Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AFIBRINOGENEMIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,387 records · Page 77Linked to original sources
PubMed2005

The past decade: fibrinogen.

This paper reviews the advances in understanding of fibrinogen structure and function, its genetic and environmental determinants, role in the process of hemostasis, platelet aggregation, plasma viscosity and erythrocyte aggregation, cellular and matrix interactions, inflammation, wound healing, tumor development, atherogenesis and involvement in pathogenesis of diseases, that have been made over the past decade. Future studies will seek to define precise mechanisms of complex gene-environment interactions that influence fibrinogen levels and its complex role in the pathogenesis of fibrinogen-associated diseases.

Afibrinogenemia↗
PubMed1976

Dysfibrinogenaemia and primary hepato-cellular carcinoma.

The mechanisms of blood coagulation and fibrinolysis have been evaluated in 28 black adult Africans with primary hepato-cellular carcinoma (HCC). A characteristic pattern of abnormalities has been defined. Dysfibrinogenaemia appears to be a useful biological marker for the disease. The reptilase test (RT) is a simple, reliable and sensitive means of detection of this metabolic abnormality. It is suggested that the RT should be used to screen populations at high risk of developing HCC, such as cirrhotics, in conjunction with alpha fetoprotein determinations, which, alone, are inadequate for the purpose. The haemostatic defect may have relevance to the pathogenesis of HCC, and further suggests a potentially useful, additional, therapeutic modality.

Adult↗
PubMed1991

Dimeric ristocetin flocculates proteins, binds to platelets, and mediates von Willebrand factor-dependent agglutination of platelets.

Ristocetin in aqueous solution dimerizes with an equilibrium dissociation constant of 5.0 x 10(-4) M, i.e. approximately 1.1 mg ml-1 (Waltho, J.P., and Williams, D. H. (1989) J. Am. Chem. Soc. 111, 2475-2480). At concentrations of about 1.0 mg ml-1 ristocetin flocculates many proteins, lyses platelets and, in the presence of von Willebrand factor, agglutinates both fresh and formalin-fixed platelets. Because ristocetin exists as both monomeric and dimeric species, we sought to determine which of these forms flocculates proteins and agglutinates platelets. We found that: 1) the initial rate of flocculation of certain proteins, 2) the initial rate of agglutination of formalin-fixed platelets, and 3) the binding of ristocetin to formalin-fixed platelets are higher order solely with respect to the concentration of ristocetin dimers. As to the operative mechanism, it appears that bifunctional dimers cross-link proteins that possess multiple copies of a common recognition site. Preliminary evidence indicates that a recognition site is a beta-turn of the form X-P-G-X'.

Afibrinogenemia↗
PubMed1991

Effect of systemic fibrinogen depletion on intraabdominal abscess formation.

Deposition of fibrin within the peritoneal cavity is an integral host response to local infection. To directly assess the role of fibrin deposition in the pathogenesis of intraabdominal abscess formation, the ability to induce abscesses in fibrinogen-depleted mice was examined. We hypothesized that systemic defibrinogenation with ancrod would limit the availability of fibrinogen for deposition within the peritoneal cavity and would therefore impair intraabdominal abscess formation. A gelatin capsule containing 50% sterile feces plus Bacteroides fragilis 1 x 10(9) CFU was inserted IP into control or defibrinogenated mice. System defibrinogenation resulted in alteration of the character of abscess formation, as manifested by reduced abscess size and degree of purulence. Abscesses were significantly smaller (0.18 +/- 0.02 gm [n = 29] vs. 0.09 +/- 0.02 gm [n = 11], p less than 0.01) and less purulent (p less than 0.001) in the ancrod-treated mice than in control animals, despite equal numbers of bacteria in the abscesses recovered from both groups. The effect of ancrod was specific for defibrinogenation, because IP repletion with fibrinogen reversed the ancrod effect on abscess size. In addition to its local effects, systemic fibrinogen depletion resulted in a significant elevation in mortality following IP infection (1 of 30 control animals vs. 10 of 23 ancrod-treated animals, p less than 0.01). However, this was not due to an increase in the magnitude of the B. fragilis bacteremia. These studies demonstrate that fibrin deposition contributes to the pathogenesis of purulent abscess formation and that systemic depletion of fibrinogen may alter host susceptibility to the consequences of infection.

Abdomen↗
PubMed1990

Fibrinogen Stony Brook II: partial characterization of a heterozygously transmitted peptide A anomaly.

We describe preliminary studies of a new familial dysfibrinogen, fibrinogen Stony Brook II, present in a propositus and his mother. Both presented with a history of unexplained and chronic joint swelling following trauma, and the propositus suffered recurrent knee haemarthroses following arthroscopic surgery. Prolonged plasma thrombin times required a 3-5 fold excess of normal plasma for correction. Isolated fibrinogen displayed prolonged clotting times and delayed onset of clot turbidity. Also, an abnormal peptide could be released by thrombin but not by batroxobin along with approximately half the expected amounts of normal A peptide. Assessed by its thrombin release and by its early HPLC retention position, the abnormal peptide suggests a possible A alpha-16-Arg----His substitution. The data suggests an association in these probands between this heterozygously transmitted anomaly and the apparently impaired healing in hypovascular sites.

Afibrinogenemia↗
PubMed1990

Significance of viral coinfections by HIV, HTLV-I, Epstein-Barr virus, and cytomegalovirus for immunological abnormalities in hemophiliacs.

In order to clarify the influence of viral coinfection on the immunological abnormalities of hemophiliacs infected with human immunodeficiency virus (HIV), 69 patients were examined. Of the 69, 35 (50.7%) were HIV-antibody positive (HIV-Ab+). Two of them were acquired immunodeficiency syndrome (AIDS) and the remaining 33 were asymptomatic carriers (AC). Anti-HTLV-I was found in 6 of 43 (14.3%), and 2 of these 6 were also HIV-Ab+. The frequencies of positive anti-viral capsid antigen (VCA) IgG against Epstein-Barr virus (EBV) and anti-cytomegalovirus (CMV) IgG were 47 of 51 (92.2%) and 42 of 49 (85.7%), respectively, while the titer of the former was higher in the HIV-Ab+ group than in the HIV-Ab- group (p less than 0.02). Nevertheless, no significant difference between these two groups was found as to the frequencies of these antibodies and of such early markers as anti-VCA IgM, early antigen (EA)-DR, and anti-CMV IgM. The results obtained showed no significant evidences that these viral superinfections facilitate the immunosuppression due to the HIV itself as correlated with the HIV antigenemia (thus accelerating the development of AIDS), or that they promote its autoantibody production. However, such possibilities did seem to be undeniable in some HIV-infected patients.

Adolescent↗