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Objective @#To investigate the economic burden of cervical cancer and precancerous lesions, so as to provide the evidence for improving the management of cervical cancer and formulating the policies for reducing the economic burden of cervical cancer and precancerous lesions. @*Methods@#The hospitalized patients with cervical cancer and precancerous lesions were recruited from four hospitals in Xinjiang Uygur Autonomous Region from September 2020 to June 2021. The direct medical expenditures, direct non-medical expenditures, duration of absence from work in patients and their family members as carers were collected using a questionnaire designed by the Cancer Hospital of the Chinese Academy of Medical Sciences, and the economic burdens of cervical cancer and precancerous lesions were estimated. The factors affecting the economic burden of cervical cancer were identified using a multivariable linear regression model.@*Results@#Totally 265 patients with cervical cancer and precancerous lesions were included, with an average age of ( 49.80±10.07 ) years. There were 170 patients with cervical cancer, including 64 cases with stage I, 79 cases with stage II, and 27 cases with stages III/Ⅳ, and 95 patients with precancerous lesions, including 33 cases with low-grade squamous intraepithelial lesion ( LSIL ) and 62 cases with high-grade squamous intraepithelial lesion ( HSIL ). The median economic burdens (interquartile range) were 11 481 ( 4 523 ), 17 850 ( 9 096 ), 112 883 ( 59 623 ), 150 875 ( 105 206 ) and 197 842 ( 61 844 ) Yuan per patient among cases with LSIL, HSIL, and stage I, II and III/Ⅳ cervical cancer, respectively, among which the direct medical expenditures accounted for 85.89% to 93.86%. The median economic burdens (interquartile range) were 708 ( 1 711 ), 11 678 (6 590), 2 557 ( 19 472 ), and 14 943 ( 27 773 ) Yuan per patient with precancerous lesions, and were 910 (1 530), 105 770 ( 91 019 ), 39 765 ( 30 490 ), and 146 445 ( 123 039 ) Yuan per patient with cervical cancer during the diagnostic phase, the clinical treatment phase, the follow-up phase, and in total, respectively. Multivariable linear regression analysis results showed that pathological stage ( β'=0.202, P=0.003 ) and duration of hospital stay ( β'=0.695, P<0.001 ) correlated with the economic burden among patients with cervical cancer. @*Conclusion@#There is a high economic burden among patients with cervical cancer and precancerous lesions. Advanced pathological stage and long duration of hospital stay may increase the economic burden among cervical cancer patients.
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Objective @#To identify biomarkers for esophageal squamous cell carcinoma (ESCC) using bioinformatics tools, so as to provide insights into diagnosis and targeted therapy of ESCC. @*Methods@#The gene expression datasets GSE23400, GSE45670, GSE20347 and GSE17351 were screened and downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) of ESCC were screened using the online tool GEO2R, and the common DEGs among the four datasets were determined using Venn diagram. Gene Ontology (GO) annotations and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed using the DAVID database, and protein-protein interaction (PPI) analysis was performed using the STRING database. The key modules were identified using molecular complex detection (MCODE) plugin in the Cytoscape software, and hub genes with the highest connectivity degree were identified using the CytoHubba plugin, and the gene expression was validated on the UALCAN platform. Survival analysis of hub genes was performed using the Kaplan-Meier plotter database.@*Results@#Totally 146 common DEGs were screened, including 102 up-regulated genes and 44 down-regulated genes. GO annotation analysis showed that the common DEGs were mainly enriched in biological processes of cell cycle, sister chromatid separation in the late mitotic phase and cell cycle regulation, enriched in cellular components of spindle and centrosome, and molecular functions of enzyme binding and ATP binding. KEGG pathway analysis showed that DEGs was significantly enriched in cell cycle, extracellular matrix (ECM)-receptor interactions and oocyte meiosis. A total of 10 hub genes were screened, and gene expression validation and survival analysis identified 7 genes associated with prognosis of ESCC, including CCNB1, CDK1, BUB1B, ZWINT, AURKA, MAD2L1 and MCM4, which were all highly expressed in ESCC specimens. @*Conclusion@#Seven hub genes of ESCC are identified based on bioinformatics, which may serve as biomarkers and therapeutic targets for ESCC.
