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Objective To examine the role of LMO4 in the regulation of endothelial cell differentiation and angio- genesis in murine embryonic stem cells (mESC) ．Methods Mouse Lmo4 cDNA was obtained from MEL cells by using the reverse transcription-polymerase chain reaction (RT-PCR) and subcloned into the expression vector pFG to generate the pFLG ，in which contained Flk-1 promoter to drive Lmo4 expresses in only FLK-1 + cells．The mESC were transfected with pFG or pFLG plasmids and subsequently screened with geneticin ( G418) to produce cell clones． These cell clones were named mESC /pFG and mESC /pFLG ，respectively． The mESC /pFG and mESC /pFLG were cultured in the differentiation medium for either 4 days or 10 days to generate embryoid bodies (EB) ．The 10-day embryoid bodies ( 10 d-EBs) carrying the pFG and pFLG vectors were subsequently stimulated to generate the blast-colony forming cells (BL-CFC) ，which indicated the presence of hemangioblasts．The endo- thelial cell sprouting analysis was performed by using 10 d-EBs．The expression of the interest genes was detected by using qualitative RT-PCR or Western blot analysis. Results The pFLG expression vector was successfully con- structed through PCR identification．The mESC /pFG and mESC /pFLG cells were obtained after transfected with the pFG or pFLG vectors and selected by G418．The cells spontaneously differentiate to generate EBs，in which some green fluoresce cells were present．Western blot analysis showed that a significant increase in LMO4 expression in both 4 d-EB and 10 d-EB when compared to mESC．BL-CFC analysis showed that the 4 d-EB/ pFLG had a higher cloning efficiency ( 7. 70% ± 1. 27% ) ，comparing with that of the 4 d-EB/ pFG ( 1. 15% ± 0. 48% ) ( P = 0. 021) ．Quantitative RT-PCR results showed that the expression of Flk-1，C-kit，Tie-2 and Ve-cad genes in 10 d- EBs /pFLG increased more than 2-fold compared to 10 d-EBs /pFG．The endothelial cell sprouting analysis result showed a significant increase in the number and length of new blood vessels in 10 d-EB/ pFLG compared to 10 d- EB/ pFG (P＜0. 05) ．Conclusion Overexpression of LMO4 promotes hemangioblast differentiation from mESC， and benefits for endothelial cell differentiation and angiogenesis.

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Objective To use linear PCR fragment containing antibiotic resistance cassette to carry out homologous recombination and replacement of target gene fragment ofAcinetobacter baumanniito achieve rapid gene knockout and functional verification. Methods Acinetobacter baumanniiAb4294 was used as the research object, and the upper(901 bp) and lower(1 028 bp) reaches offimgene cluster(4 980 bp in length) were amplified by PCR, which was used as the recombinant homologous arm. Kanamycin antibiotic resistance cassette(KanR) was amplified from pUC57 plasmid. The above three fragments were connected by overlapping extended PCR technique, and the connected fragments were transformed into wildAcinetobacter baumanniistrains. The gene deletion mutant was screened, and the plasmid complement strain was constructed. The phenotype of the obtained strains was identified, and the function offimgene cluster was explored. Results A mutant strain ofAcinetobacter baumanniiAb4294 with deletion offimgene cluster was successfully constructed by homologous substitution of linear PCR fragment containing antibiotic resistance cassette. Compared with the wild strain, the growth curve of the deletion strain had no significant difference, and the rubbing ability significantly decreased, and the phenotype recovered after complementing the gene cluster. Conclusion Thefimfamily genes ofAcinetobacter baumanniiAb4294 is successfully knocked out by homologous substitution of linear PCR fragment containing antibiotic resistance cassette, which encodes the product involved in the motile movement ofAcinetobacter baumannii.

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Objective To investigate the impact of dexmedetomidine on the oncological behavior of hepatocellular carcinoma and explore the role of NF-E2-related factor 2(Nrf2) at bothin vitroandin vivolevels. Methods In vivoexperiment, Male C57BL/6J mice were randomly divided into a control group(Ctrl group), a hepatocellular carcinoma group(HCC group), and a hepatocellular carcinoma+dexmedetomidine group(HCC+Dex group). Hepatocellular carcinoma was induced in mice by combining N-Nitrosodiethylamine(DEN)/carbon tetrachloride(CCl4), followed by daily intraperitoneal injection of 10% dexmedetomidine for two weeks. After feeding the mice for one month, the mice were assessed for the quantity and size of liver tumors. The proliferation ability of liver cancer was evaluated using Ki67 immunohistochemistry. Additionally, the expression level of Nrf2 protein in tumor tissue was measured through immunofluorescence.In vitroexperiment, Hepa1-6 cells were incubated with different concentrations of dexmedetomidine(0.1, 1, 5 nmol/L) for 48 hours to examine their effects. The proliferation, migration and invasion abilities of Hepa1-6 cells were evaluated using the MTT and Transwell methods. The expression level of Nrf2 protein in the Hepa1-6 cells was measured using Western blot and immunofluorescence. Additionally, the proliferation, migration and invasion abilities of cells were assessed after Nrf2 knockdownviasi-RNA transfection, in combination with incubation with 1 nmol/L dexmedetomidine for 48 hours. Results Compared to the HCC group, the anatomical examination results revealed an increase in the number of liver tumors and the longest diameter in the HCC+Dex group(P<0.05). Ki67 immunohistochemistry results indicated the number of Ki67 positive cells in liver cancer tissue increased in the HCC+Dex group(P<0.01). The immunofluorescence assay demonstrated an upregulation of Nrf2 expression level in the HCC+Dex group(P<0.05). MTT results showed that 1 nmol/L of dexmedetomidine increased the cell viability of Hepa1-6 cells(P<0.05). Transwell results indicated that 0.1, 1, and 5 nmol/L of dexmedetomidine enhanced the invasive ability of Hepa1-6 cells, while 0.1 and 1 nmol/L of dexmedetomidine enhanced the migration ability(P<0.05). Western blot and immunofluorescence results showed an upregulation of Nrf2 expression level in cells after treatment with 1 nmol/L dexmedetomidine(P<0.01). The Nrf2 expression level of cells was reduced using si-RNA, followed by treatment with 1 nmol/L dexmedetomidine. The results from MTT and Transwell assays revealed a decrease in the viability, invasion and migration ability of Hepa1-6 cells(P<0.01). Conclusion Dexmedetomidine may enhance the proliferation, invasion and migration capacity of hepatocellular carcinoma by upregulating the expression of Nrf2.

