Objective To explore the related factors influencing the condensate infection level in order to provide a reference for ventilator pipe care and reducing condensate infections.Methods A total of 80 patients using ventilator in ICU of the First Hospital of Liaoning Medical University was chosen as the research object,and the related factors influencing the condensate infection using correlation and regression analysis method were explored,and the regression model was estabhshed as well.Results Condensate infection were correlated with pipe length (r=0.837,P＜0.01),temperature difference between ward and gas in the pipe (r=0.875,P＜0.01),exhaled gas humidity (r=0.793,P＜0.01) and ventilation (r=0.932,P＜0.01),but the pipe length could not enter the regression equation (t=-0.09,P＞0.05),and the regression equation was y=-168.08 +9.96x1 (temperature difference) +0.33x2 (exhaled gas humidity) +20.98x3 (ventilation).Conclusions Pipe length,temperature difference between ward and gas in the pipe,exhaled gas humidity and ventilation were the influencing factors,and medical personnel can control the infection of condensate considering the influencing factors.

Objective:To observe the effect of Gemcitabine ( GEM) on the viability and apoptosis of non-small cell lung cancer HCC827 in vitro. Methods:The cell viability,apoptosis and cell cycle of HCC827 cells induced by Gemcitabine were detected with cell counting kit-8 assay (CCK-8),Annexin V-FITC/PI staining and flow cytometry. The expression of Bcl-2 protein of cells treated with GEM was examined by Western blot assay. Results: There was significant inhibition effect on HCC827 cells treated with 0. 1-1 000 ng/ml of GEM,which can promote the occurrence of HCC827 cell apoptosis and arrest cell in the S phrase. The apoptosis induced by GEM was accompanied with the down regulation of Bcl-2 protein. Conclusion: GEM can inhibit the cell viability and induce the HCC827 cell apoptosis and S phrase arrest. Its cell dead type was apoptosis,which was related with the expression of Bcl-2 protein.

Scientific research is important for the improvement of the health-care techniques,and is certainly important for the health of women and children of the whole society.With the development of medical science,research ability of maternal and child healthcare professionals is deemed essential.And the evaluation of their research ability,stimulation,and creativity have been important topics to address.Here we introduce an evaluation system for research capacity of maternal and child healthcare professionals established in our hospital,which is the fruit of constant exploration and practice for several years.It is proved to be practical,simple and feasible.The establishment methods,practices and experiences of the evaluation system are presented in this paper.

Objective To investigate the effect of high altitude hypoxia on chronic inflammation in rats.Methods Forty SD rats were randomly divided into 4 groups: control group (Con),chronic inflammation group (CI),high altitude hypoxia group (HH),high altitude hypoxia+chronic inflammation group (HH+CI).Rats in CI group were injected with lipopolysaccharide (LPS) (0.5 mg/kg) through the caudal vein twice a week for 4 weeks.Rats in HH+CI group were treated just as CI group was,but together with HH group rats were settled in a hypoxic environment of 6000 m altitude for three days.Pathological changes in lung tissues were observed by hematoxylin eosin stain.The peripheral white blood cell count and classification were measured.The levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in serum and lung tissues were detected by enzyme-linked immunosorbent assay (ELISA).Changes in IL-6 expression in rat lung tissues were observed by Western blotting.Results After LPS and high altitude hypoxia exposure,inflammatory cells infiltration and alveolar capillary expansion were observed in rats' lung tissue.Compared with Con group,not only the peripheral white blood cell count,but also the level of IL-6 and TNF-α in serum and lung tissue increased in CI and HH group(P<0.01).IL-6 expression levels observed by Western blotting were also increased in HH and CI group(P<0.01).High altitude hypoxia and chronic inflammation interacted(P<0.01).The peripheral white blood cell count was higher in HH+CI group than in other groups,and IL-6 and TNF-α expressions in lung tissue were increased(P<0.05).Conclusion An LPS-induced chronic inflammation model in rats is successfully obtained,and high altitude hypoxia could aggravate chronic inflammation.

