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As one of the most widely used anti-diabetic drugs for type II diabetes, metformin has been shown to exhibit anti-cancer activity in recent years. Epidermal growth factor (EGF) and its receptor, EGFR, play important roles in cancer metastasis in various tumors, including breast cancer. Epithelial-mesenchymal transition (EMT) is a critical process for cancer invasion and metastasis. In this study, we use EGF as a metastatic inducer to investigate the effect of metformin on cancer cell migration, invasion and EMT.Human breast cancer MCF-7 cells were exposed to EGF with or without metformin or N-acetyl cysteine (NAC). The effects of metformin on breast cancer cell proliferation were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. The production of reactive oxygen species (ROS) was tested using 2,7-dichlorodihydrofluorecein diacetate (DCFH-DA). The migratory and invasive abilities of tumor cells were analyzed using wound healing assay and transwell invasion assay, respectively. The expressions of E-cadherin, N-cadherin and Snail were tested using real-time quantitative polymerase chain reaction (qRT-PCR) and western blotting at mRNA and protein levels. The activation of protein kinase B (Akt) and nuclear factor kappa B (NF-κB) were measured by western blotting.Our results showed that metformin inhibited breast cancer cell proliferation in a dose-dependent manner with or without EGF. EGF-induced alterations in cell morphology that are characteristic of EMT were reversed by metformin. Metformin also inhibited the EGF-modulated expression of E-cadherin, N-cadherin and Snail and further suppressed cell invasion and migration. In addition, metformin suppressed EGF-induced phosphorylation of Akt and NF-κB. ROS is involved in EGF-induced cancer invasion and activation of phosphatidylinositol 3-kinase (PI3K)/Akt/NF-κB pathway.Taken together, these data indicate that metformin suppresses EGF-induced breast cancer cell migration, invasion and EMT through the inhibition of the PI3K/Akt/NF-κB pathway. These results provide a novel mechanism to explain the role of metformin as a potent anti-metastatic agent in breast cancer cells.

Objective Skill competence is essential for nursing students and experiential teaching method has become increasingly popular in China's nursing education. To systematically evaluate the effects of experiential teaching method on the development of nursing students’ skill competence, and to provide evidence for nursing education. Methods The China National Knowledge Infrastructure, VIP, Wanfang Data, PubMed, and Web of Science databases were searched from their inception until November 28, 2019. We screened the studies according to inclusion and exclusion criteria, extracted the data, and assessed the quality. Then, a meta-analysis was conducted. Results Totally 15 studies were included, and 1,633 nursing students were analyzed by Review Manager5.3 and Stata15.1 software. The results show that the experiential teaching method can significantly improve nursing students’ nursing skills such as training (SMD = 1.05, 95% CI: 0.95–1.16, P = 0.000), learning interest (ES = 0.93, 95% CI: 0.79–1.06), ability to analyze and solve problems (ES = 0.75, 95% CI: 0.55–0.94), ability to judge and innovative thinking (ES = 1.01, 95% CI: 0.77–1.25), abilities of understanding and perception (ES = 0.59, 95% CI: 0.34–0.83), and teaching satisfaction (ES = 1.26, 95% CI: 1.13–1.4). Conclusions The results suggest that the experiential teaching method is more effective for the nursing students’ skill competence than traditional teaching in China. However, due to the heterogeneity and bias risk, a large sample and high-quality studies are needed in future to confirm its effectiveness.