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Objective To investigate the protective effect of melatonin(MT) on formaldehyde(FA) inhalation-induced acute lung injury(ALI) in rats and its mechanism through the regulation of nuclear factor E2-related factor 2(Nrf2) signaling pathway. Methods Fifty female Wistar rats were randomly divided into Control group, FA group, FA+MT 5 mg/kg group, FA+MT 10 mg/kg group and FA+MT 20 mg/kg group, with 10 rats in each group. Except for the Control group, all other groups inhaled 3 mg/m3FA daily for 21 d consecutively to construct the tainted model, and then treated with different MT doses for 14 d. The tainting was continued during the MT treatment. Hematoxylin-eosin(HE) staining was used to observe the histopathological changes in lung tissue, lung water content and lung coefficient were weighed and measured, glutathione(GSH), superoxide dismutase(SOD) and 8-hydroxydeoxyguanosine(8-OHdG) levels were measured by absorbance photometric method, and enzyme linked immunosorbent assay(ELISA) was used to measure the levels of tumor necrosis factor-alpha(TNF-α), interleukin(IL)-6, and IL-1β concentrations, Western blot to detect the protein expression levels of Nrf2, heme oxygenase-1(HO-1), nuclear factor-κB(NF-κB), and phosphorylated nuclear factor-κB(p-NF-κB) in lung tissues, and quantitative polymerase chain reaction(qPCR) to detect the Nrf2, HO-1, and Kelch-like ECH-associated protein 1(Keap1) mRNA expression levels. Results Compared with the control group, lung injury was obvious in rats in the FA group; lung tissue GSH and SOD levels were reduced, and 8-OHdG levels were elevated(P<0.05); alveolar lavage fluid TNF-α, IL-6, and IL-1β levels were elevated(P<0.05); Nrf2 and HO-1 protein expression levels were reduced in the lung tissue( P<0. 05),and p-NF-κB protein expression levels were was elevated( P<0. 05); the relative mRNA expression of Nrf2 and HO-1 in lung tissue was decreased,and the relative mRNA expression of Keap1 was elevated( P<0. 05). Compared with the FA group,the lung injury of rats in the MT group was improved; the levels of GSH and SOD in the lung tissue were increased( P<0. 05),and the level of 8-OHd G was decreased( P<0. 05); the levels of TNF-α,IL-6,and IL-1β in the alveolar lavage fluid were decreased( P<0. 05); and the expression levels of the Nrf2 and HO-1 proteins in the lung tissue were increased( P<0. 05). p-NF-κB protein expression level was decreased( P<0. 05); the relative mRNA expression levels of Nrf2 and HO-1 in lung tissues were increased( P<0. 05),and the relative mRNA expression level of Keap1 was decreased( P<0. 05) in lung tissues,and all of them were in a dose-dependent manner. Conclusion MT can alleviate oxidative stress and inflammatory responses and mitigate FA exposure-induced acute lung injury by regulating the Nrf2/Keap1/HO-1 signaling pathway.

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Objective Mendelian randomization analysis was used to explore the causal relationship ofT.gondiiinfection and the cyst distribution and inflammation in brain tissue by immunohistochemistry. Methods Genome-wide association analysis data ofT.gondiiinfection and encephalitis were obtained, single nucleotide polymorphisms(SNPs) were selected, Mendelian randomization analysis was conducted by inverse variance weighting, and the causal relationship betweenT.gondiiinfection and encephalitis was evaluated byORvalue and 95%CI. Quality control was carried out by using heterogeneity test, horizontal multi-efficiency test and leave-one-out sensitivity test. Immunohistochemical staining was performed using brain sections of mice infected with tissue cysts of Wh6 strain for image analysis using Image J software. Results A total of 29 SNPs were associated with toxoplasmic encephalitis. The results of IVW method suggested thatT.gondiiinfection made encephalitis risk 0.98 times higher(OR=0.98, 95%CI=0.76 to 1.27), indicating no causal relationship between the two. The quality control results suggested that the selected SNPs were stable and reliable.Toxoplasmacysts were distributed in various parts of the brain tissue. Conclusion T.gondiiinfection and encephalitis are related, but there is no sufficient evidence to prove the causal relationship between the two.

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Objective To explore the effects of microRNA-155(miR-155) on apoptosis of chronic myeloid leukemia( CML) cells,and the influence of miRNA-155 regulating the expression of heat shock proteins( HSP) 27,HSP60,HSP70. Methods Reverse transcription-quantitative real-time PCR( RT-q PCR) was used to detect the expression levels of miR-155 in CML-resistant imatinib( IM) cell line K562-G and CML cell line K562. K562-G cells were infected with the lentivirus carrying miR-155 or the negative control lentivirus,and they were named miR-155 group and control group. The effect of miR-155 on the proliferation of drug-resistant cells was detected by cell counting kit-8( CCK-8) method. RT-q PCR and Western blot were used to detect the effect of miR-155 on the expression of heat shock proteins HSP27,HSP60,HSP70. Flow cytometry was used to detect the percentage of cell apoptosis in miR-155 group and control group. Results Compared with K562 cells,miR-155 showed low expression in K562-G cells( P<0. 05). The proliferation of miR-155 group cells decreased significantly from the 36th hour( P<0. 05). Compared with the control group,in the miR-155 group,HSP60 and HSP70 increased( P<0. 05),while HSP27 decreased( P<0. 01). The apoptosis rate of miR-155 group was higher than that of control group( P<0. 05). Conclusion miR-155 promotes the apoptosis of chronic myeloid leukemia cells,increases the expression of HSP60 and HSP70,and decreases the expression of HSP27.

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Objective To investigate the phenotype of amoxicillin(AMX) unstable resistantHelicobacter pylori(Hp) evolving into AMX stable high level resistance and the detection of its mutated genes. Methods Using the frozen Hp strain H390 as the starting strain, the clones resistant to AMX were continuously cultured on the medium with increasing AMX concentration, and the minimum inhibitory concentration(MIC) of the resistant clones was detected. After frozen at-80 ℃ for 3 months, the drug resistance was stable according to whether the MIC decreased after frozen storage. Genome sequencing analysis and efflux pump inhibition assay were performed on cloned H390r and parental strain H390 with the highest AMX MIC value, and gene mutations associated with the high level AMX resistance obtained by H390r were detected and identified. Results Four AMX high level resistant clones were obtained by AMX screening with MICs of 12, 32, 64 and ≥256 mg/L, respectively, and none of the MICs were altered after freezing at-80 ℃. Compared to the parental strain H390, the AMX stable resistant clone H390r had mutations in several genes, includinghefCencoding the RND efflux system,hopBandhopCencoding the pore proteins andftsIencoding the penicillin binding protein, which were associated with AMX resistance. H390r was substantially reduced in MIC to AMX in the presence of efflux pump inhibitors. Conclusion AMX can screen stable resistant clones from unstable resistant Hp. H390r had mutations inhefC,hopB,hopC, andftsIassociated with AMX resistance. These mutations may be the main reason why H390r acquired a stable high level of resistance to AMX.

