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Xenotransplantation of Galactosyl-Transferase Knockout, CD55, CD59, CD39, and Fucosyl-Transferase Transgenic Pig Kidneys Into Baboons

Identifieur interne : 001737 ( PascalFrancis/Corpus ); précédent : 001736; suivant : 001738

Xenotransplantation of Galactosyl-Transferase Knockout, CD55, CD59, CD39, and Fucosyl-Transferase Transgenic Pig Kidneys Into Baboons

Auteurs : S. Le Bas-Bernardet ; X. Tillou ; N. Poirier ; N. Dilek ; M. Chatelais ; J. Devalliere ; B. Charreau ; D. Minault ; J. Hervouet ; K. Renaudin ; C. Crossan ; L. Scobie ; P. J. Cowan ; A. J. F. D'Apice ; C. Galli ; E. Cozzi ; J. P. Soulillou ; B. Vanhove ; G. Blancho

Source :

RBID : Pascal:12-0017503

Descripteurs français

English descriptors

Abstract

Galactosyl-transferase knockout (GT-KO) pigs represent the latest major progress to reduce immune reactions in xenotransplantation. However, their organs are still subject to rapid humoral rejection involving complement activation requiring the ongoing development of further genetic modifications in the pig. In a pig-to-baboon renal transplantation setting, we have used donor pigs that are not only GT-KO, but also transgenic for human CD55 (hCD55), hCD59, hCD39, and fucosyl-transferase (hHT). We studied kidney xenograft survival, physiological and immunologic parameters, xenogeneic rejection characteristics, as well as viral transmission aspects among two groups of baboons: control animals (n = 2), versus those (n = 4) treated with a cocktail of cyclophosphamide, tacrolimus, mycophenolate mofetil, steroids, and a recombinant human C1 inhibitor. Whereas control animals showed clear acute humoral rejection at around day 4, the treated animals showed moderately improved graft survival with rejection at around 2 weeks posttransplantation. Biopsies showed signs of acute vascular rejection (interstitial hemorrhage, glomerular thrombi, and acute tubular necrosis) as well as immunoglobulin (Ig)M and complement deposition in the glomerular and peritubular capillaries. The low level of preformed non-Gal-α1.3Gal IgM detected prior to transplantation increased at 6 days posttransplantation, whereas induced IgG appeared after day 6. No porcine endogenous retrovirus (PERV) transmission was detected in any transplanted baboon. Thus, surprisingly, organs from the GT-KO, hCD55, hCD59, hCD39, and hHT transgenic donors did not appear to convey significant protection against baboon anti-pig antibodies and complement activation, which obviously continue to be significant factors under a suboptimal immunosuppression regimen. The association, timing, and doses of immunosuppressive drugs remain critical. They will have to be optimized to achieve longer graft survivals.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