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Objective To construct a shRNA lentiviral vector targeting the gene encoding tumor necrosis factor alpha-induced protein 8 (TNFAIP8) in RAW264. 7 cells, a mouse macrophage cell line, and to investigate the effects of TNFAIP8 gene silencing on the functions of mouse macrophages. Methods The shRNA sequence targeting TNFAIP8 gene was designed and DNA oligos containing small hairpin frame was synthesized. The double-stranded DNA was cloned into pLKO. 1-TRC vector after annealing. The recombi-nant vector was verified by using double enzyme digestion and gene sequencing. Lentiviruses were prepared by transfecting the constructed vector into 293T cells. Fluorescent quantitative RT-PCR and Western blot as-say were performed to detect the expression of TNFAIP8 at mRNA and protein levels after infecting the RAW264. 7 cells with lentiviruses. Flat dish adhesion experiment and wound-healing assay were used to evaluate the effects of TNFAIP8 gene silencing on the adhesion and migration of RAW264. 7 cells. Results The recombinant lentiviral vector was successfully constructed as indicated by double enzyme di-gestion and gene sequencing analysis. The expression of TNFAIP8 in RAW264. 7 cells at both mRNA and protein levels were significantly down-regulated after lentivirus infection (P<0. 05). Moreover, TNFAIP8 gene silencing significantly impaired the cell adhesion ability of RAW264. 7 cells after 15 min, 30 min or 2 hours of culture. Compared with the cells in control group, the RAW264. 7 cells harboring silenced TN-FAIP8 gene looked round with a smaller number of cellular extensions. The wound-healing assay showed that less TNFAIP8 gene-silenced RAW264. 7 cells migrated into the wounded area as compared with the cells in control group after 24 hours of culture (P<0. 05). The wound-healing rates of the experimental and control groups were 25% and 50%, respectively. Conclusion The recombinant lentiviral vector containing shRNA targeting the TNFAIP8 gene was successfully constructed. Transfecting the RAW264. 7 cells with the con-structed vector significantly silenced the expression of TNFAIP8 gene and inhibited the adhesion and migra-tion of these cells.
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Objective:In order to get recombinant protein OCILRP 2-Fc and anti-OCILRP2 antibody for further study of OCILRP2.Methods:Eukaryotic expression vector pIg-CD5-OCILRP2 which fused with extracellular domain of OCILRP 2 and human IgG1 Fc fragment was constructed.G418 was used for stable expression cell strain after pIg-CD5-OCILRP2 transfected into CHO cells.Recombinant protein OCILRP 2-Fc purified from CHO cell supernatant was used to immunize rabbit and anti-OCILRP2 polyclonal antibody was purified from rabbit serum by using protein G column.Results: ELISA data showed that we got a high-titer anti-serum and anti-OCILRP2 antibody purified from the rabbit serum.Western blot indicated this antibody could specifically bind to OCILRP 2-Fc and OCILRP2 in NIH/3T3 lysate.OCILRP2 expression in murine bone marrow derived dendritic cells ( DC) was detected by this polyclonal antibody ,too.Compared to immature DC ,OCILRP2 expression was elevated in LPS induced-mature DC.Conclusion: This study has offered an available tool and provided a clue for further study of the roles of OCILRP 2 in immune response.
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Objective To explore the effect of TNF related apoptosis inducing ligand (TRAIL) in apoptosis induced by LPS. Methods After LPS injected mice blocking TRAIL with soluble death receptor 5 (sDRS), detecting ALT, AST and LDH of mice serum at different times, apoptotic effects of LPS to mice hepatocyte were detected by HE and flow eytometry (FCM) with Annexin V-FITC/PI staining. The expres-sion of DR5 in mice hepatocyte was assayed with immunohistochemistry and FCM. Results Apoptotic effect was promoted by up-regulated DR5 expression on hepatocyte. Blocking TRAIL with sDR5 markedly amelio-rated the hepatocyte damage and reduced apoptosis. Conclusion These results establish a critical role for TRAIL in apoptosis during disease process of LPS.