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Objective To investigate the effects of immunoglobulin gene superfamily 10(IGSF10) on proliferation, migration and invasion of lung adenocarcinoma cells. Methods Bioinformatics was applied to study the expression levels ofIGSF10in tumor tissues and normal tissues. Western blot and quantitative real-time PCR(qPCR) were used to detect the expression level ofIGSF10in lung adenocarcinoma cell lines and normal lung epithelial cells. Knockdown ofIGSF10, the effect of knockdown ofIGSF10on proliferation, migration and invasion of lung adenocarcinoma A549 cells was examined using cell counting kit-8(CCK-8), Transwell migration and invasion assay, scratch assay and plate cloning assay. The effects of knockdown ofIGSF10on the expression of invasion and migration-related genes in A549 cells were examined by Western blot and qPCR assays. Results IGSF10expression in lung adenocarcinoma tissues was lower than that in normal tissues(P<0.05).IGSF10expression in lung adenocarcinoma cell lines was lower than that in lung epithelial cells(P<0.05). Knockdown ofIGSF10promoted the ability of lung adenocarcinoma A549 cells to proliferate, proliferation, migration and invasion(P<0.05). Knockdown ofIGSF10promoted the expression of regulatory epithelial-mesenchymal transition marker Neural-cadherin(N-cadherin) and key transcription factors Snail family transcriptional repressor 1(Snail) and Snail family transcriptional repressor 2(Slug)(P<0.05) and inhibited the expression of Epithelial-cadherin(E-cadherin)(P<0.05). Conclusion Knockdown ofIGSF10may promote proliferation, migration and invasion of lung adenocarcinoma cells through activation of Snail, Slug/E-cadherin signaling axis, and this result may provide a potential new target for clinical diagnosis and treatment of lung adenocarcinoma.

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Objective To investigate the expression difference and potential clinical significance of 83 sequence similar member A(FAM83A) and β-catenin in cervical lesions. Methods UALCAN and GEPIA2.0 online databases were used to analyze the difference ofFAM83Aexpression in normal cervix and cervical squamous cell carcinoma(CSCC) and the relationship betweenFAM83Aexpression and the prognosis of CSCC patients, LinkedOmics database was used to analyzeFAM83AmRNA co-expression genes, and R language was used for KEGG enrichment analysis. Immunohistochemistry was used to detect FAM83A and β-catenin expression in 60 cases of normal cervix, 80 cases of low-grade squamous intraepithelial lesion(LSIL), 90 cases of high-grade squamous intraepithelial lesion(HSIL) and 70 cases of cervical squamous cell carcinoma(CSCC). The relationship between FAM83A, β-catenin expression and clinicopathological features and the correlation between FAM83A and β-catenin expression were analyzed. Results UALCAN database analysis showed thatFAM83Awas highly expressed in CSCC tissues, and GEPIA 2.0 database analysis suggested that those with highFAM83Aexpression had a poor prognosis. LinkedOmics database performing KEGG enrichment analysis suggested that expression ofFAM83Awas positively correlated with aberrant activation of Wnt/β-catenin signaling pathway. The expression rate of FAM83A in CSCC was higher than that in LSIL and normal cervical tissues(P<0.001), but there was no significant difference compared with HSIL(P=0.401); the expression of FAM83A was not correlated with age(P=0.231), but was significantly different from the correlation with differentiation(P=0.001) and clinical stage(P=0.038). The abnormal expression rate of β-catenin in CSCC was higher than that in LSIL and normal cervical tissues(P<0.001), but there was no significant difference compared with HSIL(P=0.734); the expression of β-catenin was not related to age(P=0.088), related to differentiation(P=0.001) and clinical stage(P<0.001), and FAM83A was positively correlated with β-catenin expression(P<0.05). Conclusion FAM83A and β-catenin are highly expressed in both HSIL and CSCC tissues, and there is a positive correlation between the expression of FAM83A and β-catenin. The high expression of FAM83A has some correlation with the prognosis of CSCC patients and can be used as a potential marker to determine the prognosis of CSCC.

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Objective To investigate the role and related molecular mechanisms of vitamin D3(VitD3) in airway inflammation and oxidative stress response in bronchial asthma mice. Methods Twenty-eight female C57BL/6 mice were randomly divided into a control group(Ctrl) and a model group. The model group mice were sensitized using ovalbumin(OVA) to establish an asthma model, and were further divided into an asthma(Asthma) group, VitD3treatment(Asthma+VitD3) group, and Forkhead Box O1(FOXO1) inhibitor AS1842856 treatment(Asthma+AS) group. Lung resistance(LR) changes were measured in each group of mice. Enzyme-linked immunosorbent assay(ELISA) was used to detect the levels of tumor necrosis factor-alpha(TNF-α), interleukin(IL)-1β, and IL-18 in bronchoalveolar lavage fluid(BALF). Western blot was used to determine the expression levels of FOXO1, NOD-like receptor pyrin domain containing 3(NLRP3), Caspase-1, and apoptosis-associated speck-like protein(ASC) in lung tissue. Results Compared to the Ctrl group mice, LR increased in the Asthma group mice(P<0.01). Compared to the Asthma group, LR decreased in the Asthma+VitD3and Asthma+AS group mice(P<0.05), with no significant difference in LR change between Asthma+VitD3and Asthma+AS group mice. Compared to the Ctrl group, TNF-α, IL-1β, and IL-18 levels in BALF, as well as NLRP3, Caspase-1, and ASC protein expression levels in lung tissue, increased in the Asthma, Asthma+VitD3, and Asthma+AS group mice(P<0.05). Compared to the Asthma group, the Asthma+VitD3and Asthma+AS group mice showed decreased levels of the mentioned inflammatory factors in BALF and reduced protein expression of NLRP3, FOXO1, Caspase-1, and ASC in lung tissue(P<0.05). Compared to the Asthma+VitD3group, the Asthma+AS group showed increased FOXO1 protein expression(P<0.05), with no statistically significant differences in the other measured indicators. Conclusion VitD3can alleviate asthma symptoms induced by OVA in mice, improve the degree of airway inflammation, and reduce oxidative stress levels. The mechanism may be related to the downregulation of the FOXO1/NLRP3 axis.