Background/Aims: The accurate staging of pancreatic cancer (PanCa) is crucial in the development of a stage-specific treatment plan for PanCa patients. We aimed to perform a meta-analysis of endoscopic ultrasonography (EUS) in the tumor node (TN) staging and evaluation of vascular invasion in PanCa. Methods: A meta-analysis of diagnostic accuracy parameters was performed to evaluate the EUS-based TN staging, and vascular invasion by PanCa was compared to the results of intraoperative staging or to the histopathology of resected specimens. Results: Twenty studies with 726 PanCa cases were identified from 281 articles. The pooled sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), and diagnostic odds ratio (DOR) were 0.72, 0.90, 6.27, 0.28, and 24.69, respectively, for T1-2 staging and 0.90, 0.72, 3.58, 0.16, and 24.69, respectively, for T3-4 staging. The overall sensitivity, specificity, PLR, NLR, and DOR were 0.62, 0.74, 2.54, 0.51, and 6.67, respectively, for N staging (positive vs. negative) and 0.87, 0.92, 7.16, 0.20, and 56.19, respectively, for vascular invasion. The area under the curve was 0.90, 0.90, 0.79, and 0.94 for T1-2 staging, T3-4 staging, N staging, and vascular invasion, respectively. Conclusions: EUS is a reliable and accurate diagnostic tool for the TN staging and evaluation of vascular invasion in PanCa. The nodal staging accuracy using EUS is less satisfactory. i 2014 S. Karger AG, Basel

Smoking and chronic stress are well-documented risk factors that are associated with β-adrenoceptors in the development of pancreatic cancer. Stimulation of β-adrenoceptors can activate cyclic adenosine monophosphate (cAMP)/ protein kinase A (PKA) and mitogen-activated protein kinase (MAPK) pathways in pancreatic cancer cells. Many recent studies have focused on the function of β-adrenoceptors in cancer invasion. Thus, we hypothesized that β-adrenoceptors may play a role in pancreatic cancer invasion, and β-blockers may suppress the pancreatic cancer invasion and proliferation. MIA PaCa-2 and BxPC-3 cell lines express mRNA and protein of both β1 and β2-adrenoceptors. β2-adrenergic antagonist ICI118,551 and β1/2-adrenergic antagonist propranolol significantly suppressed cell invasion and proliferation in comparison to β1-adrenergic antagonist metoprolol and control in a Matrigel invasion assay and subrenal capsular assay. Treatment with β2-adrenoceptor antagonists inhibited activation of transcription factors nuclear factor κB (NF-κB), activator protein 1 (AP-1) and cAMP response element binding protein (CREB) as demonstrated by electrophoretic mobility shift assays and Western blotting. β2-adrenoceptor antagonists also significantly altered vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2), matrix metalloproteinase 2 (MMP-2) and MMP-9 expression. The β2-adrenergic antagonists suppressed invasion and proliferation by inhibiting both cAMP/PKA and Ras, which regulate activation of the MAPK pathway and transcription factors, such as NF-κB, AP-1 and CREB, as well as expression of its target genes, MMP-9, MMP-2 and VEGF. However, β1-adrenergic antagonists suppressed invasion by inhibiting only the cAMP/PKA pathway, suggesting that they may be useful as novel preventive and therapeutic strategies for pancreatic cancer.

This study examined the association between hector battifora mesothelial antigen-1 (HBME-1) expression and papillary thyroid carcinoma (PTC). A total of 206 patients were enrolled in the current study including 96 PTC patients and 110 patients with benign thyroid nodules (BTN). Immunohistochemistry (Envision) were performed to assess the expression of HBME-1. Receiver operating characteristic curve (ROC) curves were applied to evaluate the diagnostic tumor node metastasis (TNM) value of HBME-1. Specimens from 96 patients with PTC and 110 patients with BTC were reviewed. HBME-1 was positively immunostained in PTC tissue, which was significantly higher than that in BTN tissues (77.1 vs. 5.77 %, P 0.05). Immunohistochemistry also identified that HBME-1 expression did not show any statistically significant differences based on gender, age, tumor size, TNM stage, and lymph node metastasis (P 0.05). Importantly, HBME-1 expression was correlated with infiltration levels and differential levels in PTC (both P 0.05). HBME-1 was found to have high sensitivity (94.5 %) and specificity (77.08 %) for PTC diagnosis. Moreover, HBME-1 had a high specificity (83.33 %) at identifying the differential levels of PTC, but a low sensitivity (22.92 %). The sensitivity and specificity of HBME-1 identifying the infiltration levels of PTC were, respectively, 72.70 and 72.00 %. HBME-1 was highly expressed in PTC tissues, and HBME-1 can serve as a potential biomarker in the diagnosis of PTC.

