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Complement splitting

Brandshund I, Siersted SE, Teisner B. Double-decker rocket immunoelectrophoresis for direct quantitation of complement split products with C3d specificities in plasma. J Immunol Methods 1981 44 63-71. [Pg.240]

Complement Activation. With 2-h infusions at a dose of 2 mg/kg, no increases in complement-split products were observed in more than 300 patients with inflammatory diseases treated with ISIS 2302, a 20-nucleotide phosphorothioate antisense inhibitor of ICAM-1. Similarly, ISIS 5132, an inhibitor of C-raf kinase was dosed from 0.5 to 6.0 mg/kg and no meaningful increases in complement-split products were observed. ISIS 3521, a PKCa inhibitor gave equivalent data and both of these drugs were studied in patients with various malignant diseases. Similar data were observed with all the phosphorothioate oligodeoxynucleotides administered on this... [Pg.142]

Inspired by reports from Craddok, the effects of different membranes on hemodialysis Induced leukopenia and complement activation were studied (Table I). The results were disappointing. There was no definite correlation between the reduction in neutrophil count and complement activation. Unfortunately, however, these studies did not include a measure of complement split products. Serum hemolytic complement assays were performed to evaluate the consumption of complement. Since complement component levels represent a dynamic balance between synthesis and degradation of components, their assay will fail to detect a state of increased complement consumption, if such consumption is balanced by an increased synthesis (17). [Pg.166]

Mo(V) paramagnetic species is also an argument to exclude an interaction between the Mo site and Fe-S center I. These studies were further complemented by detailed study of the observable splitting and its temperature dependence, EPR saturation, and the effect of differential reduction of the Fe-S centers. A magnetic interaction was also seen in xanthine oxidase, between various Mo(V) EPR species and one of the Fe-S centers. A study on the... [Pg.408]

Histamine Serotonin Platelet-activating factor (PAF) Eicosanoids (various prostaglandins and leukotrienes) C3a, C4a, and C5a from the complement system Bradykinin and fibrin split products from the coagulation system... [Pg.621]

The chromatid separation process has also remained mysterious. It is an autonomous process that does not direcdy depend on the mitotic spindle (Wilson 1925, Mazia 1961). This is most vividly seen in cells whose spindles have been destroyed by spindle poisons such as colchicine. In many organisms, in particular in plant cells, the cell cycle delay induced by colchicine is only transient and chromatids eventually split apart in the complete absence of a mitotic spindle (Mole-Bajer 1958, Rieder Palazzo 1992) (Fig. 2). Mitosis in the presence of colchicine or colcemid (known as c-mitosis) leads to the production of daughter cells with twice the normal complement of chromosomes. This process is routinely used for manipulating plant genomes and may contribute to the therapeutic effects of taxol in treating breast cancer. [Pg.116]

Verification is the complement of calibration model predictions are compared to field observations that were not used in calibration or fidelity testing. This is usually the second half of split-sample testing procedures, where the universe of data is divided (either in space or time), with a portion of the data used for calibration/fidelity check and the remainder used for verification. In essence, verification is an independent test of how well the model (with its calibrated parameters) is representing the important processes occurring in the natural system. Although field and environmental conditions are often different during the verification step, parameters determined during calibration are not adjusted for verification. [Pg.156]

The effects of Lp(a) on the fibrinolytic system are based on the homology between plasminogen and Lp(a) (E3, E5, K4). Inactive Glu-plasminogen is converted to inactive glutamine-plasmin or inactive lysine-plasmin. Both can be converted to active lysine-plasmin, the activity of which is based on the serine protease part that splits fibrin and fibrinogen, but also factors V and Villa. In addition, Lp(a) is able to activate factor XII, factor VII, and the complement factors Cl and C3. [Pg.97]

Example UV photodiode array (PDA) and ESI-TOF detection can be combined if the effluent is split or the PDA precedes the ESI interface. The detection methods complement each other in that their different sensitivities towards components of a mixture prevent substances from being overlooked. RICs help to differentiate a targeted compound - an unknown impurity in this case - from others and to identify eventually present isomers. Finally, accurate mass measurement helps in the identification of the unknown (Fig. 12.9). [25]... [Pg.486]

Complement. Complement is an extensive series of glycoproteins and protein inhibitors whose function includes major cytolytic effects, mediation of opsonization, and modulation of inflammatory responses. Activation of this system plays an important role in host defense leading to destruction of microorganisms. It also results in generation of anaphylotoxins which induce mediator release and "split products" that mediate membrane damage, either directly through structural alteration or indirectly, via cell chemotaxis and regulation. [Pg.148]

A number of proteins are known that can be split into two fragments, which when recombined form functional, though usually less stable, folded structures (Michnick, 2001). This is known as fragment complementation. For proteins that cannot be split and reconstituted so straightforwardly, there is the possibility that reassembly might be directed by additional reagents such as ligands. Such systems present a potential route to new biosensors. [Pg.104]

In experimental serum sickness, a fall in serum complement level occurs at the time immune complexes form and inflammatory lesions develop (D6). However, levels of complement do not always reflect activation or consumption by immune complexes. The rate of synthesis of complement proteins may be sufficient to replace the amount being consumed, and several of the complement components are so-called acute-phase reactants, i.e., their levels rise with inflammation. Thus, activation may occur despite normal or even elevated levels in the serum. Turnover studies provide more direct evidence of complement utilization but are technically cumbersome (K4). A simpler approach is the detection of split products of complement components, which provides direct evidence of complement activation, or the examination of effusions for evidence of complement depletion (H31, N7, P7). [Pg.8]

Alas, things are not as simple as they may have appeared. From the discussions in Chapters 6 and 7 you might be under the impression that typical H NMR spectra exhibit just one sharp signal line for each 1H nucleus (or each set of equivalent H nuclei) and that the same thing is true for 13C spectra as well as for spectra of any other isotope. Actually, this is not usually the case. Instead, the individual signals expected on the basis of the molecule s symmetry are themselves often split into symmetrical patterns (multiplets) consisting of two or more lines. While these extra lines do make a spectrum appear more complex, they also offer valuable structural information that complements the chemical shift data. This chapter explains the source of these extra lines and shows how useful they can be for confirming the structures of molecules. [Pg.110]

The information obtained from the phosphorescence microwave double resonance (PMDR) spectroscopy nicely complements the results deduced from time-resolved emission spectroscopy. (See Sect. 3.1.4 and compare Ref. [58] to [61 ].) Both methods reveal a triplet substate selectivity with respect to the vibrational satellites observed in the emission spectrum. Interestingly, this property of an individual vibronic coupling behavior of the different triplet substates survives, even when the zero-field splitting increases due to a greater spin-orbit coupling by more than a factor of fifty, as found for Pt(2-thpy)2. [Pg.112]


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See also in sourсe #XX -- [ Pg.3 ]




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