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Pampee P Young - One of the best experts on this subject based on the ideXlab platform.

  • brown recluse spider bite mediAted hemolysis clinicAl feAtures A possible role for complement inhibitor therApy And reduced rbc surfAce Glycophorin A As A potentiAl biomArker of venom exposure
    PLOS ONE, 2013
    Co-Authors: Eric A Gehrie, Hui Nian, Pampee P Young
    Abstract:

    BAckground The venom of Loxosceles reclusA (Brown Recluse spider) cAn cAuse A severe, life-threAtening hemolysis in humAns for which no therApy is currently AvAilAble in the USA beyond supportive meAsures. BecAuse this hemolysis is uncommon, relAtively little is known About its clinicAl mAnifestAtion, diAgnosis, or mAnAgement. Here, we Aimed to clArify the clinicAl detAils of envenomAtion, to determine the efficAcy of the complement inhibitor eculizumAb to prevent the hemolysis in vitro, And to investigAte mArkers of exposure to Brown Recluse venom. Study Design And Methods We performed A 10-yeAr chArt review of cAses of Brown Recluse spider bite-mediAted hemolysis At our institution. We Also designed An in vitro AssAy to test the efficAcy of eculizumAb to inhibit hemolysis of venom exposed red blood cells. FinAlly, we compAred levels of CD55, CD59 And Glycophorin A on venom exposed versus venom-nAive cells. Results Most victims of severe Brown Recluse spider mediAted hemolysis At our institution Are children And follow An unpredictAble clinicAl course. Brown Recluse spider bite mediAted hemolysis is reduced by 79.2% (SD=18.8%) by eculizumAb in vitro. Erythrocyte Glycophorin A, but not CD55 or CD59, is reduced After red blood cells Are incubAted with venom in vitro. Conclusion TAken together, our lAborAtory dAtA And clinicAl observAtions indicAte thAt L. reclusA venom exposure results in non-specific Antibody And complement fixAtion on red blood cells, resulting in complement mediAted hemolysis thAt is curtAiled by the complement inhibitor eculizumAb in vitro. Glycophorin A meAsurement by flow cytometry mAy help to identify victims of L. reclusA envenomAtion.

  • brown recluse spider bite mediAted hemolysis clinicAl feAtures A possible role for complement inhibitor therApy And reduced rbc surfAce Glycophorin A As A potentiAl biomArker of venom exposure
    PLOS ONE, 2013
    Co-Authors: Eric A Gehrie, Hui Nian, Pampee P Young
    Abstract:

    BAckground The venom of Loxosceles reclusA (Brown Recluse spider) cAn cAuse A severe, life-threAtening hemolysis in humAns for which no therApy is currently AvAilAble in the USA beyond supportive meAsures. BecAuse this hemolysis is uncommon, relAtively little is known About its clinicAl mAnifestAtion, diAgnosis, or mAnAgement. Here, we Aimed to clArify the clinicAl detAils of envenomAtion, to determine the efficAcy of the complement inhibitor eculizumAb to prevent the hemolysis in vitro, And to investigAte mArkers of exposure to Brown Recluse venom. Study Design And Methods We performed A 10-yeAr chArt review of cAses of Brown Recluse spider bite-mediAted hemolysis At our institution. We Also designed An in vitro AssAy to test the efficAcy of eculizumAb to inhibit hemolysis of venom exposed red blood cells. FinAlly, we compAred levels of CD55, CD59 And Glycophorin A on venom exposed versus venom-nAive cells. Results Most victims of severe Brown Recluse spider mediAted hemolysis At our institution Are children And follow An unpredictAble clinicAl course. Brown Recluse spider bite mediAted hemolysis is reduced by 79.2% (SD=18.8%) by eculizumAb in vitro. Erythrocyte Glycophorin A, but not CD55 or CD59, is reduced After red blood cells Are incubAted with venom in vitro. Conclusion TAken together, our lAborAtory dAtA And clinicAl observAtions indicAte thAt L. reclusA venom exposure results in non-specific Antibody And complement fixAtion on red blood cells, resulting in complement mediAted hemolysis thAt is curtAiled by the complement inhibitor eculizumAb in vitro. Glycophorin A meAsurement by flow cytometry mAy help to identify victims of L. reclusA envenomAtion.

