Objective To study the effect of cholecystokinin-octapeptide(CCK-8) on the proliferation of fibroblast-like synovial cell line RSC-364 and p38 MAPK activity induced by TNF-? in rat.Methods The proliferation of RSC-364 cells was measured by monotetrazolium(MTT) colourmetric assay and the level of activation of p38 MAPK was deteced by Western blot.Results An increase in p38 MAPK phosphorylation was detected 5 min after TNF-?((50 ?g/L))addition,and reached a plateau at(15 min),finally returned to the basic level at(2 h).TNF-?(10,25,(50 ?g/L)) increased p38 MAPK phosphorylation in a dose dependent manner at 15 min.CCK-8((10~(-10))～(10~(-6)mol/L))could inhibit the proliferation and the level of phosphorylation of p38 MAPK in a dose dependent manner.Moreover the inhibitory effects were partly reversed by CCK-A receptor specific antagonist CR1409 or CCK-B receptor specific antagonist CR2945.SB203580 inhibited TNF-?-stimulated RSC-364 proliferation.Conclusion CCK-8 inhibited TNF-?-stimulated proliferation by decreasing p38 MAPK phosphorylation in RSC-364 cells,which was mediated through CCK-A receptor or CCK-B receptor.

Pregnancy and the puerperium have been recognized to increase the risk of stroke, particularly from late pregnancy and through the puerperium. The reported incidences of stroke during pregnancy and the puerperium varied widely, but when it occurs, there may be implications for management of the patient and delivery of the child. Important causes of stroke during pregnancy and the puerperium include preeclampsia and eclampsia, cardioembolism, rapture of cerebral vascular anomaly, cerebral aneurysm rupture and antiphospholipid syndrome, thrombotic thrombocytopenic purpura. Management of patients with pregnancy-related stroke is largely the same as that of nonpregnant patients, including thrombolysis, atntiplatelets and anticoagulants, with more consideration on maternal and fetal risks.

Objective To analyze the etiological changes of atrial fibrillation(AF) in Zhanjiang. Methods The etiology of 592 AF cases during 1990～1997 were analyzed, and 610 cases during 2000～2007 were analyzed as comparison. Results Rheumatic heart disease(36.8%) was main etiology of AF during 1990～1997. But coronary artery disease(33.1%) has surpassed rheumatic heart disease recently, and the hyperthyroidism and undetermined-e-tiology of atrial fibrillation were decreasing. The etiology of atrial fibrillation in different age groups was significantly different(P <0.05 or P <0.01). Conclusion The etiology of atrial fibrillation changes every year,and age is a pre-dictable factor to the etiology of atrial fibrillation.

Objective To discuss the influence of μ-opioid receptor ( OPRM1) and CYP3A gene polymor-phism on analgesic effect of fentanyl for abdominal hysterectomy patients .Methods 198 cases of gynecologic anes-thesia patients who were treated by elective abdominal hysterectomy surgery ,were selected in the hospital .The rela-tionship between the fentanyl consumption of intravenous analgesia and OPRMI and CYP 3A gene polymorphisms was detected by using polymerase chain reaction-restriction fragment length polymorphism detection .Results In 198 pa-tients,OPRM1 genotyping was 186 cases,the other 10 patients failed to typing were excluded ,including 89 cases of type A/A,type A/G 76 cases,type G/G 21 cases,OPRM1 the frequency of A118G allele was 31.7%.No statistically significant differences were found in mean VAS score of CYP 3A4*1/*1,CYP3A4*1/*1G,CYP3A4*1G/*1G instantly after operation in the three groups and 24h postoperation.By using analysis of variance with body mass ,age and intraoperative volume as a covariate factors after first 24h fentanyl consumption ,the difference was statistically sig-nificant among the three groups (P<0.05),CYP3A4*1G/*1G group was significantly lower than that in CYP3A4*1/*1G group and CYP3A4*1/*1 group,there was no significant difference between CYP 3A4*1/*1G group and CYP3A4*1/*1 group (P>0.05).In addition,because the OPRM1 A118G interacts with CYP3A4*1G, reducedthe quantity of expression of opioid receptor carrying CYP 3A4*1 and OPRM1 A118G/G,and thus more fent-anyl was needed postoperation to achieve the same effect .Conclusion It provided a theoretical basis and reference for clinical application of personalized medicine by analyzing the gynecological patients μopioid receptor gene A118G and CYP3A4*1G polymorphism.

Objective To explore the effects of Nimodipine on oncogene c-fos and c-jun mRNA expressions in dorsal root ganglia of rats following acute sciatic nerve injury.Methods Nimodipine at a dose of 10 mg/kg at 5,15,30,60 and 120 min and at a different dose of 2.5,5 and 10 mg/kg at 60 min was given to each rat through intraperitoneal injection before transection of sciatic nerve.Using reverse transcription PCR(RT-PCR) technique,the c-fos and c-jun mRNA expressions were detected at 5,15,30,60 and 120 min after injection of Nimodipine and following acute sciatic nerve injury.Results Compared with control group,the expressions of c-fos mRNA in injury group were obviously increased at 30,60 and 120 min after injury(all P

