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.

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.

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 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

ObjectiveTo explore the effect of TLR4,PI3K and NF-κB on the migration of asthmatic airway smooth muscle cell(ASMCs) induced by airway epithelial cells.MethodsPrimary ASMCs were cultured by the method of cell digestion.Cell culture supernatant of RTE cells were collected by TNF-α stimulation of epithelial cells.Detected the IL-8 and RANTES levels in the supernatant.The effect of TLR4/PI3K-related signaling molecules on the migration of asthmatic ASMCs induced by epithelial cells were detected by Modified Boyden chemotaxis chamber with anti-TLR4 antibody,Wortmannin and PDTC drugs as a tool.ResultsThe levels of IL-8 and RANTES in the supernatant of TNF-αgroups were significantly increased,and that in the 20 ng/ml group was significantly higher than other groups ( P＜0.01 ).Compared with control group,the transmembrane migration of asthmatic ASMCs from other groups was significantly increased (P＜0.01 ).The transmembrane migration of asthmatic ASMCs from treated groups was significantly increased than asthma group (P＜0.01).The migration of asthmatic ASMCs from TNF-α+anti-TLR4 antibody group,TNF-α+Wortmannin group and TNF-α+Wortmannin+PDTC were significantly decreased than that of TNF-αgroup( P＜0.01 ).The migration of asthmatic ASMCs from TNF-α+Wortmannin+PDTC were significantly decreased than that of TNF-α+Wortmannin group (P＜0.05).ConclusionTLR4/PI3K-related signaling molecules involved in the transmembrane migration of asthmatic ASMCs induced by airway epithelial cells and may be one of the mechanisms of airway remodeling of asthma.

Objective To establish normative data for the fetal cisterna magna septa (CMS) at various gestational age,and to evaluate its clinical significance.Methods A total of consecutive fetal between 14 and 40 gestational week(GW) were included in this prospective study.The length and width of CMS were measured by two-dimensional ultrasonography.Regression analysis was used to study the relationship between the width and length of the fetal cisterna magna septa and gestational age.Twenty-five case of fetuses with the absence of CMS and 12 case of fetuses with the enlargement of CMS were retrospectively analyzed in the past six years in our hospital.Results ①The fetal CMS length and width increased gradually between 14 and 22 GW,then plateaued between 23 GW and 36 GW,and decreased after 37 GW.This ultrasonographic pattern was in agreement with normal development of rhombencephalon.②The absence of CMS in the fetuses were common in Dandy-Walker syndrome,holoprosencephaly,severe hydrocephalus,neural tube defects,rhombencephalon synapsis and Arnold-Chiari malformation.The enlargement of CMS in the fetuses may be shown in physiologic enlargement of posterior fossa.ConclusionsCMS is a potential new marker for normal development of rhombencephalon.The enlargement and absence of CMS are related to various malformations of central neural system,especially in the abnormalities of posterior fossa.

Objective To explore the time of application of hemoperfusion (HP) for the treatment of acute serious organophosphorus pesticide (ASOPP). Methods One hundred and four patients with ASOPP were randomly divided into two groups, 46 patients accepted traditional treatment(control group), 58 patients were treated with traditional treatment and HP (HP group). The patients in HP group were again divided into three groups according the different time of treatment (time of beginning HP after poisoning), the 4-8 hours group (HP-1 group, 27 patients), the 9-16 hours group (HP-2 group, 19 patients), the 17-32 hours group (HP-3 group, 12 pafients).Tbe coma period, the dosage of atropine, the time of regaining the vitality of cholinesterase, the time of hospitalization and the rate of fatality and curing among groups were observed. Results The coma period, the dosage of atropine, the time of regaining the vitality of cholinesterase, the time of hospitalization and the rate of fatality of the HP group were less than those of the control group (P<0.05). Compared with HP-1 group, the eoma period, the dosage of atropine, the time of regaining the vitality of eholinesterase and the time of hospitalization of the HP-2 group and the HP-3 group were higher (P<0.05), but the difference of the rate of fatality and curing between the HP-1 group and the other HP groups was not statistically significant (P>0.05). The difference of all of the above indicators between HP-2 group and HP-3 group was not statistically significant (P>0.05). Conclusion Application of hemoperfusion among 4-32 hours after poisoning for the treatment of ASOPP can improve the efficacy of therapy, and the efficacy of application of hemoperfusion among 4-8 hours is the best.