Objective To summarize the recent pathogenetic researches on the acute pancreatitis. Methods Relevant references about the pathogenesis of acute pancreatitis, which were published recently domestic and abroad were collected and reviewed. Results Recent experimental data indicated that the synthesis and release of pro-inflammatory cytokines and chemotactic factors were responsible for local injury and systemic dissemination of the inflammatory mediators. Experimental studies also provided evidences implying that the immune system might play a role in the development of pancreatitis, such as the activation of lymphocyte and neutrophil. Additionally, the pancreas may completely recover or become fibrotic after an attack of acute pancreatitis and the presence of pancreatic stellate cell was known as a crucial factor in the fibrogenesis. Conclusion The pathogenesis of acute pancreatitis is very complicated, the factors that determine the ultimate severity of the attack are still unknown.
The synthesis and secretion of inflammatory cytokines in the monocytes of 68 cases of multiple system organ failure (MSOF) patients was investigated by the method of MTT stained in cytokines dependent defferential cell strain. The data showed that the serum levels of tumor necrosis factor, interleukine 1 and interleukine 6 were increased (Ｐ＜0.01) in the monocytes of MSOF patients. The synthesis and secretion of these inflammatory cytokines gradually increased in the monocytes after onset of MSOF. After 5 days of treatment with antibiotics and electrolytes intravenous infusion, the secretion of TNF, IL-1 and IL-6 were decreased respectively. These results suggested that the TNF, IL-1 and IL-6 are integrated into system inflammatory responese and caused the injury to the tissues and organs. The production levels of these cytokines can be regarded as the index of MSOF and its severity.
The study of relation between hepatogenic peptic ulcer and portal hypertension,transmitter metabolic disturbance,hepatic insufficiency and infection;and the therapeutic principles of complications of peptic ulcer are described.Twenty four of 58 patients with hepatogenic peptic ulcer were examined by color Doppler ultrasound.Portal venous flow volume (24 cases) was 1060.9±96ml/min.Portal venous pressure(8 cases)was 3.77±2.51kPa tested during operation.Histamine concentration (8 cases) was 0.70±0.31μmol/L in peripheral blood.The gastrin contents of 9cases tested 3cm,5cm away from the ulcer were 2195.6±1043.89ng/L and 2140.3±978.5ng/L respectively. H pylori positive rate was 80% in 58 cases.The therapeutic results were satisfactory with no death.The results suggest that pathogenesis of hepatogenic peptic ulcer is closely related to these factors foresaid.The treatment is nonsurgical and massive hemorrhage or perforation once occurs,surgical treatment is necessary.
Objective To explore the etiological mechanism of Kashin-Beck disease (KBD) and? the changes of bone on X-ray photography in preschool children in the KBD endemic area. Methods Children of 1-6 years old in Naidang village of Jinchuan county, Sichuan province, China were included; and their wrist and knee joints X-ray photos were collected. The photos were bl indly diagnosed. Results Of the 22 children aged 1-6 years old in the village, 17 were included and another 3 aged 6-8 years old asked for examination. All children showed changes in bone metaphysis around wrist or/and knee joints based on the results of X-ray examination. Conclusion The 20 children in mild type KBD area show common changes in bone metaphysis This result coincides with our hypothesis that hypoplastic cartilage should occur in the population of preschool children in the KBD endemic area.
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.
【Abstract】ObjectiveTo investigate the role of PPARδ in the pathogenesis of colorectal cancer. MethodsLiteratures about PPARδ and the pathogenesis of colorectal cancer were reviewed and analyzed.ResultsPPARδ is expressed in the nucleuses of glandular epithelia lining colon and rectum. It is normally suppressed by wild-type adenomatous polyposis coli (APC) but is up-regulated by enhanced β-catenin/T cell factor-4 (TCF-4) binding to TCF-4-responsive elements in the PPAR promoter when an inactivating APC mutation occurs, which indicates PPAR is a potential downstream target of the APC/β-catenin/TCF-4 signaling pathway in colorectal cancer. Consistent with PPAR’s role as an APC/β-catenin/TCF-4 target, some studies reported that PPAR mRNA is frequently overexpressed in colorectal cancers of both humans and rodent animals, which indicates that PPAR is relevant to the tumorigenesis of colorectal cancer. ConclusionPPARδ is closely related with the pathogenesis of colorectal cancer.
【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.
ObjectiveTo explore the pathogenesis of acute pancreatitis during pregnancy, differential diagnosis, and standardized treatment. MethodsThe related literatures at home and abroad in recent years were reviewed, and the progress of pathogenesis and treatment of acute pancreatitis during pregnancy were summarized. ResultsThe common cause of acute pancreatitis during pregnancy include biliary system diseases, hyperlipidemia, hyperparathyroidism, the direct effect of pregnancy on the pancreas, etc. According to the different pathogenic factors of acute pancreatitis during pregnancy, the laparoscopic cholecystectomy (LC), endoscopic retrograde cholangiopancreatography (ERCP), low-fat diet combined with Omega-3 fatty acids, parathyroid adenoma resection, or terminal pregnancy could be use. ConclusionAcute pancreatitis during pregnancy is dangerous, the cause, general condition of patients, and the growth of fetus should be give full consideration, and the diagnosis and treatment are standardized.