Objective To study the relation between expressions of transforming growth factor β1 （TGF-β1）, transforming growth factor receptor type Ⅰ (TβRⅠ) and cell proliferation, cell cycle in gallbladder carcinomas, to disclose the mechanism of TGF-β1 and TβRⅠin the gallbladder carcinogenesis，and to evaluate their values in the prognosis of gallbladder carcinomas. Methods Thirty five gallbladder carcinomas 〔age （57.94± 4.61） years, 14 male cases and 21 female cases〕 comprised 32 adenocarcinomas, 2 adenosquamous carcinoma and 1 squamous cell carcinomas. Formalin fixed, paraffin embedded sections from gallbladder carcinomas were immunostained with TGF-β1, TβRⅠ, PCNA, cyclin E antibodies by immunochemical assays. Gallbladder adenoma and chronic cholecystitis were collected as non-malignant controls. Patients of gallbladder carcinomas were followed up. Results Positive immunostaining rate of TGF-β1 was 57.14% in gallbladder carcinomas, which was significantly higher than that in gallbladder adenomas and chronic cholecystitis (P＜0.01, respectively). Expression of TGF-β1 was associated with Nevin stage, lymph nodes and distant metastasis (P＜0.05, P＜0.01, respectively). Expression of TGF-β1 was positively correlated with expression of PCNA LI and cyclin E (r=0.523 2, P=0.001 3; r=0.406 5, P=0.015 4), and 34.29% of gallbladder carcinomas were immunostained positively for TβRⅠ. Expression of TβRⅠwas significantly lower in gallbladder carcinomas than that in gallbladder adenomas and cholecystitis (P＜0.05, respectively). It was significantly lower in gallbladder carcinomas patients with lymph nodes and distant metastases than in those without (P＜0.05). Expression of TβRⅠwas negatively correlated with PCNA LI (r=-0.402 4, P=0.016 6). Patients with negative expression of TGF-β1 and/or positive expression of TβRⅠ had significant longer survival rates than those with positive expression of TGF-β1 and/or negative expression of TβRⅠ(P＜0.01, P＜0.05, respectively). Expressions of TGF-β1 and TβRⅠ correlated with prognosis of gallbladder carcinomas closely. Conclusion TGF-β1 and TβRⅠ have close correlation with cell proliferation, cell cycle of gallbladder carcinomas and are important biological markers of carcinogenesis and progress of gallbladder carcinomas. The escape of growth inhibition of TGF-β1 due to low expression of TβRⅠand carcinogenesis of TGF-β1 may play an important role in gallbladder carcinogenesis. TGF-β1 and TβRⅠare valuable indices for judging the prognosis of gallbladder carcinoma.
ObjectiveTo study the mechanism, diagnosis and treatment of spontaneous rupture of hepatocellular carcinoma (HCC) for the purpose of screening out the effective methods of diagnosis and treatment. MethodsArticles have been reviewed to find out the difference among many kinds of diagnosis and treatment. ResultsThe mechanism of spontaneous rupture was not clear. Possible factors included tumor necrosis, coagulopathy, cirrhosis and portal hypertension. Diagnosis of spontaneous rupture of HCC can be made by abdominal paracentesis, ultrasonography and CT. Judging from the reported results the first choice of emergency treatment for hemostasis was transcatheter arterial embolization (TAE). The rational treatment of patients with ruptured HCC was TAE followed by hepatectomy if the lesion was resectable. ConclusionThe prognosis of patients with ruptured HCC could be improved if the correct diagnosis and treatment can be adopted.
【Abstract】ObjectiveTo review the research advance of intestinal barrier changes and its pathogenesis in stress conditions.MethodsThe literatures in recent years on the changes of the intestinal barrier,and its pathogenesis in stress conditions were reviewed.Results In some severe stress conditions, such as trauma, severe inflammation and acute severe pancreatitis, etc, a series of pathophysiologic disorders of intestinal barrier， even systemic inflammatory response syndrome and multiple organ dysfunction syndrome or multiple organ failure were induced. The pathogenesis was a result of a series of neurologic, immunologic and endocrine factors making one another. ConclusionRecognizing the changes and pathogenesis have an important clinical significance for treating and preventing the intestinal barrier dysfunction induced by stress.
Objective To assess the tolerance of preoperative carbohydrate-rich beverage, to determine its effect on postoperative insulin resistance and analyze its potential mechanism. Methods Thirty-two patients undergoing elective colorectal cancer resection were recruited to this randomized controlled study and assigned to two groups at random. Patient in control group was fasted before operation, while patient in study group was given oral water. Homeostasis model assessment (HOMA) indexes, activity of PTK, and mRNA and (or) protein expressions of PKB, PI3K and GluT4 were measured before and (or) immediately after surgery. Furthermore preoperative well-beings of patients were studied. Results Among well-beings, feeling of thirst, hunger and anxiety tended to be better in patients receiving carbohydrate-rich beverages compared with fasted ones (P＜0.05). Whole body insulin sensitivity decreased by 33% in the study group while 38% in the control group (P=0.007 2), and the activity of PTK, expressions of PI3K and PKB in study group were higher than those in control group (P＜0.05， P＜0.01), but no significantly difference was observed about GluT4 in both groups (Pgt;0.05）. Conclusion Preoperative consumption of carbohydrate-containing fluids is safe and effective. Provision of carbohydrate energy source prior to surgery may attenuate immediate postoperative insulin resistance. A carbohydrate-rich drink enhances insulin action at the time of onset of anaesthesia or surgery by activating three kinases named PTK, PI3K, PKB which are key enzymes in pathway of insulin signal transduction. It is likely to explain the effects on postoperative insulin resistance.
【Abstract】Objective To investigate the relationship between the development of pancreatic cancer and inflammation, and the therapy strategy.Methods Related articles were reviewed.Results The pathogenesis of inflammation in pancreatic cancer development involves cytokines, NF-κB, COX-2, PPAR-γ, DNA damage, gene changes，etc. Based on these mechanisms some medications are under developing. Conclusion Accumulative effects of pancreatic inflammation may lead to DNA changes, and even pancreatic cancer development. Medications aimed at suppressing pancreatic inflammation may help with prevention and treatment of pancreatic cancer.