Objective To explore the effects of prenatal exposure to lead on learning and memory of rats' offspring. Methods The pregnant rats were randomly divided into 4 groups provided with double evaporated water, 50, 100 and 200 mg/L lead acetate solution via drinking water respectively. The lead-exposure period for exposure groups was limited from the 1st day after pregnancy to the 20th day when the offspring began to be weaned. For learning ability 20-day old offspring were tested by water maze. For active learning and memory ability, the 20-day old, 40-day old and 60-day old offspring were tested by Y maze. Results The frequency of the mistakes in water maze made by offspring increased with the increase of the prenatal lead-exposure doses of their mothers and showed significantly higher levels in 100 and 200 mg/L groups compared with that of control group (P0.05). But the qualified rates of 0-min and 24-h escape for 100 and 200 mg/L groups showed sigificantly lower levels compared with that of control group when they were 60-day old (P

Objective To observe the toxicity of diesel exhaust particles extracts(DEPE) on V79 cell in cell viability, membrane and oxidative stress. Methods Cell exposed different concentrations of DEPE for different time , the change of cell viability, the leakage of intracellular lactate dehydrogenase(LDH), intracellular glutathione(GSH) and glutathione peroxidase (GPX)content were determined respectively, and analyzed the relation between GSH and GPX. Results The results showed that the viability of V79 cell decreased and the leakage rate of lactate dehydrogenase increased gradually in according with the increasing dosage of DEPE,and that DEPE could impair V79 cell by oxidative stress, included intracellular GSH content decreased and the activity of GPX increased, indicating that GPX might play a important role in DEPE induced GSH depletion. Conclusion DEPE may impair cell viability and the cell membrane integrity, also impair cell by oxidative stress.

Objective To improve the diagnosis and treatment of liver trauma. Methods We retrospectively analyzed different therapeutic means on liver trauma including 79 cases with operative treatment and 27 cases with nonoperative treatment. Results In nonoperative treatment group, 25 cases were cured, 2 cases died. In operative treatment group, 73 cases were cured, 6 cases died. Cure rate was 92.5%(98/106), mortality was 7.5%(8/106). 5 cases died of major blood vessels rupture, 3 cases died on multiple organ function failure. Postoperative complications included 3 cases of subphrenic infection, 10 cases of hepatic abscess, 8 cases of pleural hydrops, 7 cases of incisional infection. Conclutions Type I of liver trauma can be treated by nonoperation, type Ⅱ～Ⅳ of blunt liver trauma can be treated by nonoperation on the condition of intensive monitoring. Type Ⅱ～ Ⅵ of liver trauma should be operated on emergently in case of massive intraabdominal bleeding and combined organ injury.

Objective: To investigate the effect and mechanism of emodin (EMO) on human pancreatic cancer cell line BxPC-3 in vivo. Methods: After the pancreatic cancer model in nude mice was established, the mice were divided into four groups: control group (NS 0.2mL/d by i.p. injection), EMO group (EMO 40mg?kg-1?d-1 by i.p. injection), and Gemcitabine (GEM) group (GEM 80mg/kg, twice/week by i.p. injection) with 8 mice each group. After 2 weeks of administration, the mice were sacrificed, detected the body-weight change of nude nice before and after the experiment, and recorded the growth inhibition rate of tumor (TGI). Immunohistochemical (IHC) staining for ki-67 and terminal deoxynucleotidyl transferase-mediated nicked labeling assay (TUNEL) were undertaken to detect the cell proliferation and cell apoptosis in tumor tissue in xenograft nude mice. Results: The inter-group comparisons in body-weight of nude mice showed no significant difference in comparing group NS(27.0?1.64)g with group EMO(25.1?1.58)g and GEM(25.6? 1.47)g.The EMO group was 38.46%, the GEM group was 44.23%. The inter-group comparisons in immunohistochemical analysis of ki-67 showed significant difference in comparing group NS IOD(219.5?17.98) with group EMO IOD(146.6? 11.57)and GEM IOD(139.5?12.55), (P

Objective To study the effects of arsenic trioxide ( As2 O3 ) on inhibiting the proliferation of pancreatic carcinoma cell lines. Methods The inhibiting rate of As2O3 and Fluorouracin(5-Fu) ,Gemcitabine(GEM) on pancreatic carcinoma cell lines PC-3 were detected by using CCK-8 assay. Results As compared with 5-Fu、GEM,the inhibiting rate of As2O3 was the highest one( P ＜ 0.01 or P ＜ 0.05). Conclusion As2O3 can inhibit pancreatic carcinoma cell lines PC-3 effectively in vitro. The effects of As2O3 on inhibiting the proliferation of pancreatic carcinoma cell lines was stronger than 5-Fu and GEM. This is possibly due to the extensive and unique anticancer mechanism of As2O3.