Aim To observe the influence of CCK-8 on expression of MMPs/TIMP-1 in TNF-α-induced rat fibroblast-like synovial cell line RSC-364.Methods The secretion levels of MMP-1, MMP-3, MMP-9 and TIMP-1 were determined using ELISA;MMP-3 and MMP-9 mRNA expressions were detected by RT-PCR.Results MMP-3 and MMP-9 could not be examined in RSC-364 incubated with CCK-8 and unstimulated RSC-364, which was able to product a little MMP-1, TIMP-1 and express even less MMP-3,-9 mRNA.CCK-8 inhibited the increase in MMP-1, MMP-3, MMP-9 secretion and MMP-3,-9 mRNA expression in TNF-α-induced RSC-364.TIMP-1 production was also increased in TNF-α-induced RSC-364.CCK-8 had no effect on TIMP-1 production in TNF-α-induced RSC-364, but was able to reduce the ratios of MMP-1, MMP-3, MMP-9 to TIMP-1.Conclusion The inhibitory effect of CCK-8 on MMPs activity may be related to the decrease of MMPs mRNA expression, MMPs secretion and the ratios of MMPs to TIMP-1 in TNF-α-induced RSC-364, which indicates that CCK-8 might be a possible regulator in the pathogenesis of rheumatoid arthritis.

AIM: To investigate the inhibitory effects of cholecystokinin octapeptide(CCK-8) on nuclear factor-?B(NF-?B) activities stimulated by lipopolysaccharide(LPS) by using forskolin,the activator of adenylate cyclase,and PKA inhibitor H-89 in rat pulmonary interstitial macrophages(PIMs).METHODS: PIMs were isolated and purified.EMDA was applied to detect NF-?B activities and Western blotting was used to analyze the I?B-? protein level in rat PIMs.RESULTS: The NF-?B activity was not detected in normal control rat PIMs.The NF-?B activity in LPS-treated rat PIMs was obviously higher than that in control group(P0.05).The NF-?B activity in CCK+LPS group and LPS+Fsk group were obviously lower than that in LPS group(P

Objective To evaluate the effect of high-level spinal cord injury (SCI) on the myocardial energy metabolism in rats.Methods Sixty healthy male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 2 groups (n=30 each) using a random number table:sham operation (group S) and SCI group.SCI was induced in anesthetized rats by dropping a 10 g weight onto C7 spinal cord from 5 cm height falling freely inside a vertical hollow glass tube.At 6,12,24,48 and 72 h after SCI,6 rats in each group were chosen and arterial blood samples were taken for measurement of serum creatine kinase (CK) and creatine kinase isoenzyme-MB (CK-MB) activities.The rats were then sacrificed and myocardial specimens were obtained for examination of myocardial ultrastructure and for determination of ATP weight ratio,levels of Na+-K+-ATPase,Ca2+-Mg2+-ATPase,non-esterified fatty acids (NEFA) and lactic acid (LD),and expression of peroxisome proliferator-activated receptor alpha (PPARα) mRNA and protein (using fluorescent quantitative PCR and Western blot).Results Compared with group S,the serum CK and CK-MB activities were significantly increased,the ATP weight ratio,activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase and levels of NEFA and LD were decreased,and the expression of PPAR-α mRNA and protein was down-regulated in SCI group.No pathological changes of myocardium were found in group S,and the pathological changes of myocardium were obvious in SCI group.Conclusion High-level SCI can lead to decrease in the myocardial energy metabolism in rats,and down-regulated expression of PPARα is involved in the mechanism.

Objective To analyze and compare efficacy and safety of different chemotherapy regimens in the treatment of elderly patients with advanced gastric cancer. Methods 60 elderly patients admitted to our hospital with advanced gastric cancer were selected as research subjects , and divided into experimental group and control group depending on the treatment of chemotherapy. The experimental group were treated with Gio oxaliplatin (SOX), and patients in the control group accepted Olivier Elizabeth, leucovorin and fluorouracil (FOLFOX6) treatment. Compare and analyze the efficacy of the two groups after two cycles of therapy. Results By chemotherapy, recent efficiency and disease control rate were not significantly different (P>0.05) between the two groups;and there was also no significant difference in the incidence of adverse reactions,such as adverse reactions, fatigue weakness, gastrointestinal reactions, hand-foot syndrome, oral mucositis (P > 0.05). Conclusion The efficacy was equivalent between FOLFOX6 chemotherapy SOX test group and the control group in the treatment of elderly patients with advanced gastric , and there was no significant difference in the incidence of adverse reactions.

AIM:To observe the effects of cholecystokinin octapeptide(CCK-8) on the expression of proinflammatory cytokines IL-1?,IL-6 and anti-inflammatory cytokines IL-10,IL-4 in LPS-attacked mice.METHODS: Kunming mice were randomly assigned and injected intraperitoneally with LPS alone or/and CCK-8 at different time points.The expression of IL-1?,IL-6,IL-10 and IL-4 in the serum and lung tissues were assayed by ELISA and RT-PCR.RESULTS: The expression of IL-1?,IL-6,IL-10 and IL-4 were upregulated in LPS-attacked mice.Pre-treatment of CCK-8 decreased both IL-1? and IL-6 expression and augmented IL-10 and IL-4 expression in LPS-attacked mice.CONCLUSIONS: CCK-8 exerts an anti-inflammatory effect by inhibiting the expression of IL-1?,IL-6 and increasing the expression of IL-10,IL-4 in LPS-attacked mice,which could alleviate the inflammatory response in lung tissue.