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Objective To investigate the effect of(exchange protein directly activated by cAMP-1) on inner ear hair cell injury with noise-induced hearing loss and its potential mechanism in rats. Methods Twenty Specific pathogen-free(SPF) Sprague-Dawley(SD) rats were randomly divided into normal control group and noise exposure group. The rats of noise exposure were exposed to 4 kHz at 101 dB sound pressure level(SPL) for 8 h. Auditory brainstem responses(ABR)were measured in animals before noise exposure and 24 h after noise exposure. Surface preparation, transmission electron microscopy and immunohistochemistry were performed on cochlea tissuesto elucidate changes in Epac expression in rat after noise exposure. The expression levels of Epac1、Rap1、CaMK-Ⅱ、Bax、Bcl-2、cleaved caspase3(CC3) and cleaved caspase9(CC9)were analyzed using Western blot. Results There was found a stable temporary threshold shift after noise exposure(P<0.05). The missing of outer hair cells occurred after noise exposure(P<0.05). Transmission electron microscopy indicated that the epidermis plate of HCs was partially dissolved, with loss or fusion of stereocilia, some HC organelles showed serious injuries after noise exposure. Epac1 immunostaining intensities were substantially enhanced in OHCs after noise exposure(P<0.05). The expression levels of Epac1, CaMK-Ⅱ and Rap1 protein were significantly up-regulated after noise exposure(P<0.05). The expression level of Bcl-2 was significantly down-regulated after noise exposure(P<0.05). The expression levels of Bax, CC3 and CC9 were significantly up-regulated after noise exposure(P<0.05). Conclusion Epac1-Rap1 signaling pathway mediates the early pathological damage in noise-exposed cochlea, and participates in the regulation of inner ear hair cells apoptosis. Epac1-Rap1 pathway is expected to become a new target for intervention in noise-induced hearing loss.

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Objective To investigate whether the application of melatonin(MT) in embryo culturein vitrocan improve the treatment effect ofin vitrofertilization embryo transfer(IVF-ET) in patients with decreasing ovarian reserve(DOR). Methods 128 DOR patients receiving assisted reproductive therapy were collected. All patients were treated with an antagonist scheme of super-ovulation. Patients were divided into melatonin group(n=56) and control group(n=72) according to whether melatonin(melatonin concentration 10-9mol/L) was added into embryo culture medium. Results There was no statistically significant difference in oocytes fertilization rate and cleavage rate between the two groups during later embryo culture, but blastocyst formation rate(65.22%vs56.16%) and high-quality blastocyst rate(52.96%vs40.94%) in the melatonin group were higher than those in the control group, and the differences were statistically significant(P<0.05). There were no significant differences in the implantation rate(50.00%vs38.67%) and clinical pregnancy rate(48.39%vs46.00%) of blastocysts after freezing-thawing between the two groups, but the cycle number of high-quality blastocysts obtained in the melatonin group was higher than that in the control group(85.71%vs69.44%), and the difference was statistically significant(P<0.05). Conclusion In a way, the application of melatonin in thein vitroculture of early embryos can promote the development of oocytes in patients with DOR, improve the quality of embryos, and finally substantially improve the therapeutic effect of such patients.

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Objective To explore whether miR-9 affects the proliferation of neural stem cells(NSCs) by regulating β-tubulin Ⅲ and glial fibrillary acidic protein(GFAP). Methods NSCs cells were isolated and cultured on the purchased healthy pregnant mice and the isolated cells were divided into NO group(non-transfected NSCs cell line), NN group(NSCs transfected with miR-9-NC), NM group(NSCs transfected) transfected with miR-9 mimics), NI group(transfected with miR-9 inhibitor). Nestin was identified by immunofluorescence, the contents of Mir-9, β-tubulin Ⅲ and GFAP were measured by QRT-PCR, the proliferation of NSCs was measured by MTT method, the apoptosis of NSCs was measured by flow cytometry, and the protein expressions of Mir-9, β-tubulin Ⅲ and GFAP were detected by Western blot. Results The detection index Nestin of NSCs for 24 h after cell passage was positive in 90% of the NSCs, and co-localized with the nucleus, indicating the successful isolation of NSCs. The expression of miR-9 mRNA in NSCs of the NM group was the highest among the four groups, indicating that the transfection was successful. Among the four groups, β-tubulin Ⅲ mRNA and protein expression was the highest in the NM group, and the GFAP mRNA and protein expression was the lowest. The NI group was the opposite(P<0.05). In the four groups after 24 h, the cell activity of NSCs in the NM group was the strongest and showed a trend of gradually increasing with time(P<0.05). The cell activity of NI was significantly weaker than that of the other three groups(P<0.05). Among the four groups, the apoptosis rate of the NM group was lower than that of the other three groups(P<0.05), and the apoptosis rate of NI was higher than that of the other three groups(P<0.05). The difference in the above indicators between the NO group and the NN group was smaller. Conclusion Overexpressed miR-9 promotes the proliferation of NSCs by promoting the expression of β-tubulin Ⅲ and inhibiting the expression of GFAP.

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Objective To analyze and compare the gene chip data of normal people and patients with acute myocardial infarction through GEO gene expression database, to screen out differentially expressed genes(DEGs), and to predict potential Chinese medicines for the treatment of acute myocardial infarction. Methods GSE66360 gene microarray was downloaded, DEGs information was obtained by analysis, gene ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) analysis of differential genes were performed, key genes were further analyzed by String database and Cytoscape software, and key genes were mapped to the medical ontology information retrieval platform(Coremine Medical) to screen potential Chinese medicines for the treatment of acute myocardial infarction. Results A total of 943 differentially expressed genes were screened. The biological process was mainly enriched in myeloid leukocyte activation, regulation of cytokine production, leukocyte chemotaxis, etc. The cellular component was mainly focused on secretory granule lumen, membrane surface, and extrinsic components of the membrane, etc. Molecular function was mainly in chemokine receptor binding, pattern recognition receptor activity, cytokine binding, etc. KEGG analysis showed that the main signaling pathways involved were tumor necrosis factor(TNF), hypoxia inducible factor-1(HIF-1), and JAK-STAT signaling pathways, etc. The key genes to be screened are formyl peptide receptor 2(FPR2), signal transducer and activator of transcription 3(STAT3), chemokine(C-X-C motif) ligand 1(CXCL1), chemokine(C-X-C motif) ligand 8(CXCL8), ubiquitin protein ligase E3 component n-recognin 4(UBR4), jun proto-oncogene(JUN), platelet-activating factor receptor(PTAFR), Fc fragment of IgE, high affinity I, receptor for; gamma polypeptide(FCER1 G), G protein-coupled receptor 84(GPR84), plasminogen activator, urokinase(PLAU). The potential herbs predicted for the treatment of acute myocardial infarction were Centipede(P=0.003 30), Rithoma Curcuma(P=0.002 39), Curcuma(P=0.002 40), Paris polyphylla Smith(P=0.002 48), Salviae miltiorrhizae(P=0.002 72), Fritillary bulb(P=0.003 71), and Panax ginseng(P=0.001 59). Conclusion Traditional Chinese medicines such as Rithoma curcuma in activating blood and removing blood stasis medicine, Panax ginseng in nourishing Qi, and Fritillary bulb in medicine for the treatment of cough and asthma have protective effects on acute myocardial infarction. The mechanism of action may be related to the regulation of immune and anti-inflammatory signaling pathways.