pA  
A01 01  1    @0 0041-1345
A02 01      @0 TRPPA8
A03   1    @0 Transplant. proc.
A05       @2 43
A06       @2 9
A08 01  1  ENG  @1 Xenotransplantation of Galactosyl-Transferase Knockout, CD55, CD59, CD39, and Fucosyl-Transferase Transgenic Pig Kidneys Into Baboons
A11 01  1    @1 LE BAS-BERNARDET (S.)
A11 02  1    @1 TILLOU (X.)
A11 03  1    @1 POIRIER (N.)
A11 04  1    @1 DILEK (N.)
A11 05  1    @1 CHATELAIS (M.)
A11 06  1    @1 DEVALLIERE (J.)
A11 07  1    @1 CHARREAU (B.)
A11 08  1    @1 MINAULT (D.)
A11 09  1    @1 HERVOUET (J.)
A11 10  1    @1 RENAUDIN (K.)
A11 11  1    @1 CROSSAN (C.)
A11 12  1    @1 SCOBIE (L.)
A11 13  1    @1 COWAN (P. J.)
A11 14  1    @1 D'APICE (A. J. F.)
A11 15  1    @1 GALLI (C.)
A11 16  1    @1 COZZI (E.)
A11 17  1    @1 SOULILLOU (J. P.)
A11 18  1    @1 VANHOVE (B.)
A11 19  1    @1 BLANCHO (G.)
A14 01      @1 Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643 @2 Nantes @3 FRA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 7 aut. @Z 8 aut. @Z 9 aut. @Z 17 aut. @Z 18 aut. @Z 19 aut.
A14 02      @1 Pathology Laboratory, CHU-Hôtel Dieu @2 Nantes @3 FRA @Z 10 aut.
A14 03      @1 Department of Biological and Biomedical Sciences, Glasgow Caledonian University @2 Glasgow @3 GBR @Z 11 aut. @Z 12 aut.
A14 04      @1 Immunology Research Centre, St Vicent's Hospital @2 Victoria @3 AUS @Z 13 aut. @Z 14 aut.
A14 05      @1 The Laboratorio di Tecnologie della Riproduzione, LTR @2 Cremona @3 ITA @Z 15 aut.
A14 06      @1 Consorzio per la Ricerca sul Trapianto d'Organi, CORIT @2 Padua @3 ITA @Z 16 aut.
A20       @1 3426-3430
A21       @1 2011
A23 01      @0 ENG
A43 01      @1 INIST @2 14765 @5 354000507348890670
A44       @0 0000 @1 © 2012 INIST-CNRS. All rights reserved.
A45       @0 14 ref.
A47 01  1    @0 12-0017503
A60       @1 P @2 C
A61       @0 A
A64 01  1    @0 Transplantation proceedings
A66 01      @0 NLD
C01 01    ENG  @0 Galactosyl-transferase knockout (GT-KO) pigs represent the latest major progress to reduce immune reactions in xenotransplantation. However, their organs are still subject to rapid humoral rejection involving complement activation requiring the ongoing development of further genetic modifications in the pig. In a pig-to-baboon renal transplantation setting, we have used donor pigs that are not only GT-KO, but also transgenic for human CD55 (hCD55), hCD59, hCD39, and fucosyl-transferase (hHT). We studied kidney xenograft survival, physiological and immunologic parameters, xenogeneic rejection characteristics, as well as viral transmission aspects among two groups of baboons: control animals (n = 2), versus those (n = 4) treated with a cocktail of cyclophosphamide, tacrolimus, mycophenolate mofetil, steroids, and a recombinant human C1 inhibitor. Whereas control animals showed clear acute humoral rejection at around day 4, the treated animals showed moderately improved graft survival with rejection at around 2 weeks posttransplantation. Biopsies showed signs of acute vascular rejection (interstitial hemorrhage, glomerular thrombi, and acute tubular necrosis) as well as immunoglobulin (Ig)M and complement deposition in the glomerular and peritubular capillaries. The low level of preformed non-Gal-α1.3Gal IgM detected prior to transplantation increased at 6 days posttransplantation, whereas induced IgG appeared after day 6. No porcine endogenous retrovirus (PERV) transmission was detected in any transplanted baboon. Thus, surprisingly, organs from the GT-KO, hCD55, hCD59, hCD39, and hHT transgenic donors did not appear to convey significant protection against baboon anti-pig antibodies and complement activation, which obviously continue to be significant factors under a suboptimal immunosuppression regimen. The association, timing, and doses of immunosuppressive drugs remain critical. They will have to be optimized to achieve longer graft survivals.
