Thrombin and Singlet Oxygen (1ΔO2*) Main Factors of Hemostasis

$45.00 – $179.00

Thomas Stief (Editor)
Specialist for Laboratory Medicine, Institute of Laboratory Medicine and Pathobiochemistry
University Hospital, Baldingerstr, Marburg, Germany

Series: Cell Biology Research Progress, Biochemistry Research Trends
BISAC: SCI017000

Neutrophil granulocytes (PMN) are our primary defense 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 1ΔO2* being the two daughter ROS. 1ΔO2* is the most important ROS because it is harmful against “non-self” and harmless against “self”. 1ΔO2* is highly reactive against S-H, S-S, or C=C groups and releases photons (hν). The activation of the assembly of their NADPH-oxidase, one main trigger (zymosan A) and one main primer (1ΔO2*/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. The present book examines further research on the respective altered matrix (AM=intrinsic=contact phase) – coagulation and regulation of the neutrophil´s ROS generation by important substances, e.g. singlet oxygen (the excited “pro-drug” of photons), or photons. 1ΔO2* releases a photon by • dimol emission (634 nm red fluorescence, by collision of two 1ΔO2* molecules), • monomol emission (1270 nm near infra-red phosphorescence, spontaneous), • excited carbonyl (R-C=O*) emission (around 400 nm, after alkene oxidation); this emission is shifted to higher wavelenghts by certain atoms such as fluor or phosphor. PMN are activated by kallikrein, generated in AM-coagulation activation. The best way to quantify intrinsic thrombin generation/blood ROS modulation of xenobiotics (drugs or physiologic substances at unphysiologic concentrations) is to perform a recalcified coagulation activity assay (RECA) or a contact phase assay (CPA) in combination with the blood ROS generation assay (BRGA).
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Table of Contents

Table of Contents

Preface – Hemostasis Activation in Inflammation: kAllikrein, Thrombin, <sup>1</sup>ΔO<sub>2</sub><sup>*</sup>/hv
(T. Stief)

Triggering Thrombin Generation by Low Dose Dexamethasone
(J. Klassen and T. Stief)

Modulation of Blood ROS Generation by Low Dose Dexamethasone
(R. Stumpf and T. Stief)

Modulation of Blood ROS Generation by Preincubated Low Dose Dexamethasone
(R. Dannhäuser and R. Stief)

Triggering Thrombin Generation by High Dose Dexamethasone
(C. Dippel and T. Stief)

Modulation of Blood ROS Generation by High Dose Dexamethasone
(S. Blumenau and R. Stief)

Pre-Incubation Transforms Dexamethasone into a Neutrophil Stimulator
(D. Petri and T. Stief)

Triggering Thrombin Generation by Low Dose Hydrocortisone
(A.L. Neumeier and T. Stief)

Modulation of Blood ROS Generation by Low Dose Hydrocortisone
(Y. Eroglu and T. Stief)

Paradoxical Increase of Blood ROS Generation by Pre-Incubated Low Dose Hydrocortisone
(I. Grischenkov and T. Stief)

Reactive Oxygen Species (ROS) Generation Modulation by Prolonged Blood Incubation with Low Dose Hydrocortisone
(D. Heinrich and T. Stief)

Triggering Thrombin Generation by High Dose Hydrocortisone
(K. Spengler and T. Stief)

Modulation of Blood ROS Generation by High Dose Hydrocortisone
(F. Englert and T. Stief)

Modulation of Blood ROS Generation by Pre-Incubated High Dose Hydrocortisone
(A. Süzer and T. Stief)

Imipenem/Cilastatin at Lowest Concentrations Triggers Thrombin Generation
(A. Köster, K. Zylius, and T. Stief)

Imipenem/Cilastatin Inhibits the ROS Generation of Blood Neutrophils
(K. Zylius, A. Köster, and T. Stief)

Pre-Incubated Imipenem/Cilastatin Stimulates Blood ROS Generation
(J. Drajt and T. Stief)

Imipenem/Cilastatin: A Pathophysiologic Trigger of Altered Matrix Coagulation
(A. Busch, I. Bogun, and T. Stief)

High Dose Imipenem/Cilastatin Suppresses Blood ROS Generation
(I. Bogun, A. Busch, and T. Stief)

Luminescence Kinetic in the Blood ROS Generation Assay (BRGA)
(T. Stief)

Urate Added at Ultra-Low Concentrations (0.1 µM) to Normal Plasma Triggers Thrombin Generation
(D. Stenzel and T. Stief)

Urate Triggers Thrombin Generation
(L. Schorge and T. Stief)

Urate Inhibits ROS Generation
(C. Lichtenwald and T. Stief)

Urate Stimulates ROS Generation in Pre-Incubated Blood
(J. Grass and T. Stief)

Urate Stimulates ROS Generation in Stressed Blood
(A. Mühling and T. Stief)

Urate Enhances Ros Generation in Pre-Incubated Oxidatively Stressed Blood
(T. Stief)

Blood Reactive Oxygen Species and Urate
(T. Stief, C. Lichtenwald, A. Mühling, L. Schorge, D. Stenzel, J. Grass, H. Schudarek, D. Heinrich)

Acetaminophen Suppresses the ROS Generation in Freshest Blood
(R. Stumpf and T. Stief)

Taurine Strongly Enhances the ROS Generation of Blood Neutrophils
(A. Busch and T. Stief)

Caffeine Modulates Blood ROS Generation
(A. Mühling and T. Stief)

Arginine Suppresses Blood ROS Generation
(C. Lichtenwald and T. Stief)

Some α2-Macroglobulin/Thrombin Complexes Open by Contact Activation
(T. Stief)

Singlet Oxygen uprEgulates Neutrophils´ Blue – Opsin
(T. Stief)

Violet Light Upregulates Blood Opsin (OPN1SW)
(T. Stief)

The Light Information Signal in Blood is Quenched by Erythrocytes
(T. Stief and U. Heukrath)

Diatrizoate/Dextran 500 (Polymorphprep®) Modulates Blood ROS Generation
(T. Stief)

Hydrocortisone Modulates Blue – Opsin Expression on Blood Neutrophils
(T. Stief)

Acetaminophen Modulates Blue – Opsin Expression on Blood Neutrophils
(T. Stief and S. Butzmann)

Pre-Incubated Metamizole Suppresses Blood ROS Generation about 10fold Stronger than Metamizole
(T. Stief)

Trigger Zymosan A Upregulates the Neutrophil´s Blue – Opsin
(T. Stief)

Quantification of Blood ROS Generation by Trigger Zymosan A or Primer Singlet Oxygen
(T. Stief and P. Becker)

Rhodopsin or UV-Opsin Upregulation in Blood by Singlet Oxygen
(T. Stief)

Index

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