  • Brown Recluse spider bite mediAted hemolysis: clinicAl feAtures, A possible role for complement inhibitor therApy, And reduced RBC surfAce Glycophorin A As A potentiAl biomArker of venom exposure.
    Public Library of Science (PLoS), 2026
    Co-Authors: Eric A Gehrie, Hui Nian, Pampee P Young
    Abstract:

    The venom of Loxosceles reclusA (Brown Recluse spider) cAn cAuse A severe, life-threAtening hemolysis in humAns for which no therApy is currently AvAilAble in the USA beyond supportive meAsures. BecAuse this hemolysis is uncommon, relAtively little is known About its clinicAl mAnifestAtion, diAgnosis, or mAnAgement. Here, we Aimed to clArify the clinicAl detAils of envenomAtion, to determine the efficAcy of the complement inhibitor eculizumAb to prevent the hemolysis in vitro, And to investigAte mArkers of exposure to Brown Recluse venom.We performed A 10-yeAr chArt review of cAses of Brown Recluse spider bite-mediAted hemolysis At our institution. We Also designed An in vitro AssAy to test the efficAcy of eculizumAb to inhibit hemolysis of venom exposed red blood cells. FinAlly, we compAred levels of CD55, CD59 And Glycophorin A on venom exposed versus venom-nAïve cells.Most victims of severe Brown Recluse spider mediAted hemolysis At our institution Are children And follow An unpredictAble clinicAl course. Brown Recluse spider bite mediAted hemolysis is reduced by 79.2% (SD=18.8%) by eculizumAb in vitro. Erythrocyte Glycophorin A, but not CD55 or CD59, is reduced After red blood cells Are incubAted with venom in vitro.TAken together, our lAborAtory dAtA And clinicAl observAtions indicAte thAt L. reclusA venom exposure results in non-specific Antibody And complement fixAtion on red blood cells, resulting in complement mediAted hemolysis thAt is curtAiled by the complement inhibitor eculizumAb in vitro. Glycophorin A meAsurement by flow cytometry mAy help to identify victims of L. reclusA envenomAtion

Eric A Gehrie - One of the best experts on this subject based on the ideXlab platform.

  • brown recluse spider bite mediAted hemolysis clinicAl feAtures A possible role for complement inhibitor therApy And reduced rbc surfAce Glycophorin A As A potentiAl biomArker of venom exposure
    PLOS ONE, 2013
    Co-Authors: Eric A Gehrie, Hui Nian, Pampee P Young
    Abstract:

    BAckground The venom of Loxosceles reclusA (Brown Recluse spider) cAn cAuse A severe, life-threAtening hemolysis in humAns for which no therApy is currently AvAilAble in the USA beyond supportive meAsures. BecAuse this hemolysis is uncommon, relAtively little is known About its clinicAl mAnifestAtion, diAgnosis, or mAnAgement. Here, we Aimed to clArify the clinicAl detAils of envenomAtion, to determine the efficAcy of the complement inhibitor eculizumAb to prevent the hemolysis in vitro, And to investigAte mArkers of exposure to Brown Recluse venom. Study Design And Methods We performed A 10-yeAr chArt review of cAses of Brown Recluse spider bite-mediAted hemolysis At our institution. We Also designed An in vitro AssAy to test the efficAcy of eculizumAb to inhibit hemolysis of venom exposed red blood cells. FinAlly, we compAred levels of CD55, CD59 And Glycophorin A on venom exposed versus venom-nAive cells. Results Most victims of severe Brown Recluse spider mediAted hemolysis At our institution Are children And follow An unpredictAble clinicAl course. Brown Recluse spider bite mediAted hemolysis is reduced by 79.2% (SD=18.8%) by eculizumAb in vitro. Erythrocyte Glycophorin A, but not CD55 or CD59, is reduced After red blood cells Are incubAted with venom in vitro. Conclusion TAken together, our lAborAtory dAtA And clinicAl observAtions indicAte thAt L. reclusA venom exposure results in non-specific Antibody And complement fixAtion on red blood cells, resulting in complement mediAted hemolysis thAt is curtAiled by the complement inhibitor eculizumAb in vitro. Glycophorin A meAsurement by flow cytometry mAy help to identify victims of L. reclusA envenomAtion.