Background:Suppression of tumor suppressor genes plays a key role in the pathogenesis and progress of tumors. Some microRNAs may contribute to tumorigenesis by regulating tumor suppressor genes. Aims:To investigate the targeted regulatory effect of miR-483-3p on deleted in liver cancer 1(DLC1)gene in colorectal cancer. Methods:Sixteen patients with colorectal cancer admitted from October 2012 to April 2013 at Nanjing Drum Tower Hospital were enrolled. Expression of DLC1 in cancerous and adjacent noncancerous tissues was determined by Western blotting,and expression of miR-483-3p was determined by qRT-PCR. Dual luciferase reporter gene plasmid containing the 3’untranslated region(3’UTR)of DLC1 was constructed to validate the regulation of DLC1 by miR-483-3p in human colon cancer cell line HCT116. MiR-483-3p mimic was transfected into HEK293T cells and expression of DLC1 was determined by Western blotting;MiR-483-3p mimic was transfected into HCT116 cells and cell proliferation was measured by CCK-8 assay. Results:Expression of DLC1 was significantly lower in cancerous tissue than in noncancerous tissue,while expression of miR-483-3p was significantly higher in cancerous tissue than in noncancerous tissue(P<0. 05). MiR-483-3p mimic reduced the expression of DLC1 through directly binding to the 3’UTR of DLC1. Transfection of miR-483-3p mimic enhanced the proliferation of HCT116 cells significantly(P<0. 05). Conclusions:DLC1 is a target gene of miR-483-3p. MiR-483-3p might promote the development of colorectal cancer by down-regulating DLC1 expression at post-transcriptional level.

[ ABSTRACT] AIM:To investigate the effect of HOX transcript antisense RNA ( HOTAIR) on the migration and invasion abilities of liver carcinoma HepG 2 cells.METHODS:The expression of phosphoinositide-3-kinase regulatory sub-unit 3 (PIK3R3) in the liver cancer and normal liver tissues was detected by immunohistochemistry .The efficiency of gene silencing of HOTAIR or PIK3R3 by LV3-shHOTAIR or LV3-shPIK3R3 was determined by qPCR and Western blot .The mi-gration and invasion abilities of HepG 2 cells after silencing of HOTAIR and PIK3R3 were measured by wound healing assay and Transwell Matrigel invasion assay .The expression of miR-214 after silencing of HOTAIR and PIK3R3 was analyzed by qPCR.The expression of HOTAIR and PIK3R3 in the HepG2 cells was also evaluated by qPCR after transfected with miR-214 mimics or miR-214 inhibitor .Dual-luciferase reporter assay system was used to determine the regulatory effect of miR-214 on HOTAIR and PIK3R3 expression.RESULTS:PIK3R3 expression increased significantly in the liver cancer tissues compared with normal liver tissues .The abilities of invasion and metastasis of hepatocellular carcinoma were reduced after silencing of HOTAIR and PIK3R3.miR-214 expression was increased when silencing of HOTAIR and PIK3R3 was per-formed.HOTAIR and PIK3R3 expression was reduced after transfection with miR-214 mimics.HOTAIR and PIK3R3 ex-pression was increased after transfection with miR-214 inhibitor.The results of dual-luciferase reporter assay test showed that miR-214 directly regulated HOTAIR and PIK3R3 transcription activity .CONCLUSION: HOTAIR regulates the ex-pression of PIK3R3 through miR-214, thus promoting the migration and invasion abilities in the liver cancer cells .

Objective To study the diagnosis and treatment of omental torsion.Methods 73 patients with omental torsion from Jan 1995 to Dec 2009 in literatures together with the one we reported were reviewed and analyzed The range of ages was from 3 to 65 years,and the median age was 25.3 years.Among them,35 cases were less than 18 years old(47%,and 27 with obesity) and others more than 18 years old(53%,1 with obesity).The accurate diagnosis before operation exsited in 9 patients.49 patients(66%) were diagnosed as primary omental torsion,and childhood obesity was the most related factor.Conversely,25(34%) were diagnosed as secondary omental torsion,while the most common reason was adhersion.In contrast with other clinical symotoms and signs,abdominal pain and tenderness were occurred in almost every people.Bultro sonography(positive rate:24%,6/25) was hardly useful in diagnosis but CT (positive rate:96%,23/24) and MRI(positive rate:100%,2/2) were beniticial.Operation was applied in all patients,while laparoscopy was uesed in 23 patients.As a rule,the appendix was removed together in 61 persons.The cobort of patients was recoverd fully without serious complications such as hemorrhage and intestinal infarction.Conclusion Omental torsion was a relatively rare disease,and the diagnosis should be easy with the help of CT and MRI,and the laparoscopy was the better choice for surgeons.

