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OBJECTIVE@#To explore the therapeutic mechanism of Liushen Wan (LSW) against colitis-associated colorectal cancer (CAC) by network pharmacology.@*METHODS@#TCMSP, BATMAN-TCM, CNKI, PubMed, Genecards, OMIM, and TTD databases were used to obtain the related targets of LSW and CAC. The common targets of LSW and CAC were obtained using Venny online website. The PPI network was constructed using Cytoscape 3.8.2 to screen the core targets of LSW in the treatment of CAC. GO and KEGG enrichment analysis were conducted using DAVID database. The therapeutic effect of LSW on CAC was evaluated in a C57BL/6J mouse model of AOM/DSS-induced CAC by observing the changes in body weight, disease activity index, colon length, and size and number of the tumor. HE staining and RT-qPCR were used to analyze the effect of LSW on inflammatory mediators. Immunohistochemistry and TUNEL staining were used to evaluate the effect of LSW on the proliferation and apoptosis of AOM/DSS-treated colon tumor cells. Immunohistochemistry and Western blotting were used to detect the effects of LSW on the expression of TLR4 proteins in CAC mice.@*RESULTS@#Network pharmacology analysis identified 69 common targets of LSW and CAC, and 33 hub targets were screened in the PPI network. KEGG pathway enrichment analysis suggested that the effect of LSW on CAC was mediated by the Toll-like receptor signaling pathway. In the mouse model of AOM/DSS-induced CAC, LSW significantly inhibited colitis-associated tumorigenesis, reduced tumor number and tumor load (P < 0.05), obviously improved histopathological changes in the colon, downregulated the mRNA levels of proinflammatory cytokines, and inhibited the proliferation (P < 0.01) and promoted apoptosis of colon tumor cells (P < 0.001). LSW also significantly decreased TLR4 protein expression in the colon tissue (P < 0.05).@*CONCLUSION@#LSW can inhibit CAC in mice possibly by regulating the expression of TLR4 to reduce intestinal inflammation, inhibit colon tumor cell proliferation and promote their apoptosis.
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Ratones , Animales , Receptor Toll-Like 4 , Neoplasias Asociadas a Colitis , Farmacología en Red , Ratones Endogámicos C57BL , Neoplasias del Colon/patologíaRESUMEN
Objective @#To study the effect of bufalin on the proliferation and apoptosis of human colorectal cancer cell line HCT116，and to explore the role of endoplasmic reticulum stress ( ERS) in this process．@*Methods @#The effect of bufalin on the proliferation of HCT116 cells was determined by CCK-8 assay．After HCT116 cells were treated with different concentrations of bufalin for 48 hours，cell apoptosis was detected by Annexin V / PI assay， and the expression of apoptosis-related proteins Bax and Bcl-2 was detected by Western blot．At the same time，the expression of ERS-related proteins glucose regulated protein 78 ( GRP78) ，phosphorylated protein kinase R like endoplasmic reticulum kinase ( p-PERK) ，eukaryotic translation initiation factor 2 α ( eIF2 α) ，phosphorylated eukaryotic translation initiation factor 2 α (p-eIF2 α) and C / EBP homologous protein ( CHOP) was detected by Western blot．HCT116 cells were divided into control group，bufalin group and combination group (bufalin + 4-phenylbutyric acid) ，and the expression of apoptosis-related proteins Bax and Bcl-2 was observed by Western blot. @*Results@#CCK-8 assay showed that bufalin could inhibit the proliferation of HCT116 cells．Apoptosis assay showed that bufalin could induce apoptosis of HCT116 cells．The results of Western blot showed that bufalin could up-regulate the expression of pro-apoptotic protein Bax and down-regulate the expression of anti-apoptotic protein Bcl-2．It could also induce ERS and activate PERK / eIF2 α/ CHOP pathway．When bufalin combined with 4-phenylbutyric acid，the apoptosis-promoting effect of bufalin was inhibited．@*Conclusion@#Bufalin can effectively inhibit the prolif- erative activity and induce apoptosis of HCT116，which is achieved to some extent by activating ERS.