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Objective To investigate the expression of genes and proteins in the peripheral blood mononuclear cell(PBMC) cystine/glutamate antiporter system(System Xc-)/glutathione(GSH)/glutathione peroxidase 4(GPX4) ferroptosis pathway and its influence on inflammatory factors in patients with rheumatoid arthritis(RA). Methods 30 patients with RA and 30 healthy participants were enrolled. PBMCs were isolated using Ficoll-hypaque density gradient centrifugation. The cells were categorized into the healthy control, RA, ferroptosis inhibitor, ferroptosis inducer group. The cell viability was checked using the cell counting kit-8(CCK-8) method. Intracellular Fe2+relative fluorescence intensity and reactive oxygen species(ROS) levels were detected using the FerroOrange and Dihydroethidium(DHE) fluorescent probes, respectively. Western blot and real-time quantitative PCR(qPCR) detected the expression of nuclear factor erythroid 2-related factor 2(Nrf2), solute carrier family 7 member 11(SLC7A11), GPX4 proteins and mRNA. And the flow cytometry quantified the levels of tumor necrosis factor α(TNF-α), Interleukin(IL)-1, and IL-6 in the supernatant of each cell group. Results Compared to the healthy control group, the RA group showed a significantly increased Fe2+concentration and elevated ROS levels, reduced expression of Nrf2, SLC7A11 and GPX4 proteins and mRNA, and increased contents of TNF-α, IL-1 and IL-6 in PBMC supernatant, and the differences were statistically significant. The concentration of Fe2+and ROS levels in the inhibitor group were lower than those in the RA group, the proteins expressions of Nrf2, SLC7A11 and GPX4 increased, the mRNA expressions of SLC7A11 and GPX4 increased, the content of IL-6 in the PBMC supernatant decreased but the content of TNF-α increased, and the differences were statistically significant. In contrast, the inducer group, when compared to the RA group, displayed increased ROS levels, reduced expression of SLC7A11 protein and mRNA and decreased expression of Nrf2 protein, and the contents of TNF-α and IL-1 in the PBMC supernatant increased, but the expression of GPX4 protein increased, and the differences were statistically significant. The inducer group, compared to the RA group, showed increased cell viability, and the difference was statistically significant(P<0.000 1). Conclusion The presence of ferroptosis in PBMC in RA patients, inhibiting or inducing PBMC ferroptosis in RA patients, will inhibit or promote the secretion of inflammatory factors. Inhibition of PBMC ferroptosis in RA patients may be helpful in the treatment of RA.

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Objective To investigate the drug resistance and pathogenicity of six clinical isolates ofKlebsiella pneumoniae(Kp), and to provide a basis for prevention and treatment of Kp infection. Methods The six strains from different hospitals were isolated, cultured, and identified by species-specific genekhe. Their whole genome sequences(WGS) were obtained using next-generation sequencing technology(NGS). Based on the WGS, the capsular serotypes, sequence types(ST) and drug-resistance genes of six strains were identified. The capsular serotype genes and virulence genes were validated or identified using PCR. Broth microdilution tests were conducted to validate their drug susceptibility, and mice were challenged with Kp aerosols by MicroSprayer aerosolizer to evaluate their pathogenicity. Results The six strains were all serotype K2 but belonged to four ST types(ST14, ST65, ST700, and ST86), and collectively carried six virulence genes and 23 drug-resistance genes. All the six strains were resistant to ampicillin, but only one strain was multidrug-resistant. Four strains exhibited high mucoid characteristics. Five strains could cause mortality in mice, which were preliminary identified as high virulence strains. Conclusion For the six Kp clinical isolates from different sources, only one strain named NY 13294 is both multidrug-resistant and highly virulent, and other four highly virulent strains are resistant to one or two types of antibiotics.

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Objective To investigate the changes of lipid biomarkers and lipid metabolic pathways related to liver injury in BTBR ob/ob mice with type 2 diabetes mellitus by biochemical and metabolomics methods. Methods 16 BTBR wild-type(WT) mice(WT group) and 14 BTBR ob/ob obese mice(ob/ob group) at 7 weeks of age were selected and fed in SPF environment until 20 weeks of age. Liver injury was compared between the two groups: The activities of mitochondrial respiratory enzyme complex in liver tissue were detected by high-resolution respirators,and the lipid metabolomic analysis of liver tissue samples in the two groups of mice was performed by ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry,mainly detecting endogenous metabolites.Principal component analysis( PCA),orthogonal partial least squares discriminant analysis( OPLS-DA) and other models were used to screen potential biomarkers,and the metabolic pathway analysis of the identified metabolites was performed by Metabo Analyst 5. 0. Results Compared with the WT group,the ob/ob group had significantly increased body weight,fasting blood glucose,serum levels of aspartate aminotransferase( AST),alanine aminotransferase( ALT),low-density lipoprotein( LDL-C) and cholesterol( CHO)( P<0. 01). Liver hematoxylin-eosin staining( HE) staining showed that the mice in ob/ob group had structural disorder of liver lobules,swelling of liver cells,a large number of fat vacuoles in cells,diffuse distribution and loose cytoplasm. Oil red O staining showed that there was a large amount of lipid deposition in the hepatocytes of ob/ob mice. The high resolution spirometer showed that the ob/ob mice had mitochondrial oxidative phosphorylation disorder and the activity of complexⅣ decreased. Lipid metabolomic analysis showed that the lipid metabolic profile of ob/ob mice changed,and the metabolic pathways involved mainly included glycerophospholipid metabolism,glycosylphosphatidylinositol( GPI)anchor biosynthesis,triglyceride metabolism,linoleic acid metabolism,α-linolenic acid metabolism and arachidonic acid metabolism. Conclusion The liver injury of ob/ob group mice may be related to the disorder of lipid metabolism,in which the disorder of glycerophospholipid metabolism is the most critical metabolic pathway.

