scholarly journals Inactivation of factor XII active fragment in normal plasma. Predominant role of C-1-inhibitor.

1984 ◽  
Vol 73 (6) ◽  
pp. 1542-1549 ◽  
Author(s):  
A de Agostini ◽  
H R Lijnen ◽  
R A Pixley ◽  
R W Colman ◽  
M Schapira
Keyword(s):  
Factor Xii ◽  
Predominant Role ◽  
Normal Plasma ◽  
Active Fragment

scholarly journals Rapid Loss of Factor XII- and XI-Activity in Ellagic Acid Activated Normal Plasma: Role of Plasma Inhibitors and Implications for Automated Aptt-Recording

1977 ◽  
Author(s):  
J. H. Joist ◽  
J. F. Cowan ◽  
M. Khan
Keyword(s):  
Ellagic Acid ◽  
Clinical Laboratory ◽  
Coagulation Factors ◽  
Activation Process ◽  
Factor Xii ◽  
Naturally Occurring ◽  
Normal Plasma ◽  
Factor Xiia ◽  
Loss Of Contact

Rapid prolongation of the activated partial thromboplastin time (aPTT) of normal plasma upon incubation with ellagic acid containing aPTT reagents was observed. The aPTT prolongation was not due to time dependent changes in pH in the incubation mixtures or loss of activity of the labile coagulation factors VIII and V, but occurred as a result of rapid progressive inactivation of ellagic acid activated factors XII and XI. Prolongation of the aPTT and loss of contact factor activities was not observed in plasma incubated with particulate activator reagents. This finding seemed to indicate that adsorption of factors XII and XI to larger particles during the activation process may protect these factors from inactivation by naturally occurring plasma inhibitors. Evidence is presented which supports previous observations that Ci-inhibitor, α1-antitrypsin and antithrombin III (in the presence of heparin contribute to factor XIIa- and XIa-inactivation in ellagic acid activated plasma and that plasma albumin may compete with factor XII for ellagic acid binding. The findings indicate that ellagic acid containing aPTT reagents have unfavorable properties which seriously limit their usefulness in the clinical laboratory, particularly in respect to recording of the aPTT with certain fully automated clot timers.

scholarly journals Mechanism of transient adsorption of fibrinogen from plasma to solid surfaces: role of the contact and fibrinolytic systems

Blood ◽  
1988 ◽  
Vol 71 (4) ◽  
pp. 932-939 ◽  
Author(s):  
JL Brash ◽  
CF Scott ◽  
P ten Hove ◽  
P Wojciechowski ◽  
RW Colman
Keyword(s):  
Solid Surfaces ◽  
Factor Xii ◽  
Contact Activation ◽  
Transient Detection ◽  
Normal Plasma ◽  
Plasma Factor ◽  
Factor Xiia ◽  
Factor Xia ◽  
Specific Proteins

The transient detection of fibrinogen on surfaces has been described (Vroman effect) and high-mol-wt kininogen (HK) has been shown to play a role in this reaction. In this study, we attempted to identify the form of HK responsible for preventing detection of the fibrinogen initially adsorbed from plasma to various artificial surfaces and to determine if other plasma components were involved. We compared 125I-fibrinogen adsorption in the presence of normal plasma to plasma deficient in specific proteins. On all surfaces tested, we found that fibrinogen was displaced from the surface. The extent of displacement was greatly reduced, however, but not eliminated in HK-deficient plasma. Factor XII- deficient plasma also showed reduced fibrinogen displacement. These data indicate that HK can actually displace fibrinogen; however, factor XII, or a factor XII-mediated reaction also appears to be necessary for this displacement to occur. Furthermore, when normal plasma was first subjected to extensive contact activation by dextran sulfate, during which the HK was extensively degraded to components smaller than the light chain (as assessed by Western blotting), we observed greatly reduced displacement of fibrinogen. Extensive contact activation of Factor XI-deficient plasma failed to show low-mol-wt derivatives, however, and displacement of fibrinogen was similar to normal plasma that had not undergone extensive activation. These data indicate that HKa (active cofactor produced during contact activation by factor XIIa or kallikrein) is primarily responsible for displacing fibrinogen, and that HKi (inactive cofactor generated by factor XIa) cannot displace fibrinogen. The fibrinogen from all plasma samples looked similar by Western blot analysis, suggesting that fibrinogenolysis was not a component of the Vroman effect. In addition, experiments performed with plasma prechromatographed on lysine agarose showed that a lysine- agarose adsorbable protein may be minimally involved in fibrinogen desorption and a synergism may exist between HK and that protein.

scholarly journals Mechanism of transient adsorption of fibrinogen from plasma to solid surfaces: role of the contact and fibrinolytic systems

Blood ◽  
1988 ◽  
Vol 71 (4) ◽  
pp. 932-939 ◽  
Author(s):  
JL Brash ◽  
CF Scott ◽  
P ten Hove ◽  
P Wojciechowski ◽  
RW Colman
Keyword(s):  
Solid Surfaces ◽  
Factor Xii ◽  
Contact Activation ◽  
Transient Detection ◽  
Normal Plasma ◽  
Plasma Factor ◽  
Factor Xiia ◽  
Factor Xia ◽  
Specific Proteins