C02 01  X    @0 002B25
C02 02  X    @0 002A06F
C03 01  X  FRE  @0 Hétérotransplantation @5 01
C03 01  X  ENG  @0 Heterotransplantation @5 01
C03 01  X  SPA  @0 Heterotrasplante @5 01
C03 02  X  FRE  @0 Transferases @2 FE @5 02
C03 02  X  ENG  @0 Transferases @2 FE @5 02
C03 02  X  SPA  @0 Transferases @2 FE @5 02
C03 03  X  FRE  @0 Gène @5 03
C03 03  X  ENG  @0 Gene @5 03
C03 03  X  SPA  @0 Gen @5 03
C03 04  X  FRE  @0 Mutation @5 05
C03 04  X  ENG  @0 Mutation @5 05
C03 04  X  SPA  @0 Mutación @5 05
C03 05  X  FRE  @0 Facteur accélérateur dissociation @5 06
C03 05  X  ENG  @0 Decay accelerating factor @5 06
C03 05  X  SPA  @0 Factor acelerador disociación @5 06
C03 06  X  FRE  @0 Animal transgénique @5 08
C03 06  X  ENG  @0 Transgenic animal @5 08
C03 06  X  SPA  @0 Animal transgénico @5 08
C03 07  X  FRE  @0 Porc @5 09
C03 07  X  ENG  @0 Pig @5 09
C03 07  X  SPA  @0 Cerdo @5 09
C03 08  X  FRE  @0 Rein @5 11
C03 08  X  ENG  @0 Kidney @5 11
C03 08  X  SPA  @0 Riñón @5 11
C03 09  X  FRE  @0 Primates @2 NS @5 12
C03 09  X  ENG  @0 Primates @2 NS @5 12
C03 09  X  SPA  @0 Primates @2 NS @5 12
C03 10  X  FRE  @0 Singe @5 17
C03 10  X  ENG  @0 Monkey @5 17
C03 10  X  SPA  @0 Mono @5 17
C03 11  X  FRE  @0 Médecine @5 18
C03 11  X  ENG  @0 Medicine @5 18
C03 11  X  SPA  @0 Medicina @5 18
C03 12  X  FRE  @0 Transplantation @5 19
C03 12  X  ENG  @0 Transplantation @5 19
C03 12  X  SPA  @0 Trasplantación @5 19
C03 13  X  FRE  @0 Greffe @5 25
C03 13  X  ENG  @0 Graft @5 25
C03 13  X  SPA  @0 Injerto @5 25
C03 14  X  FRE  @0 Traitement @5 26
C03 14  X  ENG  @0 Treatment @5 26
C03 14  X  SPA  @0 Tratamiento @5 26
C03 15  X  FRE  @0 Antigène CD55 @4 INC @5 86
C03 16  X  FRE  @0 Antigène CD59 @4 INC @5 87
C03 17  X  FRE  @0 Antigène CD39 @4 INC @5 88
C03 18  X  FRE  @0 Babouin @4 CD @5 96
C03 18  X  ENG  @0 Baboon @4 CD @5 96
C07 01  X  FRE  @0 Enzyme @2 FE
C07 01  X  ENG  @0 Enzyme @2 FE
C07 01  X  SPA  @0 Enzima @2 FE
C07 02  X  FRE  @0 Artiodactyla @2 NS
C07 02  X  ENG  @0 Artiodactyla @2 NS
C07 02  X  SPA  @0 Artiodactyla @2 NS
C07 03  X  FRE  @0 Ungulata @2 NS
C07 03  X  ENG  @0 Ungulata @2 NS
C07 03  X  SPA  @0 Ungulata @2 NS
C07 04  X  FRE  @0 Mammalia @2 NS
C07 04  X  ENG  @0 Mammalia @2 NS
C07 04  X  SPA  @0 Mammalia @2 NS
C07 05  X  FRE  @0 Vertebrata @2 NS
C07 05  X  ENG  @0 Vertebrata @2 NS
C07 05  X  SPA  @0 Vertebrata @2 NS
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C07 06  X  ENG  @0 Surgery @5 37
C07 06  X  SPA  @0 Cirugía @5 37
C07 07  X  FRE  @0 Génétique @5 38
C07 07  X  ENG  @0 Genetics @5 38
C07 07  X  SPA  @0 Genética @5 38
C07 08  X  FRE  @0 Appareil urinaire @5 39
C07 08  X  ENG  @0 Urinary system @5 39
C07 08  X  SPA  @0 Aparato urinario @5 39
N21       @1 002
N44 01      @1 OTO
N82       @1 OTO
pR  
A30 01  1  ENG  @1 The French Speaking Society of Transplantation and Transplantation Sans Frontières. Congrès @3 Geneva CHE @4 2000-12-15