BackgroundResveratrol is a natural compound suggested to have beneficial health effects. However, people are consuming resveratrol for this reason without having the adequate scientific evidence for its effects in humans. Therefore, scientific valid recommendations concerning the human intake of resveratrol based on available published scientific data are necessary. Such recommendations were formulated after the Resveratrol 2010 conference, held in September 2010 in Helsingør, Denmark.MethodologyLiterature search in databases as PUBMED and ISI Web of Science in combination with manual search was used to answer the following five questions: (1)Can resveratrol be recommended in the prevention or treatment of human diseases?; (2)Are there observed "side effects" caused by the intake of resveratrol in humans?; (3)What is the relevant dose of resveratrol?; (4)What valid data are available regarding an effect in various species of experimental animals?; (5)Which relevant (overall) mechanisms of action of resveratrol have been documented?Conclusions/significanceThe overall conclusion is that the published evidence is not sufficiently strong to justify a recommendation for the administration of resveratrol to humans, beyond the dose which can be obtained from dietary sources. On the other hand, animal data are promising in prevention of various cancer types, coronary heart diseases and diabetes which strongly indicate the need for human clinical trials. Finally, we suggest directions for future research in resveratrol regarding its mechanism of action and its safety and toxicology in human subjects.

To study the effects of L-arginine (L-Arg) on human colon carcinoma cell line LS174 through NO pathway and the mechanism.LS174 cells were cultured in the presence of L-Arg at different concentrations for different time. MTT assay was employed to evaluate the cell proliferation, and the cell morphological changes were observed by optical and electron microscopy. The apoptosis of L-Arg-treated cells was observed by the Annexin V/PI staining. The expression levels of VEGF, COX-2, p53, bcl-2 and bax in the cells were determined using Western blotting and immunocytochemical staining.L-Arg promoted the growth of LS174 cells at a low concentration (0.125 mmol/L) and inhibited the cell growth at higher concentrations (0.5, 2, 8, and 32 mmol/L). Under electron microscope, ultrastructual changes in the cytoplasm and nuclei of LS174 cells were observed 48 h after exposure to L-Arg. Some of the cells showed morphological changes characteristic of cell apoptosis such as cell size reduction, condensation and margination of the nuclear chromatin. Low concentration of L-Arg resulted in a cell apoptosis rate of 2.29%, as compared with the rate of 2.84% in the control group; at higher concentrations, L-Arg caused significantly increased cell apoptosis rates to 26.88%, 28.95%, 63.36%, and 84.51%, respectively. In cells treated with a low concentration of L-Arg, the expressions of VEGF and COX-2 were increased as compared with those in the control cells; higher concentrations of L-Arg obviously decreased the expressions of p53 and bcl-2 and increased the expression of bax.Low-concentration L-Arg can promote the growth of LS174 cells probably by up-regulating VEGF and COX-2 protein under the influence of NO, the metabolite of L-Arg. The inhibitory effect of high concentrations of L-Arg is probably mediated by inducing cell apoptosis via NO. The mechanism of L-Arg- induced cell apoptosis may be related to the up-regulation of bax protein and the down-regulation of p53 and bcl-2 proteins.

To examine whether beta-adrenoceptor (beta-AR) agonists can induce hypoxia-inducible factor (HIF)-1alpha accumulation which then up-regulate the expression of its target genes in pancreatic cancer cells at normoxia, and to further elucidate the mechanism involved.Pulse-chase assay, RT-PCR, and Western blot were employed to detect the effects of beta-AR agonists and antagonists, siRNA as well as several inhibitors of signal transduction pathways on MIA PaCa2 and BxPC-3 pancreatic cancer cells.Treatment of pancreatic cancer cell lines with beta-AR agonists led to accumulation of HIF-1alpha and then up-regulated expression of its target genes independently of oxygen levels. The induction was partly or completely inhibited not only by beta-AR antagonists but also by inhibitors of PKA transduction pathways and by siHIF-1alpha. Both beta1-AR and beta2-AR agonists produced the above-mentioned effects, but beta2-AR agonist was more potent.Activation of beta-AR receptor transactivates epidermal growth factor receptor (EGFR) and then elicits Akt and ERK1/2 in a PKA-dependent manner, which together up-regulate levels of HIF-1alpha and downstream target genes independently of oxygen level. Our data suggest a novel mechanism in pancreatic cancer cells that links beta-AR and HIF-1alpha signaling under normoxic conditions, with implications for the control of glucose transport, angiogenesis and metastasis.