Objective To obtain the recombinant corticotropin releasing hormone (CRH) protein with soluble, high purity protein through optimizing prokaryotic expression condition and purifying glutathione thiol transferase (GST)-CRH protein. Methods To detect the expression of soluble CRH protein through grope of the host strain GST-CRH temperature of induction expression, the host strain concentration (OD600), IPTG concentration and induction time, the purification of GST-CRH was performed by GST-CRH agarose gel. Western Blot assay was used for the expression identification of the target protein. Results The optimal conditions for the induction of CRH protein were determined: temperature of 30 ℃, IPTG induced concentration 0.1 mmol/L, bacteria density (OD600) 0.8, the induction time of 8 hours, purified GST-CRH>95% fusion protein was obtained. Conclusion The optimal expression conditions of GST-CRH are obtained, and the soluble protein of high purity GST-CRH is also obtained.

BACKGROUNDTo construct a DC-Ad-Ki-ras(V12) vaccine and investigate the anti-tumor activities of lung cancer dendritic cell vaccine modified by mutant Ki-ras gene in vitro.

METHODSKi-ras(V12) cDNA was transfected into cultured bone marrow-derived DC with the recombinant adenovirus [(Ad-Ki-ras(V12)] containing human mutant Ki-ras gene. Anti-tumor activity of the vaccine was studied in vitro by flow cytometry, PCR, MLR and cytotoxicity assay.

RESULTS(1) The DC vaccine was confirmed not only to express Ki-ras(V12) gene, but also to remarkably stimulate lymphocyte proliferation and improve CTL activity. (2) The DC vaccine modified by mutant Ki-ras gene could induce specifical CTL activity of immunized mice against Lewis lung carcinoma that could express Ki-ras(V12) gene, but not to B16.

CONCLUSIONSThe DC vaccine modified by mutant Ki-ras gene can induce obvious anti-tumor activities against Lewis lung carcinoma that can express Ki-ras(V12) gene.

Objective To investigate the effects of microRNA497 (miR-497) on the metastasis of gastric cancer and its possible molecular mechanism. Methods SGC-7901 gastric cancer parent cells were cultured in an ultra-low adhesion environment, and the anoikis resistance model of SGC-7901 cells was created after re-adhesion. Clone formation assay, flow cytometry, Transwell^TM test and scratch healing test were used to detect the differences of biological behavior compared with their parent cells. Fluorescence quantitative PCR was performed to detect the expression of miR-497. Western blot analysis was used to detect the changes of key proteins of Wnt/β-catenin signaling pathway and epithelial mesenchymal transformation (EMT) related proteins such as vimentin and E-cadherin. Parent cells and anoikis resistant SGC-7901 cells were transfected with miR-497 inhibitor or miR-497 mimic, and CCK-8 assay was used to detect the proliferation activity. Transwell^TM invasion assay was performed to detect the invasion ability of cells. Transwell^TM migration test and scratch healing assay was used to determine the migration ability. Western blot analysis was used to detect the expressions of Wnt1, β-catenin, vimentin and E-cadherin. By transfecting miR-497 mimic into the anoikis resistance SGC-7901 cells and inoculating them subcutaneously in nude mice, the changes in the volume and mass of tumor tissues were measured and recorded. Western blot analysis was used to determine the expressions of Wnt1, β-catenin, vimentin and E-cadherin of tumor tissues. Results Compared with the parent cells, the anoikis resistance SGC-7901 gastric cancer cells had faster proliferation rate, stronger colony formation, lower apoptosis rate, stronger invasion and migration ability. The expression of miR-497 was significantly decreased. After down-regulation of miR-497, the proliferation ability, invasion and migration ability were significantly enhanced. The expressions of Wnt1, β-catenin and vimentin increased significantly, while E-cadherin decreased notably. The results of up-regulation miR-497 were the opposite. The tumor growth rate, tumor volume and mass of miR-497 overexpression group were significantly lower than those of control group. The expressions of Wnt1, β-catenin and vimentin decreased significantly, while the expression of E-cadherin increased significantly. Conclusion The expression of miR-497 is low in the anoikis resistance SGC-7901 cells. miR-497 can inhibit the growth and metastasis of gastric cancer cells by blocking Wnt/β-catenin signaling pathway and EMT.
Animals ; Mice ; Humans ; beta Catenin/metabolism* ; MicroRNAs/metabolism* ; Vimentin/metabolism* ; Stomach Neoplasms/pathology* ; Anoikis/genetics* ; Wnt Signaling Pathway/genetics* ; Mice, Nude ; Cell Proliferation/genetics* ; Cadherins/genetics* ; Cell Line, Tumor ; Epithelial-Mesenchymal Transition/genetics* ; Cell Movement/genetics*