Format Inist (serveur)

NO : PASCAL 12-0017503 INIST
ET : Xenotransplantation of Galactosyl-Transferase Knockout, CD55, CD59, CD39, and Fucosyl-Transferase Transgenic Pig Kidneys Into Baboons
AU : LE BAS-BERNARDET (S.); TILLOU (X.); POIRIER (N.); DILEK (N.); CHATELAIS (M.); DEVALLIERE (J.); CHARREAU (B.); MINAULT (D.); HERVOUET (J.); RENAUDIN (K.); CROSSAN (C.); SCOBIE (L.); COWAN (P. J.); D'APICE (A. J. F.); GALLI (C.); COZZI (E.); SOULILLOU (J. P.); VANHOVE (B.); BLANCHO (G.)
AF : Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643/Nantes/France (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut., 17 aut., 18 aut., 19 aut.); Pathology Laboratory, CHU-Hôtel Dieu/Nantes/France (10 aut.); Department of Biological and Biomedical Sciences, Glasgow Caledonian University/Glasgow/Royaume-Uni (11 aut., 12 aut.); Immunology Research Centre, St Vicent's Hospital/Victoria/Australie (13 aut., 14 aut.); The Laboratorio di Tecnologie della Riproduzione, LTR/Cremona/Italie (15 aut.); Consorzio per la Ricerca sul Trapianto d'Organi, CORIT/Padua/Italie (16 aut.)
DT : Publication en série; Congrès; Niveau analytique
SO : Transplantation proceedings; ISSN 0041-1345; Coden TRPPA8; Pays-Bas; Da. 2011; Vol. 43; No. 9; Pp. 3426-3430; Bibl. 14 ref.
LA : Anglais
EA : Galactosyl-transferase knockout (GT-KO) pigs represent the latest major progress to reduce immune reactions in xenotransplantation. However, their organs are still subject to rapid humoral rejection involving complement activation requiring the ongoing development of further genetic modifications in the pig. In a pig-to-baboon renal transplantation setting, we have used donor pigs that are not only GT-KO, but also transgenic for human CD55 (hCD55), hCD59, hCD39, and fucosyl-transferase (hHT). We studied kidney xenograft survival, physiological and immunologic parameters, xenogeneic rejection characteristics, as well as viral transmission aspects among two groups of baboons: control animals (n = 2), versus those (n = 4) treated with a cocktail of cyclophosphamide, tacrolimus, mycophenolate mofetil, steroids, and a recombinant human C1 inhibitor. Whereas control animals showed clear acute humoral rejection at around day 4, the treated animals showed moderately improved graft survival with rejection at around 2 weeks posttransplantation. Biopsies showed signs of acute vascular rejection (interstitial hemorrhage, glomerular thrombi, and acute tubular necrosis) as well as immunoglobulin (Ig)M and complement deposition in the glomerular and peritubular capillaries. The low level of preformed non-Gal-α1.3Gal IgM detected prior to transplantation increased at 6 days posttransplantation, whereas induced IgG appeared after day 6. No porcine endogenous retrovirus (PERV) transmission was detected in any transplanted baboon. Thus, surprisingly, organs from the GT-KO, hCD55, hCD59, hCD39, and hHT transgenic donors did not appear to convey significant protection against baboon anti-pig antibodies and complement activation, which obviously continue to be significant factors under a suboptimal immunosuppression regimen. The association, timing, and doses of immunosuppressive drugs remain critical. They will have to be optimized to achieve longer graft survivals.
CC : 002B25; 002A06F
FD : Hétérotransplantation; Transferases; Gène; Mutation; Facteur accélérateur dissociation; Animal transgénique; Porc; Rein; Primates; Singe; Médecine; Transplantation; Greffe; Traitement; Antigène CD55; Antigène CD59; Antigène CD39; Babouin
FG : Enzyme; Artiodactyla; Ungulata; Mammalia; Vertebrata; Chirurgie; Génétique; Appareil urinaire
ED : Heterotransplantation; Transferases; Gene; Mutation; Decay accelerating factor; Transgenic animal; Pig; Kidney; Primates; Monkey; Medicine; Transplantation; Graft; Treatment; Baboon
EG : Enzyme; Artiodactyla; Ungulata; Mammalia; Vertebrata; Surgery; Genetics; Urinary system
SD : Heterotrasplante; Transferases; Gen; Mutación; Factor acelerador disociación; Animal transgénico; Cerdo; Riñón; Primates; Mono; Medicina; Trasplantación; Injerto; Tratamiento
LO : INIST-14765.354000507348890670
ID : 12-0017503