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Objective To explore the protective effect and mechanism of salvianolic acid salt on acute lung injury induced by one lung ventilation(OLV) in rabbits. Methods 24 rabbits were randomly divided into three groups: control group, model group and treatment group, with 8 rabbits in each group. The W/D value of lung was measured, and the morphological changes of lung tissue were observed by HE staining and electron microscopy; The contents of arachidonic acid(AA),leukotriene B4(LTB4),thromboxaneA2(TXA2) and prostacyclin 2(PGI2) in rabbit lung tissue were detected by ELISA; The expressions of cyclooxygenase-2(COX-2),5-lipoxygenase(5-LOX) in lung tissue were detected by RT-qPCR; The expressions of COX-2, 5-LOX, clara cell secretory protein(CCSP)and cytoplasmic phospholipase A2(C-PLA2) in lung tissue were detected by Western blot. Results The W/D ratio of model group was higher than that of control group, but decreased after treatment(P<0.05); HE staining showed that in the model group, the capillaries were dilated and congested, there were red exudates in the alveoli, the walls of alveoli were thickened, and inflammatory cells were infiltrated, but the treatment of salvianolic acid salt was relieved; The mitochondria swelling, crista breaking and even disappearing were observed by transmission electron microscope in the model group, and alveolar epithelial cell Ⅰ(AT-Ⅰ) ultrastructural damage in the treatment group significantly improved compared with that in the model group; The AA, LTB4, TXA2 and PGI2 contents in the treatment group were lower than those in the model group(P<0.05). RT-qPCR showed that the expression of COX-2 and 5-LOX in model group was higher than that in control group(P<0.05), while the expression of COX-2 and 5-LOX decreased after Salvianolic acid salt treatment(P<0.05); Western blot showed that the expression of COX-2, 5-LOX and C-PLA2 in treatment group was lower than that in model group, while the expression of CCSP increased(P<0.05). Conclusion Salvianolic acid salt has protective effect on lung injury induced by one-lung ventilation. Its mechanism may be related to down-regulation of COX-2, 5-LOX and C-PLA2 expression, up-regulation of CCSP expression.

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Objective To investigate the expression and prognosis of(progestin and adipoQ receptor family member 4,PAQR4) in hepatocellular carcinoma(HCC) and its effect on the proliferation, invasion, migration and apoptosis of HepG2 cells. Methods The HCC data in the cancer genome atlas(TCGA) database was used to analyze the expression of PAQR4 mRNA in the tissues of HCC and its prognostic significance. HepG2 cell lines of pcDNA3.1-PAQR4 experimental group and pcDNA3.1-vector control group were established. CCK-8 assay was used to detect the effect of overexpression PAQR4 on the proliferation of HepG2 cells. The scratch assay and Transwell assay were used to detect the effects of PAQR4 overexpression on the migration and invasion of HepG2 cells.PI and Annexin V double staining experiment was used to observe the effect of PAQR4 overexpression on HepG2 cell apoptosis.Results TCGA database data analysis results showed that the expression of PAQR4 mRNA in HCC tissues was higher than that in adjacent tissues(P<0. 05), and the overall survival rate of HCC patients with PAQR4 mRNA high expression group was lower than that of low expression group(P= 0. 012). Univariate regression analysis showed that PAQR4 mRNA expression level(HR:1. 104, 95%CI: 1. 051-1. 160,P<0. 001), T stage(HR:1. 816, 95%CI:1. 442-2. 287,P<0. 001), M stage(HR:3. 924, 95%CI:1. 230-12. 519,P=0. 021), pathological staging(HR:1. 879, 95%CI: 1. 466-2. 408,P<0. 001) had a significant impact on the prognosis of HCC patients. Multivariate regression analysis showed that PAQR4 mRNA expression level(HR:1. 396, 95%CI: 1. 081-1. 804,P= 0. 011) was an independent risk factor of the prognosis of HCC patients. The results of CCK-8 assay, scratch assay and Transwell assay showed that the proliferation, migration, invasion and invasion ability of HepG2 cells in the experimental group were significantly improved compared with the control group(P<0. 05). Overexpression PAQR4 could inhibit HepG2 cell apoptosis(P<0. 05).Conclusion PAQR4 is significantly up-regulated in HCC tissue and is related to the prognosis of the patients. Overexpression PAQR4 promotes the proliferation, invasion and migration of HepG2 cells, and inhibits HepG2 cells apoptosis. PAQR4 maybe a new marker for the diagnosis and prognosis of HCC.

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Objective To explore the effect of C2-ceramide, one of the sphingomyelin substances, on apoptosis of non-small cell lung cancer cells(A549 and PC9). Methods Non-small cell lung cancer cell lines(A549 and PC9) were cultured, total proteins were extracted and Western blot was performed to detect the expression of apoptotic protein Caspase-3 and cleaved Caspase-3 in the two cells. CCK-8 colorimetric method was used to screen drug concentration. Hoechst 33258 apoptosis staining was used to detect apoptosis. The apoptosis rate was detected by flow cytometry, and the expression of apoptotic protein Caspase-3 was detected by RT-PCR. Results The cell viability was about 70% when ceramide was treated at 50 μmol/L. Compared with the control group, the expression of apoptotic proteins increased in the ceramide group(P<0.05).Flow cytometry and apoptosis staining showed that the rate of apoptosis increased in the ceramide treatment group compared with the control group(P<0.05). mRNA detection at gene level showed increased the expression of apoptotic protein Caspase-3(P<0.05). Conclusion C2-ceramide can promote the apoptosis of non-small cell lung cancer cells, thus providing a new therapeutic target for clinical lung cancer chemotherapy.

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Objective To investigate the protective effect of adiponectin APN on myocardial injury caused by sepsis and its possible mechanism. Methods According to the experimental design, 30 healthy C57 BL/6 male mice were randomly divided into 3 groups: sham operation group(sham group), lipopolysaccharide treatment group(LPS group), adiponectin treatment group(APN+LPS group). HE staining was used to observe the injury of mouse heart. Immunohistochemical staining and Western blot were used to observe the expression of connexin 43(Cx43), Caspase3, Bax, Bcl-2 proteins. Results Compared with sham group, the expression of Bax, cleaved Caspase3 protein increased and the expression of Bcl-2 protein decreased in LPS group. Compared with LPS group, the injury in APN+LPS group was significantly alleviated, showing that the expression of Bax, cleaved caspase3 protein decreased and the expression of Bcl-2 protein increased. Meanwhile, compared with sham group, the expression of Cx43 increased in LPS group and decreased in APN+LPS group. Conclusion Adiponectin can attenuate LPS-induced cardiac injury in septic mice. The mechanism may be through the inhibition of apoptotic signal pathway and the expression of Cx43.

