptosis increased, tumorigenicity reduced in nude mice, cyclinD1 and CDK6 proteins expression decreased, and anti-apoptotic protein Bcl-2 expression decreased, the pro-apoptotic protein Bax expression increased, and the key proteins of PI3 K/AKT signaling pathway pPI3 K and pPAKT expression decreased. Conclusion Silencing the expression of lncRNA PCAT-1 may inhibit the proliferation and promote apoptosis of pancreatic cancer cells by regulating the PI3 K/AKT signaling pathway. lncRNA PCAT-1 may be a new target for the treatment of pancreatic cancer.

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Objective To investigate the effects of chloride intracellular channel 4(CLIC4) on the proliferation and migration ability of gastric cancer cell line SGC-7901. Methods Lentiviral plasmids with CLIC4 shRNA were transfected into HEK 293 T cells and the supernatant with virus particles were collected and infected into SGC-7901 cells to construct stable CLIC4 low-expression cell lines with puromycin selection, and the protein levels of CLIC4 was detected by Western blot. Colony formation assays and CCK-8 assays were conducted for the proliferation of SGC-7901 cells after CLIC4 knockdown. The expressions of epithelial-mesenchymal transition( EMT)-related proteins such as E-cadherin and Vimentin were checked by Western blot in SGC-7901 cells after CLIC4 knockdown.Results A stable CLIC4 low-expressing SGC-7901 cell line was successfully constructed. The expression of CLIC4 did not affect the proliferation of SGC-7901 cells,while the EMT associated protein E-cadherin was up-regulated and Vimentin was down-regulated with CLIC4 knockdown. Conclusion CLIC4 does not affect the proliferation but promote the migration capacity of SGC-7901 cells.

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Objective To study the possible regulation mechanism of overexpression of salt-inducible kinase 1(SIK1) on hepatic lipid metabolism disorders(LMD) in obese rats induced by high-fat diet(HFD). Methods Forty SD rats were randomly divided into Control group(10 cases) and modeling group(30 cases). They were fed with HFD for 12 weeks, and those with successful modeling were randomly divided into Obesity group, Obesity+LV group and Obesity+LV-SIK1 group. Obesity+LV group and Obesity+LV-SIK1 group were injected with lentiviral blank plasmid and lentivirus-mediated SIK1 overexpression plasmid through tail vein, respectively, and then fed with HFD for 8 weeks. Fasting blood from tail vein was applied to detect levels of liver function indexes [(alanine aminotransferase, ALT),(aspartate aminotransferase, AST)], lipid metabolism indexes [(total cholesterol, TC),(triglycerides, TG),(high density lipoprotein cholesterol, HDL-C),(low density lipoprotein cholesterol, LDL-C)]and inflammatory cytokines [(tumor necrosis factor-α,TNF-α),(inducible nitric oxide synthase, iNOS),(interleukin-6,IL-6), IL-10]. The pathological damage and fat accumulation in liver tissues were observed by HE staining and oil red O staining. The expression of apoptosis marker proteins(Caspase-3, Caspase-9) and adipogenesis genes(SREBP-1 c, FASN, ACC1) in liver tissue was detected by Western blot. Results Compared with Control group, body mass, levels of serum ALT, AST, TC, TG, LDL-C, TNF-α, iNOS, IL-6 and IL-10 increased in Obesity group(P<0.05), while HDL-C level decreased(P<0.05). There was significant structural damage and fat accumulation in liver tissues, and the expression levels of cleaved-Caspase-3/Caspase-3, cleaved-Caspase-9/Caspase-9, SREBP-1 c, FASN and ACC1 proteins in liver tissues increased(P<0.05). Compared with Obesity group, body mass, levels of serum ALT, AST, TC, TG, LDL-C, TNF-α, iNOS and IL-6 decreased in Obesity+LV-SIK1 group(P<0.05), while levels of HDL-C and IL-10 increased(P<0.05). The structure destruction and fat accumulation in liver tissues reduced. The expression levels of cleaved-Caspase-3/Caspase-3, cleaved-Caspase-9/Caspase-9, SREBP-1 c, FASN and ACC1 proteins decreased(P<0.05). Conclusion There are damage and large amount of fat accumulation in liver tissues of HFD induced obese rats. SIK1 overexpression can reduce the expression of adipogenesis genes, improve LMD, and reduce damage to liver tissue caused by fat accumulation.

