Prevention Of Shwartzman’S Phenomenon In Factor XIII Deficiency

1981 ◽  
Author(s):  
Soo Young Lee ◽  
Sung Keun Chang ◽  
Soo II Chung
Keyword(s):  
Factor Xiii ◽  
Rabbit Platelet ◽  
Factor Xiii Deficiency ◽  
Platelet Factor ◽  
Cortical Necrosis ◽  
Rate Of Increase ◽  
Shwartzman Reaction

Cross-linked clots formed in vitro are reported to be more resistant to fibrinolysis but the relevance of these observations to the situation in vivo is uncertain. The possible role of Factor XIII in the formation of diffuse intravascular fibrin deposition was examined in experimentally induced Factor XIII deficient rabbits. Factor XIII deficiency was induced by intravenous infusion of IgG isolated from goat anti-rabbit platelet Factor XIII. Control received normal goat IgG. The Shwartzman reaction was produced by two injections of bacterial endotoxin given 24 hours apart.The most striking histological differences were observed after 48 hours. A large number of glomerular loops were enlarged and engorged with red blood cells and platelet- fibrin thrombi; extensive bilateral cortical necrosis was observed in 8 out of 10 endotoxin injected control rabbits but none in the Factor XIII deficient group.Fibrinogen levels in control rabbits were increased 3-4 fold (1.1g/100 ml), at 24 hours and slightly decreased at 48 hours after endotoxin injection, whereas in Factor XIII deficient animals, the rate of increase was slower but reached similar levels at 48 hours. Fibrinolytic activity in vivo, studied by the degradation of infused 125I-fibrinogen, was significantly increased in both endotoxin injected groups, irrespective of Factor XIII levels.These results strongly suggest that cross-linked thrombi are more resistant to fibrinolysis in vivo as well as in vitro.

Studies on the Pathogenesis of the Generalized Shwartzman Reaction

1964 ◽  
Vol 12 (02) ◽  
pp. 471-483 ◽  
Author(s):  
F Rodríguez-Erdmann
Keyword(s):  
Clotting Factor ◽  
Factor V ◽  
Clotting System ◽  
Platelet Factor ◽  
Trigger Mechanism ◽  
Haemorrhagic Diathesis ◽  
Shwartzman Reaction ◽  
Ca Ions

SummaryThe rôle of the clotting system in the pathogenesis of the generalized Shwartzman reaction (gSr) has been stressed in recent years. The clotting system is activated ubiquitously and as a result of it, fibrin is deposited intravascularly and a haemorrhagic diathesis develops. Evidence is presented herein, that endotoxin does not activate purified prothrombin, nor does endotoxin influence the convertion of prothrombin when it is activated in the presence of purified platelet-factor 3 (or caephalin) purified Ac-G (factor V) and Ca-ions.The trigger mechanism of the gSr also seems to be in the so-called prephase of clotting mechanism. Data are presented, which show that endotoxin activates the Hageman factor in vitro. The importance of this clotting factor and of platelet-factor 3 is discussed. Also the rôle played by the RES and cardiodynamic and vascular components are taken in consideration in the discussion.

Participation of Soluble Fibrin Monomer Complexes and Platelet Factor 4 in the Generalized Shwartzman Reaction

1968 ◽  
Vol 20 (01/02) ◽  
pp. 285-295 ◽  
Author(s):  
B Lipiński ◽  
K Worowski ◽  
J Jeljaszewicz ◽  
S Niewiarowski ◽  
L Rejniak
Keyword(s):  
Blood Platelets ◽  
Aminocaproic Acid ◽  
Salmonella Typhi ◽  
Platelet Factor 4 ◽  
Platelet Factor ◽  
Soluble Fibrin ◽  
Fibrin Monomer ◽  
Shwartzman Reaction

SummaryThe generalized Shwartzman reaction was produced in rabbits by the typical way of 2 consecutive injections of Salmonella typhi endotoxin. Generalized Shwartzman reaction was also induced by “preparation” of the rabbits with epsilon-aminocaproic acid or mercuric chloride intoxication, followed by a single injection of the endotoxin. Significant impairment of blood fibrinolytic activity resulting from inhibition by endotoxin of a release of the kidney plasminogen activator, was demonstrated in the classical generalized Shwartzman reaction. Inhibition of fibrinolysis led to the accumulation of soluble fibrin monomer complexes in the circulation, detectable in plasma by protamine sulfate precipitation. It is postulated that hypercoagulability, regularly occurring in the generalized Shwartzman phenomen, is due to fibrinolysis inhibition. Endotoxin causes release of platelet factor 4 from rabbit blood platelets both in vitro and in vivo. This factor is thought to be responsible for nonenzymatic intravascular precipitation of fibrin from circulating soluble fibrin monomer complexes. Bilateral cortical necrosis in kidneys is due by fibrin deposition resulting from the disturbance in the equillibrium between blood clotting and fibrinolytic systems and the interaction of accumulated soluble fibrin monomer complexes with platelet factor 4.