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Objective To explore the significance of circular RNAs(circRNAs) underlining the molecular biological pathogenesis of Uyghur type 2 diabetes(T2 DM) by observing the difference of circRNAs expression in the peripheral blood of Uyghur T2 DM patients. Methods High-throughput nucleotide sequencing was utilized to screen out differentially expressed circRNAs from peripheral blood mononuclear cells of 5 Uyghurs volunteers with healthy adults and 5 Uyghurs with T2 DM.To further verify the differentially expressed circRNAs, additional samples from 20 NC Uyghur volunteers and 22 T2 DM Uyghur patients were analyzed by real-time fluorescent quantitative-PCR(RT-qPCR). Results A total of 134 differentially expressed circRNAs were screened out by high-throughput nucleotide sequencing, of which 87 were up-regulated and 47 were down-regulated.hsa-circ-0139634 andhas-circ-0005414 were obviously up-regulated andhsa-circ-0032491 andhsa-circ-0002922 were obviously down-regulated and they were selected for further verification by RT-qPCR of the additional samples.The study found that the differential expression ofhsa-circ-0139634、hsa-circ-0032491、hsa-circ-0002922 in peripheral blood samples was statistically significant, which was consistent with the sequencing results. Among them, the area under the receiver operating characteristic(ROC) curve ofhsa-circ-0139634 was 0.935 [95%confidence interval(0.884-1.000),P<0.001], Youden index was 0.867, sensitivity was 1.000, specificity was 0.867 and cutoff value was 0.169;the area under the receiver operating characteristic(ROC) curve ofhas-circ-0005414 was 0.575[95%confidence interval(0.370-0.779),P=0.910], Youden index was 0.278, sensitivity was 0.412, specificity was 0.867 and cutoff value was 5.749; the area under the ROC curve ofhsa-circ-0032491 was 0.316[95% confidence interval(0.086-0.440),P=0.017], Youden index was 0.056, sensitivity was 1.000, specificity was 0.056 and cutoff value was 0.230; the area under the ROC curve ofhsa-circ-0002922 was 0.263[95% confidence interval(0.078-0.428),P=0.014], Youden index was 0.080, sensitivity was 0.955, specificity was 0.125 and cutoff value was 0.011. Conclusion Uyghur T2 DM patients and NC populations have differentially expressed circRNAs profiles. Of note,hsa-circ-0139634 has potential value in the molecular biological pathogenesis of Uyghur T2 DM.

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Objective To investigate the effect of motile cilia of ependymal cells on cerebral edema induced by ischemic stroke. Methods SD rats(n=60)were randomly divided into sham group and ischemia-reperfusion model group. In the model group, a 2 h reperfusion 24 h model of ischemia was constructed by the method of suture. The Longa′s-5 point method and the 2, 3, 5-triphenyltetrazolium chloride(TTC) staining were used to assess neurological function and the cerebral infarction volume, respectively. The dry and wet weight method was used to measure brain water content. The morphological changes of motile cilia were observed by HE staining and scanning electron microscope(SEM). The level of SPAG6 expressed in tissues with motile cilia was measured by Western blot. Immunofluorescence was used to detect the structure of motile cilia and the expression distribution of SPAG6 in brain. Results Compared with the sham group, the infarct volume and neurological function score of the model group increased significantly, and the brain edema was obvious(P<0.05). HE staining and SEM results showed that the brain tissue structure of the sham group was tight and regular and the ependymal cell nucleus was round and full. The motile cilia in sham group were arranged orderly and the structure was complete. The brain tissue structure of the model group was loose and the ependymal cell nucleus was wrinkled、condensed and dyed. A large number of necrotic cells were generated, and the structure of motile cilia was disordered. The number and density of motile cilia were significantly reduced, and the arrangement was disordered. Western blot results showed that the total protein content of SPAG6 in the model group was higher than that in the sham group, but the results were not statistically different. Immunofluorescence results showed that compared with the sham group, the length of motile cilia in the model group was significantly shorter(P<0.05). The fluorescence intensity of SPAG6 in the model group was higher than that in the sham group, but the results were not statistically different. Compared with the sham group, the average fluorescence intensity of SPAG6 in ependymal cells of the model group significantly increased, and the difference was statistically significant(P<0.05); and cerebral ischemia-reperfusion injury reduced the expression of SPAG6 fluorescence in the cilia(P<0.05). Conclusion Cerebral ischemia-reperfusion down-regulates the expression of SPAG6 in motile cilia of ependymal cells, resulting in abnormal structure and dysfunction of motile cilia, and subsequent brain edema injury.

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Objective To investigate the effect and mechanism of overexpression of miR-370 on immune injury in asthmatic mice induced by ovalbumin(OVA). Methods 40 female BALB/c mice were divided into control group, model group(OVA), negative control group(OVA+miR-NC) and miR-370 overexpression group(OVA+miR-370). Except for the control group, the other groups were sensitized and stimulated to establish the asthma mouse model.After successful modeling, the OVA+miR-NC group and the OVA+miR-370 group were injected with miR-NC adenovirus and miR-370 overexpression adenovirus respectively by caudal vein. RT-PCR was commended to detect the expression level of miR-370, the bronchoalveolar lavage fluid(BALF) was collected, and Wright-Giemsa staining was used to determine the BALF number of leukocytes. Enzyme-linked immunosorbent assay(ELISA) was employed to detect the expression levels of immunoglobulin E(IgE) and immunomodulatory factor protein in BALF of asthmatic mice; hematoxylin-eosin(HE) staining and terminal labeling method(TUNEL) were used to observe the degree of lung tissue pathological damage and cell apoptosis; Western blot was used to detect the protein expression levels of Bax/Bcl-2 and cleaved cas3/cas3. Results Compared with the control group, mice in the OVA group expressed low miR-370(P<0.05), the number of leukagtes increased(P<0.05), the level of IgE increased(P<0.05), the levels of immunomodulatory factor γ-Interferon(INF-γ), interleukin-13(IL-13), interleukin-12(IL-12) and interleukin 4(IL-4) were up-regulated(P<0.05), and lung tissue was severely damage(P<0.05), the expression ratio of Bax/Bcl-2 and cleaved cas3/cas3 increased(P<0.05); Compared with the OVA group, there was no difference in the indicators of the OVA+miR-NC group. Ove-rexpression of miR-370 up-regulated the expression of miR-370(P<0.05), decreased the number of leukagtes(P<0.05) and the level of IgE(P<0.05), down-regulated immunoregulatory factors INF-γ and IL-12(P<0.05), up-regulated IL-13 and IL-4(P<0.05), and improved lung tissue damage, decreased cell apoptosis, and reduced the expression ratio of Bax/Bcl-2 and cleaved cas3/cas3(P<0.05). Conclusion Overexpression of miR-370 inhibits the production of BALF inflammatory cells in OVA-induced asthmatic mice and relieves lung injury in mice.