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Objective To explore the effect of ASH2 L, an important component of the core subunit of the mixed lineage leukemia(MLL) methyl transferase complex, on the proliferation of ovarian epithelial carcinomacell line SKOV-3. Methods Immunohistochemistry was used to detect the localization of ASH2 L protein expression in epithelial cancer tissue specimens. Western blot was used to detect the expression level of ASH2 L in ovarian cancer tissue samples and normal ovarian tissue samples, and the expression level of ASH2 L in ovarian malignant tumor cell lines. Polyplus reagent was used to mediate ASH2 L plasmid transfection, the transfection efficiency of ASH2 L was verified by Western blot, and the proliferation of SKOV-3 cells after transfection was detected by CCK-8 method. Results The expression of ASH2 L was located in the nucleus of ovarian cancer tissues. Compared with normal ovarian tissues, the expression level of ASH2 L protein in ovarian epithelial cancer tissues was up-regulated(P<0.01). Compared with 293 T cell line, the expression level of ASH2 L protein in SKOV-3 cell line was up-regulated(P<0.05). After SKOV-3 cell line was transfected with ASH2 L plasmid, the expression of ASH2 L protein in the cells increased. Compared with SKOV-3 cells transfected with empty plasmid, the proliferation of SKOV-3 cells transfected with ASH2 L plasmid increased(P<0.01). Conclusion ASH2 L is highly expressed in epithelial ovarian cancer. Increased expression of ASH2 L can promote the proliferation of ovarian epithelial tumor cells SKOV-3.

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Objective To explore the effect of Icariin on pathological injury and oxidative stress in renal ischemia-reperfusion rats. Methods The rat model of renal ischemia-reperfusion was established and the rats were randomly divided into 5 groups: Control group, RIRI group, RIRI+icariin 25 mg/kg group, RIRI+icariin 50 mg/kg group and RIRI+icariin 100 mg/kg group for follow-up experiments. The kit was used to detect the levels of proteinuria, serum creatinine and urea nitrogen. HE staining was used to detect the degree of pathological damage. The contents of iNOS and IL-10 in peripheral blood and kidney tissues were detected by ELISA. The content of SOD and GSH was detected by the kit. Western blot was used to detect the expression levels of Caspase-3, Caspase-9, Bax, Bcl-2, Nrf2, p-Nrf2 and HO-1. Results The results showed that, compared with the Control group, the levels of proteinuria, serum creatinine and urea nitrogen in the RIRI group significantly increased(P<0.05), presenting significant renal ischemia-reperfusion injury, the cleaved Caspase-3/Caspase-3, cleaved Caspase-9/Caspase-9, and Bax/Bcl-2 ratios significantly increased(P<0.05), and the levels of inducible nitric oxide synthase(iNOS) and interleukin-10(IL-10) in the peripheral blood and renal tissues significantly increased(P<0.05). The contents of superoxide dismutase(SOD)and glutathione(GSH) significantly reduced(P<0.05), and the p-Nrf2/Nrf2 ratio and HO-1 protein level significantly reduced(P<0.05). Compared with the RIRI group, the levels of proteinuria, serum creatinine and urea nitrogen in the RIRI+icariin 50 and 100 mg/kg groups significantly reduced(P<0.05), and the degree of pathological damage was significantly improved. The ratios of cleaved Caspase-3/Caspase-3, cleaved Caspase-9/Caspase-9 and Bax/Bcl-2 significantly reduced(P<0.05), the iNOS content significantly reduced(P<0.05), and the IL-10 content significantly increased(P<0.05). The contents of SOD and GSH significantly increased(P<0.05). The p-Nrf2/Nrf2 ratio and HO-1 protein level significantly increased(P<0.05). Conclusion Icariin alleviates renal ischemia reperfusion injury and oxidative stress in rats by mediating Nrf2/HO-1 signaling pathway.

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Objective To study the distribution of genotype and allele frequencies of ABCB1 C3435 T and ABCB1 T2677 G in Uygur, Han and Hui patients with dyslipidemia. Methods The ABCB1 C3435 T and ABCB1 T2677 G genotypes were detected by fluorescence in-situ hybridization in 311 Uygur, 409 Han and 53 Hui patients with dyslipidemia. The genotypes were compared with people of different races and then analyzed the difference in frequencies of genotypes and alleles. Results The difference of ABCB1 C3435 T genotype frequency and allele frequency of Uighur and Han patients with dyslipidemia was statistically significant(P<0.05), and the difference of ABCB1 C3435 T allele frequency of Uighur and Hui patients with dyslipidemia was statistically significant(P<0.05). The difference of ABCB1 T2677 G genotype frequency in Uyghur and Han patients with dyslipidemia was statistically significant(P<0.05). Conclution The distribution of ABCB1 gene polymorphism in patients with dyslipidemia in different ethnicities of Xinjiang is different. Ethnic difference is important factors in studying the mechanism of ABCB1 and statin efficacy.