Abstract The transient detection of fibrinogen on surfaces has been described (Vroman effect) and high-mol-wt kininogen (HK) has been shown to play a role in this reaction. In this study, we attempted to identify the form of HK responsible for preventing detection of the fibrinogen initially adsorbed from plasma to various artificial surfaces and to determine if other plasma components were involved. We compared 125I-fibrinogen adsorption in the presence of normal plasma to plasma deficient in specific proteins. On all surfaces tested, we found that fibrinogen was displaced from the surface. The extent of displacement was greatly reduced, however, but not eliminated in HK-deficient plasma. Factor XII- deficient plasma also showed reduced fibrinogen displacement. These data indicate that HK can actually displace fibrinogen; however, factor XII, or a factor XII-mediated reaction also appears to be necessary for this displacement to occur. Furthermore, when normal plasma was first subjected to extensive contact activation by dextran sulfate, during which the HK was extensively degraded to components smaller than the light chain (as assessed by Western blotting), we observed greatly reduced displacement of fibrinogen. Extensive contact activation of Factor XI-deficient plasma failed to show low-mol-wt derivatives, however, and displacement of fibrinogen was similar to normal plasma that had not undergone extensive activation. These data indicate that HKa (active cofactor produced during contact activation by factor XIIa or kallikrein) is primarily responsible for displacing fibrinogen, and that HKi (inactive cofactor generated by factor XIa) cannot displace fibrinogen. The fibrinogen from all plasma samples looked similar by Western blot analysis, suggesting that fibrinogenolysis was not a component of the Vroman effect. In addition, experiments performed with plasma prechromatographed on lysine agarose showed that a lysine- agarose adsorbable protein may be minimally involved in fibrinogen desorption and a synergism may exist between HK and that protein.

scholarly journals Assess the Effectiveness of protective Concrete coatings of microbiological sulfuric acid Aggression

2019 ◽  
Vol 97 ◽  
pp. 02022
Author(s):  
Viktor Sopov ◽  
Julia Danchenko ◽  
Ekaterina Latorez
Keyword(s):  
Sulfuric Acid ◽  
Building Structures ◽  
Predominant Role ◽  
Microbiological Processes ◽  
Repair Materials ◽  
Bactericidal Properties ◽  
Mineral Acids ◽  
Concrete Building ◽  
Modified Epoxy

Specification of corrosion processes in sewerage networks, the predominant role of microbiological processes in them requires the protection of concrete with materials resistant to specific biogenic sulfuric acid aggression. The effective protective materials, in this case, are those that, in addition to acid-proofing materials, have bactericidal properties. Polymer composite materials (PCM) of cold curing based on modified epoxy-resin, resins with dispersed oxides as fillers are widely used in construction. Unique properties and simple technologies make it possible to use them as injection formulations for repair, restoration and restoration of building structures and structures, waterproofing and facing materials, for impregnating, gluing and coating metal, wooden, brick and concrete building structures and parts. In the reconstruction and restoration of sewerage collectors operating under conditions of exposure to liquid biochemically aggressive media with mineral acids and organic substances, particular attention is paid to the permeability of repair materials. Based on the results of the study, PCM compositions were chosen whose estimated lifetime is about 20 years, ensuring reliable protection of the sewage collectors from corrosion.

scholarly journals Predominant role of alpha 4-integrins for distinct steps of lymphoma metastasis.

1996 ◽  
Vol 93 (10) ◽  
pp. 4821-4826 ◽  
Author(s):  
U. Gosslar ◽  
P. Jonas ◽  
A. Luz ◽  
A. Lifka ◽  
D. Naor ◽  
...  
Keyword(s):  
Predominant Role

Abstract 207: Unc-51-like Kinase 1 (ULK1) Plays A Crucial Role In Mitophagy In Cardiomyocytes

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Toshiro Saito ◽  
Junichi Sadoshima
Keyword(s):  
Glucose Deprivation ◽  
High Ratio ◽  
Control Mechanisms ◽  
Oxygen Species ◽  
Predominant Role ◽  
Mitochondrial Quality Control ◽  
Over Expression ◽  
Pathological Conditions

The mitochondrion is an essential organelle that supplies ATP in cardiomyocytes (CMs). However, damaged mitochondria are harmful via the production of reactive oxygen species and induction of apoptosis in pathological conditions. Therefore, quality of mitochondria should be controlled tightly through various mitochondrial quality control mechanisms. Mitochondrial autophagy (mitophagy) is considered an integral part of this mechanism, and recent investigations uncovered the role of PINK1 and Parkin in mitophagy. However, these observations were made under artificial conditions, such as over-expression of Parkin or treatment with CCCP, and thus the precise mechanism has not been fully elucidated in more pathophysiologically relevant conditions. Recent evidence suggests that mitophagy can take place independently of ATG7, a molecule essential for the conventional form of autophagy, and that this form of autophagy is ULK1-dependent. We investigated the role of ULK1 and ATG7 in mediating mitophagy using mitochondria-targeted Keima (Mito-Keima) in cultured rat neonatal CMs. Keima has a bimodal excitation spectrum peaking at 440 and 560 nm, corresponding to the neutral and acidic pH, respectively. In CMs transfected with Mito-Keima, the fluorescent dots with a high 560nm/440nm ratio represent the mitochondria incorporated into autolysosomes which indicate mitophagy. Here we report that ULK1 plays a more predominant role in glucose deprivation (GD) -induced mitophagy than ATG7. Control CMs exhibited 8.7±1.0 % of the area of high-ratio dots per cells after GD. Knockdown of ULK1 significantly reduced the area to 2.3±0.9 % in CMs after GD (p<0.01, vs sh-Control). The reduction was significantly greater in CMs with knockdown of ULK1 than that of ATG7 (7.0±1.6 %, p<0.05, sh-ULK1 vs sh-ATG7). In addition, knockdown of Beclin1 and Drp1 also significantly decreased the area of high-ratio dots (about 1.0 % and 0.5 %, respectively). Overexpression of ULK1 was sufficient to induce mitophagy without starvation, whereas that of ATG7 was not. These results suggest that ULK1, Beclin1 and Drp1 play an essential role in mediating GD-induced mitophagy in CMs.

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