To investigate the expression of survivin in acute pancreatitis in rats.Acute pancreatitis was induced in rats by retrograde injection of sodium taurocholate into the pancreaticobiliary duct. The expressions of survivin in the pancreatic tissues was detected by immunohistochemisty, Western blotting and RT-PCR, and the apoptotic ratio of the acinar cells was determined by TUNEL assay.Survivin was not detected in the control group, and in rat models of acute pancreatitis, the expressions of survivin protein and mRNA increased but the apoptotic index of the acinar cells decreased gradually with the severity of inflammation.Survivin is involved in the regulation of acinar cell apoptosis and also the necrosis of the apoptotic acinar cells through its anti-apoptosis activity to aggravate acute pancreatitis, suggesting its value as a promising marker in predicting the severity of acute pancreatitis.

To investigate the effect of resveratrol on the apoptosis of pancreatic acinar cells in rats with severe acute pancreatitis (SAP) and explore the mechanism of such effect.SD rats with 3.5% sodium taurocholate-induced SAP were treated with resveratrol, and the serum amylase was detected with automatic biochemistry analyzer. The apoptosis of the pancreatic acinar cells in the rats was detected by TUNEL assay, and the expression of Fas and FasL genes was determined by RT-PCR and Western blotting. The pathological changes of the pancreas were observed under optical microscope.Compared with SAP group, the resveratrol-treated rats showed obviously decreased serum amylase and scores for pancreatic histopathological lesions. Resveratrol treatment significantly increased the apoptotic indices of pancreatic acinar cells and the levels of FasL mRNA and protein in rats with SAP.Resveratrol produces important therapeutic effect on SAP in rats by inducing pancreatic acinar cell apoptosis possibly as a result of up-regulated FasL gene expression.

To test the effect of resvertrol on protecting the intestinal mucosal barrier in rats with severe acute pancreatitis.Twenty four SD rats were randomly divided into three groups: severe acute pancreatitis without treatments (SAP group), severe acute pancreatitis with sham-operations (SO group), and severe acute pancreatitis treated with resveratrol (RES group). Specimen were obtained 6 hours after the severe acute pancreatitis was induced. The endotoxin level in the blood taken from portal vein was measured with turbidimetry. Apoptosis of mucosal cells was detected by TUNEL methods. The expressions of Bax and Bcl-2 mRNA in intestinal mucosal cells were determined by semi-quantitative RT-PCR. Mitochondrial membranous electric potential of intestinal mucosal cells was measured by confocal microscopy.The RES group had less serum endotoxin in portal vein than the SAP group (P0.01). The SAP group had higher apoptotic index of mucosal cells than the RES group (P0.01). The SAP group had higher expression of Bax mRNA in intestinal mucosal cells and lower expression of Bcl-2 mRNA than the RES group (P0.01). The SAP group had lower mitochondrial membranous electric potential of intestinal mucosal cells than the REA group (P0.01).Resvertrol inhibits the apoptosis of intestinal mucosa cells and protects the intestinal barrier function, which might prevent the translocation of bacteria and endotoxin in patients with severe acute pancreatitis.

To investigate the antitumor effect of a benzoquinone ansamycin antibiotic, geldanamycin (GA), against HER2 /neu tyrosine kinase-overexpressing human breast cancer cell line SKBr3.To evaluate the antitumor activity of GA, the degradation of HER2 /neu tyrosine kinase in GA-treated SKBr3 cells was analyzed by Western blotting, their proliferation assessed using MTT assay, and the cell cycle distribution identified by flow cytometry. RT-PCR and Real-time PCR were employed to detect cyclin D1 mRNA expression and cell culture inserts model was used to evaluate the motility of the cells.GA induced a dose- and time-dependent degradation of HER2 /neu tyrosine kinase and cell proliferation inhibition. GA treatment obviously decreased the survival rates of the cancer cells, leading also to a dose-dependent G(1) arrest. The antitumor effects of GA proved to be relevant with declined transcription of cyclin D1. The GA-treated cells also exhibited reduced motility.GA can efficiently destabilize HER2 /neu tyrosine kinase and inhibit the proliferation and motility of human breast cancer cell line SKBr3 overexpressing HER2 /neu tyrosine kinase.