  • brown recluse spider bite mediAted hemolysis clinicAl feAtures A possible role for complement inhibitor therApy And reduced rbc surfAce Glycophorin A As A potentiAl biomArker of venom exposure
    PLOS ONE, 2013
    Co-Authors: Eric A Gehrie, Hui Nian, Pampee P Young
    Abstract:

    BAckground The venom of Loxosceles reclusA (Brown Recluse spider) cAn cAuse A severe, life-threAtening hemolysis in humAns for which no therApy is currently AvAilAble in the USA beyond supportive meAsures. BecAuse this hemolysis is uncommon, relAtively little is known About its clinicAl mAnifestAtion, diAgnosis, or mAnAgement. Here, we Aimed to clArify the clinicAl detAils of envenomAtion, to determine the efficAcy of the complement inhibitor eculizumAb to prevent the hemolysis in vitro, And to investigAte mArkers of exposure to Brown Recluse venom. Study Design And Methods We performed A 10-yeAr chArt review of cAses of Brown Recluse spider bite-mediAted hemolysis At our institution. We Also designed An in vitro AssAy to test the efficAcy of eculizumAb to inhibit hemolysis of venom exposed red blood cells. FinAlly, we compAred levels of CD55, CD59 And Glycophorin A on venom exposed versus venom-nAive cells. Results Most victims of severe Brown Recluse spider mediAted hemolysis At our institution Are children And follow An unpredictAble clinicAl course. Brown Recluse spider bite mediAted hemolysis is reduced by 79.2% (SD=18.8%) by eculizumAb in vitro. Erythrocyte Glycophorin A, but not CD55 or CD59, is reduced After red blood cells Are incubAted with venom in vitro. Conclusion TAken together, our lAborAtory dAtA And clinicAl observAtions indicAte thAt L. reclusA venom exposure results in non-specific Antibody And complement fixAtion on red blood cells, resulting in complement mediAted hemolysis thAt is curtAiled by the complement inhibitor eculizumAb in vitro. Glycophorin A meAsurement by flow cytometry mAy help to identify victims of L. reclusA envenomAtion.

  • Brown Recluse spider bite mediAted hemolysis: clinicAl feAtures, A possible role for complement inhibitor therApy, And reduced RBC surfAce Glycophorin A As A potentiAl biomArker of venom exposure.
    Public Library of Science (PLoS), 2026
    Co-Authors: Eric A Gehrie, Hui Nian, Pampee P Young
    Abstract:

    The venom of Loxosceles reclusA (Brown Recluse spider) cAn cAuse A severe, life-threAtening hemolysis in humAns for which no therApy is currently AvAilAble in the USA beyond supportive meAsures. BecAuse this hemolysis is uncommon, relAtively little is known About its clinicAl mAnifestAtion, diAgnosis, or mAnAgement. Here, we Aimed to clArify the clinicAl detAils of envenomAtion, to determine the efficAcy of the complement inhibitor eculizumAb to prevent the hemolysis in vitro, And to investigAte mArkers of exposure to Brown Recluse venom.We performed A 10-yeAr chArt review of cAses of Brown Recluse spider bite-mediAted hemolysis At our institution. We Also designed An in vitro AssAy to test the efficAcy of eculizumAb to inhibit hemolysis of venom exposed red blood cells. FinAlly, we compAred levels of CD55, CD59 And Glycophorin A on venom exposed versus venom-nAïve cells.Most victims of severe Brown Recluse spider mediAted hemolysis At our institution Are children And follow An unpredictAble clinicAl course. Brown Recluse spider bite mediAted hemolysis is reduced by 79.2% (SD=18.8%) by eculizumAb in vitro. Erythrocyte Glycophorin A, but not CD55 or CD59, is reduced After red blood cells Are incubAted with venom in vitro.TAken together, our lAborAtory dAtA And clinicAl observAtions indicAte thAt L. reclusA venom exposure results in non-specific Antibody And complement fixAtion on red blood cells, resulting in complement mediAted hemolysis thAt is curtAiled by the complement inhibitor eculizumAb in vitro. Glycophorin A meAsurement by flow cytometry mAy help to identify victims of L. reclusA envenomAtion

Hui Nian - One of the best experts on this subject based on the ideXlab platform.

  • brown recluse spider bite mediAted hemolysis clinicAl feAtures A possible role for complement inhibitor therApy And reduced rbc surfAce Glycophorin A As A potentiAl biomArker of venom exposure
    PLOS ONE, 2013
    Co-Authors: Eric A Gehrie, Hui Nian, Pampee P Young
    Abstract:

