Objective To investigate the expression and clinical significance of CDx2 and hepatocyte antigen(Hep) in gastric carcinoma.Methods The expression of CDx2 and Hep in 9 cases of nomal gastric mucosa,15 cases of small intestinal mucosa,8 cases of colon mucosa,15 cases of intestinal metaplasia of the stomach and 130 cases of gastric carcinoma were detected with immuohistochemical EnVisionTM Systems measures.Results The positive rates of CDx2 expressed in the nomal gastric mucosa were 0,small intestinal mucosa 80%(12/15),colon mucosa 87.5%(7/8),intestinal metaplasia of the stomach 86.7%(13/15),gastric carcinoma 37.7%(49/130);The positive rate of Hep was 11.1%(1/9),86.7%(13/15),12.5%(1/8),100%(15/15),55.4%(72/130) respectively.There was much higher positive expression of CDx2 in intestinal-type carcinoma than in diffuse-type gastric carcinoma(P

Designed experiment teaching fits well with characteristic of naval hygiene training subjects on the sea.Attention should be paid to several key points including content selection,training plan design and teaching effect evaluation.It was proved that designed experiments enhanced the practical ability of the undergraduates and significantly improved the effect of naval hygiene training subjects.

AIM: To study the mechanism responsible for ONOO --induced the airway epithelial injury. METHODS: Effects of 3-aminobenzamide(3-AB), a poly-(ADP-ribose) polymerase(PARP) inhibitor, and Ac-DEVD-CHO, a caspase-3 inhibitor, on LDH release and apoptosis of cultured rat tracheal epithelial (RTE) cells induced by ONOO - were examined. The cleavage of PARP was analysed by Western blot. RESULTS: 3-AB inhibited the release of LDH induced by ONOO - partially, and had no effect on the apoptosis of RTE cells. Caspase-3 inhibitor Ac-DEVD-CHO obviously prevented the apoptosis of RTE cells induced by ONOO - in a dose-dependent manner. The cleavage of PARP was observed in the process of apoptosis of RTE cells induced by ONOO -. CONCLUSIONS: PARP activation represents one of the pathways of ONOO --mediated epithelial injury, and the excessive activation of PARP contributes to the necrosis in RTE cells induced by ONOO -. Cleavage of PARP by activated caspase-3 plays a crucial role in the apoptosis of RTE cells induced by ONOO -.

AIM: To elucidate the anti-inflammatory mechanism of cholecystokinin octapeptide (CCK-8). METHODS: The pulmonary interstitial macrophages (PIMs) from rats were stimulated with LPS (1 mg?L~(-1)) in the presence or absence of CCK-8 (10~(-8)-10~(-6) mol?L~(-1)) or/and CCK receptor antagonist proglumide (2 mg?L~(-1)). The expression of TNF-? mRNA was assayed by reverse transcription polymerase chain reaction (RT-PCR) at 3 h of the stimulation, and nuclear factor-?B (NF-?B) binding activity was analyzed by electrophoretic mobility shift assay (EMSA) at 1 h of stimulation. The I?B? protein level in the cytoplasma at 30 min of the stimulation was detected by Western blot. RESULTS: CCK-8, at concentrations from 10~(-8) mol?L~(-1) to 10~(-6) mol?L~(-1) obviously inhibited LPS-induced TNF-? mRNA expression and NF-?B binding activity in a dose-dependent manner. Stimulation with LPS resulted in a reduction of I?B? protein level in PIMs, which was elevated by CCK-8. The effects of CCK-8 on NF-?B activity and I?B protein level were attenuated by CCK receptor antagonist proglumide. CONCLUSION: CCK-8 inhibits LPS-induced TNF-? mRNA expression by regulating NF-?B activity in rat PIMs, which is mediated through CCK receptors and inhibition of I?B? degradation. This represents one of the anti-inflammatory mechanisms of CCK-8.

Objective To explore the variation of insulin like growth factor-I (IGF-I) and glucose and correlation in children with sepsis. Methods Forty-two children with sepsis in pediatric intense care unit were enrolled from January 2009 to January 2010. In the morning (2nd morning) after admission, the blood glucose, serum IGF-I, cortisol, insulin, IL-6, and IGF-binding protein-I (IGFBP-1) were detected. In the 3rd and 5th morning, the serum IGF-1 was detected again. According to the blood glucose level of the 2nd morning, the children with sepsis were divided into hyperglycemia group and normal group. Meanwhile, 60 healthy children were served as control group. The data had been compared among three groups. Results In the 2nd morning, the levels of blood glucose, serum IGF-I, cortisol, insulin, and IL-6 were signiifcantly different among three groups (all P<0.05), but the serum IGFBP-I was not signiifcantly different (P>0.05). Compared with control group, the sepsis children with hyperglycemia and with normal blood glucose all had signiifcantly higher serum levels of cortisol and IL-6, and signiifcantly lower serum level of IGF-I. In the 2nd, 3rd, and 5th morning, the serum levels of IGF-1 were not signiifcantly changed with time in sepsis children with hyperglycemia and with normal blood glucose (all P>0.05). Meanwhile, there were no signiifcant differ-ences in the serum levels of IGF-1 between sepsis children with hyperglycemia and with normal blood glucose in the 2nd, 3rd, and 5th morning (all P>0.05). In children with sepsis, the blood glucose and serum IGF-1 was not correlated in the next morning (r=0.152, P=0.267). Conclusions The serum level of IGF-I decreased but maintain stable in children with sepsis. The change of blood glucose may be not related with IGF-I.