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Objective To investigate the effect of Liu-Shen-Wan on transplanted tumors in mice with colon cancer based on the polarization of M2 macrophages in the tumor microenvironment. Methods We established a subcutaneous transplantation tumor model of mice with CT26 colon cancer. Mice were randomly divided into vehicle, oxaliplatin, and oxaliplatin combined with Liu-Shen-Wan groups. Treatment was administered for three weeks, and tumor volume was measured. All mice were weighed during the administration. After the end of the treatment, the mice were dissected and tumors were photographed and weighed. Spleen index was calculated. The expression levels of IFN-γ and IL-12P40 in serum and related blood biochemical indices were measured. The expression levels of M2 macrophage polarization indices, namely, IL-10 and TGF-β, in serum and tumor tissues were detected. The infiltration degree of M2 macrophages in each group was observed by immunohistochemical experiments. Results The tumor volume and mouse weight in the oxaliplatin combined with Liu-Shen-Wan group significantly decreased compared with those in the vehicle group. The spleen index increased, and the expression levels of IFN-γ and IL-12P40 in serum also significantly increased. The mice had no obvious side effects after the drug treatment. In addition, the expression levels of IL-10 and TGF-β in the serum and tissues of mice in the oxaliplatin combined with Liu-Shen-Wan group significantly decreased. The expression levels of CD68 and CD206 in tumor tissues also decreased. Conclusion The anti-tumor effect of Liu-Shen-Wan on the transplanted tumors of mice with colon cancer is related to the inhibition of M2 macrophage polarization in the tumor microenvironment.
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Objective To explore the cooperative mechanism of hospital research management and ethics review.Methods Through the analysis of current ethical conditions,as well as the relationship between hospital research management and ethical review,study on how to integrate them during the management of scientific research project.Results Research management and ethical review have different emphasis from different perspectives,however,both of them serve for research projects which makes inseparable connections.Conclusions Hospital research management and ethical review can be synergistic,according to which the management of scientific research projects will be more reasonable and scientific.
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Objective To explore the effect of Ganoderma lucidum extract (GLE) on immune function of Walker256 ascites rats and its mechanisms.Methods Sixty Wistar rats were randomly divided into 6 groups:control group,model group,high-dose GLE group,medium-dose GLE group,low-dose GLE group and cisplatin group according to different treatments,with 10 rats in each group.After the Walker-256 ascites rat model was successfully established,the rats in the low-dose,medium-dose and high-dose GLE groups were intragastrically administered with 0.84,1.68 and 3.36 g/(kg · d) GLE,respectively,twice a day,2 mL each time,for 14 days;the rats in the cisplatin group were intraperitoneally injected with 0.004 g/(kg · d) cisplatin in normal saline once a week;the rats in control group and model group were intragastrically administered with normal saline,2 mL each time,twice a day for 14 days.The general health status of the rats of each group were observed,the mass of ascites was tested,the spleen,thymus and kidney indexes were calculated,and the renal function was measured.Flow cytometry was used to measure the cell cycles of thymus and bone marrow cells,the distributions of T lymphocyte subsets and the number of NK cells in peripheral blood.Serum immune cytokine protein chip was used to measure the serum levels of immune cytokines of rots in the control group,model group and medium-dose GLE group.Results GLE significantly reduced the mass of ascites in rats (P＜ 0.05).Compared with the control group,thymus,spleen and kidney were damaged in the model group and cisplatin group,and treating rats with GLE significantly increased the thymus index and renal indexes,and significantly decreased serum creatinine and urea nitrogen (P＜0.05).G0/G1 phase arrest was significantly induced in the thymus and bone marrow cells in the model group and the cisplatin group (P＜0.05);and GLE significantly reduced the arrest of G0/G1 phase and significantly induced the transformation of thymus and bone marrow cells to G2/M and S phases (P＜0.05).GLE significantly increased the number of CD4+ cells,the ratio of CD4+ to CD8+ ceils and the number of NK cells,and significantly decreased the number of CD8+ cells in the peripheral blood of rats as compared with the model group (P＜0.05).Compared with the model groups,the expressions of interferon-γ (IFN-γ),interleukin (IL)-1α,IL-1β,IL-2,IL-4,IL-10 and tumor necrosis factor-α (TNF-α) in serum of the rats in medium-dose GLE group were significantly increased (P＜0.05).Conclusion GLE can effectively reduce the generation of ascites and improve immune function in Walker-256 ascites rats,and has no renal damage effect compared with cisplatin.
