Objective To investigate the effects of esmolol on ATPase activity in myocardial mitochondria after resuscitation in rats.Methods Sixty-six male Wistar rats were randomly allocated to three groups:sham group,AD group,AD+Es group.A cardiac arrest model was reproduced by asphyxiation in rats,and then CPR was performed in these animals after 10min asphyxia.The ATPase activity of myocardial mitochondria was determined at 30th,120th and 180th minute after resuscitation.ECG,MAP,HR and temperature were measured continuously.Results Heart rates were significantly higher after adrenaline when compared with sham group.Myocardial mitochondria ATPase activity was decreased significantly in both AD and AD+Es group compared with that of sham group(P

Objective: To investigate the effect of nerve growth factor-β(NGF-β) on the proliferation and cell cycle of human pancreatic cancer MIA PaCa-2 cells. Methods: MIA PaCa-2 cells were treated with different concentrations of NGF-β and K252a (inhibitor of NGF-β receptor TrKA) alone or in combination. Clone forming rate, proliferation, and cell cycle of MIA PaCa-2 cells treated with different strategies were examined by clone formation assay, MTT, and flow cytometry, respectively. Results: NGF-β significantly increased the clone formation and proliferation of MIA PaCa-2 cells (P<0.05, P<0.01). K252a significantly inhibited the proliferation of MIA PaCa-2 cells (P<0.05), while NGF-β combined with K252a had no significant effect on the proliferation of MIA PaCa-2 cells. NGF-β arrested MIA PaCa-2 cell cycle in S phase, K252a arrested cell cycle in G_0/ G_1 phase, and NGF-β combined with K252a arrested cell cycle in S phase. Conclusion: NGF-β can enhance the proliferation of pancreatic carcinoma MIA PaCa-2 cells.

Objective To investigate the cerebral protective effects of propofol and ketamine against ischemia-reperfusion injury induced by cardiac arrest in rats. Methods One hundred and twenty male SD rats weighing 180-250 g were randomly divided into four equal groups of 30 animals : group A served as control without cardiac arrest;group B was subjected to 10 minutes of cardiac arrest followed by resuscitation ( C-R); group C received propofol 10 mg 100 ?g-1 ip 10 min before C-R; group D received ketamine 10 mg-100? g-1 ip 10 min before C-R. The animals were anesthetized with isoflurane inhalation by mask, intubated and mechanically ventilated. Anesthesia was maintained with isoflurane inhalation. Cardiac arrest was induced by asphyxiation (vecuronium 0.01 mg - 100 g -1, disconnection of ventilator, tracheal tube clamping) and maintained for 10 min, then resuscitated. Seven animals in each group were killed at 30 min (T, ) , 120 min (T,) and 180 min (T3 ) after successful resuscitation respectively for determination of serum TNF-a and IL-Ip and cerebra) SOD activity and MDA content. Results Cerebral SOD activity in group C and D was significantly lower than that in group A but higher than that in group B, while cerebral MDA content in group C and D was significantly higher than that in group A but lower than that in group B ( P

Objective To investigate the role of the expression of prostate stem cell antigen(PSCA)in the development of perineural invasion in pancreatic carcinoma.Methods The histopathologic and immunohis-tochemical(SABC)studies were performed on 80 patients with pancreatic carcinoma.The overall incidence of PSCA expression,perineural,lymphatic and vascular vessel invasion were counted to investigate the relationships among them.Results Perineurel invasion was positively correlated with lymphatic and vascular vessel invasion (P<0.01).A positive corelation Was found between tumor PSCA expressioa(53 cases)and the perineurel in-vasion(66 cases).A definite correlation Was also found between cancer differentiation and PSCA tyxplres-sion.Conclusion PSCA is one of the most important molecules and may play a role as a "navigating" and " docking" molecule in the developmeat of perineural invasion.

pancreatic carcinoma by some signal transduction.

Objective To evaluate the efficacy and toxicity of three dimensional confoimal radiotherapy(3D-CRT)concurrent taxotere for patients with esophageal carcinoma.Methods Ninty-six patients with esophageal carcinoma were received 3D-CRT concurrent taxotere,the radiotherapy was carried out by 3D-CRT,to a total dose 95% PTV 66Gy/33f/6.6W.The trial results were evaluated by the clinical curative effect criterion.Results Complete response rate(CR)was 67.7%.Overall response rate(CR+PR)was 89.6%.The local control rates of 1 year and 3 years were 86.5% and 63% ,respectively.The survival rates of 1 year and 3 years were 76.1% and 50.0%,respectively.The main acute toxic effect was radioactive esophagitis.Conclusions 3D-CRT concurrent taxotere could improve the overall response rate and survival rate of esophageal carcinoma.Although it increased the acute toxic effect,the patients could accept the therapy.