Links to Exploration step

Pascal:12-0017503

Le document en format XML

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<inist:fA14 i1="03">
<s1>Department of Biological and Biomedical Sciences, Glasgow Caledonian University</s1>
<s2>Glasgow</s2>
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<sZ>11 aut.</sZ>
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<inist:fA14 i1="04">
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<name sortKey="D Apice, A J F" sort="D Apice, A J F" uniqKey="D Apice A" first="A. J. F." last="D'Apice">A. J. F. D'Apice</name>
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<name sortKey="Galli, C" sort="Galli, C" uniqKey="Galli C" first="C." last="Galli">C. Galli</name>
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<name sortKey="Cozzi, E" sort="Cozzi, E" uniqKey="Cozzi E" first="E." last="Cozzi">E. Cozzi</name>
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<s1>Consorzio per la Ricerca sul Trapianto d'Organi, CORIT</s1>
<s2>Padua</s2>
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<sZ>16 aut.</sZ>
</inist:fA14>
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<author>
<name sortKey="Soulillou, J P" sort="Soulillou, J P" uniqKey="Soulillou J" first="J. P." last="Soulillou">J. P. Soulillou</name>
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<name sortKey="Vanhove, B" sort="Vanhove, B" uniqKey="Vanhove B" first="B." last="Vanhove">B. Vanhove</name>
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<author>
<name sortKey="Blancho, G" sort="Blancho, G" uniqKey="Blancho G" first="G." last="Blancho">G. Blancho</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
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<idno type="RBID">Pascal:12-0017503</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">001737</idno>
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<title xml:lang="en" level="a">Xenotransplantation of Galactosyl-Transferase Knockout, CD55, CD59, CD39, and Fucosyl-Transferase Transgenic Pig Kidneys Into Baboons</title>
<author>
<name sortKey="Le Bas Bernardet, S" sort="Le Bas Bernardet, S" uniqKey="Le Bas Bernardet S" first="S." last="Le Bas-Bernardet">S. Le Bas-Bernardet</name>
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<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
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<sZ>1 aut.</sZ>
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</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Tillou, X" sort="Tillou, X" uniqKey="Tillou X" first="X." last="Tillou">X. Tillou</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
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<sZ>1 aut.</sZ>
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<sZ>18 aut.</sZ>
<sZ>19 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Poirier, N" sort="Poirier, N" uniqKey="Poirier N" first="N." last="Poirier">N. Poirier</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
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<sZ>7 aut.</sZ>
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<sZ>18 aut.</sZ>
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</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Dilek, N" sort="Dilek, N" uniqKey="Dilek N" first="N." last="Dilek">N. Dilek</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
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<sZ>7 aut.</sZ>
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<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>19 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Chatelais, M" sort="Chatelais, M" uniqKey="Chatelais M" first="M." last="Chatelais">M. Chatelais</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
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</author>
<author>
<name sortKey="Devalliere, J" sort="Devalliere, J" uniqKey="Devalliere J" first="J." last="Devalliere">J. Devalliere</name>
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<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
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<sZ>1 aut.</sZ>
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<sZ>7 aut.</sZ>
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<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
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</inist:fA14>