scholarly journals Presence of autoantibodies to interleukin-8 or neutrophil-activating peptide-2 in patients with heparin-associated thrombocytopenia

Blood ◽  
1996 ◽  
Vol 88 (2) ◽  
pp. 410-416 ◽  
Author(s):  
J Amiral ◽  
A Marfaing-Koka ◽  
M Wolf ◽  
MC Alessi ◽  
B Tardy ◽  
...  
Keyword(s):  
Cell Activation ◽  
Interleukin 8 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Platelet Factor ◽  
Elisa System ◽  
Platelet Aggregometry ◽  
Test Result

Eighty-seven patients with heparin-associated thrombocytopenia (HAT) showed either a positive heparin platelet aggregometry test result and/or the presence of antibodies to heparin-platelet factor 4 (H-PF4) complexes by enzyme-linked immunosorbent assay (ELISA). Fifteen of these patients lacked antibodies to H-PF4, and plasma from these patients was analyzed for the presence of antibodies to PF4-related chemokines, Neutrophil-activating peptide-2 (NAP-2) and interleukin-8 (IL-8). Of these 15 patients, 6 showed antibodies to IL-8 and 3 to the platelet basic protein (PBP)-derived protein, NAP-2. Antibodies to IL-8 and NAP-2 were not observed in control patients (n = 38), patients with HAT and H-PF4 autoantibodies (n = 72), patients with autoimmune diseases (n = 21), or patients with non-HAT thrombocytopenia (n = 30). Five of these nine patients with anti-IL-8 or anti-NAP-2 developed thrombosis during heparin treatment, which is not statistically different from the patients with H-PF4 antibodies. The existence of autoantibodies to IL-8 and NAP-2 in HAT patients highlights the significance of chemokines in the pathogenesis of HAT. The contribution of heparin in vitro was minimal in patients with anti-IL-8 and anti-NAP- 2 antibodies, suggesting a biologic difference from the majority of patients with HAT and anti-PF4 antibodies. It may be that antibodies to IL-8 and NAP-2 have weaker affinity for heparin and that the ELISA system may not reflect in vivo heparin-chemokine complex formation. Alternatively, antichemokine autoantibodies may predate heparin exposure, and the role of heparin in initiating HAT may be to mobilize the chemokines and to target them to platelets, neutrophils, or endothelial cells. Subsequent chemokine-binding autoantibodies then lead to cell activation resulting in thrombocytopenia and thrombosis.

scholarly journals 2508

2017 ◽  
Vol 1 (S1) ◽  
pp. 10-10
Author(s):  
Sara Blick ◽  
Craig Morrell ◽  
Sara Ture ◽  
David J. Field
Keyword(s):  
Cell Differentiation ◽  
B Cell ◽  
B Cell Differentiation ◽  
Wild Type ◽  
Platelet Factor ◽  
Cell Numbers ◽  
Study Population

OBJECTIVES/SPECIFIC AIMS: To investigate the role of platelet factor-4 (PF4) in B cell differentiation and develop strategies to better modulate B cell differentiation in vitro and in vivo. METHODS/STUDY POPULATION: We use tissue culture and flow cytometry to examine the role of PF4 in B cell differentiation. We use wild type (WT) and PF4−/− mice on a C57Bl6/J background. PF4−/− mice have reduced in vivo B cell differentiation responses. RESULTS/ANTICIPATED RESULTS: We anticipate that our studies will demonstrate that PF4 promotes B cell differentiation in the bone marrow microenvironment. DISCUSSION/SIGNIFICANCE OF IMPACT: The significance of this project may be valuable in developing efficient methods and strategies to increase or limit B cell numbers in vitro and in human disease.

Treatment of Factor XIII Deficiency with Cryoprecipitate

1968 ◽  
Vol 20 (03/04) ◽  
pp. 528-533 ◽  
Author(s):  
C. J Amris ◽  
M Hilden
Keyword(s):  
Factor Xiii ◽  
Prophylactic Treatment ◽  
Factor Xiii Deficiency ◽  
Intravenous Injections ◽  
Congenital Factor

SummaryIn in vitro and in vivo investigations of two patients with congenital factor XIII-deficiency it was demonstrated that cryoprecipitate contains a high factor XIII-activity. Cryoprecipitate in small amounts, given as intravenous injections every 3 or 4 weeks seems to be useful as a prophylactic treatment of patients with severe haemorrhagic due to factor XHI-deficiency.

