Heparin types

Type I heparin-induced thrombocytopenia is common and is characterized by a mild transient thrombocytopenia (with platelet counts that usually do not fall below 50 X 10 /1) the thrombocytopenia occurs on the first few days of heparin administration (usually 1-5 days) and requires careful monitoring but not usually withdrawal of heparin. Type I thrombocytopenia is generally harmless and very probably results from direct heparin-induced platelet aggregation. Thrombocjdopenia is most common when large doses of heparin are used, or in some particular circumstances, such as after thrombolytic therapy (35) or in the early orthopedic postoperative period (36) it can abate in spite of continued therapy. Tjrpe I thrombocytopenia is a non-immune reaction, probably due to a direct activating effect of heparin on platelets. 

Chondroitin 4-sulfate is easily differentiated from the sulfated polysaccharides of the heparin type by its negative optical rotation, and from dermatan sulfate (also called chondroitin sulfate B or /S-heparin) by the identification of L-iduronic acid in the latter. However, it is difficult to distinguish it from chondroitin 6-sulfate ( chondroitin sulfate C ), since the differences in optical rotation, solubility, and susceptibility to enzymic degradation between the two substances are minimal or non-existent. It is probable that studies made in the past with products isolated from incompletely characterized sources have dealt with mixtures of both chondroitin sulfates. 

In contrast to heparin, the coumarinic acid anticoagulants are inactive in vitw ]6k.e heparin they are active in vivo. The phenylindanedione-type compounds (7) (36) and warfarin (2) produce their in vivo inhibitory effect on the coagulation system by competitively antagonizing the normal activity of vitamin (8) (37—44). 

Basal laminas are specialized areas of the ECM that surround epithelial and some other cells (eg, muscle cells) here we discuss only the laminas found in the renal glomerulus. In that strucmre, the basal lamina is contributed by two separate sheets of cells (one endothelial and one epithelial), each disposed on opposite sides of the lamina these three layers make up the glomerular membrane. The primary components of the basal lamina are three proteins—laminin, entactin, and type IV collagen—and the GAG heparin or heparan sulfate. These components are synthesized by the underlying cells. 

Figure 48-3. Schematic representation of fibronectin. Seven functional domains of fibronectin are represented two different types of domain for heparin, cell-binding, and fibrin are shown. The domains are composed of various combinations of three structural motifs (I, II, and III), not depicted in the figure. Also not shown is the fact that fibronectin is a dimer joined by disulfide bridges near the carboxyl terminals of the monomers. The approximate location of the RGD sequence of fibronectin, which interacts with a variety of fibronectin integrin receptors on cell surfaces, is indicated by the arrow. (Redrawn after Yamada KM Adhesive recognition sequences.

Type I IgE Anaphylaxis, urticaria P-Lactam antibiotics penicillins (primarily), cephalosporins, carbapenems Non-fl-lactam antibiotics sulfonamides, vancomycin Others insulin, heparin... 

Type II IgG Hemolytic anemia, thrombocytopenia Quinidine, methyldopa, penicillins, heparin... 

Refludan Lepirudin Hoechst Marion Roussel Heparin-induced thrombocytopenia type II... 

Heparin inhibits many enzymes, including all RNases, therefore, it is criticalfor this step. It also inhibits the labeling step therefore it needs to be removed later (by a LiCl precipitation). We did not find any comparable alternative (in efficiency and cost) to heparin. The composition and concentrations of other ingredients can be changed depending on the cell type or experiment. 

Mann, W.A., Meyer, N., Weber, W., Meyer, S., Greten, H., and Beisiegel, U. (1995) Apolipoprotein E isoforms and rare mutations parallel reduction in binding to cells and to heparin reflects severity of associated type III hyperlipoproteinemia./. Lipid Res. 36, 517. 

Capacitative Ca2+ entry is the predominant mode of regulated Ca2+ entry in nonexcitable cells but it also occurs in a number of excitable cell types. This pathway of Ca2+ entry is usually associated with the activation of phospholipase C, which mediates the formation of IP3 (see Ch. 20). Intracellular application of IP3 mimics the ability of hormones and neurotransmitters to activate calcium ion entry, and activation of calcium ion entry by hormones and neurotransmitters can be blocked by intracellular application of low-molecular-weight heparin, which potently antagonizes IP3 binding to its receptor. There is considerable evidence for the presence of an IP3 receptor in the plasma membrane of some cells types. 1(1,3,4,5)P4, a product of IP3 phosphorylation, has been shown in some cells to augment this action of IP3 in activating PM calcium ion entry, but in others IP3 alone is clearly sufficient. 

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