scholarly journals The Role of the Coagulation System in Preterm Parturition

Preterm Birth ◽  
10.5772/54843 ◽  
2013 ◽  
Author(s):  
Vered Klaitman ◽  
Ruth Beer-Wiesel ◽  
Tal Rafaeli ◽  
Moshe Mazor ◽  
Offer Erez
Keyword(s):  
Coagulation System

A Re-Appraisal of the Role of Blood Coagulation and Platelets in the Generalized Shwartzman Phenomenon

1966 ◽  
Vol 15 (03/04) ◽  
pp. 519-538 ◽  
Author(s):  
J Levin ◽  
E Beck
Keyword(s):  
Blood Coagulation ◽  
The State ◽  
Coagulation System ◽  
Renal Lesions ◽  
Intravascular Coagulation ◽  
Renal Glomeruli ◽  
Coagulation Mechanism ◽  
Shwartzman Phenomenon ◽  
Do So

SummaryThe role of intravascular coagulation in the production of the generalized Shwartzman phenomenon has been evaluated. The administration of endotoxin to animals prepared with Thorotrast results in activation of the coagulation mechanism with the resultant deposition of fibrinoid material in the renal glomeruli. Anticoagulation prevents alterations in the state of the coagulation system and inhibits development of the renal lesions. Platelets are not primarily involved. Platelet antiserum produces similar lesions in animals prepared with Thorotrast, but appears to do so in a manner which does not significantly involve intravascular coagulation.The production of adrenal cortical hemorrhage, comparable to that seen in the Waterhouse-Friderichsen syndrome, following the administration of endotoxin to animals that had previously received ACTH does not require intravascular coagulation and may not be a manifestation of the generalized Shwartzman phenomenon.

scholarly journals Progress in research on the role of fibrinogen in lung cancer

2020 ◽  
Vol 15 (1) ◽  
pp. 326-330
Author(s):  
Xing Liu ◽  
Bin Shi
Keyword(s):  
Lung Cancer ◽  
Coagulation Factor ◽  
Coagulation System ◽  
Plasma Coagulation ◽  
Hepatic Cells ◽  
Tumor Growth And Metastasis ◽  
Cancer Côlon ◽  
The Relationship ◽  
Multiple Interactions

AbstractLung cancer is one of the most prevalent malignancies worldwide. Local recurrence and distant metastasis remain the major causes of treatment failure. It has been recognized that the process of tumor growth and metastasis involves multiple interactions between tumor and host. Various biomarkers have been used for predicting tumor recurrence, metastasis, and prognosis in patients with lung cancer. However, these biomarkers are still controversial and require further validation. The relationship between malignancy and coagulation system disorders has been explored for more than a century. Fibrinogen is the most abundant plasma coagulation factor synthesized mainly by hepatic cells. Increased plasma fibrinogen levels were observed in various carcinomas such as gastric cancer, colon cancer, and pancreatic cancer. Recent studies have also investigated the role of fibrinogen in patients with lung cancer. This review aimed to address the role of fibrinogen in lung cancer.

S PROTEIN/VITRONECTIN NEUTRALIZES THE ANTICOAGULANT ACTIVITY OF GLYCOSAMINOGLYCANS IN THE INHIBITION OF THROMBIN BY HEPARIN COFACTOR II

1987 ◽  
Author(s):  
K T Preissner ◽  
P Sie
Keyword(s):  
Dermatan Sulfate ◽  
Enzyme Inhibitor ◽  
Anticoagulant Activity ◽  
Coagulation System ◽  
Binary Complex ◽  
Heparin Cofactor Ii ◽  
S Protein ◽  
Adhesive Protein ◽  
Inhibition Of Thrombin

The complement inhibitor S protein, which is identical to the adhesive protein vitronectin, functions as heparin-neutralizing factor by protecting thrombin against fast inactivation by antithrombin III. The interference of S protein with glycos-aminoglycan-catalyzed inhibition of thrombin by heparin cofactor II was investigated in a purified system. In the presence of 0.3 μg/ml heparin, or 0.5 μg/ml pentosan polyphosphate (SP 54), or 2 μg/ml dermatan sulfate, S protein induced a concentration-dependent reduction of the inhibition rate of thrombin by heparin cofactor II. This resulted in a decrease of the apparent pseudo-first order rate constants by about 17-fold (heparin), or about 7-fold (SP 54), but only by about 2-fold for dermatan sulfate at a physiological ratio of S protein to heparin cofactor II. Likewise, S protein significantly counteracted the anticoagulant activity of heparin and SP 54 bot not of dermatan sulfate when tested in an inhibition assay using various concentrations of glycosaminoglycans. For heparin, the activity of S protein at the point of 50% inhibition of thrombin was expressed in the range 0.06-0.6 μg/ml (0.01-0.1 U/ml) and for SP 54 in the range 0.3-2 pg/ml. Exposure of the glycos-aminoglycan-binding region of S protein by reduction and carb-oxymethylation of the protein even increased the neutralizing activity of S protein towards heparin and SP 54. S protein not only was found together with thrombin in a binary complex. S protein also became incorporated into a ternary complex with thrombin and heparin cofactor II as judged by crossed immunoelectrophoresis, regardless whether complex formation was initiated by heparin or dermatan sulfate. These findings underline the role of S protein as potent glycosaminoglycan-neutral-izing protein in plasma and as scavenger protein which may bind to enzyme-inhibitor complexes of the coagulation system.

