scholarly journals Dimiconin, a novel coagulation inhibitor from the kissing bug, Triatoma dimidiata, a vector of Chagas disease

2012 ◽  
Vol 215 (20) ◽  
pp. 3597-3602 ◽  
Author(s):  
Y. Ishimaru ◽  
E. A. Gomez ◽  
F. Zhang ◽  
L. Martini-Robles ◽  
H. Iwata ◽  
...  
Keyword(s):  
Chagas Disease ◽  
Coagulation Inhibitor

706 B-type natriuretic peptide (BNP) and ventricular arrhythmias in Chagas disease

2007 ◽  
Vol 6 (1) ◽  
pp. 155-156
Author(s):  
J MARQUES ◽  
A KANSKY ◽  
I MENDOZA ◽  
L LOPEZGOMEZ ◽  
F MOLEIRO ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Chagas Disease ◽  
Ventricular Arrhythmias

Chagas Disease After Organ Transplantation - Los Angeles, California, 2006

2006 ◽  
Author(s):  
L. Mascola ◽  
B. Kubak ◽  
S. Radhakrishna ◽  
T. Mone ◽  
R. Hunter ◽  
...  
Keyword(s):  
Los Angeles ◽  
Organ Transplantation ◽  
Chagas Disease

(-)-Cubebin and (-)-Hinokinin: Evaluation of immunomodulatory effects in Chagas' disease

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
VR Esperandim ◽  
DS Ferreira ◽  
KCS Rezende ◽  
R Lucarini ◽  
LGR Oliveira ◽  
...  
Keyword(s):  
Chagas Disease ◽  
Immunomodulatory Effects

Heparin Cofactor II Deficiency in Patients Infected with the Human Immunodeficiency Virus

1993 ◽  
Vol 70 (05) ◽  
pp. 730-735 ◽  
Author(s):  
P Toulon ◽  
M Lamine ◽  
I Ledjev ◽  
T Guez ◽  
M E Holleman ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Absolute Number ◽  
Thrombin Inhibitor ◽  
Unusual Complication ◽  
Healthy Individuals ◽  
Heparin Cofactor Ii ◽  
Immunodeficiency Virus ◽  
Coagulation Inhibitor ◽  
The Mean ◽  
Cd4 Lymphocytes

SummaryIn human plasma, heparin cofactor II (HCII) is a thrombin inhibitor, whose deficiency has been reported to be associated with recurrent thrombosis. The finding of two cases of low plasma HCII activity in two patients infected with the human immunodeficiency virus (HIV) led us to investigate this coagulation inhibitor in the plasma of a larger population of HIV-infected patients. The mean plasma HCII activity was significantly lower in 96 HIV-infected patients than in 96 age- and sex-matched healthy individuals (0.75 ± 0.24 vs 0.99 ± 0.17 U/ml, p <0.0001). HCII antigen concentration was decreased to the same extent as the activity. The proportion of subjects with HCII deficiency was significantly higher in the HIV-infected group than in healthy individuals (38.5% vs 2.1%). In addition, HCII was significantly lower in AIDS patients than in other HIV-infected patients, classified according to the Centers for Disease Control (CDC) on the basis of an absolute number of circulating CD4+ lymphocytes below 200 x 106/1. The link between HCII and immunodeficiency is further suggested by significant correlations between HCII activity and both the absolute number of CD4+ lymphocytes and the CD4+ to CD8+ lymphocyte ratio. Nevertheless, the mean HCII level was not different in the various groups of patients classified according to clinical criteria, except in CDC IVD patients in whom HCII levels were significantly lower. In addition, no correlation could be demonstrated between HCII and protein S activities, another coagulation inhibitor whose plasma level was also found to be decreased in HIV-infected patients. A similar prevalence of HCII deficiency was also found in a small series of 7 HIV-infected patients who developed thrombotic episodes, an unusual complication of the infection. This suggests that, in HIV-infected patients, HCII deficiency is not in itself the causative factor for the development of thrombosis.

On the Natural Blood Coagulation Inhibitor System Investigations of Inhibitor Factors Based on Antithrombin Deficient Blood

1965 ◽  
Vol 14 (03/04) ◽  
pp. 473-489 ◽  
Author(s):  
O Egeberg
Keyword(s):  
Normal Level ◽  
Antithrombin Iii ◽  
Strong Support ◽  
Blood Protein ◽  
Coagulation Inhibitor ◽  
Inhibitor System ◽  
Normal Human ◽  
Partial Deficiency ◽  
Antithrombin Iii Activity ◽  
Prothrombinase Activity

SummaryNatural coagulation inhibitor factors were studied in sera, or in fractions of sera, from patients with congenital partial deficiency of antithrombin and from normal persons. In the patients’ sera the progressive antithrombin (antithrombin III) and heparin cofactor (antithrombin II) had both been measured around 50 per cent of normal level.No decreased activity could be demonstrated in the patients’ sera as to antiprothrombinase, the inhibitor against blood intrinsic prothrombinase activity.For anticonvertin, the inhibitor against the tissue convertin complex, the activity was found decreased to about the same level as that demonstrated for antithrombin III and II. The results lend strong support to the hypothesis that the activities measured as anticonvertin, antithrombin III and antithrombin II represent functions of the same blood protein, which on the other side appears to be distinct from antiprothrombinase. In accordance with this explanation, an antithrombin III concentrate had also antithrombin II and anticonvertin activity, and further, adsorption of a normal human serum with convertin appeared to specifically reduce its antithrombin III activity.The inhibitor against activated antihemophilic C factor (AHC’ = activated f. XI) was studied in sera adsorbed with BaS04 and celite. The inhibitor activity was found at normal level in the patients’ sera, consistent with the view that anti-AHC’ is distinct from antithrombin III, II and from anticonvertin. No acceleration of the anti-AHC’ activity could be demonstrated after addition to the inhibition mixture of weak solutions of heparin.The results are discussed.

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