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Objective To analyze the effects of transglutaminase 2(TGM2) gene interference on the malignant proliferation and movement of lung cancer cells. Methods A549 cells in logarithmic growth phase were divided into control group, shRNA-NC group and TGM2-shRNA1 group. After transfection, expression levels of TGM2 mRNA and protein after transfection were detected by RT-PCR and Western blot. The growth of A549 cells was detected by clone formation assay. The proliferation activity of cells was detected by CCK-8. The apoptosis rate was detected by flow cytometer. The invasion of cells was detected by Transwell. The number of tubule formation in each group was observed under microscope. The expression of E-cadherin(E-cad), N-cadherin(N-cad), fibronectin(FN) and vascular endothelial growth factor(VEGF) in each group was detected by Western blot. Results Compared with shRNA-NC group, the mRNA level and protein expression of TGM2 in TGM2-shRNA1 group were decreased(P<0.05), and the rate of clone formation, proliferation activity, number of invasive cells and number of tubules formation were decreased(P<0.05).The apoptosis rate and the expression of E-cad protein were increased(P<0.05), while the expression of N-cad, FN and VEGF protein were decreased(P<0.05). Conclusion TGM2 gene silencing can inhibit the expression of VEGF protein, inhibit the malignant proliferation and invasion of A549 cells, and promote apoptosis.

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Objective To study the effect of ubiquinol-cytochrome C reductase subunit 2(QCR2) on cell cycle arrest of cervical cancer SiHa cell line, and to explore related mechanisms. Methods The log-phase SiHa cells were taken, and QCR2 siRNA and control siRNA were transfected into SiHa cells by liposome transfection, which were set as QCR2 siRNA group and control siRNA group, and untreated cells were set as a blank group. qRT-PCR and Western blot were used to determine the relative expression of QCR2, p53 mRNA and protein. Propidium iodide(PI) staining was used to determine cell cycle. The cells in the QCR2 siRNA group were taken, and were intervened with a final concentration of 50 nmol/L ubiquitin-proteasome inhibitor PS341 as the QCR2 siRNA+PS341 group. In addition, the cells in the QCR2 siRNA group were intervened with the same amount of normal saline(NS) and set as the QCR2 siRNA+NS group. Western blot was used to determine the relative expression of p53 protein. The immunoprecipitation test was used to determine the level of p53 ubiquitination. Results Observed under a fluorescence microscope, the transfection efficiency of QCR2 siRNA group and control siRNA group were both>80%. Compared with the blank group and control siRNA group, the relative expression of QCR2 mRNA and protein in the QCR2 siRNA group decreased(P<0.05), the proportion of G0/G1increased(P<0.05), and the proportion of S, G2/M decreased(P<0.05). There was no significant difference in the relative expression of p53 mRNA between the groups. Compared with the blank group and control siRNA group, the relative expression of p53 protein in the QCR2 siRNA group increased(P<0.05). Compared with the blank group and QCR2 siRNA+PS341 group, the relative expression of p53 protein in the QCR2 siRNA group and QCR2 siRNA+NS group increased(P<0.05). Compared with the blank group and control siRNA group, the degree of p53 ubiquitination in the QCR2 siRNA group was reduced(P<0.05). Conclusion Silencing QCR2 can block SiHa cells in G0/G1phase. Its mechanism may be related to the inhibition of p53 ubiquitination and the increase of its protein expression.

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Objective To investigate the effect of miRNA-22 on cardiomyocyte apoptosis and autophagy under uremic toxin stimulation and to elucidate the underlying mechanisms of this process. Methods H9 c2 cells stimulated by indoxyl sulfate(IS) were collected and transfected with mimic-miR-22, anti-miR-22 and LeUCP2 respectively. Flow cytometry was used to analyze the survival of H9 c2 cells, and Western blot was used to analyze the expression of autophagy related proteins LC3 and p62. Results Compared with H9 c2 cells subjected to the control treatment, the number of healthy H9 c2 cells decreased(87.5%vs56.9%,P<0.01), while the number of necrotic and apoptotic cells increased(6.2%vs20.6%, 6.3%vs22.5%,P<0.01) after IS treatment. Treatment with the miR-22 mimics reduced the percentages of necrotic and apoptotic cells(11.0%vs20.6%, 11.0%vs22.5%,P<0.05), while treatment with the miR-22 inhibitors increased the percentages of necrotic and apoptotic cells(38.5%vs20.6%, 40.9%vs22.5%,P<0.01). Western blot analysis showed that H9 c2 cells transfected with miR-22 mimics exhibited a low LC3-Ⅱ-to-LC3-Ⅰ ratio[(1.24±0.15)vs(3.26±0.42),P<0.001]but high p62 protein [(0.92±0.06)vs(0.65±0.05),P<0.05]expression compared with cells transfected with corresponding negative control miRNAs; however, miR-22 inhibitors yielded contrasting results[LC3-Ⅱ/Ⅰratio:(4.53±0.42)vs(3.29±0.40),P<0.01;p62:(0.29±0.04)vs(0.58±0.05),P<0.01]. In addition, LeUCP2 transfection resulted in an increase in p62 expression(P<0.05) and a decrease in LC3-Ⅱ-to-LC3-Ⅰ ratio(P<0.05) in H9 c2 cells exposed to IS or miR-22 inhibitor-transfected H9 c2 cells compared with empty lentivirus vector. Conclusion miR-22 plays an important role in reducing IS induced cardiomyocyte apoptosis and autophagy by targeting UCP2.

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Objective To observe the effect of hydrogen sulfide(H2S) on the expression of transforming growth factor-β1(TGF-β1),E-cadherin(E-CAD), Vimentin(VIM), alpha-smooth muscle actin(α-SMA) during epithelial-mesenchymal transformation(EMT), and to explore the anti-fibrosis mechanism of it. Methods Sixty rats(male SD)were randomly divided into control group, bleomycin group, NaHS+bleomycin group and prednisolone+bleomycin group, 15 rats per group.5 rats of each group were sacrificed at random in 7 th, 14 th and 28 th day. The degree of alveolitis and pulmonary fibrosis was observed.The expression of protein and mRNA of TGF-β1,E-cad, VIM,α-SMA were determined by Immunohistochemi stry and RT-PCR. Results (1) HE and Masson staining showed that the lung tissue of fibrosis had the lowest degree in control group. and the most severe in bleomycin group.The lung tissue of NaHS+bleomycin group and prednisolone+bleomycin group also had alveolitis and fibrosis changes, but the degree Were significantly less than bleomycin group.(2) The mRNA and protein expression levels of TGF-β1, VIM and α-SMA in bleomycin group, NaHS+bleomycin group and prednisolone+bleomycin group were all higher than that in control group at 7 th, 14 th and 28 th day(P<0.05), while the expression levels of them in NaHS+bleomycin group and prednisolone + bleomycin group were all lower than that in bleomycin groupat each time(P<0.05), which was significant at 28 th day in NaHS+bleomycin.(3) The mRNA and protein expression levels of E-Cad in bleomycin group, NaHS+bleomycin group and prednisolone + bleomycin group were all lower than that in control group at 7 th, 14 th and 28 th day(P<0.05), but the expression levels of E-Cad inNaHS+bleomycin group and prednisolone+bleomycin group were higher than that in bleomycin group at each time(P<0.05), which was significant at 28 th day in NaHS +bleomycin. Conclusion H2S can reduce the degree of pulmonary fibrosis in rats, its mechanism may be related to the down-regulation of TGF-β1 and the inhibition of the EMT, which can enhance the expression of E-cad and reduce the expression of TGF-β1,VIM and α-SMA.