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Objective To investigate the effect of miR-141-3p on LPS induced A549 cell injury by targeting high mobility group protein 1(HMGB1). Methods A549 cells derived from type Ⅱ alveolar epithelial cells were taken as the study object, miR-141-3p mimics, mimics NC,HMGB1gene overexpression plasmid(pcDNA3.1-HMGB1) and empty Vector were transfected into A549 cells respectively or co-transfected, then 10 μg/ml LPS was used for 24 h. Cell proliferation activity was detected by cell counting kit-8(CCK-8). The activity of lactate dehydrogenase(LDH) in the supernatant of cell culture was detected by colorimetry. The apoptosis level of each group was detected by flow cytometry. The levels of interleukin(IL)-1β, IL-6 and tumor necrosis factor α(TNF-α) were detected by enzyme-linked immunosorbent assay(Elisa). Dual luciferase reporter gene assay verified the targeted regulatory relationship between miR-141-3p andHMGB1. Results After treatment with LPS, the proliferative activity of A549 cells and the expression level of miR-141-3p decreased(P<0.05), the apoptosis rate increased(P<0.05), the levels of IL-1β, IL-6, TNF-α and the activity of LDH in supernatant increased(P<0.05). Overexpression of miR-141-3p increased the proliferation activity of A549 cells treated with LPS(P<0.05), and decreased the apoptosis rate and the levels of IL-1β, IL-6, TNF-α in cells and LDH activity in supernatant(P<0.05). However, overexpression ofHMGB1gene could reverse the ameliorative effect of miR-141-3p on LPS-induced A549 cell injury. Dual luciferase reporter gene experiment confirmed thatHMGB1was the downstream target gene of miR-141-3p. Conclusion miR-141-3p can inhibit LPS-induced apoptosis, reduce the expression level of inflammatory factors, and improve the damage of A549 cells, which may be related to the targeted regulation ofHMGB1expression.

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Objective To investigate the possible mechanism of metformin(Met)-induced cardiomyocyte autophagy in protecting myocardial injury in septic mice. Methods The model of myocardial injury in septic mice was established by cecal ligation and puncture(CLP). Sixty Kunming mice were randomly divided into sham operation group(Sham group), model group(CLP group), model+dimethyl sulfoxide(DMSO) group(CLP+DMSO group), model+metformin(Met) group(Met group), model+Met+3-methyladenine(3-MA) group(Met+3-MA group), model+Met+compound C(CC) group(Met+CC group), with 10 mice in each group. The Met, Met+3-MA and Met+CC groups were intraperitoneally injected with Met(200 mg/kg) once a day for 2 weeks before modeling. The Met+3-MA group was intraperitoneally injected with 3-MA(10 mg/kg) 1 h before surgery. The Met+CC group was intraperitoneally injected with CC(20 mg/kg) 30 min before surgery. The model was established 24 h after the last injection of Met. The heart and blood of all mice were collected 24 h after surgery. The Western blot technique was employed to assess the relative expression levels of microtubule-associated protein 1 light chain 3(LC3) isoforms, namely LC3 I and LC3 II, autophagy effector protein 1(Beclin-1), ubiquitin-binding protein 62(p62), B-cell lymphoma/leukemia-2(Bcl-2), Bcl-2-associated X protein(Bax), adenosine monophosphate(AMP) kinase(AMPK) and phosphorylated AMPK(p-AMPK). Myocardial pathological changes were observed by hematoxylin-eosin(HE) staining. The changes of myocardial mitochondria and autophagosomes were observed by electron microscopy. Hematoxylin-eosin(HE) staining was used to observe the pathological changes of myocardium. Electron microscopy was used to observe the changes of myocardial mitochondria and autophagosomes. Results Compared with Sham group, the relative protein expression of Beclin-1, p62, p-AMPK/AMPK and LC3 II/LC3 I in CLP and CLP+DMSO groups had no statistical significance, but Bax increased and Bcl-2 decreased in CLP group(P<0.01). Compared with CLP group, the relative expression of Beclin-1 protein and LC3 II/LC3 I in Met group increased and p62 decreased(P<0.01), Bax decreased and Bcl-2 increased(P<0.01). Compared with Met group, the relative protein expression of Beclin-1 and LC3 II/LC3 I in Met+3-MA group decreased and p62 increased(P<0.05), Bax increased and Bcl-2 decreased(P<0.05). Besides, the relative protein expression of p-AMPK/AMPK in Met+CC group decreased(P<0.05). HE staining showed that there was no disorder in myocardial fibers in Sham group, and a large number of inflammatory cells infiltrated the myocardial fibers of CLP group in a clear disorder. The Met group showed vacuolar changes in the myocardium, while the Met+3-MA group showed disordered arrangement of myocardial fibers and a small amount of inflammatory cell infiltration. Under electron microscopy, the morphology of myocardial mitochondria in the Sham group was normal, while in the CLP group, the arrangement of mitochondrial cristae was disordered with vacuolar changes, and occasional autophagosomes were observed. Mitochondria in Met group showed slight swelling and a large number of autophagosomes. The mitochondria in the Met+3-MA group showed significant swelling with a small amount of autophagosomes. Conclusion The protective effect of metformin on myocardial injury in septic mice can reduce cardiomyocyte apoptosis and improve mitochondrial damage by activating AMPK signaling pathway to induce autophagy.

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Objective To explore the effect ofMPZL1knockdown in A549 Taxol resistant(A549/Tax) cells and whether it affect drug resistance and tumor cell stemness by regulating β-catenin. Methods A549 and A549/Tax cells were treated with different concentrations of doxorubicin and paclitaxel to observe the differences in drug resistance between the two cells. Quantitative real-time PCR(qRT-PCR) and Western blot were used to detect the MPZL1 expression level in A549 and A549/Tax cells. After knockdown or overexpression ofMPZL1in A549/Tax cells, cells were divided into control group, small hairpin RNA negative control(sh-NC) group,MPZL1knockdown(sh-MPZL1) group, overexpression negative control(OE-NC) group,MPZL1overexpression(OE-MPZL1) group. Cell counting kit-8(CCK-8) and clone formation assay were utilized to investigate cell proliferation and clone formation ablity. Western blot assay was used to detect the protein expression after the cells treated with Wnt/β-catenin signaling inhibitor XAV939 and activator CHIR-99201. Results The half inhibitory concentration(IC50) of doxorubicin and paclitaxel in A549/Tax cells significantly increased compared to A549 cells(P<0.01). MPZL1 presented a higher expression trend in A549/Tax cells. The IC50values of A549/Tax for doxorubicin and paclitaxel were 2.731 mg/ml and 4.939 μg/ml afterMPZL1knockdown, compared to 4.541 mg/ml and 13.55 μg/ml in the NC group(P<0.01). The results of CCK-8 and clone formation assay showed that the knockdown ofMPZL1reduced the viability of cells proliferation and clonal formation ability(P<0.05). Western blot results indicated that the expression levels of MPZL1 protein, tumor cell stemness associated proteins(CD44, CD133), β-catenin and multidrug resistance protein 1(MDR1), lung resistance-related protein(LRP) were significantly reduced in the sh-MPZL1 group. Furthermore, XAV939 could inhibit the expression levels of MPZL1, CD44, CD133, MDR1, LRP and β-catenin(P<0.01). The inhibitory effect of knockdownMPZL1on the aforementioned proteins was significantly reversed by CHIR-99201 treatment. Conclusion MPZL1 is highly expressed in A549/Tax cells. KnockdownMPZL1suppresses the tumor cell stemness and proliferation, thereby reversing the drug resistance of doxorubicin and paclitaxel in A549/Tax cells.

