From 1982 to 1991, there were 13 cases of traumatic rupture of spleen, 26 percent in a total of 50 cases of splenic rupturesin the same period. The abdominal punctures were all positive preoperatively. In general, traumatic rupture of spleen should bc first repaired, if it failed, the subsplenectomy or transplatation of autosplenic tissues in the omental sack might be adopted. We used the technique to repair the ruptured splenic tissues in order to achieve cure. They did not require a second operation. Immunoiogical evaluation was normal 3-4 week safter operation .No postoperative sepsis was encountered.The follow-up results were good (1-7years,mean 3.5years).
Purpose To investigate whether experimental autoimmune uveitis can be induced equally in different rats by urea soluble fraction of bovine melanin-associated antigen(USF-BMAA),and,if so,difference among them. Methods Lewis rats,F344 rats,Wistar rats were immunized with USF-BMAA emulsified with complete Freud is adijuvant and Bordelella pertussis to induce experimental autoimmune uveitis.The animal models were investigated clinically and histopathologically and compared with each other. Rusults Experimental autoimmune uveitis could be induced in Lewis rats,F344 rats and Wistar rats with US-BMAA.Clinical and histopathalogical examination showed that bilateral ocular inflammation developed after immunization 9-13 days.Although inflammation was mainly located in anterior uvea,a mild focal choroiditis was noted in those with severe anterior inflammation.No inflammation was observed in the retina and pineal gland.Experimental autoimmune uveieis induced with USF-BMAA was similar to experimental autoimmune anterior uveitis incited with BMAA presented by other authors.Inflammation induced with USF-BMAA in F344 rats and in Lewis rats was quite similar in the severity and course of the model.But the inflammation was less in Wistar rats compared with that in Lewis rats and F344 rats. Conclusion Experimental autoimmune anterior uveitis was successfully induced with USF-BMAA in Lewis rats,F344 rats and Wistar rats.The difference with regard to the severity among these aminals were propably attributed to their genetic bankground. (Chin J Ocul Fundus Dis,1998,14:149-152)
ObjectiveTo summarize the recent progress in studies of intestinal immunity in inflammatory bowel disease (IBD). MethodsThe literatures on studying the intestinal immunity in IBD, including ulcerative colitis and Crohn disease were reviewed and analyzed. ResultsIBD comprised two main diseases that cause inflammation of the intestines: ulcerative colitis and Crohn disease. Although the diseases had some features in common, there were some important differences in clinical symptoms and pathological features. Accumulating evidence suggested that IBD results from an inappropriate inflammatory response to intestinal microbes in a genetically susceptible host. Immunity studies highlighted the importance of host-microbe interactions in the pathogenesis of these diseases. Prominent among these findings were genomic regions containing nucleotide oligomerization domain 2 (NOD2), autophagy genes, miRNAs, and components of the interleukin-23/type 17 helper T-cell (Th17) pathway. The disfunction of the intestinal microbiome, intestinal epithelium, intestinal immune cells, and the intestinal vasculature played a key role in the process of IBD. The treatment with monoclonal antibody had been introduced to treat IBD and had been certificated effective. ConclusionThe study of basic intestinal immunity and regulation network of molecules in pathogenic process of IBD provides theory basis on prevention of IBD, while related genes of IBD can offer more gene therapy targets.