Besides BH-TiO2/SiO2, this method may also be applied to synthesize other element-self-doped TiO2 in only one step, such as kelp which contains iodine. This work is of great meaning in ICG-001 combining biological engineering and biochemistry, providing a good way combining natural hierarchical porous structure with synthetic material chemistry and extending potentials of biomass in applications such as photocatalysts, sunlight water splitting and so forth. Sepsis is the culmination of complex interactions between the infecting microorganism and the host immune, inflammatory, coagulation and anti-coagulation responses. Sepsis caused by infections with bacteria such as Staphylococcus aureus is a lifethreatening condition that may lead to septic shock, resulting in multiple organ failure and death. It is well known that disorders of coagulation and fibrinolysis play a major role in the development of organ dysfunction during sepsis. Plasmin, a potent serine protease in fibrinolysis and the key component of the plasminogen activator system, is generated by conversion from its precursor, plasminogen, by either of two physiological PAs, tissue-type PA and urokinase-type PA. Besides fibrinolysis, plasmin also degrades a large range of extracellular matrix substrates and activates pre-matrix metalloproteinases. Plasmin has therefore been suggested to be an important upstream regulator of extracellular matrix remodeling in many tissue degradation-related innate immune processes such as cell migration, tissue remodeling, inflammation, and complement activation. In addition to its roles in extracellular proteolysis, the PA system is also involved in generation of pro-inflammatory responses in the extracellular environment. Studies using plasminogen-deficient mice have provided evidence supporting a role of the PA system in mediating the migration of inflammatory cells towards inflammatory sites. In vitro studies have also indicated that plasmin cleaves components of the complement system, thereby releasing chemotactic complement fragments. Moreover, recent in vitro studies suggest that the PA system appears to be involved in the intracellular signaling events during inflammation. For instance, plasmin can activate the p38 mitogen-activated protein kinase, Janus kinase, signal transducers and activators of transcription signaling pathways in monocytes, which have been shown to be important for the inflammatory response. Plasmin is also known to stimulate the release of cytokines and other inflammatory mediators by different cell types. During severe infection, uncontrolled release of cytokines such as tumor necrosis factor-alpha and interleukin-6 may cause a so-called cytokine storm. An uncontrolled cytokine storm leads to sepsis, and is therefore fatal. However, although various mechanisms underlying the inflammatory response during infection have been proposed, the possible functional roles of the PA system during infection, and during sepsis especially, remain largely unknown. In recent years, in vitro studies have suggested that plasmin plays a role in regulating signaling pathways, and in stimulating the release of cytokines and other inflammatory mediators.