IntroductionFHR1 is a member of Factor H (FH) protein family involved in complement to regulate the innate immune response. FHR1 shares with FH highly conserved C-terminal region and considered act as competitor cause induction. also an inflammatory mediator able inhibit terminal activation. Homozygous deletion FHR1, found occur 10% healthy population, strongly associated pathologies like atypi...

BACKGROUND Heparin-induced thrombocytopenia is caused by antibody formation to heparin-platelet factor 4 complexes. It typically develops 5 to 14 days after the initiation of heparin, but it can occur up to 3 weeks after the patient stops taking it. Early recognition by monitoring platelet counts during heparin therapy can decrease associated mortality and morbidity. METHODS A case is describ...

Heparin is a widely used anticoagulant. Because of its negative charge, it forms complexes with positively charged platelet factor 4 (PF4). This can induce anti-PF4/heparin IgG Abs. Resulting immune complexes activate platelets, leading to the prothrombotic adverse drug reaction heparin-induced thrombocytopenia (HIT). HIT requires treatment with alternative anticoagulants. Approved for HIT are ...

The binding of heparin or heparan sulphate to a variety of cell types results in specific changes in cell function. Endothelial cells treated with heparin alter their synthesis of heparan sulphate proteoglycans and extracellular matrix proteins. In order to identify a putative endothelial cell heparin receptor that could be involved in heparin signalling, anti-(endothelial cell) monoclonal anti...

Heparin, a sulfated glycoconjugate, reportedly inhibits the blood-stage growth of the malaria parasite Plasmodium falciparum. Elucidation of the inhibitory mechanism is valuable for developing novel invasion-blocking treatments based on heparin. Merozoite surface protein 1 has been reported as a candidate target of heparin; however, to better understand the molecular mechanisms involved, we cha...

Although it is well established that long-term heparin therapy causes osteoporosis, it is unknown whether heparin-induced bone loss is reversible when heparin treatment is stopped. To address this question, we randomized rats to once daily subcutaneous injections of either unfractionated heparin (1.0 U/g or 0.5 U/g) or saline for 28 days and then followed the rats for an additional 28 days off ...

From experiments reported it is concluded that heparin combines with and inactivates Christman factor (C.F.) to form reversibly a heparin-C.F. complex. Apart from the effect of heparin on C.F. and on thrombin, heparin in moderate concentrations was not shown to inactivate any other coagulation factors."Available" heparin is defined as heparin in such a state that it can delay some clotting syst...

Evidence is presented that heparin pretreatment produces protective effects on myocardial tissue distinct from its anticoagulant activity. The present study examines the ability of heparin sulfate and N-acetyl heparin (a derivative of heparin devoid of anticoagulant effects) to protect the heart from injury associated with global ischemia and reperfusion. Male New Zealand White rabbits were adm...

Heparin inhibits the growth of several cell types in vitro, including bovine pulmonary artery smooth muscle cells (BPASMCs). To understand more about the heparin structure required for endogenous activity, chemically modified derivatives of native heparin and glycol-split heparin, namely, 2-O-desulfonated iduronic/glucuronic acid residues in heparin, and 2-O-desulfonated iduronic residues in gl...

Heparin is a widely used anticoagulant. Because of its negative charge, it forms complexes with positively charged platelet factor 4 (PF4). This can induce anti-PF4/heparin IgG Abs. Resulting immune complexes activate platelets, leading to the prothrombotic adverse drug reaction heparin-induced thrombocytopenia (HIT). HIT requires treatment with alternative anticoagulants. Approved for HIT are ...