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Objective To study the mechanism of neurotrophin receptor-interacting MAGE homolog(NRAGE) on the proliferation and invasion of colorectal cancer(CRC) cells. Methods The clinicopathological data of 84 CRC patients were selected. Fluorescence quantitative PCR(qPCR) and Western blot were used to detect the expression of NRAGE in CRC tissues and adjacent normal tissues. The relationship between the expression of NRAGE in cancer tissues and clinicopathological characteristics was analyzed statistically. RT-PCR and Western blot were used to detect the expression of NRAGE mRNA and protein in CRC tumor cell lines HT29, SW480, SW620, LOVO and colorectal normal cell line FHC. MTT proliferation experiment and Transwell migration experiment were used to observe the tumor cell proliferation and migration ability of the NC group, overexpression NRAGE group and NRAGE knockdown group. The expression differences of AKT, p-AKT, ERK1/2, p-ERK1/2, E-cadherin, N-cadherin and Vimentin were detected by qPCR and Western blot. Results Compared with adjacent tissues, NRAGE mRNA and protein expression in CRC cancer tissues were significantly higher. The expression of NRAGE in cancer tissues was related to tumor stage, distant metastasis and lymph node metastasis(allP<0.05). Compared with FHC cells, CRC tumor cell lines HT29, SW480, SW620, and LOVO cells had higher NRAGE mRNA and protein expression(P<0.05). Compared with the NC group, the proliferation and migration ability of CRC tumor cells in the overexpression NRAGE group was significantly enhanced, while the knockdown group was significantly weakened. Compared with the NC group, the SW480 cells in the overexpression NRAGE group had higher p-ERK1/2 protein expression, but there was no significant difference in the expression of ERK1/2, AKT and p-AKT. After the SW480 cells in the overexpression NRAGE group were treated with ERK inhibitor U0126, the proliferation and migration ability of SW480 cells significantly reduced. Conclusion NRAGE can promote the epithelial-mesenchymal transition of CRC cells and enhance the proliferation and migration of CRC tumor cells by activating ERK signaling pathway.

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Objective To analyze the effects of miR-346 on alleviating cardiac function damage and oxidative stress in rats undergoing myocardial ischemia/reperfusion(I/R).Methods A total of 48 rats were randomly divided into control group, I/R group, I/R+agomiR-NC group and I/R+agomiR-346 group. I/R model was replicated by the ligation of left anterior descending coronary artery. The recombinant adeno-associated virus miR-346 was injected through the tail vein for overexpression intervention. After 120 minutes of reperfusion, heart rate(HR), left ventricular ejection fraction(LVEF), fractional shortening(FS) and left ventricular wall thickness(LVWT), levels of serum creatine kinase MB(CK-MB), myoglobin(Mb), lactate dehydrogenase(LDH) and cardiac troponin I (cTnI), and levels of superoxide dismutase( SOD), glutathion peroxidase( GSH-Px) and malondialdehyde(MDA) in myocardial tissues were detected. The apoptosis of myocardial tissue cells was detected by TUNEL staining. The expression of B-cell lymphoma/leukemia-2(Bcl-2) gene, Bcl-associated x protein(Bax), cysteine protease 3( Cas-3) and Cas-9 in myocardial tissues was detected by Western blot.Results HR, LVEF, FS and LVWT in I/R group were lower than those in control group, the levels of serum CK-MB, LDH, Mb and cTnI were higher than those in control group, the expression of MDA, Bax/Bcl-2, cleaved Cas-3/Cas-3 and cleaved Cas-9/Cas-9 proteins in myocardial tissues was higher than that in control group, the levels of SOD and GSH-px were lower than those in control group, and the apoptosis rate of myocardial tissue cells was higher than that in control group(P<0. 05). HR, LVEF, FS and LVWT in I/R + agomiR-346 group were higher than those in I/R + agomiR-NC group, the levels of serum CK-MB, LDH, Mb and cTnI were lower than those in I/R + agomiR-NC group, the expression of MDA, Bax/Bcl-2, cleaved Cas-3/Cas-3 and cleaved Cas-9/Cas-9 proteins in myocardial tissues was lower than that in I/R + agomiR-NC group, the levels of SOD and GSH-px were higher than those in I/R + agomiRNC group, and the apoptosis rate of myocardial tissue cells was lower than that in I/R + agomiR-NC group(P<0. 05).Conclusion The miR-346 overexpression can reduce oxidative stress level in I/R rats, alleviate myocardial tissue damage, and improve cardiac function.

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Objective To investigate the effects of 6-gingerol on amyloid β-protein(Aβ) induced apoptosis, oxidative stress and neuroinflammation in Alzheimer's disease(AD) rats by regulating Wnt/β-catenin signaling pathway. Methods The rat model of AD was established by injecting Aβ into hippocampus of bilateral brain. The rats were randomly divided into six groups: control group, model group, low-dose 6-gingerol group, medium-dose 6-gingerol group, high-dose 6-gingerol group and positive control group. Nerve injury was evaluated by nerve injury score, brain water content was measured by dry/wet method, and hippocampal histological injury was measured by HE staining. The apoptosis of hippocampal cells was detected by flow cytometry and TUNEL staining. The protein levels of iNOS, IL-6, TNF-α, SOD, GSH-Px and MDA were detected by ELISA. The mRNA and protein relative expression levels of Wnt and β-catenin were detected by qRT-PCR and Western blot. Results Compared with the model group, after 6-gingerol treatment, nerve injury score decreased, brain water content decreased, the apoptosis rate decreased, the expression of iNOS, IL-6 and TNF-α decreased, SOD and GSH-Px protein content increased, while MDA protein content decreased. The mRNA and protein relative expression levels of Wnt and β-catenin were up-regulated. Conclusion 6-gingerol can reduce apoptosis, oxidative stress and neuroinflammation in AD rats by activating Wnt/β-catenin signaling pathway.