Abnormal Wound Healing in Experimentally-Induced Factor XIII Deficiency in Rabbits

1979 ◽  
Author(s):  
Soo Young Lee ◽  
S. I. Chung
Keyword(s):  
Wound Healing ◽  
Factor Xiii ◽  
Tissue Repair ◽  
Culture Media ◽  
Rabbit Platelet ◽  
Fibroblast Proliferation ◽  
Factor Xiii Deficiency ◽  
Platelet Factor ◽  
Collagenous Matrix ◽  
Matrix Accumulation

The observation of poor wound healing and abnormal scarring in Factor XIII deficiency reported by Duekert et al., (Throab. Diath. Haenorrh., 5:179, 1960) aroused great interest in the role of this factor in tissue repair. In the present atudy, Factor XIII deficiency was induced in rabbits by intravenous infusion of IgC isolated from goat anti-rabbit platelet Factor XIII, and the deficient state vaa maintained by daily infusion. Control rabbits were given normal goat IgG. After production of standard akin wound the progress of eptthellalizacion, fibroblast proliferation, and collagenous matrix formation was monitored by histology and immunohiscocherais try. In normal rabbits, epithelialization was complete by day 6; fibroblast proliferation by day 10; maximal collagenous matrix accumulation was observed on day 14. In Factor XIII deficient animals, epithelialixation was not completed until day 14; fibroblast proliferation and collagenous matrix accumulation were retarded beyond day 20. These observations suggest that Factor XIII is involved in early phases of wound healing. In an initial attempt to study the mode of Factor XIII in tissue repair, the effect of Factor XIII ou the growth of fibroblast was examined in vitro. However, contrary to an earlier report, the addition of Factor XIII to the culture media shoved no effect on the growth of cells.

The Role of Polyphenols in the Modulation of Plasma Non-Enzymatic Antioxidant Capacity (NEAC)

2012 ◽  
Vol 82 (3) ◽  
pp. 228-232 ◽  
Author(s):  
Mauro Serafini ◽  
Giuseppa Morabito
Keyword(s):  
Antioxidant Capacity ◽  
Dietary Intervention ◽  
Ex Vivo ◽  
The Body ◽  
Dietary Polyphenols ◽  
Enzymatic Antioxidant ◽  
Endogenous Antioxidant

Dietary polyphenols have been shown to scavenge free radicals, modulating cellular redox transcription factors in different in vitro and ex vivo models. Dietary intervention studies have shown that consumption of plant foods modulates plasma Non-Enzymatic Antioxidant Capacity (NEAC), a biomarker of the endogenous antioxidant network, in human subjects. However, the identification of the molecules responsible for this effect are yet to be obtained and evidences of an antioxidant in vivo action of polyphenols are conflicting. There is a clear discrepancy between polyphenols (PP) concentration in body fluids and the extent of increase of plasma NEAC. The low degree of absorption and the extensive metabolism of PP within the body have raised questions about their contribution to the endogenous antioxidant network. This work will discuss the role of polyphenols from galenic preparation, food extracts, and selected dietary sources as modulators of plasma NEAC in humans.

Anti-obesity role of Aster glehni extract: in vivo and in vitro effects

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
HM Lee ◽  
TG Ahn ◽  
CW Kim ◽  
HJ An
Keyword(s):  
In Vitro Effects

A Molecular Approach to Immunoscintigraphy: A Study of the T-Antigen Conformation on the Surface of Tumors

1987 ◽  
Vol 26 (01) ◽  
pp. 1-6 ◽  
Author(s):  
S. Selvaraj ◽  
M. R. Suresh ◽  
G. McLean ◽  
D. Willans ◽  
C. Turner ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Tumor Cell ◽  
T Antigen ◽  
Human Carcinomas ◽  
Animal Tumor ◽  
Synthetic Antigens

The role of glycoconjugates in tumor cell differentiation has been well documented. We have examined the expression of the two anomers of the Thomsen-Friedenreich antigen on the surface of human, canine and murine tumor cell membranes both in vitro and in vivo. This has been accomplished through the synthesis of the disaccharide terminal residues in both a and ß configuration. Both entities were used to generate murine monoclonal antibodies which recognized the carbohydrate determinants. The determination of fine specificities of these antibodies was effected by means of cellular uptake, immunohistopathology and immunoscintigraphy. Examination of pathological specimens of human and canine tumor tissue indicated that the expressed antigen was in the β configuration. More than 89% of all human carcinomas tested expressed the antigen in the above anomeric form. The combination of synthetic antigens and monoclonal antibodies raised specifically against them provide us with invaluable tools for the study of tumor marker expression in humans and their respective animal tumor models.

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