Objective To investigate the effect of NS-398, a selective cyclooxygenase-2 (COX-2) inhibitor, on the expression of P-glycoprotein(P-gp) in a gastric cancer cell line SGC-7901. Methods SGC-7901 cells were treated with NS-398 in different concentrations (0, 10 ?mol/L and 100 ?mol/L) respectively. Prostaglandin E2(PGE2) was detected by ELISA. Twenty four hs and 48 hs later, the expression of mdr1 mRNA were detected by RT-PCR. P-gp protein expression in SGC-7901 cells was detected by immunocytochemical technique after NS-398 treatment.Results NS-398 can inhibit the expression of PGE2 in a dose-dependent manner(P

OBJECTIVE: To investigate the effect and mechanism of TLR4 monoclonal antibody (TLR4mAb) on mmLDL induced impairment of endothelium-dependent vasodilatation in mouse mesenteric artery. METHODS: The experiment established three groups of normal saline group, mmLDL treatment group and TLR4mAb intervention group. The concentration of IL-1β and TNF-α in plasma was determined by enzyme-linked immunosorbent assay (ELISA). Measurement of endothelium-dependent vasodilatation was achieved by microvascular tension mapping. Western blot and RT-PCR were used to investigate the expression level of protein and mRNA expressions in vascular tissues. In addition, ultra-structure of mesenteric artery endothelial cells was observed by transmission electron microscope. RESULTS: TLR4mAb could improve the damage of mmLDL induced impairment of endothelium-dependent vasodilatation in a dose-dependent manner. Besides, TLR4mAb obviously up-regulated protein expressions in KCa3.1-channel and KCa2.3-channel, and down-regulated the expression of inflammatory factors TNF-α and IL-1β. Furthermore, the improvement of mmLDL impaired vascular endothelial cells and endothelium-dependent vasodilatation might be correlated with its competitive antagonism of mmLDL-activated TLR4 signal transduction pathway and its downstream NF-κBp65 and p-38 MAPK pathway. CONCLUSION: Administration of TLR4mAb in advance can alleviate the impairment of endothelial cells and the decrease of endothelium-dependent vasodilatation induced by mmLDL, and inhibit the overexpression of inflammatory factors. Regulation of TLR4 pathway as well as its downstream NF-κBp65 and P-38 MAPK pathways may be effective targets for the prevention and treatment of cardiovascular diseases.

Objective To discuss the efficacy of omeprazole and pantoprazole in treatment of peptic ulcer hemorrhage.Methods 80 patients with peptic ulcer hemorrhage were selected,they were divided into two groups randomly.The observation group (41 cases) was given pantoprazole by intravenous drip.The control group (39 cases) was given omeprazole by intravenous drip.The efficacy and safety of omeprazole and pantoprazole in treatment of peptic ulcer hemorrhage was evaluated by efficacy,pH before and after treatment,bleeding time,hospitalization and bleeding volume,and adverse reaction during treatment.Results The effective rate was 92.7％ in the observation group and 89.7％ in the control group.There was no statistical significance on effective rate between two groups.But the excellent rate of observation group was higher than that of the control group (P ＜ 0.05).Before treatment,the gastric acid was acidic.There were no statistical significance on pH value between two groups.After treatment,the pH value was increased in two groups.The pH value of observation group was higher than that of the control group (P ＜ 0.05).The hospitalization,hemostasis time and bleeding volume was shorter than that of the control group (P ＜ 0.05).During treatment,the patients given pantoprazole had less adverse reaction (P ＜ 0.05).Conclusion Pantoprazole and omeprazole are suitable for treating peptic ulcer hemorrhage.But the antacid and hemostatic effect of pantoprazole was better with high safety.It was worthy of clinical application.