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</author>
<author>
<name sortKey="Charreau, B" sort="Charreau, B" uniqKey="Charreau B" first="B." last="Charreau">B. Charreau</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
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</author>
<author>
<name sortKey="Minault, D" sort="Minault, D" uniqKey="Minault D" first="D." last="Minault">D. Minault</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
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</author>
<author>
<name sortKey="Hervouet, J" sort="Hervouet, J" uniqKey="Hervouet J" first="J." last="Hervouet">J. Hervouet</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
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<author>
<name sortKey="Renaudin, K" sort="Renaudin, K" uniqKey="Renaudin K" first="K." last="Renaudin">K. Renaudin</name>
<affiliation>
<inist:fA14 i1="02">
<s1>Pathology Laboratory, CHU-Hôtel Dieu</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Crossan, C" sort="Crossan, C" uniqKey="Crossan C" first="C." last="Crossan">C. Crossan</name>
<affiliation>
<inist:fA14 i1="03">
<s1>Department of Biological and Biomedical Sciences, Glasgow Caledonian University</s1>
<s2>Glasgow</s2>
<s3>GBR</s3>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Scobie, L" sort="Scobie, L" uniqKey="Scobie L" first="L." last="Scobie">L. Scobie</name>
<affiliation>
<inist:fA14 i1="03">
<s1>Department of Biological and Biomedical Sciences, Glasgow Caledonian University</s1>
<s2>Glasgow</s2>
<s3>GBR</s3>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
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</affiliation>
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<name sortKey="Cowan, P J" sort="Cowan, P J" uniqKey="Cowan P" first="P. J." last="Cowan">P. J. Cowan</name>
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<inist:fA14 i1="04">
<s1>Immunology Research Centre, St Vicent's Hospital</s1>
<s2>Victoria</s2>
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<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
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</affiliation>
</author>
<author>
<name sortKey="D Apice, A J F" sort="D Apice, A J F" uniqKey="D Apice A" first="A. J. F." last="D'Apice">A. J. F. D'Apice</name>
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<inist:fA14 i1="04">
<s1>Immunology Research Centre, St Vicent's Hospital</s1>
<s2>Victoria</s2>
<s3>AUS</s3>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Galli, C" sort="Galli, C" uniqKey="Galli C" first="C." last="Galli">C. Galli</name>
<affiliation>
<inist:fA14 i1="05">
<s1>The Laboratorio di Tecnologie della Riproduzione, LTR</s1>
<s2>Cremona</s2>
<s3>ITA</s3>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Cozzi, E" sort="Cozzi, E" uniqKey="Cozzi E" first="E." last="Cozzi">E. Cozzi</name>
<affiliation>
<inist:fA14 i1="06">
<s1>Consorzio per la Ricerca sul Trapianto d'Organi, CORIT</s1>
<s2>Padua</s2>
<s3>ITA</s3>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Soulillou, J P" sort="Soulillou, J P" uniqKey="Soulillou J" first="J. P." last="Soulillou">J. P. Soulillou</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
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</affiliation>
</author>
<author>
<name sortKey="Vanhove, B" sort="Vanhove, B" uniqKey="Vanhove B" first="B." last="Vanhove">B. Vanhove</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
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</author>
<author>
<name sortKey="Blancho, G" sort="Blancho, G" uniqKey="Blancho G" first="G." last="Blancho">G. Blancho</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
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</analytic>
<series>
<title level="j" type="main">Transplantation proceedings</title>
<title level="j" type="abbreviated">Transplant. proc.</title>
<idno type="ISSN">0041-1345</idno>
<imprint>
<date when="2011">2011</date>
</imprint>
</series>
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</sourceDesc>
<seriesStmt>
<title level="j" type="main">Transplantation proceedings</title>
<title level="j" type="abbreviated">Transplant. proc.</title>
<idno type="ISSN">0041-1345</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Baboon</term>
<term>Decay accelerating factor</term>
<term>Gene</term>
<term>Graft</term>