To construct the replication-incompetent recombinant adenovirus mediated shRNA to inhibit the neurite growth-promoting factor (Pleiotrophin, PTN) in pancreatic carcinoma and to study the inhibitory effect of shRNA-PTN recombinant adenoviruses on the neurite's growth of dorsal root ganglion neurons (DRGn).Four pairs of complementary single-stranded oligonucleotides (ss oligo) were designed and synthesized and then they were annealed to create a double-stranded oligonucleotide (ds oligo). The ds oligos were cloned into pENTR/U6 vector to produce the shuttle plasmid pENTR/U6-shRNA, which was transduced into pancreatic carcinoma cells by liposome after sequencing. The plasmid with good silence effect was chosen by RT-PCR to perform the LR recombination reaction to the adenovirus backbone plasmid. The expression clone was transfected into HEK293A cell to produce adenovirus. The silence of the recombinant adenovirus against PTN was detected by Western blot. After DRGn was co-cultured with pc-2 cell infected by shRNA-PTN recombinant adenovirus, the morphological changes of DRGn were observed.The pENTR/U6-shRNA shuttle plasmid was constructed and confirmed by sequencing. The recombinant adenovirus mediated shRNA against PTN was constructed. The best silence effect of the adenovirus against PTN was detected by Western blot on the 7th day after the pancreatic carcinoma cell was transfected. The growth of DRGn neurites was inhibited after the co-culture of DRGn with pc-2 cell which was infected by shRNA-PTN recombinant adenovirus.The PTN SiRNA recombinant adenovirus has been constructed and the silence effect against PTN in pancreatic carcinoma cell has been confirmed. The growth of DRGn neurites can be inhibited by shRNA-PTN recombinant adenovirus.

To investigate the efficacy of different interventional therapies for primary hepatic cell cancer (HCC).1126 HCC patients before or after hepatectomy were treated by different kinds of interventional therapies: transcatheter arterial chemoembolization (TACE), TACE and radio-frequency ablation (RFA), Chinese traditional medicine and biotherapy after TACE or the transcatheter arterial infusion (TAI). The results of liver function, alpha-fetoprotein, imaging, color-ultrasonography and survival rate were reviewed.874 patients were followed up for 2 to 63 months. The overall 1-, 3-, 5-year survival rate was 67.8% , 28.7% and 18.8%, respectively. The 1-, 3-, 5-year survival rate of patients who received TACE before hepatectomy was 74.7%, 41.4% and 36.9% ; after hepatectomy 78.9%, 40.4% and 37.5%, respectively. The response rate ( PR + NC) of TACE and RFA was 93.4%, and the 1-, 3-year survival rate was 74.5% and 36.8%, respectively, after TACE and RFA. The response rate (PR + NC) of TACE was 83.2% with 1-, 3-, 5-year survival rate of 69.3%, 21.7%, 8.4% after TACE, respectively. The response rate (PR + NC) of TAI was 27.5% with 1-, 2-year survival rate of 11. 6% and 0 after TAI. The Child grade of liver function, color-ultrasonography and alpha-fetoprotein of TACE + RFA group, TACE and TAI were compared. There was no significant difference between each above mentioned index among TACE, RFA or TACE groups.Compared with other modalities, transcatheter arterial chemoembolization (TACE) before or after hepatectomy is more effective than other interventional therapies for primary hepatocellular cancer, whereas, if combined with radiofrequency ablation (TAI), it is much more effective than TACE alone.