The apoptosis was observed under a fluoroscope when the tested tumor cells were treated with the supernatant derived from the liquid culture of an actinomyces strain AK 11, which had showed cell toxicity by means of MTT assay, and was further confirmed by the correspondent band of ”DNA ladder” in the agarose gel electrophoresis. In a bioassay employed nude mouse, the pure compound produced by the strain AK 11 showed tumor inhibition in rates of 52.01% and 33.64% corresponding to the dosages of 0.016 ?g?kg -1 and 0.008 ?g?kg -1 ip, respectively. According to the indexes IC 50 of human hepatocarcinoma SMMC7721 and stomach cancer MGC 803 cells, it was estimated that the inhibition effect of the pure compound was slightly stronger than that of Adriamycin. The results showed high antitumor effect of the tested compound from the strain AK 11. When the cells were treated with AK 11, it was found by flow cytometry analysis that cell division was ceased at S phase due to the DNA synthesis block .

Bile Duct Neoplasms ; surgery ; Bile Ducts, Intrahepatic ; Cholangiocarcinoma ; surgery ; Humans

Objective To investigate the corresponds between NF-κB p65 activation and k-ras mutations.Methods NF-κB p65 activation was analyzed by immunochemistry in 167 colorectal cancer specimens in which the k-ras mutation status was confirmed.Resluts Among 167 colorectal cancer specimens screened,59 (35.3 ％) had k-ras mutations and 63 (37.7 ％) had NF-κB p65 activation.k-ras mutations and NF-κB p65 nuclear expression were no significant difference in different sex,age,ECOG score,pathological types,degrees of pathological differentiation,TNM stage,and metastases on lymph nodes (P＞ 0.05).The positive nuclear expression rate of NF-κB p65 was 50.8 ％ (30/59) in specimens with k-ras mutations and 30.6 ％ (33/108) in specimens with wild type k-ras.There was obviously statistical difference between them (P =0.010).Conclusion NF-κB p65 activation in coloretal cancer was associated with k-ras mutations.

Acupuncture Therapy ; instrumentation ; Adult ; Breathing Exercises ; Combined Modality Therapy ; Dysmenorrhea ; therapy ; Exhalation ; Female ; Humans ; Needles

In order to improve the reference service, the necessity to provide reference service for translational medicine in academic library was analyzed and the translational medicine-based reference service in Library of Qingdao University was elaborated from the aspects of its contents and ways with the existing problems and weaknesses summarized.

Prostaglandin E1 ( PGE1) , derived from D-HLA and controlled by phospholipidase A2, is a kind of strong endogeneous vasodilator and platelet inhibitor. Its effects on vasculars and platelets are just inferior to prostacyclin only, which is the strongest physiological vasodilator and platelet inhibitor, and the common receptors exits.Now it is found that exogeneous PGE1 can central some kinds of paletet supra-activation in illnesses such as cardiovascular disease, renal disease and diabetes mellitus. So PGE1 may be benificial to those patients.

Objective To investigate the effect of bifidobacteria on dextran sulphate sodium(DSS)- induced acute ulcerative colitis in mice.Methods Thirty BALB/C mice were randomly divided into nor- mal control group (n=10),0501 strain group (n=10) and c122 strain group (n=10).Fifty BALB/ C mice received 5% dextran sulphate sodium(DSS) for 7 days to induce ulcerative colitis.The mice were then divided to model group,negative control group(perfused with 0.9 NaCl solution ),positive control group(perfused with SASP of 20 mg/ml),DSS + 0501 strain group(perfused with 1?10~9 CFU/ml bifidobacteria 0501 strain solution and DSS + c122 strain group (perfused with 1?10~9 CFU/ml bifidobacteria c122 strain solution).All mice were sacrificed 9 days later.The colon specimens were measure by histoehemical staining with H-E.The expressions of interleukin-10 (IL-10) and its protein were detected by RT-PCR and immunohistochemistry respectively.Results The degree of colon inflam- mation in mice both in DSS+ 0501 strain and DSS+ c122 strain groups were aggravated and expressions of IL-10 mRNA and protein were reduced compared to model group.No colon inflammation was found in 0501 strain and c122 strain groups.Conclusion Some strain of bifidobaeteria may aggravate colon in- flammation in mice when mucosal harrier is destroyed.