The platelets bind to the human red cells, containing the malaria parasites, and kill the parasites by releasing into the red cell
PF4.
The exact pathophysiology remains unclear but is thought to be due to the interaction of negative polyanions such as nucleic acids and lipopolysaccharides with
PF4 [9, 10].
The activated platelets could result in forming platelet factor 4 (
PF4), while the formed thrombin could couple with antithrombin III to generate thrombin-antithrombin III (TAT) complexes [31].
C-K O-K Al-K Si-K S-K Ti-K V-K Base(495)_pf1 1-2 0.00 0.0- 0.62 0.05 0.00 0.13 Base(49;)_pf2 1.26 0.00 0.04 0.54 0.00 0.00 0.12 Base(495) pf3 1.66 0.00 0.07 0.60 0.00 0.00 0.17 Base(495)
pf4 1.64 0.00 0.04 0.56 0.05 0.00 0.09 Base(495) pt5 3.60 0.00 0.00 0.47 0.00 0.00 0.10 Base(495) pt6 1.53 0.00 0.06 0.58 0.02 0.00 0.08 Cr-K Mn-K Fe-K Ni-K Mo-L Base(495)_pf1 12.53 0.79 83.94 j 0.15 0.00 Base(49;)_pf2 11.49 1.33 84.-2 0.43 0.07 Base(495) pf3 11.85 0.65 84.69 i 0.22 0.09 Base(495)
pf4 12.07 0.89 84.36 i 0.30 0.00 Base(495) pt5 11.68 0.84 82.77 i 0.46 0.08 Base(495) pt6 12.56 0.46 84.43 i 0.27 0.00 Fig.
Heparin binds to
PF4, and the heparin-PF4 complex is immunogenic, which induces the expression of IgG, as well as IgA and IgM antibodies against the heparin-PF4 complex.
Item Loading SE [alpha] [rho] AVE Construct Anonymous communication AC1 .82 (***) .03 .79 .87 .62 AC2 .84 (***) .02 AC3 .72 (***) .05 AC4 .76 (***) .04 Perceived freedom PF1 .83 (***) .03 .85 .89 .63 PF2 .74 (***) .04 PF3 .83 (***) .03
PF4 .74 (***) .04 PF5 .82 (***) .03 Perceived need for legal protection LP1 .77 (***) .05 .72 .85 .64 LP2 .83 (***) .04 LP3 .80 (***) .04 Propensity to trust PT1 .75 (***) .15 .82 .88 .63 PT2 .85 (***) .17 PT3 .83 (***) .11 PT4 .75 (***) .13 Note: SE = standard error, [alpha] = Cronbach's alpha, [rho] = Dillon Goldstein's rho, AVE = average variance extracted.
Heparin-induced thrombocytopenia (HIT) is a serious complication from heparin use, arising from the binding of antibody against heparin-platelet factor 4 (
PF4) complexes onto platelets.
The pathogenesis of HIT has been recently better defined: duringthe early phase heparin binds to platelet factor 4 (
PF4), generating a complex (heparin-PF4) toward which IgG antibodies are produced and this complex is also able to activate platelets via FcyRIIa receptor, causing microthrombosis and thrombocytopenia.