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Figure 5　ATP level and CD11b expression after fMLP stimulation in healthy control subjects. a Changes in the mean fluorescence intensity (MFI) of PMAP-1 after stimulation with the indicated fMLP concen-trations; MFI values were normalized to those of controls (no fMLP) (n = 8 per group). The data shown are the mean ± SEM, and groups were compared with one-way ANOVA and Tukey’s post hoc test (*p < 0.01). b Changes in CD11b expression of polymorphonuclear neutrophils after fMLP stimulation; expression levels were normalized to those of controls (no fMLP) (n = 8 per group). The data shown are the mean ± SEM, and groups were compared with one-way ANOVA with Tukey’s post hoc test (*p < 0.01). c Changes in MFI of MitoAP-1 after stimulation with the indicated fMLP concentrations; MFI values were normalized to those of controls (no fMLP) (n = 8 per group). The data shown are the mean ± SEM, and groups were compared with one-way ANOVA with Tukey’s post hoc test (*p < 0.01, **p < 0.05)oped a hypothesis that one of the causes for multiple organ failure in sepsis patients is complement acti-vation. The complement system is a term denoting a series of more than 20 proteins that circulate in the blood and tissue fluids. Complement causes the killing of bacteria and the recycling of dead cells in the body and is essential to an effective immune response in the human body. Complement activa-tion occurs during a range of alien invasions, such as viral infection, allergy, severe trauma, heat stroke and sepsis. In recent years, it has become clear that excessive complement activation can cause thrombotic microangiopathy (TMA), which is a condition that can lead to organ damage. Knowing this, we set about working to understand the extent to which complement activation is involved in multiple organ failure during biological infection. It is known that when the protein complement compo-nent 3 (C3) is activated by the immune system in response to infection, foreign objects or external stimulus, it becomes C3a and C3b, the latter of which binds to the surface of the cell membranes of microorganisms and reacts with factor B and factor D to form C3 converting enzymes. Moreover, when this particular pathway weakens the function of complement regulators in the body, it becomes amplified and becomes C5a and C5b which leads to the development of a variety of pathological condi-tions. We are therefore working on aspects of this knowledge with a view to determining whether uncontrolled complement activation occurs during biological infection and whether TMA is triggered, eventually leading to multiple organ failure. To achieve their aims, we have investigated the suppression of multiple organ failure in both clin-ical and basic research by studying the quantita-tive evaluation of the complement activation, its relationship with TMA, the relationship between complement activation and leukocyte/platelet and the control of complement activity. To perform the experiments, we used tools that are common to immunology, such as ELISA (enzymelinked immu-nosorbent assay) and FACS (flow cytometry) (7).-A joint research course (Emergency AI Color Image Information Standardization Course)-Additionally, a joint research course (Emergency AI Color Image Information Standardization Course) was established with Toppan Printing Co. Ltd since 329