Plays important roles in regulating cytokine expression, inflammatory signal transduction, bacterial killing ability, and mice survival rate during infection and sepsis. Based on these results, we propose that the available level of plasmin is critical for the onset of death, bacterial killing ability, and cytokine production in the development of sepsis. STAT3 is a key molecule in mediating the signaling of many inflammatory cytokines such as TNF-a, IL-6, and IL-10 during inflammatory responses. TNF-a and IL-6 have been considered to be the primary mediators of sepsis, and a positive correlation has been found between serum IL-6 and TNF-a levels and multiple organ failure. IL-10 has a pronounced antiinflammatory effect by reducing the level of superoxide production in neutrophils, which interferes with neutrophil-mediated cellular cytotoxicity. Previous in vitro studies have shown that plasmin stimulates the expression of cytokines in human monocytes. The data presented here suggest that reducing or removing functional plasmin in mice, leads to a higher survival rate during sepsis due to an impaired cytokine production. Studies of how plasmin regulate cytokine expression and downstream signal pathways during sepsis are being carried out in our laboratory. Several studies have shown that mice with low complement activity have impaired host defense during infection, whereas during sepsis excessive complement activation leads to compromised innate immune functions. Blockade of C5a or the C5a receptor with antibodies has been shown to greatly improve survival of rodents during sepsis. plg and WT mice during infection and sepsis. In summary, the current study reveals a contrasting role of plasminogen deficiency in infection and sepsis, and suggests that pro-inflammatory plasmin plays deleterious roles during systemic inflammation. This pro-inflammatory function of plasmin is distinctly different from its classical roles as a protease that degrades fibrin and extracellular matrix. Our findings may be potentially useful for the development of novel therapeutic strategies against infection and sepsis in humans. It has been also shown that C/ EBPb plays an important role in the consolidation of long-term memory, suggesting a very important role for this protein in the hippocampus and Menard et al have defined a MEK-C/EBP pathway as being essential for the differentiation of cortical progenitor cells into postmitotic neurons. In this regard, we have demonstrated that C/EBPb serves as a critical factor in neuronal differentiation. In the central nervous system, developing neurons are derived from quiescent multipotent or neural stem cells. The hippocampus is a unique structure in that it is one of the two brain regions where adult neurogenesis persists throughout adulthood. New neurons are continuously generated in the subgranular zone of the dentate gyrus of the hippocampus, migrate into the granule layer, and differentiate into new dentate granule cell neurons.