The pathogenesis of acute pancreatitis(AP)has been a hot issue around the world.Regarding the pathogenesis of AP,there are mainly the trypsin autodigest doctrine,microcirculation theory,inflammation and cell-medium theory,theory of intracellular calcium overload,bacterial translocation and the "two-hit" theory,oxidative stress and doctrine of NO role,and so on.Resveratrol,a natural plant extraction with a wide therapeutic effect of anti-inflammation and anti-oxidation,inhibits platelet aggregation,improves microcirculation and has other pharmacological effects.In recent years,we have carried out extensive and in-depth literature-based studies on the mechanisms for AP and the therapeutic effect of resveratrol on rat AP models,and confirmed that resveratrol could relieve AP-caused damage to the pancreas and the resulting multiple-organ injury.

Objective:To improve the recognition of bleeding risk in the anticoagulant process by analyzing one case of senior patient with deep vein thrombosis occurred severe bleeding during the anticoagulant therapy.Methods:The possible causes of hemorrhage were analyzed after the brief introduction of medical history,lab test report and treatment process of the patient.Results:The reasons of hemorrhage might be as follows:① the combination of warfarin and dalteparin induced the adverse drug reaction;② albumin decreased during the treatment process resulting in the effect enhancement of warfarin;③ the clearance of warfarin decreased resulting from the low creatinine clearance of the elderly patient.Conclusion:Clinical anticoagulant practice should be more careful in senior patients.The frequency of related laboratory tests should be increased in order to find potential risks timely.

Objective To investigate the effects of resvertrol on apoptosis and the expression of apoptosis-regulated genes Bax in rats with experimental severe acute pancreatisis.Methods Totally 54 SD rats were randomly divided into 3 groups: sham-operation group(SO),severe acute pancreatitis group(SAP),and resveratrol-treated group(RES).In SO group the pancreases were slightly flipped only.The SAP model was set up by giving 40g/L sodium chrolate(1mL/kg) through pancreatic duct,and resveratrol(5mg/mL,10mg/kg) was given intravenously.Apoptosis of mucosal cells was detected by TUNEL methods,and the expression of Bax protein was determined by SP immunohistochemical technique.Results The apoptotic index of mucosal cells in SAP group at 3,6 and 12 hours after induction of severe acute pancreatitis was significantly higher than that in resveratrol-treated group((P

?-adrenoceptor,whose subtypes ?1-and ?2-adrenoceptor are expressed on panreatic cancer cells,is closely related to the occurrence and development of pancreatic cancer.?-adrenoceptor agonists epirenamine,isopropylarterenol and the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK) induce pancreatic cancer proliferation.Research on the molecular mechanism is as follows: Activating ?-receptor can stimulate protein kinase A(PKA)/arachidonic acid(AA) pathway in pancreatic cancer cells.NNK also stimulates mutation of Ras and the activation of Src tyrosine kinase and Ras,followed by activation of mitogen activated protein kinase(MAPK) pathway.?-adrenoceptor can make the epidermal growth factor(EGFR) pathway transactivated,and the EGFR and ?-adrenergic signalling pathways might synergize to activate Src and Ras.Increased evidence suggests that patients with pancreatic adenocarcinoma share many risk factors,such as smoking and chronic depression,with cardiovascular disease patients.Drugs to block ?-adrenoceptor in cardiovascular diseases might be used for the prevention and treatment of pancreatic cancer.

Objective To explore the protective effect of resveratrol on rat brain injury resulting from severe acute pancreatitis (SAP). Methods Ninety-six male Sprague-Dawley rats were randomly divided into four groups:sham-operation (SO) group,severe acute pancreatitis (SAP) group,resveratrol-treated (RES) group and dexamethasone-treated (DEX) group,with eight rats in each group evaluated at 3,6 and 12 h. Levels of serum myelin basic protein (MBP),tight junction protein zonula occludens 1 (Zo-1),TNF-? and IL-6 were determined by ELISA. The ultrastructural changes of the brain and pancreatic tissues were examined using a transmission electron microscope. Results MBP,Zo-1,TNF-? and IL-6 levels in RES group were lower than those in SAP group at all time points (P0.05). Conclusion The degradation of Zo-1 is involved in the pathophysiology of brain injury in SAP; MBP can be used as a marker of brain injury in SAP rats. Resveratrol can inhibit brain injury associated with SAP.