Objective To evaluate different treatment modaltities for limited (local) hepatic metastasis in patients of colonic carcinoma Methods We conducted a retrospective analysis on 81 cases of colonic cancer suffering from hepatic local metastasis from 1987 to 2000 Results The 1、3、5 year survival rate was 85%、 46% and 32% respectively for patients underwent resection of metastatic liver cancer, and 26%、 0 and 0, respectively for those not having the metastatic liver cancer resected ( P 0 05) Conclusion Resection or ablation therapy promises a much longer long term survival than do nothing in colonic cancer patients with local liver metastatic tumor

Objective:To evaluate the effect of emodin on acute rejection after orthotopic liver transplantation(OLT) in rats.Methods:The LEW→BN OLT models were established.A total of 45 rats were divided randomly and equally into 3 groups:group A was treated with normal saline at dose of 0.5 ml/d intraperitoneally from 1st day to 8th day after operation;Group B,CsA at dose of 10.0 mg?kg-1?d-1;Group C,emodin at dose of 50.0 mg?kg-1?d-1.8 days after operation,6 recipients of each groups were killed for confirming rejection-active index(RAI) and hepatocellular apoptosis index(AI) by observing the pathologic change of transplanted liver in recipients.The other recipients were raised for observing the survival time.Results:Respectively,the survival time(days) of group A,B,C was 9.50?1.64,21.57?2.15,21.29?2.21.The survival time of group B,C was significantly longer than that of group A(P0.05).Respectively,the RAI of group A,B,C was 7.67?0.9,5.17?0.40,5.83?0.75 and the AI of group A,B,C was 35.83?2.32,15.83?1.33,16.50?2.35.The RAI and AI of group B,C was significantly lower than that of group A(P0.05).Conclusion:Emodin can reduce the hepatocellular apoptosis and suppress the acute rejection after OLT in rats.

In view of gemcitabine resistance has limited clinical activity of gemcitabine as a cellulotoxic drug in pancreatic cancer patients, this study is designed to investigate the effect of emodin on the sensitivity of pancreatic cancer to gemcitabine as well as its mechanism. After gemcitabine-resistant pancreatic cancer cell line (SW1990/GZ) was established by escalating doses of gemcitabine serially in pancreatic cancer cell line (SW1990). The cellular proliferation was detected by cell counting kit-8 (CCK-8) assay. Flow cytometry (FCM) was used to determine apoptosis of pancreatic cancer cells. The activity of NF-kappaB in pancreatic cancer cells was measured by electrophoretic mobility shift assay (EMSA). Western blotting was used to detect the protein expression of Bcl-2 and Survivin in SW1990/GZ cells. Metastatic model simulating human pancreatic cancer was established by orthotopic implantation of histologically intact human tumor tissue into pancreatic wall of nude mice. Also, immunohistochemistry was used to detect the positive expression of Ki-67, NF-kappaB, Bcl-2 and Survivin in the tumors. The results show that pretreatment of cells with emodin followed by gemcitabine induced a higher percentage of growth inhibition and apoptosis of pancreatic cancer cells than that of gemcitabine alone. In addition to in vitro results, emodin in combination with gemcitabine is much more effective as an antitumor agent compared to either agent alone in the orthotopic tumor model. Further study showed that the emodin with or without gemcitabine significantly down-regulates NF-kappaB and its regulated molecules such as Bcl-2 and Survivin proteins both in vitro and in vivo. It is concluded that inactivation of NF-kappaB signaling pathway by emodin resulting in the chemosensitization of pancreatic cancer to gemcitabine, which is likely to be an important and novel strategy for the treatment of pancreatic cancer.

Objective To explore the prevention and treatment of lymphorrhagia due to lymph node dissection in gastric carcinoma. MethodsClinical data of 743 patients undergoing radical gastrectomy plus lymphadenectomy from January 1997 to March 2004 were analyzed retrospectively. ResultsThe patients in D3 or D4 lymphadenectomy suffered from a higher lymphorrhagia rate than those in D2 lymphadenectomy(P

Objective To explore the clinicopathological characteristics of early gastric cancer (EGC),surgical treatment, and prognosis in elderly patients. Methods The clinicopathological and follow-up data in 83 elderly patients with EGC treated by gastrectomy from 1989. 8-2004. 8 were studied retrospectively. Results All of 83 patients were resectable, and there was no operative death nor surgical complications. The 5-, 10-, and 15- year survival rate was 98%,95%,and 92%, respectively. Sixty-one cases (74%) were mucosal cancer without lymph node metastasis, 22 cases were submucosal cancer with node metastasis in 4 cases. 7 cases were multiple primary carcinoma. Conclusions Local resection and partial gastrectomy are not suitable for multiple primary carcionoma in elderly patieats with EGC. Subtotal gastrectomy, and total gastrectomy should be the procedure of choice when foci were scattered about. Lymph node metastasis,multiple primary cancer foci and invasion of submucosal layer are all among factors impacting postoperative prognosis.