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Objective To study the association between ERCC1 C8092 A polymorphism and genetic susceptibility to lung cancer, and to screen the markers of genetic susceptibility to lung cancer. Methods A case-control study was used to select 264 cases of lung cancer as the case group, and 264 cases of non-lung cancer patients as the control group. Mass spectrometry was used to detect the polymorphism of the ERCC1 gene at C8092 A. The control group was tested by the Hardy-Weinberg law of genetic balance. The frequency distribution of ERCC1 C8092 A SNP between the case group and the control group was analyzed by the χ2test. Multivariate Logistic regression analysis was used to calculate the corrected odds ratio(OR) and 95% confidence interval(CI). Results Genetic susceptibility to lung cancer in individuals carrying the CA genotype of ERCC1 C8092 A had low susceptibility(CAvsCC,OR=0.380, 95%CI: 0.267～0.541,P<0.001). After adjusting for confounding factors such as age, gender, smoking and drinking, polymorphism of ERCC1 C8092 A was still associated with genetic susceptibility to lung cancer. Compared with the CC genotype, the risk of lung cancer with the CA genotype reduced(adjustedOR=0.380, 95%CI: 0.262～0.538,P<0.001). Stratified analysis found that in the age group ≥61 years old, regardless of gender, smoking or drinking, compared with CC genotype, the risk of lung cancer of CA genotype also reduced, and the difference was statistically significant(P<0.05). Conclusion ERCC1 C8092 A SNP is related to the genetic susceptibility to lung cancer. The CA population has a lower risk of developing lung cancer.

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Objective To investigate the social support status and its influencing factors of patients with gestational diabetes mellitus(GDM). Methods 499 GDM patients and 353 normal pregnant women were included as the subjects of the study. The general demographic characteristics were collected and the Social support rating scale(SSRS) was used for the questionnaire. Results The objective support score, the subjective support score, the degree of support score and the total score of the social support of the GDM group were not significantly different from that of the control group. Multivariate analysis showed that education level, work situation, family income, production history, early pregnancy response were related factors affecting the social support level of GDM patients(P<0.05). High education, employment during pregnancy, high family income, multipara, no early pregnancy reaction of GDM patients received more social support. Conclusion The social support level of GDM patients is affected by many factors, and the attention to the social support of GDM patients should be further strengthened, with a special focus on the social support of pregnant women with low education, non-employment, low family income, primary production and early pregnancy reaction.

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Objective To investigate the influence of prior cesarean section on the pregnancy, delivery and neonatal outcomes ofin vitrofertilization and embryo transfer. Methods 235 patients with prior cesarean section were collected from the assisted reproductive center, and their clinical information were retrospectively analyzed. Patients were divided into two groups according to the previous cesarean scar defect(PCSD) with 158 cases in NPCSD group and 77 cases in PCSD group. The control group consisted of 219 patients who had only previous vaginal delivery in the same period. The basic data, pregnancy, delivery and neonatal outcomes were compared among the three groups of patients. Results The basic data, Gn duration, Gn dosage, estradiol(E2) level on human chorionic gonadotrophin(hCG) injection day, mean number of retrieved oocytes, number of high-quality embryo, endometrial thickness on ovulation day and number of transfer embryos were similar between previous cesarean section group and previous vaginal delivery group. The embryo implantation rate, clinical pregnancy rate and take-home baby rate were significantly lower in PCSD group than NPCSD group and previous vaginal delivery group(P<0.05). Twin deliveries had lower gestational age and neonatal birth weight compared with singleton deliveries in previous cesarean section group and previous vaginal delivery group. Twin deliveries had higher preterm birth rate compared with singleton deliveries in both groups(P<0.05). Conclusion From the clinical data, it should be the cesarean scar defect rather than the previous cesarean history that causes significant decrease of implantation rate, clinical pregnancy rate and take-home baby rate. But it does not affect abortion rate and neonatal outcomes. And it is an important factor affecting the outcome of assisted reproductive technology. It should reduce the number of transfer embryos to control multiple pregnancy in patients with previous cesarean section.