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Objective To explore the effect of esketamine on anxiety-depressive-like behavior in mice and its relationship with inflammation. Methods SPF grade healthy adult male C57BL/6J mice, weighing 20-24 g, were used in the exprement. The random number table method was used to divide into 5 groups(n=8): control group(Con group), esketamine group(ESK group), model group(LPS group), model+esketamine prevention group(LPS+ESK1 group) and model + esketamine treatment group(LPS+ESK2 group). An inflammation-induced anxiety-depression model was prepared by intraperitoneal injection of LPS 0.83 mg/kg. The ESK group was injected with esketamine 10 mg/kg; LPS group was injected with LPS 0.83 mg/kg; LPS+ESK1 group was injected with LPS 0.83 mg/kg before 24 hours intraperitoneal injection of esketamine 10 mg/kg; and the LPS+ESK2 group was injected with LPS 0.83 mg/kg and 30 minutes later with esketamine 10 mg/kg. 24 h after intraperitoneal injection of LPS, the anxiety-depression-like behaviors of mice were measured using behavioral experiments. At the end of behavioral experiments, the spleen was taken immediately; hippocampal tissues were taken and enzyme-linked immunosorbent assay(ELISA) was used to detect the contents of interleukin-1β(IL-1β), tumor necrosis factor alpha(TNF-α) and interleukin 6(IL-6) and neuronal pathological changes in hippocampal tissues were observed by HE staining. Results Compared with the Con group, mice in the LPS group showed increased anxiety and depression-like behavior(P<0.05), increased spleen weight/body weight(P<0.05), increased hippocampal tissue concentrations of IL-1β, TNF-α and IL-6(P<0.05), and increased neuronal degeneration necrosis, there was no statistically significant difference in these indicators in the ESK group compared with the Con group. Compared with the LPS group, mice in the LPS+ESK1 and LPS+ESK2 groups showed reduced anxiety-depression-like behavior(P<0.05), decreased splenic weight/body weight(P<0.05), hippocampal tissue IL-1β, TNF-α, IL-6 concentrations were reduced(P<0.05), and neuronal degeneration necrosis was reduced. Compared with the LPS+ESK1 group, the LPS+ESK2 group showed an increase in the distance travelled in the central area of the open field experiment and the distance into the open arm of the elevated cross maze experiment(P<0.05), a decrease in IL-6 and TNF-α concentrations(P<0.05), and a reduction in the degree of neuronal damage. Conclusion Esketamine ameliorates LPS-induced anxiety-depression-like behavior and neuronal damage in mice by a mechanism that may be related to reduced inflammation.

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Objective To study the effect and mechanism of action of Silibinin on the differentiation of 3T3-F442A preadipocytes in murine. Methods The effects of 0-400 μmol/L Silibinin on the proliferation of 3T3-F442A adipocytes at 24, 48 and 72 h were detected by 3-(4,5-dimethylthiazol-2)-2,5-diphenyltetrazolium bromide(MTT) assay, and the effects of Silibinin on the adipogenesis of 3T3-F442A adipocytes were visualized by Oil Red O staining; RT-qPCR, Western blot and ELISA assays were used to detect the effects of Silibinin on 3T3-F442A adipocyte differentiation-associated transcription factor CCAAT/enhancer binding protein(C/EBP) α, C/EBP β, peroxisome proliferator-activated receptor γ(PPARγ), adipocyte protein 2(aP2), adipose generation-associated vascular endothelial growth factor( VEGF)-α and VEGF receptor 2( VEGFR-2),matrix metalloproteinase( MMP)-2and MMP-9,mitogen-activated protein kinase( MEK) and phosphorylated MEK( p-MEK),and extracellular regulated protein kinase( ERK) and phosphorylated ERK( p-ERK) expression. Results MTT assay showed that the cell proliferation rate of 3T3-F442A preadipocytes decreased after 100,200,and 400 μmol/L Silibinin treatment compared with the control group( P<0. 001); Oil Red O staining assay showed that the accumulation of red lipid droplets of the cells in the 160 μmol/L Silibinin assay group significantly decreased; RT-q PCR assay showed that mRNA expression of C/EBPα,C/EBPβ,PPARγ,a P2,VEGF-α,VEGFR-2,MMP-2,and MMP-9 was down-regulated in 3T3-F442A adipocytes treated with 160 μmol/L Silibinin compared with the control group( P<0. 001);Western blot assay showed that protein expression of C/EBPα,C/EBPβ,PPARγ and a P2 was down-regulated in 3T3-F442A adipocytes treated with 160 μmol/L Silibinin( P<0. 001),and the phosphorylation level of p-MEK/MEK and p-ERK/ERK proteins was down-regulated compared with the control group(P<0. 001); ELISA assay showed that the protein concentrations of MMP-2 and MMP-9 in the cell supernatant were down-regulated( P<0. 001) in 3T3-F442A adipocytes treated with 160 μmol/L Silibinin. Conclusion Silibinin inhibited 3T3-F442A adipocyte differentiation and adipogenesis through inhibition of the MEK/ERK pathway and matrix metalloproteinase activity.

