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Thurman, Joshua M.,Kraus, Damian M.,Girardi, Guillermina,Hourcade, Dennis,Kang, Hee J.,Royer, Pamela A.,Mitchell, Lynne M.,Giclas, Patricia C.,Salmon, Jane,Gilkeson, Gary,Holers, V. Michael Elsevier 2005 Molecular immunology Vol.42 No.1
<P><B>Abstract</B></P><P>Studies in gene-targeted mice have demonstrated that factor B of the alternative complement pathway plays an important role in several disease models, but an exogenous inhibitor of factor B has not previously been available. We have developed an inhibitory monoclonal antibody directed against a critical epitope on mouse factor B and have tested it in a model of antiphospholipid (aPL) antibody (Ab)-induced fetal loss. Gene-targeted factor B-deficient mice (fB<SUP>−/−</SUP>) were injected with a fusion protein comprised of the second and third short consensus repeat (SCR) domains of mouse factor B linked to a mouse IgG<SUB>1</SUB> Fc domain. Hybridomas were made from splenocytes of the immunized mouse. One mAb, designated 1379, produced an IgG<SUB>1</SUB> antibody that inhibited alternative pathway activation in vitro and in vivo by preventing formation of the C3bBb complex. Strikingly, this mAb inhibited alternative pathway activation in serum from mice, rats, humans, monkeys, pigs and horses. Fab fragments made from this mAb also inhibited alternative pathway activation. Epitope mapping demonstrated that this antibody binds to factor B within the third SCR domain. When mAb 1379 was administered to mice that also received human IgG containing antiphospholipid antibodies, it provided significant protection from antiphospholipid antibody-induced complement activation and fetal loss. Thus, this mAb to factor B has broad species reactivity and effectively inhibits alternative pathway activation. The mAb protects mice in an in vivo model of antiphospholipid antibody syndrome, demonstrating the therapeutic potential for the inhibition of factor B in this disease.</P>
Optically-Activated Gold-Compensated Silicon V-Groove P-I-N Diodes : I-Optical Gating Model
Nam Ki Min,Seong Jae Lee,H. Thurman Henderson 한국정보과학회 1998 Journal of Electrical Engineering and Information Vol.3 No.5
Simple physical and mathematical models of the optical switching of gold-compensated silicon p-i-n devices were developed using a single level approach (only the gold acceptor level was considered). The expressions for concentrations of electrons, holes, and negatively-charged and neutral gold acceptors were derived and calculated as a function of photon flux for three different cases of photon energy. A variation of switching voltage with photon flux was also calculated. These calculations showed clearly that the concentration of neutral gold acceptor and the hole lifetime increase with increasing photon flux, and thus the gold-compensated p-i-n device can be optically triggered, and the switching voltage can be easily controlled with photon energies larger than 0.55 eV. The maximum optical gating effect of gold-compensated silicon p-i-n devices will be obtained when the sample is closely compensated with gold and the light has a photon energy hv>1.12 eV as a optical source.