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Objective To investigate clinical prediction value of BNP combined with cardiac structural index in hypertension patients with heart failure. Methods 320 patients with hypertension were divided into control group(n=52), septal thickening group(n=48), left ventricular wall thickening group(n=40), left atrial enlargement group(n=46), left ventricular hypertrophy group(n=66), left atrial and left ventricular enlargement group(n=68). General data, BNP level, left atrial diameter(LAD), interventricular septal(IVS), left ventricular end diastolic diameter( LVEDD),left ventricular ejection fraction( LVEF) and left ventricular posterior wall( LVPW)were recorded. The differences of each index in six groups were compared,and the correlation among these indexes,the changes of cardiac structure and the occurrence of heart failure in patients with hypertension was analyzed.Results BNP,LAD and LVEDD in each group of cardiac remodeling were higher than those in the control group.BNP,LAD and LVEDD increased with the severity of cardiac remodeling( P<0. 05). The correlation analysis of LVEF with BNP and cardiac structure showed that LVEF was negatively correlated with BNP,LAD and LVEDD( r=-0. 584,-0. 430,-0. 764,P<0. 001,P<0. 001,P<0. 001). ROC curve analysis showed that the area under the curve of BNP,LAD,LVEDD alone and combined diagnosis of HFREF was 0. 845,0. 725,0. 940 and0. 954,respectively. The sensitivity and specificity of combined detection of BNP,LAD and LVEDD for HFREF were 94. 6% and 89. 5% respectively,which were higher than that of single detection of each index. Conclusion The plasma BNP level has a good clinical predictive value for the changes of cardiac structure and function in patients with hypertension. Combining BNP,LAD and LVEDD can improve the diagnosis of HFREF in hypertension patients.

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Objective To investigate the factors affecting therapeutic effect and short-term prognosis of anlotinib in the treatment of advanced lung cancer by comparing the efficacy and prognosis between different groups so as to provide theoretical basis for improving anlotinib's clinical treatment. Methods The general data, efficacy data and prognosis data of 81 advanced lung cancer patients treated with anlotinib were collected retrospectively. The efficacy and prognosis were compared between different groups. Logistic and Cox regression models were used to analyze the factors affecting efficacy and short-term prognosis. Results After anlotinib treatment, the objective response rate among 81 patients was 8.6%(7/81), the disease control rate was 56.8%(46/81), the follow-up time was 0.7～10.0 months and the median progression free survival time was 3.2 months(95%CI=2.149～4.317 months). Logistic regression analysis showed that influencing factors of the efficacy of anlotinib in the treatment of advanced lung cancer were gender(OR=3.034, 95%CI=1.072～8.584,P=0.037) and Eastern Cooperative Oncology Group(ECOG) score before treatment(OR=5.523, 95%CI=1.557～19.588,P=0.008). Cox regression analysis showed that influencing factors of the short-term prognosis of patients with advanced lung cancer treated with anlotinib were gender(HR=2.317, 95%CI=1.312～4.091,P=0.004), family history of cancer(HR=4.556, 95%CI=1.562～13.285,P=0.005) and ECOG score before treatment(HR=2.187, 95%CI=1.178～4.060,P=0.013). Conclusion The efficacy of anlotinib in the treatment of advanced lung cancer is influenced by gender and ECOG score before treatment. Female, family history of cancer and high ECOG score before treatment are the important factors leading to poor prognosis of anlotinib in the treatment of advanced lung cancer patients.

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Objective To analyze the changes of Antithrombin Ⅲ(AT-Ⅲ) activity in patients with HBV-related acute liver failure(HBV-ACLF) and to study its potential correlation with liver function and coagulation function. Methods 80 subjects with HBV-ACLF and 48 subjects with chronic hepatitis B(CHB) as the controls were enrolled in our hospital. The level of AT-Ⅲ was detected with chromogenic substrate method, the relationships between AT-Ⅲ and total bilirubin(TBIL),albumin(ALB), alanine aminotransferase(ALT), aspartate aminotransferase(AST),prothrombin time activity(PTA), international normalized ratio of prothrombin time(PT-INR) and end-stage liver disease(MELD) score were analyzed by using Spearman rank correlation, and the receiver operating characteristic(ROC) curve was used to evaluate whether AT-Ⅲ could be used as a laboratory test to influence the clinical prognosis of HBV-ACLF. Results The activity level of AT-Ⅲ in patients with HBV-ACLF decreased than those of patients with CHB. Compared with CHB patients, other markers of liver function and coagulation function increased except for the decrease of ALB and PTA in patients with HBV-ACLF, and the differences were significant(P<0.05). The level of AT-Ⅲ activity was correlated with TBIL, PT-INR and PTA in patients with HBV-ACLF. And it was negatively correlated with MELD score in the prognosis of patients with HBV-ACLF. The ROC curve showed that the area under the curve predicted by AT-Ⅲ was 0.686, the sensitivity was 75.0%, the specificity was 52.9%, and the boundary value was 16.4%; the area under the curve predicted by MELD core was 0.698, the sensitivity was 76.5%, the specificity was 55.9%, and the boundary value was 28.5; the area under the curve predicted by MELD core and AT-Ⅲ was 0.756, the sensitivity was 62.5%, the specificity was 88.2%, the boundary value were 25 and 20.1%. Conclusion AT-Ⅲ is associated with the severity and progression of liver injury in patients with HBV-ACLF. The clinical combination of AT-Ⅲ and MELD score is useful in predicting the prognosis of HBV-ACLF.