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0.1 ?mol?L-1), inducing differentiation through enhancement of melanogenesis and increase of the activity of tyrosinase at lower doses(
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<p><b>OBJECTIVE</b>To study whether previously intravenous injection of anisodamine can prevent endotoxemia of heat stroke of rats.</p><p><b>METHODS</b>Experimental animals were randomly divided into two groups, their average artery pressure, heart rate, survival time, survival rate and rectal temperature were measured at an environmental temperature of 38 degrees C-40 degrees C and 50%-60% retative humidity. Blood samples for endotoxins analyses were taken both before and after heat-stress.</p><p><b>RESULTS</b>During heat stress, the animals of rectal temperature of the experimental and control groups continuously increased and two hours later, separately to (42.7 +/- 0.6) degree C and (43.1 +/- 0.5) degree C, without statistic difference(P > 0.05), and to (44.6 +/- 0.4) degree C and (44.2 +/- 0.3) degree C prior to death, with statistic difference(P < 0.05). Before the experiment, the contents of endotoxins of portal vein blood were (45.7 +/- 5.2) pg/ml and (42.6 +/- 5.4) pg/ml, and that of systemic blood was (14.8 +/- 4.5) pg/ml and (13.9 +/- 7.2) pg/ml, without statistic difference(P > 0.05). Two hours later, the contents of portal vein blood separately increased to (122.2 +/- 16.7) pg/ml and (49.7 +/- 10.2) pg/ml, obviously higher than that before heat-stress(P < 0.01). And there were clear statistic difference between the two groups(P < 0.01). The changing tendency of the heart rhythm is almost the same in two groups, that is, first rose and then fell. But it is without statistic difference before and two hours later(P > 0.05): before heat-stress, the average artery pressures were (13.3 +/- 0.6) kPa and (13.6 +/- 0.5) kPa, without statistic difference(P > 0.05), and two hours later, were (9.6 +/- 0.5) kPa and (8.6 +/- 0.6) kPa, with obvious statistic difference(P < 0.01). The survival time of the animals were (166.5 +/- 16.9) min and (144.5 +/- 18.2) min with obvious statistic difference(P < 0.01), the survival rate of heat stressed rats in the experimental group were obviously higher than control group(P < 0.01 or P < 0.05).</p><p><b>CONCLUSIONS</b>Anisodamine can prevent endotoxemia in rats suffering heat stroke.</p>
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Animals , Rats , Blood Pressure , Body Temperature , Endotoxemia , Endotoxins , Blood , Heat Stress Disorders , Drug Therapy , Mortality , Hot Temperature , Solanaceous Alkaloids , Therapeutic Uses , Survival RateABSTRACT
Objective:To determine the sensitivity of SMMC-7721 cells to mDRA-6,the synergistic damage effect of mDRA-6 and adriamycin on human hepatocellular carcimoma cell lines and its possible mechanism.Methods:SMMC-7721 cells were cultured with RPMI1640 medium in regular condition.The morphology was observed by microscope.Cytotoxicity was examined by MTT assay. Apoptosis were detected by flow cytometry.Results:(1)The apoptosis of SMMC-7721 cells could be induced by mDRA-6,1.89 ?g/ml of mDRA-6 cound kill 36% of the cells;(2)Concentration-dependent cytotoxicity of adriamycin was exhibited in SMMC-7721 cells;(3)The combination of mDRA-6 and adriamycin exhibited synergistic effect on SMMC-7721 cells.2 ?g/ml of mDRA6 and 40 ng/ml of adriamycin killed 60%SMMC-7721.Conclusion:MDRA-6 can induce SMMC-7721 cell apoptosis.The combination of mDRA-6 and adriamycin exhibit synergistic effect on SMMC-7721 cells.