Cholecystectomy is the most commonly performed procedure in general surgery. However, bile duct injury is a rare but still one of the most common complications. These injuries sometimes present variably after primary surgery. Timely detection and appropriate management decrease the morbidity and mortality of the operation.Five cases of iatrogenic bile duct injury (IBDI) were managed at the Department of Surgery, First Affiliated Hospital, Xi'an Jiaotong University. All the cases who underwent both open and laparoscopic cholecystectomy had persistent injury to the biliary tract and were treated accordingly.Recovery of the patients was uneventful. All patients were followed-up at the surgical outpatient department for six months to three years. So far the patients have shown good recovery.In cases of IBDI it is necessary to perform the operation under the supervision of an experienced surgeon who is specialized in the repair of bile duct injuries, and it is also necessary to detect and treat the injury as soon as possible to obtain a satisfactory outcome.

Solid-cystic pseudopapillary tumor of the pancreas (SCPT) is a rare type of pancreatic tumor with low grade of malignancy. Its diagnosis and treatment remain controversial. This study was to discuss the diagnosis criteria and treatment strategy of SCPT.Clinical data, including general history, medical history, treatment history and treatment outcome, of 9 SCPT patients, treated in the Department of Hepatobiliary Surgery of the First Affiliated Hospital of Xi'an Jiaotong University from Jan. 1997 to Feb. 2005, were analyzed retrospectively, and the related literature was reviewed to summarize the clinical characteristics, diagnosis, and treatment of SCPT.Among the 9 patients, 7 (77.8%) were women under 44 years old. The laboratory tests of liver function, serum amylase, and CEA, CA199 were normal. The accurate diagnosis rate of ultrasound was 22.2%, while that of CT was 77.8%. Most patients received local resection of the tumor. All patients were followed-up till Oct. 2005 and no metastasis was detected.SCPT is a rare disease with good prognosis. It occurs mainly in young women. In spite of unspecific laboratory tests, CT and fine needle aspiration method are useful to diagnose the disease. Based on literatures, operation could achieve satisfactory efficacy for SCPT patients.

To investigate nuclear factor kappa B (NF-kappaB) activation induced by lipopolysaccharide (LPS) in rat peritoneal macrophages (PMAs) and the inhibitory effect of resveratrol on NF-kappaB activation.PMAS from normal SD rats were randomly divided into 7 groups, including a control group, a LPS group and 5 resveratrol groups (I-V). PMAs of the control group were incubated in DMEM, and those in LPS group in DMEM containing LPS (10 microg/ml). PMAS of resveratrol groups I-V were incubated in DMEM containing LPS (10 microg/ml) and different concentrations of resveratrol. After 24 h of incubation, NF-kappaB activation in the PMAs was determined, and the expression levels of tumor necrosis factor alpha (TNF-alpha), interleukin-1 (IL-1) and nitric oxide (NO) in the culture medium were measured.Exposure to LPS resulted in an excessive enhancement of cytokine and NO expressions in the PMAs. Resveratrol at 1.25-10 microg/ml produced a dose- dependent inhibition of cytokine and NO expressions and on NF-kappaB activation in LPS-stimulated PMAs.Resveratrol can inhibit LPS-induced NF-kappaB activation in rat PMAs and subsequently suppress the expressions of TNF-alpha, IL-1 and NO.

To study the expressions of Fas and Fas-Ligand (FasL) genes in rats with acute pancreatitis (AP) and their relation to apoptosis of pancreatic acinar cells.Rat models of acute pancreatitis with varied severity were established by retrograde injection of sodium taurocholate at different concentrations via the apancreatobiliary duct. The expressions of Fas and FasL mRNAs and proteins were detected by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. The apoptosis of acinar cells was quantified by in situ nick ending-labeling technique.of expressions fas, FasL mRNA and protein were colocalized in normal pancreatic acinar cells. In pancreatic tissue with less severe inflammation, the expressions of Fas and FasL mRNA increased significantly, and the apoptosis index of the acinar cells was also elevated; with the increase in the severity of the pancreatitis, the expression of Fas and FasL mRNAs were gradually lowered and apoptosis index of the acinar cells was increased.Fas/FasL system might be involved in the renewal and homeostasis of normal pancreatic tissue, and constitute an important pathway mediating the apoptosis of pancreatic acinar cells in AP.