Objective To establish a stable brain injury model with pancreatitis and explore the mechanism of brain injury resulting from severe acute pancreatitis (SAP) in experimental rat models. Methods Twenty-four adult male Sprague-Dawley rats were randomly divided into three groups: sham operation (SO) group, SAP group and trypsin group, with eight rats in each. Brain tissue and pancreas tissue specimens were collected at 12 h after treatment. Death rate in each group was evaluated; the level of tight junction protein zonula occludens 1 (Zo-1) was determined by enzyme-linked immunosorbent assay. The ultrastructure of the brain tissues was examined using transmission electronic microscope; pathological changes in the brain tissues were observed with HE staining. Results The death rate was increased significantly in SAP group compared with that in trypsin group; no rats in SO group died. Zo-1 level was obviously lower in SO group than in SAP group and trypsin group (P<0.05). The ultrastructural changes were seen in the latter two groups, including obvious neuronal cell swelling, capiliary stasis, increased vascular permeability, thrombosis and cell apoptosis. Conclusion Trypsin may cause brain injury with pancratitis. The death rate of SAP model established by trypsin was low. We have provided a stable animal brain injury model for further study and treatment of brain injury.

Objective To investigate the relationship between peritoneal macrophages (PMAs) and inflammatory reaction in a rat model of severe acute pancreatitis (SAP). Methods Sprague-Dawley rats were randomly divided into control group and SAP group. To induce SAP in rats, 40 g/L sodium taurocholate (0.1 mL/100 g) was injected into the pancreatic duct through retrograde exposure of pancreatic bile duct in hepatic porta. One-third of rats were sacrificed at 3, 6 or 12 h after modeling. PMAs were extracted, and incubated for 24 h in a humidified 5% carbon dioxide incubator. The expressions of tumor necrosis factor alpha (TNF-α) and interleukin-1β (IL-1β) mRNA in PMAs were measured by semi-quantitative RT-PCR. The levels of TNF-α and IL-1β in culture medium and serum were evaluated.The histological changes of pancreas were examined. Rosults The expressions of TNF-α mRNA and IL-1β mRNA in PMAs were significantly higher in SAP group than in control group at each time point (P<0.01). The concentrations of TNF-α and IL-1β in culture medium and serum were significantly elevated in SAP group compared with control group (P<0.01). The histological analysis of pancreas indicated that the damage was more severe in SAP group than in cuntrol group (P<0.01). Conclusion PMAs secrete cytokines into pancreatitis-associated ascitic fluid, and this study demonstrates a correlation between SAP and the activation of PMAs.

Animals ; Antibiotics, Antineoplastic ; administration & dosage ; toxicity ; Apoptosis ; drug effects ; Daunorubicin ; administration & dosage ; toxicity ; Disease Models, Animal ; Female ; In Situ Nick-End Labeling ; Male ; Myocardium ; cytology ; metabolism ; pathology ; ultrastructure ; Neuregulins ; metabolism ; pharmacology ; RNA, Messenger ; metabolism ; Rats ; Rats, Wistar ; Receptor, ErbB-2 ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction

Objective To observe the characteristics of electro-neurophysiology in diabetic patients with early peripheral neuropathy. Method The nerve conduction velocity ( NCV ) and quantitative sensory test (QST) were examined in 175 diabetic patients without clinical peripheral neuropathy and in 50 normal subjects, and their results were compared. Results In 175 diabetic patients, the abnormal ratio of NCV was 7% (13/175).While using QST,the abnormal ratio was 45% (79/175). There was significant difference between two methods (P< 0.01). Compared diabetic patients with normal subjects,there was no significant difference between motor conduction velocity and sensory conduction velocity (P > 0.05 ).While using QST, the threshold values of cold sensation, warm sensation, and thermalgesia showed significant difference between diabetic patients and normal subjects (P< 0.01). Conclusion QST is more sensitive than NCV in diagnosing diabetic peripheral neuropathy, which suggests that small nerve fibers are more likely to be damaged than large fibers in early stage.