AIM and METHODS: to elucidater the effect of poly(ADP-ribose) polymerase(PARP) on tracheal hyperreactivity of guinea - pig induced by peroxynitrite, the responses of guinea pig tracheas to histamine af- ter incubation with peroxynitrite in the absence and presence of 3 - aminobenzamide(3 - AB), a highly selective inhibitor for PARP, were observed in vitro. RESULTS: The exposure of tracheal strips to peroxynitrite led to epithelial damage and hyperreacitivity to histamine, both of which were reversed by 3 - AB(l mmol/L or 5mmol/L), whereas incubation of tracheal strips with 3 - AB(5 mmol/L) had no effect on the reponses. CONCLUSION:PARP is involved in the epithelial damage and hyperreactivity of guinea - pig tracheas induced by peroxynitrite. The results suggested that inhibition of excessive activation of PARP may represent a novel strategy for the prevention and therapy of airway hyperreactivity in asthma.

AIM: To explore the effect of peroxynitrite (ONOO -) on pulmonary microvascular endothelial barrier and roles of ONOO - in the pathogenesis of acute lung injury in vivo. METHODS: SD rats in different groups were insufflated with various concentrations of ONOO -, decomposed ONOO - or vehicle (alkaline normal saline), respectively. Then permeability changes in pulmonary microvascular walls were detected and the pathological alterations of pulmonary tissue were examined under light microscope. Malondialdehyde(MDA) contents were measured in normal lung homogenate pretreated with various concentration of ONOO -. RESULTS: Intratracheal insufflation of ONOO - resulted in dose-dependent increase in lung coefficient, lung wet/dry ratio, lung water contents and Evans blue contents, together with significant pulmonary pathological changes such as diffuse alveolar collapse, capillary congestion, focal hemorrhage, and endothelial swollen. In addition, ONOO - can also elicit increase in MDA contents in normal lung homogenate. CONCLUSION: ONOO - may induce dysfunctions of pulmonary microvascular endothelial barriers, it is suggested that enhanced endogenous ONOO - generation may take part in the pathogenesis of acute lung injury.

Objective To investigate the variation of interleukin-6 ( IL-6 ) , vascular endothelial growth factor(VEGF),E-selectin and intercellular adhesion molecule-1(ICAM-1)in children with sepsis and the clinical significance. Methods This was a prospective and control study. Thirty-two children diagnosed as sepsis in PICU from December 2008 to December 2009 served as the sepsis group. According to whether there was a shock, sepsis group were divided into shock subgroup and no shock subgroup. Fifteen healthy children served as control group. The serum levels of IL-6,VEGF,E-selectin and ICAM-1 were detected with enzyme linked immunosorbent assay. Results The serum level of IL-6 was 65. 00(30. 49~237. 14) ng/L in shock subgroup and 48. 68(30. 25~75. 00) ng/L in no shock subgroup,which were significantly higher than that in control group[0. 80(0. 60 ~1. 00) ng/L](P<0. 05). There was no significant difference between shock subgroup and no shock subgroup. The serum levels of VEGF and E-selectin showed no significant differences among the three groups. The serum level of ICAM-1 was 998. 72(666. 93~1 526. 44) ng/ml in shock subgroup,and 925. 71(683. 53~1 225. 12) ng/ml in no shok subgroup,which were significantly high-er than that in control group[660. 59(525. 48~685. 47) ng/ml]. Compared with those who survived in sep-sis group,the serum levels of VEGF and E-selectin in the died children with sepsis showed no significant difference,but IL-6 and ICAM-1 significantly increased(P<0. 05). Conclusion IL-6 and ICAM-1 increase greatly and accentuate inflammation in septic patients,the changes of which may help to determine the prog-nosis of sepsis.

Objective To study the signification of p57kip2 immunostaining to distinguish molar gestations from hydropic abortions.Methods To observe the p57kip2 immunohistochemical expression in 58 cases of histological hydropic villi which were divided into complete mole(18 cases) ,partial mole(19 cases),hydropic abortion(11 cases)and undetermined hydropic abortion or molar gestations(10 cases) and in 3 normal placentas.Results Normal villi,partial mole and hydropic abortions show positive staining for p57kip2, which expressed in the nuclei of cytotrophoblast and villous mesenchyme,and complete moles show complete absence of staining in the cytotrophoblast and villous mesenchyme.According to the comparison of the diagnosis based on morphology and the one based on p57kip2 stai-ning,the later whose sensitivity is 96% (46/48) confirmed the earlier diagnosis in 58 cases studied and the later conformed to the earlier very well.Conclusion The immunohistochemical staining for p57kip2 is a valuable diagnostic mean to distinguish molar gestations from hydropic abortions and is a sensitive and specific marker for the diagnosis of complete mole.

AIM:To study the effect of ONOO- on the airway epithelial injury. METHODS: The mitochondrial respiration, the amount of lactate dedydrogenase (LDH) release into the cell culture medium, the levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG), and the cellular apoptosis were examined after exposure of cultured rat tracheal epithelial (RTE) cells to ONOO-. RESULTS: Exposure of RTE cells to 0.25, 0.5 and 1 mmol/L ONOO- caused a dose-dependent suppression of the mitochondrial respiration . ONOO- also caused a dose-dependent increase in the percentage of LDH release. Exposure of RTE cells to ONOO- resulted in an increased generation of 8-OHdG in a dose-dependent manner. ONOO- caused an increase in apoptotic percentage in RTE cells in a time-dependent manner at different concentrations. CONCLUSION: ONOO- could cause necrosis and apoptosis in cultured RTE cells. Low concentration of ONOO- caused apoptosis in a time-dependent manner. Whereas exposure to high concentration of ONOO- resulted in cell necrosis, ONOO- caused a dose-dependent increase in the percentage of LDH release. Suppression of mitochondrial respiration and oxidative DNA damage by ONOO- may be the major cause of cellular injury induced by ONOO-.