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Objective To explore the mechanism of hippocampal corticotropin-releasing hormone(CRH) receptor type 1(CRHR1) in chronic stress-induced learning and memory impairment in early aged mice. Methods C57BL/6J mice aged 12-14 months were divided into two groups according to gender, and then divided into wild type(WT) group and hippocampal CRHR1 conditional gene knockout(KN) group according to genotype. Mice in each group were randomly divided into control group and stress group, and the stress group was subjected to chronic unpredictable stress(CUS) for 30 days. Genotyping of mice was performed using polymerase chain reaction(PCR), agarose gel electrophoresis and real-time fluorescence quantitative PCR(RT-qPCR). The new object recognition experiment and Morris Water maze measured learning and memory ability. Golgi-Cox staining was used to observe damage to hippocampal neuronal dendrites. The protein expressions of target protein of rapamycin(mTOR), p-mTOR(Ser2448), ribosomal protein S6 kinase(p70S6K) and p-p70S6K(Thr389/Thr412) were detected by Western blot. Serum levels of corticotropin releasing hormone(CRH) were measured by ELISA. Results Compared to mice without chronic stress, the cognitive coefficient of WT stress groups decreased after chronic stress, and the difference was statistically significant(P<0.05), while there was no significant difference in cognitive coefficient of KN stress groups before and after chronic stress. Compared with the WT stress group, the escape latency of the WT control group was shortened(P<0.05), and the number of crossing the platform and target quadrant increased(P<0.01), and there was no significant difference in the KN groups above. Compared with the WT control group, the WT stress group had a significant reduction in the neuronal complexity in the hippocampal CA1, CA3 and DG regions(P<0.05) and significant reductions in the expression of p-mTOR and p-p70S6K in the hippocampus(P<0.05). There was no significant difference in the expression of p-mTOR between the KN stress group and the KN control group(P>0.05), except that the expression of p-mTOR in the hippocampus of the female group decreased(P<0.05). In addition, the serum level of CRH in the stress group was higher than that in the control group(P<0.01). Conclusion Hippocampal CRHR1 regulates learning and memory impairment and neuronal dendrite damage in early aged mice induced by chronic stress. The mechanism may be that high levels of CRH induced by chronic stress cannot bind to CRHR1 receptor, thereby enhancing the expression of down-regulated mTOR/p70S6K signaling pathway.

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Objective To explore the role of long non-coding RNA XR＿378418(LncRNA XR＿378418) in the biological behavior of hepatic stellate cells line JS-1 and to probe the potential molecular mechanism of LncRNA XR＿378418 involved in liver fibrosis based on transcriptome sequencing. Methods In this study, the recombinant plasmid of pcDNA-LncRNA XR＿378418 and control plasmid pcDNA-NC were constructed and transfected into JS-1 cells respectively. Then, the expression level of LncRNA XR＿378418 was analyzed by quantitative real-time PCR(RT-qPCR). The effect of overexpression of LncRNA XR＿378418 on proliferation and migration of JS-1 cells were detected by cell counting kit-8 assay(CCK-8) and scratch assay, respectively. Finally, by high-throughput sequencing analysis, the effect of XR＿378418 on the transcriptomics of JS-1 cells was analyzed. Results RT-qPCR results showed that the expression level of LncRNA XR＿378418 in the overexpression group was significantly higher than that in the control group(P<0.05). The results of CCK-8 and scratch experiment suggested that the proliferation and migration in the pcDNA-LncRNA XR＿378418 group significantly increased. Furthermore, the high-throughput sequencing analysis showed that a total of 248 genes were screened by gene differential analysis, of which 127 were up-regulated, and 117 were down-regulated. Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses revealed that LncRNA XR＿378418 could regulate cell adhesion, autophagy and Ca2+signaling, etc. Conclusion LncRNA XR＿378418 promotes the proliferation and migration of JS-1 cells and affects the expression of genes related to cell adhesion and calcium signaling in JS-1 cells.

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Objective To explore the effect of PAT family proteins homolog 1(PATL1) on the proliferation and migration of gastric cancer cells and its potential mechanism. Methods The expression levels ofPATL1in pancarcinoma, gastric cancer and normal tissues were analyzed by TCGA database. The expression level ofPATL1in 40 human gastric cancer tissues and paired adjacent tissues was evaluated by quantitative real-time PCR(RT-qPCR). The Kaplan-Meier Plotter database was used to analyze the prognosis of PATL1 in gastric cancer patients. The gastric cancer cell line AGS was transfected with PATL1 interference vector, and the interference effect was evaluated by RT-qPCR. The effects ofPATL1on the proliferation and migration of AGS were detected by cell counting kit-8(CCK-8), Transwell test and scratch healing test. The effects of interference withPATL1on the expression of cellular-myelocytomatosis viral oncogene(c-Myc) and autophagy related 7(ATG7) proteins in gastric cancer cells were detected by Western blot assay. Results RT-qPCR showed that the expression ofPATL1in human gastric cancer tissue was higher than that in normal gastric tissue(P<0.001), andPATL1was correlated with the prognosis of patients with enteric gastric cancer(P<0.000 1). AfterPATL1was knocked down, the number of proliferating and migrating gastric cancer cells decreased(P<0.05). Western blot test results showed that the expression level of ATG7 protein decreased afterPATL1was knocked down(P<0.05). Conclusion PATL1 may inhibit the proliferation and migration of gastric cancer cells through crosstalk with c-Myc and ATG7.

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Objective To investigate the correlation between the expression level ofYTHDF1in oral squamous cell carcinoma(OSCC) and clinicopathologic features and its potential prognostic value. Methods The expression ofYTHDF1in 132 OSCC tissues and 66 paracancerous tissues was detected by immunohistochemistry(IHC), and the expression ofYTHDF1protein in OSCC cell lines was detected by Western blot. The correlation betweenYTHDF1and clinicopathological features was analyzed by chi-square test. Kaplan-Meier and Cox factors were used to analyze the factors affecting the survival time of the patients and draw the survival curves of theYTHDF1gene to evaluate its potential clinical significance. Results The expression ofYTHDF1in OSCC tissues was higher than that in paracancerous tissues(P<0.001), and the expression of YTHDF1 protein increased in OSCC cell lines compared with normal oral epithelial keratinocytes(P<0.001). The expression ofYTHDF1was correlated with the TNM stage and T stage of patients with OSCC(P<0.05), and the patients with high expression ofYTHDF1had a shorter survival time compared with those with low expression(P<0.001). Conclusion High expression ofYTHDF1may be associated with poor patient prognosis andYTHDF1may be able to serve as a target for OSCC treatment.