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Objective To investigate the effect and mechanism of Src homology 2 domain-containing protein tyrosine phosphatase inhibitor PHPS1 on atherosclerotic plaque vulnerability in ApoE knockout mice, and to provide a new idea for the study of atherosclerosis.Methods Sixteen 8-week-old ApoE-/-mice were randomly divided into control group and PHPS1 group. The aortic root was fixed with formalin and sectioned. The collagen and macrophage contents in the plaque were evaluated by Movat and Sirius red staining. The activity of ERK and the expression of MMP-9 in the descending aorta were detected by Western blot.Results The plaque area(0. 52 ± 0. 05),(0. 31 ± 0. 03), collagen content(0. 062 ± 0. 013),(0. 136 ± 0. 022) and macrophage cell ratio(0. 799 ±0. 031),(0. 621 ± 0. 043) were different between PHPS1 group and control group(P<0. 01). The results of western blot showed that PHPS1 inhibited the activity of ERK and decreased the protein expression of MMP-9(P<0. 01).Conclusion PHPS 1, an inhibitor of SHP-2, can inhibit ERK activity and decrease the expression of MMP-9, thus reducing the degradation of collagen in fibrous cap and stabilizing vulnerable atherosclerotic plaque.

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Objective To investigate the effect of lentivirus mediated silencing ofNIPBLgene on osteogenic differentiation of mouse bone marrow mesenchymal stem cells(BMSCs). Methods The third generation C57 Mouse Bone marrow mesenchymal stem cells were divided into experimental group, negative control group and blank control group. The lentiviral vector was transfected into mouse bone marrow mesenchymal stem cells, the transfection results were observed by inverted fluorescence microscope, and the expression ofNIPBLgene was detected by real-time PCR. The cells of each group were cultured by osteogenic induction. The alkaline phosphatase activity was detected. Real-time PCR and Western blot were used to measure the mRNA and protein expression ofOCN,BMP-2 andRUNX-2. Results The expression ofNIPBLmRNA decreased in the experimental group(P<0.05). The activity of alkaline phosphatase in experimental group was lower than that in negative control group and blank control group(P<0.05). The gene transcription and protein expression levels ofOCN,BMP-2 andRunx-2 in experimental group were lower than those in negative control group and blank control group(P<0.05). Alizarin red staining results showed that the negative control group and blank control group had more red calcium nodules than the experimental group. Conclusion Lentivirus mediated silencing ofNIPBLgene reduces the proliferation of mouse bone marrow mesenchymal stem cells, inhibits the expression of osteogenic differentiation related genes, and reduces the osteogenic differentiation ability.

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Objective To investigate the effect of chemotherapeutic drug resistance induced by CLDN18-ARHGAP26 fusion mutation gene in gastric cancer cells, and to investigate the sensitization effect of ginsenoside in the treatment of chemotherapeutic drug resistance caused by the expression of CLDN18-ARHGAP26 fusion mutation gene. Methods The side population(SP) cells and non-side population(NSP) cells of gastric cancer cell line BGC-823 were labeled with immunomagnetic bead antibody, and the lentiviral vector with overexpression of CLDN18-ARHGAP26 fusion mutation gene was selected for transfection with NSP cells.qPCR was used to detect the mRNA levels of CLDN18-ARHGAP26 fusion mutation and ATP Binding Cassette Subfamily G Member 2(ABCG2).The expression of EMT-related proteins E-Cadherin and Vimentin was detected by Western blot. The sensitivity of transfected cells to oxaliplatin was detected by CCK-8. The effect of ginsenoside on drug resistance of transfected cells was detected by CCK-8. The expression of E-Cadherin and Vimentin in transfected cells was detected by Western blot after ginsenoside treatment.Results qPCR detection showed that the expression ofCLDN18-ARHGAP26 fusion mutant gene in NSP cells transfected with overexpressedCLDN18-ARHGAP26 fusion mutant gene was significantly higher than that of the non-transfected group, and the expression of ABCG2 mRNA was significantly higher than that of the non-transfected group. Western bolt showed that the expression of E-Cadherin protein in NSP cells with over-expressedCLDN18-ARHGAP26 fusion mutation gene was lower than that in the non-transfected group, the expression of Vimentin protein was higher than that in the non-transfected group, and the sensitivity of transfected cells to oxaliplatin was lower than that in the non-transfected group. The survival rate of transfected cells treated with ginsenoside and oxaliplatin was significantly lower than that treated with oxaliplatin alone. The expression of E-Cadherin protein in the transfected cells treated with ginsenoside was higher than that in the untreated group, and the expression of Vimentin protein was lower than that in the untreated group.Conclusion Ginsenoside can reverse cell EMT transformation and oxaliplatin resistance induced byCLDN18-ARHGAP26 fusion mutated gene expression in gastric cancer tissues.

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Objective To investigate the changes of liver renin-angiotensin(RAS) system as well as its relationship with liver function in endotoxemia rats. Methods Totally 90 rats were randomly divided into control group and 2, 4, 8, 12, 24, 48, 72 h and 7 d after injection group, which were prepared for sepsis model by tail vein injection of LPS except for the control group. Animals in the control group were collected samples at 8 h after injection, while animals in the model group were collected samples at each time points(2, 4, 8, 12, 24, 48, 72 h and 7 d). Heart blood was collected to measure liver markers alanine amine aminotransferase(ALT), aspartate aminotransferase(AST), lactate dehydrogenase(LDH), RAS markers renin-angiotensin(PRA), angiotensin converting enzyme(ACE) and angiotensin Ⅱ(Ang Ⅱ). Liver tissues were extracted to observe the pathology characteristics and detect PRA, ACE, Ang Ⅱ and angiotensin type 1 receptor(AT1 R) mRNA. Results The levels of AST, ALT and LDH in the model group gradually increased after LPS injection, and AST and LDH in the model group were higher than those in the control group at 4～48 h, ALT in the model group was higher than that in the control group at 2 to 48 h, and the differences were statistically significant(P<0.05). The circle and liver PRA level in the model group increased rapidly after injection, which was higher than that in the control group at 2 to 48 h. The circle and liver levels of ACE and Ang Ⅱ increased after injection too, which were both higher than those in the control group at 2 to 28 h, and the difference was statistically significant(P<0.05). The expression of AT1 R mRNA in the model group gradually increased after injection, which was higher than that in the control group at 4 to 48 h, and the difference was statistically significant(P<0.05). Conclusion Liver function damage caused by endotoxemia may be related to the activation of local RAS in the liver.

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Objective To investigate the effect of glycyrrhizin on the fibrosis of silica-treated mice. Methods C57 BL/6 male mice were randomly divided into control group, silicosis model group and glycyrrhizin treatment group, with 6 mice in each group. The pathological changes of lung tissues were observed by HE and Sirius red staining. Lung function indexes were detected by respiratory function instrument. The content of hydroxyproline in the lung tissues was detected by corresponding kit. The mRNA levels of monocyte chemotactic protein 1(MCP-1), fibronectin(FN) and alpha-smooth muscle actin(α-SMΑ) were detected by real-time fluorescent quantitative PCR.The number of leukocytes in the bronchoalveolar lavage fluid(BALF) was counted and the secretion of transforming growth factor-β1(TGF-β1) in BALF was detected by ELISA.Results HE and Sirius red staining showed that the inflammatory cells and the collagen were accumulated in the lung tissue of mice in silicosis model group. After treatment with glycyrrhizin, the accumulation of inflammatory cells and the collagen was ameliorated. Compared with the control group, pause(PAU) and enhanced pause(Penh) increased in the model group(P<0. 05). Glycyrrhizin treatment improved the respiratory function in mice. Furthermore, glycyrrhizin also effectively reduced the increase in the content of hydroxyproline, the expression of MCP-1, FN and α-SMΑ mRNA, the number of leukocytes and the secretion of TGF-β1 induced by silica treatment in mice(P<0. 05).Conclusion Glycyrrhizin can improve the pulmonary function and alleviate the fibrosis in mice with silicosis.