To investigate the therapeutic effects of resveratrol (RESV) as a free radical scavenger on experimental severe acute pancreatitis (SAP).Seventy-two male Sprague-Dawley rats were divided randomly into sham operation group, SAP group, and resveratrol-treated group. Pancreatitis was induced by intraductal administration of 0.1 mL/kg 4% sodium taurocholate. RESV was given intravenously at a dose of 20 mg/kg body weight. All animals were killed at 3, 6, 12 h after induction of the model. Serum amylase, pancreatic superoxide dismutase (SOD), malondialdehyde (MDA), and myeloperoxidase (MPO) were determined. Pathologic changes of the pancreas were observed under optical microscope.The serum amylase, pancreatic MPO and the score of pathologic damage increased after the induction of pancreatitis, early (3, 6 h) SAP samples were characterized by decreased pancreatic SOD and increased pancreatic MDA. Resveratrol exhibited a protective effect against lipid peroxidation in cell membrane caused by oxygen free radicals in the early stage of SAP. This attenuation of the redox state impairment reduced cellular oxidative damage, as reflected by lower serum amylase, less severe pancreatic lesions, normal pancreatic MDA levels, as well as diminished neutrophil infiltration in pancreas.RESV may exert its therapeutic effect on SAP by lowering pancreatic oxidative free radicals and reducing pancreatic tissue infiltration of neutrophils.

A quantitative multiple-marker reverse transcriptase (RT)-polymerase chain reaction (PCR) assay for sensitive detection of cancer cells in axillary drainage fluid was developed to examine whether the presence of cancer cells in axillary drainage fluid can be used as a predictor of locoregional recurrence (LRR) in patients with breast cancer who had T1/2 primary tumors and one to three positive axillary lymph nodes treated with modified radical mastectomy without adjuvant radiotherapy.Axillary drainage fluid was collected from 126 patients with invasive ductal carcinoma of the breast who were treated with modified radical mastectomy and were found to have one to three positive axillary nodes. Cancer cells in axillary drainage fluid were detected by RT-PCR assay using primers specific for carcinoembryonic antigen (CEA) and cytokeratin-19 (CK-19) together with numerous clinicopathologic and treatment-related factors and were analyzed for their impact on LRR.A total of 38 patients suffered LRR during follow-up and the multimarker RT-PCR assays for CEA and CK-19 in the axillary drainage fluid both were positive in 34 patients (27.0%), of which 29 patients had LRR. In univariate analysis, the 5-year LRR-free survival showed higher rates in patients with PCR-negative findings in axillary drainage fluid (p0.0001), ageor=40 years old (p0.0001), tumor size2.5 cm (p0.0001), negative lymph-vascular space invasion (p=0.026), and T1 status (0.0001); in multivariate analysis, PCR-positive findings together with age and tumor size were found to be independent predictors of LRR (all p0.05).Multiplex RT-PCR assay for CEA and CK-19 was highly sensitive for detection and might be useful for prediction of LRR in such subgroup breast cancer patients.

To evaluate the effect of bronchial artery embolization (BAE) with polyvinyl alcohol (PVA) foam and gelatinum sponge (GS) for serious hemoptysis.Of 46 patients with severe hemoptysis, BAE with only GS was performed in 21 cases and with both PVA and GS in 25 cases.The total efficacy rate of BAE was 91.3%; and comparable between PVA+GS and GS groups (92.0%; vs 90.5%;, P0.05). The total recurrence rate after BAE was 26.2%;, but lower in PVA+GS group than in GS group (11.3%; vs 42.1%;, P0.05). No serious complications occurred in these patients after BAE.BAE is effective and safe for management of serious hemoptysis, and treatment with PVA+GS may effectively lower the recurrence rate.