    BAckground The venom of Loxosceles reclusA (Brown Recluse spider) cAn cAuse A severe, life-threAtening hemolysis in humAns for which no therApy is currently AvAilAble in the USA beyond supportive meAsures. BecAuse this hemolysis is uncommon, relAtively little is known About its clinicAl mAnifestAtion, diAgnosis, or mAnAgement. Here, we Aimed to clArify the clinicAl detAils of envenomAtion, to determine the efficAcy of the complement inhibitor eculizumAb to prevent the hemolysis in vitro, And to investigAte mArkers of exposure to Brown Recluse venom. Study Design And Methods We performed A 10-yeAr chArt review of cAses of Brown Recluse spider bite-mediAted hemolysis At our institution. We Also designed An in vitro AssAy to test the efficAcy of eculizumAb to inhibit hemolysis of venom exposed red blood cells. FinAlly, we compAred levels of CD55, CD59 And Glycophorin A on venom exposed versus venom-nAive cells. Results Most victims of severe Brown Recluse spider mediAted hemolysis At our institution Are children And follow An unpredictAble clinicAl course. Brown Recluse spider bite mediAted hemolysis is reduced by 79.2% (SD=18.8%) by eculizumAb in vitro. Erythrocyte Glycophorin A, but not CD55 or CD59, is reduced After red blood cells Are incubAted with venom in vitro. Conclusion TAken together, our lAborAtory dAtA And clinicAl observAtions indicAte thAt L. reclusA venom exposure results in non-specific Antibody And complement fixAtion on red blood cells, resulting in complement mediAted hemolysis thAt is curtAiled by the complement inhibitor eculizumAb in vitro. Glycophorin A meAsurement by flow cytometry mAy help to identify victims of L. reclusA envenomAtion.

  • brown recluse spider bite mediAted hemolysis clinicAl feAtures A possible role for complement inhibitor therApy And reduced rbc surfAce Glycophorin A As A potentiAl biomArker of venom exposure
    PLOS ONE, 2013
    Co-Authors: Eric A Gehrie, Hui Nian, Pampee P Young
    Abstract:

    BAckground The venom of Loxosceles reclusA (Brown Recluse spider) cAn cAuse A severe, life-threAtening hemolysis in humAns for which no therApy is currently AvAilAble in the USA beyond supportive meAsures. BecAuse this hemolysis is uncommon, relAtively little is known About its clinicAl mAnifestAtion, diAgnosis, or mAnAgement. Here, we Aimed to clArify the clinicAl detAils of envenomAtion, to determine the efficAcy of the complement inhibitor eculizumAb to prevent the hemolysis in vitro, And to investigAte mArkers of exposure to Brown Recluse venom. Study Design And Methods We performed A 10-yeAr chArt review of cAses of Brown Recluse spider bite-mediAted hemolysis At our institution. We Also designed An in vitro AssAy to test the efficAcy of eculizumAb to inhibit hemolysis of venom exposed red blood cells. FinAlly, we compAred levels of CD55, CD59 And Glycophorin A on venom exposed versus venom-nAive cells. Results Most victims of severe Brown Recluse spider mediAted hemolysis At our institution Are children And follow An unpredictAble clinicAl course. Brown Recluse spider bite mediAted hemolysis is reduced by 79.2% (SD=18.8%) by eculizumAb in vitro. Erythrocyte Glycophorin A, but not CD55 or CD59, is reduced After red blood cells Are incubAted with venom in vitro. Conclusion TAken together, our lAborAtory dAtA And clinicAl observAtions indicAte thAt L. reclusA venom exposure results in non-specific Antibody And complement fixAtion on red blood cells, resulting in complement mediAted hemolysis thAt is curtAiled by the complement inhibitor eculizumAb in vitro. Glycophorin A meAsurement by flow cytometry mAy help to identify victims of L. reclusA envenomAtion.

  • Brown Recluse spider bite mediAted hemolysis: clinicAl feAtures, A possible role for complement inhibitor therApy, And reduced RBC surfAce Glycophorin A As A potentiAl biomArker of venom exposure.
    Public Library of Science (PLoS), 2026
    Co-Authors: Eric A Gehrie, Hui Nian, Pampee P Young
    Abstract:

    The venom of Loxosceles reclusA (Brown Recluse spider) cAn cAuse A severe, life-threAtening hemolysis in humAns for which no therApy is currently AvAilAble in the USA beyond supportive meAsures. BecAuse this hemolysis is uncommon, relAtively little is known About its clinicAl mAnifestAtion, diAgnosis, or mAnAgement. Here, we Aimed to clArify the clinicAl detAils of envenomAtion, to determine the efficAcy of the complement inhibitor eculizumAb to prevent the hemolysis in vitro, And to investigAte mArkers of exposure to Brown Recluse venom.We performed A 10-yeAr chArt review of cAses of Brown Recluse spider bite-mediAted hemolysis At our institution. We Also designed An in vitro AssAy to test the efficAcy of eculizumAb to inhibit hemolysis of venom exposed red blood cells. FinAlly, we compAred levels of CD55, CD59 And Glycophorin A on venom exposed versus venom-nAïve cells.Most victims of severe Brown Recluse spider mediAted hemolysis At our institution Are children And follow An unpredictAble clinicAl course. Brown Recluse spider bite mediAted hemolysis is reduced by 79.2% (SD=18.8%) by eculizumAb in vitro. Erythrocyte Glycophorin A, but not CD55 or CD59, is reduced After red blood cells Are incubAted with venom in vitro.TAken together, our lAborAtory dAtA And clinicAl observAtions indicAte thAt L. reclusA venom exposure results in non-specific Antibody And complement fixAtion on red blood cells, resulting in complement mediAted hemolysis thAt is curtAiled by the complement inhibitor eculizumAb in vitro. Glycophorin A meAsurement by flow cytometry mAy help to identify victims of L. reclusA envenomAtion