scholarly journals Plasma Kallikrein Contributes to Coagulation in the Absence of Factor XI by Activating Factor IX

2020 ◽  
Vol 40 (1) ◽  
pp. 103-111 ◽  
Author(s):  
Mayken Visser ◽  
René van Oerle ◽  
Hugo ten Cate ◽  
Volker Laux ◽  
Nigel Mackman ◽  
...  
Keyword(s):  
Complex Formation ◽  
Ellagic Acid ◽  
Thrombin Generation ◽  
Factor Ix ◽  
Coagulation System ◽  
Plasma Kallikrein ◽  
Factor Xia ◽  
The Difference ◽  
Long Chain

Objectives: FXIa (factor XIa) induces clot formation, and human congenital FXI deficiency protects against venous thromboembolism and stroke. In contrast, the role of FXI in hemostasis is rather small, especially compared with FIX deficiency. Little is known about the cause of the difference in phenotypes associated with FIX deficiency and FXI deficiency. We speculated that activation of FIX via the intrinsic coagulation is not solely dependent on FXI(a; activated FXI) and aimed at identifying an FXI-independent FIX activation pathway. Approach and Results: We observed that ellagic acid and long-chain polyphosphates activated the coagulation system in FXI-deficient plasma, as could be demonstrated by measurement of thrombin generation, FIXa-AT (antithrombin), and FXa-AT complex levels, suggesting an FXI bypass route of FIX activation. Addition of a specific PKa (plasma kallikrein) inhibitor to FXI-deficient plasma decreased thrombin generation, prolonged activated partial thromboplastin time, and diminished FIXa-AT and FXa-AT complex formation, indicating that PKa plays a role in the FXI bypass route of FIX activation. In addition, FIXa-AT complex formation was significantly increased in F11 −/− mice treated with ellagic acid or long-chain polyphosphates compared with controls and this increase was significantly reduced by inhibition of PKa. Conclusions: We demonstrated that activation of FXII leads to thrombin generation via FIX activation by PKa in the absence of FXI. These findings may, in part, explain the different phenotypes associated with FIX and FXI deficiencies.

scholarly journals Should We Replace the Terms Intrinsic and Extrinsic Coagulation Pathways With Tissue Factor Pathway?

2016 ◽  
Vol 23 (8) ◽  
pp. 922-927 ◽  
Author(s):  
Jan F. Vojacek
Keyword(s):  
Tissue Factor ◽  
Coagulation Cascade ◽  
Coagulation System ◽  
Bleeding Complications ◽  
Antithrombotic Agents ◽  
Risk Of Bleeding ◽  
Tissue Factor Pathway ◽  
The Common ◽  
Coagulation Pathway

Present review highlights some new aspects of the role of individual components of blood coagulation process and proposes a modified concept of hemocoagulation cascade. The role of FXII in the initiation of the so-called intrinsic coagulation system is currently questioned. Its role has been recently demonstrated mainly in the thrombus propagation and final stabilization together with factors XI and XIII. The edited concept underlines the common part of the tissue factor (TF) in the initiation of both the intrinsic and extrinsic pathways of the coagulation system and therefore may make it not improperly be called the TF coagulation pathway. The search for new antithrombotic agents shows that the level of the coagulation system blockade depends on which step in the coagulation cascade is targeted and results in different degrees of the antithrombotic efficiency and the risk of bleeding complications.

The role of pre/postoperative changes in coagulation system following carotid endarterectomy

1992 ◽  
Vol 65 ◽  
pp. S224
Author(s):  
Đ. Radak ◽  
R. Baklaja ◽  
V. Đukić ◽  
B. Petrović ◽  
E. Rosato ◽  
...  
Keyword(s):  
Carotid Endarterectomy ◽  
Coagulation System ◽  
Postoperative Changes

The role of the coagulation system in tumour angiogenesis

2001 ◽  
Vol 2 (10) ◽  
pp. 608-613 ◽  
Author(s):  
GF Nash ◽  
DC Walsh ◽  
AK Kakkar
Keyword(s):  
Coagulation System ◽  
Tumour Angiogenesis
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