To establish a rat model of liver cancer complicated by liver cirrhosis and explore the effects of the spleen on immune function in this model.Liver cirrhosis was inflicted in rats by percutaneous injection of 40% CCl4 on the back. Walker-256 tumor cells were inoculated in the cirrhotic liver and splenectomy was performed. Two weeks later, the growth and metastasis of tumor were observed and the amount of ascites and the activity of NK cells and CD25 cells were investigated.The amount of ascites and tumor volume were significantly higher in splenectomy group than in controls (P0.01). Two weeks after inoculation, the activity of NK cells in both groups was decreased as compared with that before the inoculation (P0.01). There was no significant difference between the two groups before and after the inoculation (P0.05). The number of CD25 in both groups was higher than that before the inoculation (P0.01). However, there was no significant difference between the two groups before and after the inoculation (P0.05).Splenectomy in early stage of tumor inoculation can stimulate the tumor growth and metastasis. The activity of NK cells and the number of CD25 are inhibited by tumor itself, not by splenectomy.

To explore the mechanism of benign biliary stricture caused by bile duct trauma.A model of trauma of the common bile duct was established in 28 dogs and then repaired. The anastomotic tissues were taken on 3 days, 1 week, 3 weeks, 3 months, and 6 months respectively after operation and examined by using light microscopy and electromicroscopy. Macrophage, transforming growth factor beta 1 (TGF-beta1) and alpha-smooth muscle actin (alpha-SMA) were studied immunohistochemically.The mucosal epithelium of the common bile duct restored poorly, chronic inflammation lasted for a long time, fibroblasts proliferated actively, extracellular matrix overdeposited, and myofibroblasts functioned actively during the whole healing process. Immunohistochemical test showed a high expression of macrophage, TGF-beta1 and alpha-SMA during the healing process lasting a long duration. Macrophages were found in the lamina propria under mucosa, TGF-beta1 in the granular tissue, fibroblasts and endothelial cells of blood vessels, while alpha-SMA in the myofibroblasts and smooth muscle tissue.The healing of the bile duct is in the mode of overhealing. Myofibroblast is the main cause for contracture of scar and stricture of the bile duct. The high expression of macrophage, TGF-beta1 and alpha-SMA is closely related to active proliferation of fibroblasts, extracellular matrix overdeposition and scar contracture of the bile duct.

AIM: To verify the effect of combined interventional therapy for hepatocellular carcinoma (HCC). METHODS: The clinical data of 1126 HCC patients who received combined interventional therapy for transcatheter arterial chemoembolization (TACE) before or after hepatectomy, TACE and radio-frequency ablation (RFA), Chinese medicine treatment and biotherapy after TACE or transcatheter arterial infusion (TAI), were reviewed according to the results of their liver function, alpha-fetoprotein, image data, color-ultrosonography finding and survival rate. RESULTS: A total of 874 patients were followed up for a period of 2 to 63 mo. The overall 1-, 3- and 5- year survival rates were 67.8%, 28.7% and 18.8% respectively. The 1- 3- and 5- year survival rates of patients who received TACE were 74.7%, 41.4%, 36.9% before hepatectomy and 78.9%, 40.4%, 37.5% after hepatectomy. The effective rate (PR + NC) after TACE and RFA was 93.4%, the 1- and 3- year survival rates were 74.5% and 36.8% after TACE and RFA. The effective rate of PR + NC after TACE was 83.2%. The 1-, 3- and 5- year survival rates were 69.3%, 21.7%, 8.4% after TACE. The effective rate of PR + NC after TAI was 27.5%, the 1- and 2- year survival rates were 11.6% and 0% after TAI. The liver function, color-ultrosonography finding and alpha-fetoprotein after TACE + RFA, TACE and TAI were compared. There was no significant difference in each index between TACE and RFA or TACE as well as in liver function between TACE and RFA or between TACE and TAI. CONCLUSION: The therapeutic effectiveness of TACE before or after hepatectomy is most significant, while the effect of TACE and RFA is better than that of TACE, and the effect of TAI is minimal.

Accumulating evidence demonstrates that resveratrol, a natural polyphenolic compound extracted from plants, inhibit inflammation when administered. It has direct effects on suppression of platelet coagulation and cytokines production in many experimental models. Because microcirculation occlusion and cytokines over-production is involved in many diseases such as acute pancreatitis (AP), the discovery of resveratrol as platelet and cytokines inhibitors has shed light on the treatment of AP, which still has significant mortality and morbidity. It is anticipated that this natural polyphenol could serve as a therapeutic compound in managing AP through different pathways.