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Objective Innovate scientific research management thinking,explore new scientific research management models,and enhance hospital's competitiveness.Methods The hospital insistently adheres to the path of science and education hospital development in the practice of scientific research management,and takes measures of creating academic atmosphere,innovating management concept,rationalizing incentive measures,setting supporting policies,and so on.Results The hospital has gained certain progress in the fields of key discipline construction,research project,talent plan,scientific and technological achievements,etc.Conclusions The path of science and education hospital development plays an important role in the further healthy and sustainable development of hospital.
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Colorectal cancer is currently the world's fourth incidence of malignant tumors,the early clinical manifestations are not obvious,so the early diagnosis is difficult to find,most of them are in progress.Treatment of advanced stage with chemotherapy,interventional therapy,radiotherapy and other methods,in which chemotherapy in the killing of tumor cells at the same time,the normal cells of the body also has a killing effect.In recent years,all kinds of new nano targeting delivery system has been developed,which can be targeted to the tumor tissue,so it is more and more important in the treatment of intestinal tumor,especially with metastasis.The author has made an overview of the types of nano drug carrier materials,the research status and its application in the research of colorectal cancer.
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Background and purpose:Suppression of apoptotic signaling pathways is an important factor in tumor cell resistance. Research on cell apoptosis will open up a new way of reversing drug resistance and tumor treatment. This study examined the effects of a novel naphthalimide derivative 8c on multidrug resistant colon cancer HCT116/L-OHP cells and explored the molecular mechanisms underlying the apoptosis induction. Methods: The anti-proliferative effects of 8c were detected by CCK-8 assays and the effects on apoptosis induction were examined by lfow cytometry. The mRNA expression levels of p53, Bax and Bcl-2 were measured by real-time PCR;The protein expressions of p-p53, Bax, Bcl-2 and Cyt-c were detected by Western blot. Results:8c (IC50=8.16 μmol/L) seemed to be more potent than amonaifde (IC50=28.37 μmol/L) against HCT116/L-OHP cells. 8c induced apoptosis on HCT116/L-OHP cell lines through intrinsic or mitochondria dependent pathway. The protein expression of phosphorylation of p53 at Ser-15 was increased, but the mRNA level of p53 did not increase in HCT116/L-OHP cells. Bax protein and mRNA levels were signiifcantly increased, and Bcl-2 protein and mRNA levels were decreased, suggesting an increase of Bax/Bcl-2 ratios. Meanwhile, 8c induced a substantial release of cytochrome c from the mitochondria into the cytosol in HCT116/L-OHP cells. Conclusion: 8c induced cell death signal by inducing the activation p53 phosphorylation which subsequently activated related protein expressions of apoptotic pathway, which may be an important mechanism of 8c on inhibiting proliferation of HCT116/L-OHP resistant cells. All the results suggested that 8c was a potent compound to be developed as an anti-tumor and anti-resistance agent for clinic application in the future.
