Cascade-release

De Groot, F. M. H., A. Carsten, R. Koekkoek, P. H. Beusker, and H. W. Scheeren. 2003. Cascade-release dendrimers liberate all end groups upon a single triggering event in the dendriticAngs/v. Chem. 

The syndrome of acute hypotension, adult respiratory distress syndrome, non-cardiogenic pulmonary edema, anemia, coagulopathy, and anaphylactic reactions after the administration of dextran 70 is referred to as the dextran syndrome (36-39). Factors other than acute volume overload due to intravascular absorption of dextran are thought to account for the syndrome. A combination of diverse pathophysiological factors may be responsible, namely direct pulmonary toxicity, activation of the coagulation cascade, release of vasoactive mediators, hypotension, pulmonary edema, intravascular intravasation of fluids, dilution of blood, and impaired renal and hepatic clearance. Cases of pulmonary edema are described under the section Respiratory. 

Cascade release facilitated by linear autodegradation reactions... 

Cascade Release Facilitated by Linear Autodegradation Reactions... 

B. Cascade release/activation mechanisms initiated by an enzymatic triggering step i. Linear releasing system... 

Additional studies are needed to understand the immunotoxic potential of OPs and CMs. Since e.stcrase activation has a role at various steps of complement cascade, release of histamine or other bioaetive substances from cells, and chemo-laxis of. sensitized lymphocytes, the inhibition of cstcrasc.s may produce opposite effects. Anticholinesterase pc.sticidcs have potent effects on various processes of the immune response in some cases. It has not been established whether these are mediated directly via inhibition of cholinesterases or via other esterases that mediate the immune reactions since potent anticholinesterase insecticides have the potential to inhibit different esterases in the body. It is not known if the anticholinesterase property can be effectively used for therapeutic modulation of the immune system. The cytotoxic... 

VII Proconvertin M, 45-54000. Contains Gla. Part of extrinsic cascade. Released by tissue trauma. 

As shown above, when an ion arrives at the microchannel array it releases a cascade of electrons onto the back plate. This cascade constitutes an electrical pulse from the microchannel plate, which... 

FXa complexes bind to and neutralize tissue factor/ FVIIa complexes, the key starting point of the extrinsic clotting cascade (see earlier) (Fig. 7). Heparin is able to enhance this reaction by direct binding to the complex and by releasing TFPI from the unaltered vessel wall, which then can access the TF-exposing surface. 

A cascade of proteins of the immune response that can be triggered by antigen-antibody complexes and by the innate immune system (e.g. exposure to microbial polysaccharides) to raise the immune response. Complement proteins can detect and bind to foreign material or immune complexes and label them for phagocytosis. They can also cause inflammation by directly degranulating mast cells and releasing chemokines to recruit other immune cells into the affected area. 

Many low weight compounds produced by microor-ganism-like formylated peptides as well as endogenous mediators are chemotactic for leukocytes and promote the inflammatory process. The main endogenous compounds are listed in Table 1 and are derived from activated plasma protein cascades that function as amplification mechanisms, are performed and released from activated cells or are de novo synthesized on demand by cells participating in or being affected by inflammatory events. The major modulators of leukocyte adhesion to endothelial cells are listed in Table 2. 

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