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Objective To explore the role of long non-coding RNA PITPNA-AS1 in ovarian cancer and its possible molecular mechanism. Methods Fluorescence real-time quantitative polymerase chain reaction(qPCR) technology was used to detect the expression level of PITPNA-AS1 in ovarian cancer tissues and corresponding adjacent tissues, ovarian cancer cell lines and normal ovarian epithelial cell lines. The cell lines with the least expression of PITPNA-AS1 were divided into control group and experimental group, and transfected with negative control plasmid or PITPNA-AS1 plasmid respectively. Cell counting(CCK-8) method and Transwell method were used to detect cell proliferation activity and invasion ability. Bioinformatics methods and dual luciferase activity reporter gene experiments predicted and verified the molecular mechanism of PITPNA-AS1. qPCR and Western blot were used to detect the gene expression of PITPNA-AS1 interaction. Results The expression of PITPNA-AS1 in ovarian cancer tissues was lower than that in adjacent tissues(P<0.01). The expression level of PITPNA-AS1 in ovarian cancer cell lines was lower than that in normal ovarian epithelial cells(P<0.05), and the expression in OVCAR-3 cells was the least(P<0.01). Compared with the control group, overexpression of PITPNA-AS1 could inhibit the proliferation activity(P<0.05) and invasion ability(P<0.01) of OVCAR-3 cells. PITPNA-AS1 had a targeting relationship with miR-92 a-3 p(P<0.01), and miR-92 a-3 p had a targeting relationship with transcription factor 21(TCF21)(P<0.01). Overexpression of PITPNA-AS1 caused a decrease in the expression of miR-92 a-3 p in OVCAR-3 cells(P<0.01), and an increase in the expression of TCF21 gene(P<0.01). Conclusion PITPNA-AS1 is lowly expressed in ovarian cancer tissues and cell lines. PITPNA-AS1 can inhibit the proliferation and invasion of ovarian cancer OVCAR-3 cells through targeted regulation of miR-92 a-3 p/TCF21.

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Objective To explore the material basis and mechanism of Yindan Xinnaotong soft capsule(YD) in treating myocardial ischemia-reperfusion injury(MIRI) based on network pharmacology, so as to provide theoretical reference for the treatment of MIRI. Methods The main active components and action targets of YD were searched by TCMSP, SwissTargetPrediction and China knowledge Network. The disease targets of MIRI were screened by GeneCards database. The “ drug-component-disease-target” network relationship was constructed by Cytoscape software, enrichment analysis and prediction mechanism were analyzed, and the molecular docking verification was carried out between the top three main active components and the top six targets in PPI network. Human myocardial AC-16 cells were constructed hypoxia/reoxygenation(H/R) model to initially verify the core target. Using CCK-8 assay was usedto detect cell viability and explore the optimal drugconcentration. The influence of YD on cell morphology was observed by using optical microscope. LDH content was detected to assess the integrity of cell membrane; Western blot was used to detect the expression of STAT3, p-STAT3, PI3 K, AKT1 and p-AKT1.Results A total of 105 active components, 382 drug targets, 1223 MIRI disease targets and 160 drug-disease common targets of YD were obtained. The key targets involved AKT1, STAT3, VEGFA,TNF, MAPK8, PIK3 CA and so on. GO analysis mainly involved apoptosis, lipolysis, muscle cell proliferation, cytokine-mediated inflammation,oxidative stress and so on. The results of molecular docking showed that VEGFA, APP and PIK3 CA could bind to quercetin, luteolin and kaempferol. Our results showed that 200 mg/L YD could significantly promote the proliferation of AC-16 cells and reduce LDH leakage. Western blot results showed that YD could activate STAT3 and PI3 KAKT1 signaling pathways and protect myocardium.Conclusion YD can protect MIRI through multi-components,multi-targets and multi-pathways.

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Objective This experiment was carried out to study the effects of chronic inflammatory pain on the gut flora of mice by 16 S rRNA high-throughput sequencing. Methods Twelve specific pathogen free(SPF) C57 BL/6 J mice were randomly divided into CFA group and mock group, with 6 mice in each group. Chronic inflammatory pain model was established by intraplantar injection of CFA in the right posterior pelma of C57 BL/6 J mice. In the control group, normal saline was injected by intraplantar injection in the same position. Two weeks later, the mice were euthanized, and the feces in the colon were collected. The feces of two mice in the same group were mixed, detected and analyzed by 16 S rRNA high-throughput sequencing technology. Results Compared with mock group, the abundance and diversity of gut flora in CFA group decreased. The abundance ofFirmicutesand TM7 increased at the phylum level, the abundance ofAerococcus,LactobacillusandDesulfovibrioincreased significantly at the family and genus level, while the abundance ofPsychrobacter,Prevotella,OscillospiraandBifidobacteriumdecreased significantly compared to mock group. In addition, many biomarkers were found from the level of the phylum to the genus. Conclusion The gut microflora structure, especially the dominant flora, has changed significantly in mice with chronic inflammatory pain, which can provide basis for the treatment of microecological imbalance caused by chronic inflammatory pain and the improvement of patients′ negative emotions through “gut brain axis”.

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Objective To investigate the effect of CD147 on reducing hydrogen peroxide-induced oxidative stress injury in prostate cancer LNCaP cells. Methods The lentiviral system was used to establish a CD147-silencing prostate cancer cell model(LNCaP/shCD147 cells) and a negative control cell(LNCaP/Scramble cell), and RT-qPCR was performed for verification.By detecting the activity of reactive oxygen species(ROS), superoxide dismutase(SOD), glutathione peroxidase(GSH-PX) and malondialdehyde(MDA) in LNCaP/shCD147 and LNCaP/Scramble cells to verify the changes of oxidative stress and antioxidant enzymes in prostate cancer cells after silencing CD147; hydrogen peroxide(H2O2) was added to the cells and the cell growth was detected by CCK-8; Western blot was used to detect the expression changes of nuclear factor E2 related factors(Nrf2) and heme oxygenase-1(HO-1) to verify the relationship between the oxidative stress that occurs in prostate cancer cells after silencing CD147 and the PI3 K/AKT signaling pathway. Results Successfully constructed a CD147-silencing prostate cancer cell model. Compared with LNCaP/Scramble cells, the expression of CD147 in mRNA was reduced(P<0.01).The results of oxidative stress showed that the content of ROS and MDA in cells increased after silencing CD147(ROS,P<0.01; MDA,P<0.05), while the activities of SOD and GSH-PX decreased(P<0.01), indicating that after silencing CD147, LNCaP/shCD147 cells undergo oxidative stress. In addition, with the increase of H2O2concentration, the survival rate of LNCaP/shCD147 group cells decreased(P<0.01). After inhibiting the PI3 K/AKT signaling pathway, the expressions of Nrf2 and HO-1 in the LNCaP/shCD147 group were reduced(P<0.01), indicating that CD147 inhibits the oxidative stress injury of prostate cancer cells through the PI3 K/AKT pathway. Conclusion CD147 can reduce the oxidative stress damage of PCa cells, and its inhibitory mechanism may be related to the PI3 K/AKT signaling pathway.