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Objective To investigate the effects of sorafenib combined with dendritic cells and cytokine induced killer (DC-CIK) cells on the growth,invasion and metastasis of hepatocellular carcinoma.Methods CIK cells and dendritic cells from healthy adults were cultured in vitro.Mice models with H22 hepatic cancer were established,and randomly divided into the normal saline group,sorafenib group,DC-CIK group and the sorafenib + DC-CIK group according to the random number table.There were 40 rats in each group.All the mice received intragastric gavage with sorafenib of 100 μg/g once a day.DC-CIK cells were intraperitoneally injected into the mice every 3 days with 1 × 107 cells each time.Twenty mice bearing tumors in each group were sacrificed after treatment for 3 weeks,and the peripheral venous blood and hepatic tumor tissues were harvested.The levels of alphafetoprotein (AFP) were detected by ELISA,and the necrotic degree of tumor tissues was evaluated by hematoxylin and eosin staining.The protein expressions of Ki-67 and CD34 in the tumor tissues were determined by immunohistochemical method.The survival time of the other 20 mice bearing the tumor in each group were detected.All data were analyzed using the analysis of variance or LSD test.Results CIK cells and dendritic cells were successfully cultured.The levels of AFP in the peripheral venous blood of the normal saline group,sorafenib group,DC-CIK group and sorafenib + DC-CIK group were (0.675 ± 0.177) rg/L,(0.379 ± 0.052) ng/L,(0.415 ± 0.028) ng/L,(0.288 ± 0.012) ng/L,with significant difference between the 4 groups (F =0.415,P ＜ 0.05).The numbers of intrahepatic and peritoneal metastasis of the normal saline group,sorafenib group,DC-CIK group and sorafenib + DC-CIK group were 21.2 ± 1.3 and 29.7 ± 7.6,16.4 ± 1.6 and 17.4 ± 1.8,20.2 ± 1.7 and 26.4 ± 1.7,15.2 ± 1.3 and 15.2 ± 1.3,with significant difference between the 4 groups (F =2.137,3.271,P ＜0.05).The tumor inhibition rate of the normal saline group,sorafenib group,DC-CIK group and sorafenib + DC-CIK group were 0,21％ ± 3％,9％ ± 3％ and 24％ ± 5％,with significant difference between the 4 groups (F =3.715,P ＜0.05).The survival time of mice in the normal saline group,sorafenib group,DC-CIK group and sorafenib ± DC-CIK group were (18.2 ± 2.5) days,(21.6 ± 2.1) days,(24.3 ± 2.8) days and (25.4 ± 1.4) days,with significant difference between the 4 groups (F =6.247,P ＜ 0.05).Conclusions Sorafenib combined with immunotherapy can significantly increase the therapeutic effects of molecular targeted drug on hepatocellular carcinoma.
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RIA(Rich Internet Applications) have highly interactive, rich user experience and powerful clients. Based on introducing the concept, features, and technology platform of the RIA technology, we proposed that RIA should be the highest priority in hospital medical equipment management information system construction.
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Sistemas de Administración de Bases de Datos , Internet , Servicio de Mantenimiento e Ingeniería en Hospital , Métodos , Programas InformáticosRESUMEN
There is a long history of Toad venom in the treatment of cancer in China.Bufalin,extracted from Toad venom,is one of the biologically active compounds of anticancer.We elaborate the molecular mechanism of bufalin on anticancer activity from several aspects such as inducing cell apoptosis and differentiation,inhibitting cell proliferation and angiogenesis,enhancing the sensitivity of chemotherapeutics,which can provide the basis for in-depth study of Toad venom and its development and clinical medication.
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It is to difficult to diagnose and treat hepatobiliary surgical diseases since its diverse clinical manifestations,which increases the difficulty of clinical internship.Taking clinical cases as teaching material,case-based learning was combined with teaching theme and was conducted by means of discussion and question and answer between teachers and students.Students can know about concepts or theories related to teaching theme.Case-based learning in internship can consolidate basic knowledge of hepatobiliary surgery,cultivate clinical scientific thinking and is helpful in analyzing and resolving problems of hepatobiliary surgical diseases.