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Objective To analyze the difference of urinary iodine level in Hashimoto thyroiditis(HT) patients, and to explore the possible relationship between urinary iodine level and HT under different iodine nutritional status, so as to provide some references for reasonable iodine intake in HT patients. Methods A total of 101 hospitalized HT patients were selected as HT group and divided into 3 groups according to thyroid function: HT group with hyperthyroidism(41 cases). There were 25 cases in HT group with normal thyroid function. There were 35 cases in HT combined with hypothyroidism group. In addition, 30 healthy subjects were selected as control group. Serum levels of thyroid stimulating hormone(TSH), triiodothyronine(T3), thyroxine(T4), thyroid peroxidase antibody(TPOAb) and thyroglobulin antibody(ATG) were detected by chemiluminescence assay. The size and morphological structure of thyroid organs were examined by ultrasonography. Urinary iodine was determined by catalytic spectrophotometry with arsenic and cerium. The nutritional status of iodine was classified into iodine deficiency(<100 μg/L), iodine adequacy(100-199 μg/L), iodine adequacy(200-299 μg/L) and iodine excess(≥300 μg/L). Non-parametric test was used to compare urinary iodine level between HT group and control group, one-way ANOVA and t test were used to compare urinary iodine level between HT group and control group, and Spearman correlation analysis was used to compare the correlation between urinary iodine level and T3, T4, TSH, ATG and TPOAb under different iodine nutrition status. Results Compared with control group, ATG and TPOAb levels in HT group increased(P<0.001), and urinary iodine levels increased(P<0.05), with statistical significance. Compared with the control group in different thyroid function states, only the HT group with hypothyroidism increased the urinary iodine level(P<0.01), and the difference was statistically significant. Spearman correlation analysis showed that urine iodine level was positively correlated with ATG and TPOAb levels in iodine excess condition(P<0.05), and urine iodine level was positively correlated with TSH level in iodine sufficient condition and iodine excess condition in HT patients(P<0.05). Conclusion The urinary iodine level of HT patients was higher than that of normal people. When the urinary iodine level of residents is ≥300 μg/L, iodine intake is prone to HT. When the urinary iodine level of HT patients is ≥200 μg/L, iodine consumption is prone to hypothyroidism, and iodine intake should be limited.

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Objective To detect the risk factors for bleeding in patients with cirrhosis and esophageal and gastric varices(EGV) and better understand the potentially life-threatening complications. Methods Retrospectively, and a total of 309 patients with cirrhosis and EGV were enrolled in this study and were divided into the observation group and control based on EGV bleeding or not. Meanwhile, the patients' epidemiological, clinical, laboratory, and radiological characteristics were collected and analyzed to construct a prediction model. The bootstrap method could be used to validate predictive models and the ROC curves to evaluate its forecasting ability. Results High-density lipoprotein(HDL)(P<0.001,OR=0.131, 95%CI=0.049-0.350), C-reactive protein(CRP)(P=0.010,OR=2.657, 95%CI=1.269-5.563), the width of portal vein(PVW)(P=0.050,OR=1.156, 95%CI=1.000-1.336), the thickness of spleen(P=0.035,OR=1.492, 95%CI=1.028-2.165), Child-Pugh grade B(P=0.003,OR=11.320, 95%CI=2.232-57.407) and Child-Pugh grade C(P=0.002,OR=3.888, 95%CI=1.659-9.114) were significantly associated with the occurrence of EGV bleeding. The AUC of the predictive risk model in the modeling group was 0.802, and the validation group was 0.836. Conclusion The lower HDL and higher CRP, PVW, the thickness of the spleen, Child-Pugh grade B and C are the risk factors for the occurrence of EGV bleeding.

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Objective To evaluate the prognostic value of a radiomics model based on the peritumoral region of glioma. Methods 138 patients with glioma were retrospectively analyzed, medical imaging interaction toolkit(MITK) software was used to obtain the magnetic resonance imaging(MRI) images of peritumoral area 5 mm, 10 mm and 20 mm from the tumor edge and extract texture features. The texture features were screened the radiomics model was established and the radiomic score was calculated. A clinical prediction model and a combined prediction model along with Rad-score and clinical risk factors were established. The combined prediction model was displayed as a nomogram,and the predictive performance of the model for survival in glioma patients was evaluated.Results In the validation set,the C-index value of the radiomics model based on the peritumoral region 10 mm away from the tumor edge based on T2 weighted image( T2WI) images was 0. 663( 95% CI = 0. 72-0. 78),resulting in the best prediction performance. On the training set and validation set,the C-index of the nomogram was0. 770 and 0. 730,respectively,indicating that the prediction performance of nomogram was better than those of the radiomics model and clinical prediction model. The model had the highest prediction effect on the 3-year survival rate of glioma patients( training set area under curve( AUC) = 0. 93,95% CI = 0. 83-0. 98; validation set AUC= 0. 88,95% CI = 0. 76-0. 99). The calibration curve showed that the joint prediction nomogram in both the training set and the validation set had good performance. Conclusion The combined prediction model based on the preoperative T2WI images in the peritumoral region 10 mm from the tumor edge and the clinicopathological risk factors can accurately predict the prognosis of glioma,providing the best effect of prediction on the 3-year survival rate of glioma.

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Objective To employ the EQ-5D-5L questionnaire to evaluate HRQOL in patients on peritoneal dialysis(PD) and investigate the related risk factors to provide suggestions for improving quality of life. Methods PD patients who were followed up regularly in the department of nephrology were recruited in this study. Demographic characteristics and laboratory data were collected. Exercise capacity was assessed by the 6-MWT. PHQ-9 was conducted to screen depression status. The EQ-5D-5L questionnaire was used to evaluate HRQOL. Multivariate linear regression analysis was used to examine the potential influencing factors of EQ-5D-5L health utility value. Results Among recruited 90 PD patients, the mean age was(49.44±11.41) years and range from 18 to 70. The highest health utility value of EQ-5D-5L was 1 point, while the lowest was-0.01 points. The mean EQ-5D-5L score was(0.92±0.15). The multivariate linear regression analyses showed that increased bilirubin level(β=-0.009,P=0.018), increased CRP level(β=-0.005,P<0.001), and increased PHQ-9 score(β=-0.008,P=0.014) were negatively correlated with the EQ-5D-5L health utility value. Increased 6-MWD(β=0.005,P=0.018) was positively correlated with the EQ-5D-5L health utility value. Conclusion The bilirubin and CRP levels, depression status, and exercise capacity are considered the main factors influencing HRQOL in PD patients.