Based on the scale-free network, an integrated systemic inflammatory response syndrome model with artificial immunity, a feedback mechanism, crowd density and the moving activities of an individual can be built. The e...Based on the scale-free network, an integrated systemic inflammatory response syndrome model with artificial immunity, a feedback mechanism, crowd density and the moving activities of an individual can be built. The effects of these factors on the spreading process are investigated through the model. The research results show that the artificial immunity can reduce the stable infection ratio and enhance the spreading threshold of the system. The feedback mechanism can only reduce the stable infection ratio of system, but cannot affect the spreading threshold of the system. The bigger the crowd density is, the higher the infection ratio of the system is and the smaller the spreading threshold is. In addition, the simulations show that the individual movement can enhance the stable infection ratio of the system only under the condition that the spreading rate is high, however, individual movement will reduce the stable infection ratio of the system.展开更多
AIM：To develop a novel model of colitis in rats, using a combination of iodoacetamide and enteropathogenic E. coli（EPEC）, and to elucidate the pathophysiologic processes implicated in the development of ulcerative ...AIM：To develop a novel model of colitis in rats, using a combination of iodoacetamide and enteropathogenic E. coli（EPEC）, and to elucidate the pathophysiologic processes implicated in the development of ulcerative colitis （UC）. METHODS： Hale Sprague-Dawley rats （/7 = 158） were inoculated intrarectally on a weekly basis with 4 different combinations： （a） 1% methylcellulose （HC）, （b） 100 μL of 6% iodoacetamide （IA） in 1% HC, （c） 200 p.L containing 4×10^8 colony factor units （CFU） of EPEC, and （d） combined treatment of （IA） followed by bacteria （13） after 2 d. Thirty days post treatment, each of the four groups was divided into two subgroups; the inoculation was stopped for one subgroup and the other subgroup continued with biweekly inoculation until the end of the experiment. Colitis was evaluated by the clinical course of the disease, the macroscopic and microscopic alterations, activity of myeloperoxidase （HPO）, and by TNF-α gene expression. RESULTS： Findings indicative of UC were seen in the combined treatment （IA ＋ B） as well as the IA continued treatment groups： the animals showed slow rate of increase in body weight, diarrhea, bloody stools, high colonic ulcer score, as well as histological alterations characteristic of UC, with an extensive inflammatory reaction. During the course of the experiment, the MPO activity was consistently elevated and the TNF-α gene expression was upregulated compared to the control animals. CONCLUSION： The experimental ulcerative colitis model used in the present study resembles, to a great extent, the human disease. It is reproducible with characteristics indicative of chronicity.展开更多
基金Project supported by the Natural Science Foundation of the Education Department of Guizhou Province,China (Grant No.20090133)International Cooperative Foundation of Guizhou Province,China (Grant No.20117007)
文摘Based on the scale-free network, an integrated systemic inflammatory response syndrome model with artificial immunity, a feedback mechanism, crowd density and the moving activities of an individual can be built. The effects of these factors on the spreading process are investigated through the model. The research results show that the artificial immunity can reduce the stable infection ratio and enhance the spreading threshold of the system. The feedback mechanism can only reduce the stable infection ratio of system, but cannot affect the spreading threshold of the system. The bigger the crowd density is, the higher the infection ratio of the system is and the smaller the spreading threshold is. In addition, the simulations show that the individual movement can enhance the stable infection ratio of the system only under the condition that the spreading rate is high, however, individual movement will reduce the stable infection ratio of the system.
基金The Lebanese National Council for Scientific Research and Diagnostic Laboratories, Seattle, USA
文摘AIM：To develop a novel model of colitis in rats, using a combination of iodoacetamide and enteropathogenic E. coli（EPEC）, and to elucidate the pathophysiologic processes implicated in the development of ulcerative colitis （UC）. METHODS： Hale Sprague-Dawley rats （/7 = 158） were inoculated intrarectally on a weekly basis with 4 different combinations： （a） 1% methylcellulose （HC）, （b） 100 μL of 6% iodoacetamide （IA） in 1% HC, （c） 200 p.L containing 4×10^8 colony factor units （CFU） of EPEC, and （d） combined treatment of （IA） followed by bacteria （13） after 2 d. Thirty days post treatment, each of the four groups was divided into two subgroups; the inoculation was stopped for one subgroup and the other subgroup continued with biweekly inoculation until the end of the experiment. Colitis was evaluated by the clinical course of the disease, the macroscopic and microscopic alterations, activity of myeloperoxidase （HPO）, and by TNF-α gene expression. RESULTS： Findings indicative of UC were seen in the combined treatment （IA ＋ B） as well as the IA continued treatment groups： the animals showed slow rate of increase in body weight, diarrhea, bloody stools, high colonic ulcer score, as well as histological alterations characteristic of UC, with an extensive inflammatory reaction. During the course of the experiment, the MPO activity was consistently elevated and the TNF-α gene expression was upregulated compared to the control animals. CONCLUSION： The experimental ulcerative colitis model used in the present study resembles, to a great extent, the human disease. It is reproducible with characteristics indicative of chronicity.