Objective To investigate nerve growth factor (β-NGF) and its receptors expression in human pancreatic ductal adenocarcinoma. Methods Expression and distribution of β-NGF, tyrosine kinase A (TrKA) and P75NGFR were detected in operation tissue specimens of pancreatic ductal adenocarcinoma with immunohistochemistry and real-time PCR. Relations of β-NGF and its receptors with clinicalpathological characters, especially nerve invasion were analyzed. Results β-NGF and TrKA expression are higher in pancreatic adenocarcinoma than normal pancreas, and the differences are significant (P < 0. 01). Β-NGF and TrKA expression are associated with the differentiation grades(DG), lymphatic node metastasis, nerve invasion and surgical pathological stages. Poorer of DG and later stages, more expression of β-NGF and TrKA. Β-NGF and TrKA expression have positive correlations. Β-NGF, TrKA and P75NGFR mRNA expression have significantly increased 3.84,4. 23 and 2. 41 times than normal tissues by real-time PCR, respectively. Conclusions β-NGF and TrKA might play potential rules in carcinogenesis for pancreatic cancer,have affinity with clinicopathological characters of pancreatic cancer. Β-NGF and TrKA may have mutual effect in signal transduction leading to perineural invasion of pancreatic carcinoma.

Objective To investigate the expression and the role of osteopontin(OPN)and matrix metalloproteinase-9(MMP-9)in the invasion and metastasis of pancreatic carcinoma.Methods Human pancreatic cancer cell line MIA PaCa-2 was cultured in vitro.The location of OPN protein in pancreatic tumor cell line was detected by immunofluorescence staining.100 cases of pancreatic cancer and 40 cases of adjacent normal pancreatic tissues were used to analysis.The expressions of OPN and MMP-9 were investigated by immunohistochemistry assay.Results OPN expressed in the cell membrane and cytoplasm,OPN and MMP-9 in pancreatic cancer tissues positive rates were 73.0%(73/100)and 68.0%(68/100),which were higher than that in adjacent normal pancreatic tissues(all P ＜ 0.05).OPN and MMP-9 expression were associated with pancreatic tumor grade,lymph node metastasis and perineural invasion of pancreatic cancer(P ＜ 0.05).OPN and MMP-9 in pancreatic cancer tissues were positively correlated(r,=0.39,P ＜ 0.01).Conclusions OPN and M MP-2 might play an important role in the development of invasion and metastasis of pancreatic carcinoma.OPN and MMP-2 might play synergetic roles in the progression of pancreatic carcinoma.

Objective To investigate artemin and its receptors GFRα3 expression in human pancreatic ductal adenocarcinoma and its significance. Methods Expression and distribution of artemin and GFRα3 in 100 cases of human pancreatic ductal adenocarcinoma(PDAC) and 40 cases of normal pancreatic tissue were detected by immunohistochemistry and RT-PCR, quantitative RT PCR. Relations of artemin and GFRα3 with clinicopathological characteristics, especially nerve invasion were analyzed. Results Nerve invasion was detected in 64 out of 100 cases of PDAC, and the rate of nerve invasion was 64%. The ratio of expression of Artemin, GFRα3 protein in PDAC/normal pancreatic tissue was 2.697 ± 0.231 and 2.599 ± 0.588; the ratio of expression of Artemin, GFRα3 mRNA was 7.01 and 4.63. Artemin and GFRα3 expression were associated with tumor location, differentiation degree, TNM staging, nerve invasion node metastasis, but it was not associated with age, sex and tumor size. Artemin and GFRα3 expression was more positively expressed in cancer cells close to nerve tissue than cells far from nerve tissue. Conclusions Artemin and GFRα3 were involved in the development of pancreatic cancer and their high expression was closely related to perineural invasion.

Objective To investigate the effects of artemin and its receptor GFRα - 3 on the invasion and metastasis of pancreatic cancer cells. Methods Human pancreatic cancer cell line MIA PaCa -2 was used in this study. Transwell cell culture chamber assay in vitro was used to detect the ability of invasion and metastasis of MIA PaCa -2 cells. The influence of artemin and GFRα -3 on the protein expression of MMP-2 and E-cadherin was investigated by Western blot and quantitative real time polymerase chain reaction-analyses (Q-RT-PCR). Results As the increase of artemin and GFRα -3, the invasion and metastasis of MIA PaCa- 2 was markedly increased [ 150 ng / ml concentration: Artemin group: 107.4 ± 11.4;GFRα3 group:94. 4 ± 9. 3 ;control group:34. 6 ± 7. 3, P < 0. 01 ]. With 150 ng / ml artemin and GFR-3,the synthesis of MMP-2 in MIA PaCa 2 cells was significantly increased than that in control group[ Artemin grou: (2. 17 ± 0. 05 ) × 108; GFRα3 group: (2. 02 ± 0. 03 ) × 108; control group: ( 1.02 ± 0. 02 ) × 108, t =6. 35,7. 32 ], while E-cadherin significantly decreased [ Artemin group: ( 0. 65 ± 0. 04 ) × 108; GFRα3 group: (0. 74 ± 0. 01 ) × 108; control group: ( 1. 36 ± 0. 03 ) × 108, t = 4. 27,5.61 ], the difference was statistically significant ( P <0. 01 ). Conclusions Artemin and its receptor GFRα3 could promote pancreatic cancer cell invasion and metastasis. This effect may be related to the up-regulated expression of MMP-2 and down regulated expression of E-cadherin.