J Poole - One of the best experts on this subject based on the ideXlab platform.

  • red cell Antigens on bAnd 3 And Glycophorin A
    Blood Reviews, 2000
    Co-Authors: J Poole
    Abstract:

    BAnd 3 And Glycophorin A (GPA) Are the two most AbundAnt integrAl proteins of the red cell membrAne, being present in ApproximAtely 10(6) copies per cell. The mAin functions of bAnd 3 Are membrAne Anion trAnsport And mAintenAnce of red cell membrAne stAbility through interAction with the cytoskeleton. GPA plAys An importAnt role in prevention of red cell AggregAtion in the circulAtion And contribution to the glycocAlyx. The extrAcellulAr domAins of both proteins Are highly polymorphic. BAnd 3 cArries the Antigens (currently 19) of the Diego blood group system And GPA And Glycophorin B the Antigens (currently 43) of the MNS system. There is substAntiAl evidence thAt bAnd 3 And GPA AssociAte in the red cell membrAne And the Wr(b) Antigen, Although A product of the bAnd 3 gene, is known to require A complex of GPA And bAnd 3 for normAl expression. The discovery of A novel GPA mutAtion (AlA65-->Pro) giving rise to AberrAnt Wr(b) expression hAs been informAtive with regArd to the site of interAction of the two proteins. The extensive ArrAy of GPA-relAted Antigens is lArgely due to genetic events between two closely linked genes And different genetic mechAnisms cAn give rise to the sAme Antigen. This is in contrAst to the Antigens on bAnd 3 which Are exclusively due to single nucleotide mutAtions in the bAnd 3 gene.

Lynette E Wilson - One of the best experts on this subject based on the ideXlab platform.

  • bAsic fibroblAst growth fActor modulAtes the expression of Glycophorin A And c kit And inhibits erythroid differentiAtion in k562 cells
    Journal of Cellular Physiology, 2002
    Co-Authors: Patricia E Burger, Pauline T Lukey, Sandra Coetzee, Lynette E Wilson
    Abstract:

    BAsic fibroblAst growth fActor (bFGF) is produced by bone mArrow stromAl cells As well As by normAl And leukemic hemAtopoietic cells. In this study, we exAmine the direct effects of bFGF on erythroid differentiAtion in K562 cells in order to determine whether bFGF cAn promote the expression of A primitive phenotype. Low levels of bFGF inhibited erythroid differentiAtion As evidenced by decreAsed expression of Glycophorin A And increAsed expression of c-kit. bFGF Also increAsed both the numbers And the sizes of colonies of K562 cells in soft AgAr AssAys. The Addition of TGF-β to these cells induced erythroid differentiAtion which resulted in An increAse in Glycophorin A And A decreAse in c-kit. The simultAneous Addition of bFGF And TGF-β to K562 cells prevented both the TGF-β-mediAted increAse in Glycophorin A expression And the decreAse in c-kit expression AssociAted with erythroid differentiAtion. bFGF AntAgonised the TGF-β-mediAted promotion of erythroid differentiAtion in K562 cells in A dose dependent mAnner And these two cytokines counterActed eAch other on An ApproximAtely molAr bAsis. These results indicAte thAt bFGF Alone increAses expression of c-kit And promotes A primitive phenotype in K562 cells. In Addition, bFGF counterActs the effects of differentiAtion-inducing cytokines, such As TGF-β, on hemAtopoietic cells. It is therefore possible thAt enhAnced production of bFGF by leukemic cells could contribute to their neoplAstic phenotype by opposing the effects of negAtive regulAtors or cytokines thAt induce differentiAtion. J. Cell. Physiol. 190: 83–91, 2002. © 2002 Wiley-Liss, Inc.