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Objective To investigate the significance of metastasis associated lung adenocarcinoma transcript 1 ( MALAT1 ),cyclooxygerase-2 ( COX-2 ),beta catenin ( β-catenin )、matrix metalloproteinase (MMP)-3 and MMP-9 in the occurrence and development of colorectal carcinoma.Methods Real-time PCR was used to detect MALAT1,COX-2,β-catenin,MMP-3 and MMP-9 rnRNA expression in samples from 30 fresh colorectal carcinomas and 30 corresponding adjacent tissues.And the correlation analysis of the gender and age of patients,CEA,immune cellular factors ( CD4 and CD8 ),clinical stages,and the degree of differentiation was undertaken.Results The expression levels of MALAT1,COX-2,β-catenin and MMP-9 were significantly different between colorectal carcinoma tissues and adjacent colorectal tissues (P ＜ 0.05 ).MMP-3 showed no significant difference (P ＞ 0.05).MALAT1,COX-2,β-catenin and MMP-9 expression levels showed an average 2.22-fold,1.86-fold,2.16-fold,0.58-fold ( P ＜ 0.01 ) increase in colorectal carcinoma tissues when compared with adjacent colorectal tissues respectively.There were negative correlation between MALAT1 and β-cateuin ( colorectal carcinoma tissues vs adjacent colorectal tissues) ( r =- 0.346,P =0.030).While there were positive correlation between MMP-9 and β-catenin ( colorectal carcinoma tissues vs adjacent colorectal tissues) ( r =0.312,P =0.047 ).There were significant difference between male patients and female patients in terms of COX-2 and MMP-9 (colorectal carcinoma tissues vs adjacent colorectal tissues) (P =0.047; P =0.018).There were significant difference between patients with tumor marker CEA increase and patients without CEA increase in terms of COX-2 ( colorectal carcinoma tissues vs adjacent colorectal tissues) ( P =0.021 ).Conclusion MALAT1,COX-2,MMP-9 and β-catenin have significance in the occurrence and development of colorectal carcinoma,while MMP-3 has no significant reference value. The negative correlation between MAL(A)T-1 and β-catenin and the positive correlation between MMP-9 and β-catenin might show some interaction relationship in the development of colorectal carcinoma.The expression differences of COX-2 and MMP-9 (colorectal carcinoma tissues vs adjacent colorectal tissues) in male and female patients suggest that above two genes may affect the occurrence ratio of colorectal carcinoma.Detecting of COX-2 maybe helpful to the tumor marker CEA during the diagnosis of colorectal carcinoma.
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Objective To study the effect of aquaporin 1 on intestinal capillary endothelial barrier in rats with experimental acute necrotizing pancreatitis (ANP).Methods In this study,160 male Sprague-Dawley rats were randomly divided into five groups:Control group ( n =32),ANP group (n =32),NS group,Dexamethasone group,and Acetazolamide group.Eight rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models.Volume of ascites and levels of serum amylases were deternined at each time point.Pathological changes in intestine tissues were observed under electron microscope after HE staining.Capillary permeeabilities in intestine tissues were detected by Evans blue (EB) extravasation experiment.The mRNA and protein expressions of AQP1 in intestine tissue were determined by real-time PCR and Western blotting,respectively.Results Serum amylase level in ANP group was significantly higher than that in control group.Amylase level in dexamethasone group was lower than that in ANP group,and amylase level in acetazolamide group was higher than that in ANP group at 12 h (P ＜0.05 ) ; The concentration of EB in intestine tissues at each time point in ANP group was significantly higher than those in control group,and EB in dexamethasone group was lower than those in ANP group at 6,12 and 18 h.EB in acetazolamide group was higher than that in ANP group at 3 h ( P ＜ 0.05 ) ; The mRNA expression of AQPI in ANP group was significantly lower than that in control group.The expression of AQP1 in dexamethasone group was higher than those in ANP group at 6,12 and 18 h,and the expression of AQP1 in acetazolamide group was lower than that in ANP group at 3,6,12 h in intestine tissue ( P ＜ 0.05 ).Protein expression of AQPI in tissues in ANP group was significantly lower than that in control group.The expression of AQP1 in dexamethasone group increased more than that in ANP group at 3,6,12 h,and the expression of AQP1 in acetazolamide group was lower than that in ANP group at 3 h,6 h ( P ＜ 0.05 ).Conclusions The expression of AQP1 is down-regulated in intestine tissue in rats with acute necrotizing pancreatitis,and AQP1 could play an important role in the pathogenesis of capillary endothelial barrier dysfunction.
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Extensive researches suggest that the metastasis of colorectal cancer involves multiple factors and genes.Recurrence and metastasis after surgery are the important reasons for poor prognosis of thesc patients with colorectal cancer.Tumorigenesis is a dynamic process.The levels of tumor markers are changed in different stages.It has not yet been found any kind of tumor markers specific for a certain type of colorectal cancer.The sensitivity and specificity of diagnoising colorectal cancer by detecting an individual tumor marker are not ideal.The better combination of tumor markers has its advantages,can improve the early diagnostic rate.Combining detection of tumor markers will improve the diagnostic yield.