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To compare the change of posterior corneal higher-order aberrations(HOA) of myopic eyes after four refractive surgeries including laser in situ keratomileusis(LASIK), femtosecond laser-assisted laser in situ keratomileusis(FS-LASIK), wavefront-guided LASIK with iris registration(WF-LASIK), and small incision lenticule extraction(SMILE). A total of 242 subjects(46 subjects underwent LASIK, 38 subjects underwent FS-LASIK, 68 subjects underwent WF-LASIK, and 90 subjects underwent SMILE) were involved. HOAs of each patient's right eye were measured with Pentacam device preoperatively and 6 months after surgery. The aberrations were described as zernike polynomials, and analysis was focused on total HOAs, spherical aberration(SA), coma, horizontal coma, and vertical coma over 6 mm diameter central corneal zone. In LASIK group, pre-and postoperative total HOA, SA and horizontal coma were not statistically significantly different, but postoperative coma and vertical coma were significantly different(P<0.01). In FS-and WF-LASIK groups, significant differences were found in the total HOA, SA and coma(P<0.05) while no difference was found in the horizontal coma and vertical coma. In addition, all HOAs were found to have significantdifferences between pre-and postoperative SMILE procedure(P<0.01). The result showed that SMILE induced significantly negative shift in horizontal coma compared with FS-LASIK and WF-LASIK(P<0.01). Meanwhile, SMILE group also had a significant increase in vertical coma compared with FS-LASIK and WF-LASIK(P<0.01). In LASIK and the other groups, induced total HOAs, SA, coma, horizontal coma and vertical coma were all comparable.SMILE induced more horizontal coma and vertical coma compared with FS-LASKandWF-LASIK, indicating that the centration of SMILE procedure is probably less precise.

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To explore the value of T1 mapping techniques in the evaluation myocardial fibrosis in 23 patients with hypertrophic cardiomyopathy( HCM) and 18 patients with dilated cardiomyopathy( DCM),and to study the correlation between the native T1 value and cardiac function. The native T1 values in HCM group,DCM group and control group were statistical significance [( 1 318. 4 ± 44. 7) ms,( 1 353. 7 ± 56. 9) ms and( 1 267. 0 ± 24. 3) ms,P<0. 05) ]; the native T1 value of the left ventricular myocardium in HCM and DCM patients was negatively correlated with the LVEF( r =-0. 488,P<0. 05; r =-0. 659,P<0. 01). The study showed that T1 mapping evaluated the myocardial fibrosis of HCM and DCM noninvasively. The myocardial fibrosis shown by the native T1 value of the left ventricular myocardium was negatively correlated with cardiac function in patients with HCM and DCM.

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To study the elastic fixation clinical application of orthodontic straight wire appliance combined with pad in the treatment of traumatic tooth dislocation and to evaluate the clinical effect. 36 cases with 82 teeth of traumatic tooth dislocation were studied retrospectively and the patients were divided into two groups according to the type of treatment. The study group of 44 teeth were treated with orthodontic straight wire appliance and combined with pad.The control group of 38 teeth were treated with traditional resin splint bonded metal wire. According to the functional state and the symptoms after treatment,the therapeutic effect was classified as significant,effective and ineffective. In the study group,36 teeth were markedly effective,8 teeth were effective,and the effective rate was81. 82%. In the control group,20 teeth were markedly effective,18 teeth were effective,and the effective rate was52. 63%. The differeance between the two groups was statistically significant( P = 0. 005). The treatment of tooth dislocation with orthodontic straight wire appliance combined with pad technique is expected and better,hence it is recommended.