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Objective To investigate the effects of one night of sleep deprivation on adults' cognitive performance and sleepiness. Methods The study employed a repeated-measures design. Participants performed cognitive performance tasks, which included the Continuous Performance Test and Digit Span Test and Karolinska Sleepiness Scale. The data were analyzed using one-way repeated-measures ANOVA. Results 48 participants were included in this study. Sleep deprivation during night shift had a adversely affect on sustained attention performance and alertness(P<0.05). Compared with the beginning of night shift work, the correct number decreased, the number of errors, missed number and reaction time increased, and the score of Karolinska sleepiness scale decreased after the night shift work. The sleep deprivation has no significant effect on working memory performance(P>0.05). Conclusion One night of sleep deprivation has significant deleterious effects on cognitive performance and subjective sleepiness. However, no effect on the working memory performances has been found.

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Objective To explore the correlation between α 1-antitrypsin, CXCL12, IL-15 Ralpha and the prognosis of HIV-infected patients. Methods A total of 154 HIV-infected patients were selected, and 154 healthy volunteers were randomly selected from our hospital for physical examination and divided into control group.According to the stage of the disease, the patients were divided into stage I, stage II, stage Ⅲ and stage Ⅳ. Western blot was used to detect the expression of α 1-antitrypsin and CXCL12, PC-PCR was used to detect the expression of IL-15 Rα, and indirect method was used to detect the levels of CD3 and CD4. Results Compared with the control group, the levels of CD4 and CD8 in AIDS group decreased abnormally, and the difference was statistically significant(P<0.05); compared with the control group, the expression of α 1-antitrypsin, CXCL12, IL-15 Rα in AIDS group increased(P<0.05); compared with stage I patients, the expression of α 1-antitrypsin, CXCL12, IL-15 Rα in patients with stage Ⅱ increased(P<0.05); compared with stage Ⅱ patients, the expression of α 1-antitrypsin, CXCL12, IL-15 Rα increased(P<0.05); compared with patients in stage Ⅲ, the expression of α 1-antitrypsin, CXCL12 and IL-15 Rα in patients with stage Ⅲ was higher(P<0.05); compared with patients in stage III, the expressions of α 1-antitrypsin, CXCL12 and IL-15 Rα in patients with stage IV increased(P<0.05). Conclusion α 1-antitrypsin, CXCL12 and IL-15 Rα are closely related to HIV infection and prognosis of HIV infected patients.

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Objective To study the expression and clinical significance of Wnt signal secretory protein DKK1 in cervical cancer. Methods Reverse transcription polymerase chain reaction(RT-PCR) was used to detect the expression of DKK1 mRNA in 30 pairs of cervical cancer tissues and adjacent normal tissues. The expression of DKK1 protein was detected by immunohistochemistry in 60 cases of cervical cancer and 30 cases of normal cervical tissue, and the relationship between the expression and clinicopathological characteristics of cervical cancer was analyzed. Results The expression of DKK1 in cervical cancer tissues was lower than that in adjacent tissues and normal cervical tissues(P<0.05). The expression of DKK1 was closely related to clinicopathological stage, tissue differentiation, lymph node metastasis and depth of invasion(P<0.05). Conclusion The expression of DKK1 is low in cervical cancer and plays an important role in the occurrence and development of cervical cancer.

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Objective To study the best machine learning method for early prediction of hematoma expansion in hypertensive intracerebral hemorrhage based on head CT plain scan. Methods The CT images of 130 patients with cerebral hemorrhage were retrospectively analyzed, and the texture features of the head CT plain scan were extracted. The classifier was trained by selecting the features, and the six classic machine learning methods were cross-validated to evaluate the stability and performanceof predicting cerebral hemorrhage hematoma expansion. Results The prediction performance of support vector machine(SVM-Radial)(AUC 0.714±0.144, accuracy 0.723±0.109), generalized linear model(GLM) prediction performance(AUC 0.643±0.125, accuracy 0.587±0.136), random forest(RF) prediction performance(AUC 0.686±0.128, accuracy 0.680±0.130), k-nearest neighbor(kNN) prediction performance(AUC 0.657±7 C 15, accuracy 0.639±39 performance 19), gradient boosting tree algorithm(GBM) Prediction performance(AUC 0.718±0.141, accuracy 0.670±0.126), neural network(NNet) prediction performance(AUC 0.659±0.162, accuracy 0.680±0.130), in which support vector machines showed high prediction performance, generalized linear model showed low predictive performance. Conclusion Among the six machine learning methods based on cranial CT radiomics to predict early hematoma expansion in hypertensive intracerebral hemorrhage, support vector machine(SVM-Radial) has the best predictive performance and has potential clinical application value.

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Objective To investigate the association between c.1311 C>T and c.1004 C>A of glucose-6-phosphate dehydrogenase(G6 PD) gene single nucleotide polymorphism(SNP) with the risk of G6 PD deficiency in Guangxi population. Methods 417 patients with G6 PD deficiency were randomly selected as case group, and 295 healthy patients were selected as control group. The c.1311 C>T and c.1004 C>A were genotyped using the SNPscanTM multiple SNP method, and the haplotype frequency of two sites were analyzed by SHEsis. Results In the case and control group, there were statistically significant differences in the distribution frequency of genotype TT, CC+CT and allele T at c.1311 C>T locus [TT vs CC:(P=0.001,OR=0.373, 95%CI=0.204-0.683); TTvsCC+CT:(P=0.001,OR=0.371, 95%CI=0.203-0.678); TvsC:(P=0.002,OR=0.601, 95%CI=0.435-0.829)];however, there was no significant difference in genotype and allele distribution frequency at c.1004 C>A locus(P>0.05). The results of the rate method showed that compared with genotype CC,the genotype CT at c.1311 C>T increased the expression level of G6 PD enzyme, while the genotype TT decreased the expression level of G6 PD enzyme(P<0.05), the haplotype analysis showed that C-C and T-C were associated with G6 PD risk(P<0.05). Conclusion In Guangxi population, c.1311 C>T locus genotypes TT, CC+CT and allele T were related to the decreased risk of G6 PD deficiency.