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<p><b>OBJECTIVE</b>To develop a maintenance management system for medical equipment based on HIS. The system contains some special functions( including preventive maintenance, automatic job dispatch, performance assessment, etc.) which are very useful for confirming the medical equipment in proper conditions and promoting the working efficiency of the staff. The system provides technical support for the improvement of the maintenance management level.</p><p><b>METHODS</b>The system, completed the software design using C/S, B/S combination mode.</p><p><b>RESULTS</b>The system realized clients of various sections of zero maintenance, and make the data manipulation, statistical features of equipment management department more convenient.</p><p><b>CONCLUSION</b>the system connects the subsystems closer and interacts information from time to time, forming a tight network structure. This provides a basis for future hospital-wide information integration.</p>
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Eficiencia Organizacional , Sistemas de Información en Hospital , Mantenimiento , Diseño de SoftwareRESUMEN
Colorectal cancer is a common malignancy in China.The incidence of it showed an increasing trend with the economic development,living standards improvement and lifestyle changes.The traditional treatment methods include surgery,radiotherapy and chemotherapy.In recent years,hyperthermia has become a method for treating tumor.Hyperthermia kills tumor cells by thermal effect and no-thermal effect.Not only does it have a direct therapeutic effect on tumor cells,hyperthermia also has some synergy combined with radiotherapy and chemotherapy.Hyperthermia combined with conventional therapy can improve the local control rate and extend survival for patients.In this paper,the efficacy of hyperthermia has been reviewed,combined with a variety of treatment methods for colorectal cancer in China.
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Since the laparoscopic thyroidectomy carried out in China for ten years,this technique has become more and more mature,indications gradually broadened,and playing a vital role in the field of thyroid surgery.This article will explain this technique in the aspects of approaches,the establishment and maintenance of the surgical space,indications,antiindications and complications.
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As one of the most major disease,malignant tumor is harmful to human health.Althought it' s exact pathogenesis is still not clear,it is certainly that the formation of cancer is typical of containing many factors and having gone through many steps.Resulting from the abnormal activation of a series of proto-oncogene as well as the inactivation caused by many anti-oncogene mutation,some signal pathways work abnormally.In recent years,the study of Hedgehog ( Hh),as the signal pathway,shows that Hh encodes a series of secreted signaling protein,having an important effect on the differentiation and proliferation of cells in the process of embryogenesis.The occurrence of abnormal activation of Hh signaling pathway plays a significant role in the process of tumorigenesis.Signal paths of Hh signaling protein include as much as following at least:patched(Ptch),smoothened (Smo),fused (Fu),suppressor of fused (SuFu),costaⅠ-2 (Cos)-2 and cubitus interruptus (Ci) and so on.In this paper,the function of Hh genetic family and the mechanism of its relation to many kinds of human cancers will be givien a brief overview.
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Objective To observe the therapeutic effect of brucine nanoparticles on hepatocellular carcinoma.Methods Brucine nanoparticles with block copolymer of carboxylation polyethylene glycol and polylactic acid were manufactured by ultraphonic emulsification.The effect brucine nanoparticles on growth of SMMC-7721 cell line was observed in vitro.The protein and mRNA levels of Fas were measured with Western blotting and FQ-PCR respectively after the brucine nanoparticles were added into cell culture fluid for 72 hours.Results The mean diameter,the carried drug rate and the entrapment rate of brucine nanopaticles was 146±96 nm,4.2％ and 67％,respectively.The growth inhibition of liver cancer cells was enhanced significantly with the increasing drug dose.The IC50 of growth inhibition of 5-FU,brucine and brucine nanoparticles was 16.7 μg/ml,90.3 μg/ml and 164.9 μtg/ml,respectively.There was significant difference among them (P＜0.05).The protein and mRNA expression of Fas in brucine nanoparticles treated SMMC-7721 cells increased significantly compared with that in blank control group(P＜0.05).Conclusion Brucine nanoparticles may potentially be a novel therapeutic drug for hepatocellular carcinoma.