Thrombin is the main factor of mammalian blood coagulation, a complex system generating fibrin clots that physiologically prevents critical bleeding at local areas of tissue injury. There are many diseases, situations, or drugs that critically alter the blood matrix. Then, thrombin is massively generated in the systemic circulation. The individual reader of the present book will understand a bit more the complicated thrombin generating system - called coagulation. Understanding thrombin means understanding coagulation.

Neutrophils are the cells that protect our lives against fungi, bacteria, or thrombi. In fungal or bacterial sepsis the flowing blood is exposed to unphysiologic matrices that fold factor 12 and prekallikrein into F12a and kallikrein. These two enzymes start the contact system of coagulation (altered matrix (AM) coagulation). The intrinsic ten-ase, factor 10a, thrombin, and micro-thrombi are formed. The neutrophils answer to increased blood concentrations of kallikrein (also a tissue enzyme) or micro-thrombi with intracellular NADPH-oxidase assembly and secretion of extracellular myeloperoxidase, together these enzymes generate reactive oxygen species (ROS) of the type of singlet oxygen, a selective destructor of "non-self" and light signal emitter. Two very interesting clinical routine assays quantify the pro-oxidative capacity of neutrophils in unsupplemented or supplemented blood (the blood ROS generation assay (BRGA)) and the kallikrein and thrombin-generating capacity of any material (eg: drinking water, vitamins, drugs, pathogens) that comes into contact with blood (the recalcified coagulation activity assay (RECA)). Especially the RECA is the breakthrough in innovative hemostasis diagnostic. Therefore, the present book focuses on activation of neutrophils by singlet oxygen or by kallikrein, an important starter enzyme of clinically so relevant altered matrix coagulation.

Neutrophil granulocytes are the primary defense cells of blood against bacteria, fungi, parasites, or thrombi. Their main weapons and signals are reactive oxygen species (ROS) that release photons. The activation of the assembly of their NADPH-oxidase, the few specific triggers and many specific or unspecific primers are of great physiological and pathophysiological importance in inflammation and in hemostasis. The neutrophils generate different types of photons and they can "see" them. The 300400 nm photons are the main signals and the photons of lowest wave length which seem to especially alert them in emergency. The present book presents research on the regulation of the neutrophil's ROS generation by different photons, by singlet oxygen (the excited "pro-drug" of photons), by important proteins, or by modulators of the eicosanoid metabolism that should not favor the generation of systemically circulating micro-thrombi.

Neutrophil granulocytes (PMN) are our primary defence cells against bacteria, fungi, parasites, or micro-thrombi. Their main weapons and signals are the reactive oxygen species (ROS), H2O2 being mother ROS, radicalic OH and non-radicalic 1DELTAO2* being the two daughter ROS. 1DELTAO2* is the most important ROS because it is harmful against non-self and harmless against self. 1DELTAO2* is highly reactive against S-H, S-S, or C=C groups and releases photons (hnu). The activation of the assembly of their NADPH-oxidase, one main trigger (zymosan A) and one main primer (1DELTAO2*/hv) are of great physiological and pathophysiological importance in inflammation and in hemostasis. There is photonic communication: the neutrophils generate different types of photons and they can see them in other cells. The approximate 300-400 nm photons are the main signals and the photons of lowest wave length seem to especially alert them in emergency.