<term>Heterotransplantation</term>
<term>Kidney</term>
<term>Medicine</term>
<term>Monkey</term>
<term>Mutation</term>
<term>Pig</term>
<term>Primates</term>
<term>Transferases</term>
<term>Transgenic animal</term>
<term>Transplantation</term>
<term>Treatment</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Hétérotransplantation</term>
<term>Transferases</term>
<term>Gène</term>
<term>Mutation</term>
<term>Facteur accélérateur dissociation</term>
<term>Animal transgénique</term>
<term>Porc</term>
<term>Rein</term>
<term>Primates</term>
<term>Singe</term>
<term>Médecine</term>
<term>Transplantation</term>
<term>Greffe</term>
<term>Traitement</term>
<term>Antigène CD55</term>
<term>Antigène CD59</term>
<term>Antigène CD39</term>
<term>Babouin</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Galactosyl-transferase knockout (GT-KO) pigs represent the latest major progress to reduce immune reactions in xenotransplantation. However, their organs are still subject to rapid humoral rejection involving complement activation requiring the ongoing development of further genetic modifications in the pig. In a pig-to-baboon renal transplantation setting, we have used donor pigs that are not only GT-KO, but also transgenic for human CD55 (hCD55), hCD59, hCD39, and fucosyl-transferase (hHT). We studied kidney xenograft survival, physiological and immunologic parameters, xenogeneic rejection characteristics, as well as viral transmission aspects among two groups of baboons: control animals (n = 2), versus those (n = 4) treated with a cocktail of cyclophosphamide, tacrolimus, mycophenolate mofetil, steroids, and a recombinant human C1 inhibitor. Whereas control animals showed clear acute humoral rejection at around day 4, the treated animals showed moderately improved graft survival with rejection at around 2 weeks posttransplantation. Biopsies showed signs of acute vascular rejection (interstitial hemorrhage, glomerular thrombi, and acute tubular necrosis) as well as immunoglobulin (Ig)M and complement deposition in the glomerular and peritubular capillaries. The low level of preformed non-Gal-α1.3Gal IgM detected prior to transplantation increased at 6 days posttransplantation, whereas induced IgG appeared after day 6. No porcine endogenous retrovirus (PERV) transmission was detected in any transplanted baboon. Thus, surprisingly, organs from the GT-KO, hCD55, hCD59, hCD39, and hHT transgenic donors did not appear to convey significant protection against baboon anti-pig antibodies and complement activation, which obviously continue to be significant factors under a suboptimal immunosuppression regimen. The association, timing, and doses of immunosuppressive drugs remain critical. They will have to be optimized to achieve longer graft survivals.</div>
</front>
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<s1>DILEK (N.)</s1>
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<fA11 i1="05" i2="1">
<s1>CHATELAIS (M.)</s1>
</fA11>
<fA11 i1="06" i2="1">
<s1>DEVALLIERE (J.)</s1>
</fA11>
<fA11 i1="07" i2="1">
<s1>CHARREAU (B.)</s1>
</fA11>
<fA11 i1="08" i2="1">
<s1>MINAULT (D.)</s1>
</fA11>
<fA11 i1="09" i2="1">
<s1>HERVOUET (J.)</s1>
</fA11>
<fA11 i1="10" i2="1">
<s1>RENAUDIN (K.)</s1>
</fA11>
<fA11 i1="11" i2="1">
<s1>CROSSAN (C.)</s1>
</fA11>
<fA11 i1="12" i2="1">
<s1>SCOBIE (L.)</s1>
</fA11>
<fA11 i1="13" i2="1">
<s1>COWAN (P. J.)</s1>
</fA11>
<fA11 i1="14" i2="1">
<s1>D'APICE (A. J. F.)</s1>
</fA11>
<fA11 i1="15" i2="1">
<s1>GALLI (C.)</s1>
</fA11>
<fA11 i1="16" i2="1">
<s1>COZZI (E.)</s1>
</fA11>
<fA11 i1="17" i2="1">
<s1>SOULILLOU (J. P.)</s1>
</fA11>
<fA11 i1="18" i2="1">
<s1>VANHOVE (B.)</s1>
</fA11>
<fA11 i1="19" i2="1">
<s1>BLANCHO (G.)</s1>
</fA11>
<fA14 i1="01">
<s1>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>19 aut.</sZ>
</fA14>
<fA14 i1="02">
<s1>Pathology Laboratory, CHU-Hôtel Dieu</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="03">
<s1>Department of Biological and Biomedical Sciences, Glasgow Caledonian University</s1>
<s2>Glasgow</s2>
<s3>GBR</s3>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="04">
<s1>Immunology Research Centre, St Vicent's Hospital</s1>
<s2>Victoria</s2>
<s3>AUS</s3>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
</fA14>
<fA14 i1="05">
<s1>The Laboratorio di Tecnologie della Riproduzione, LTR</s1>
<s2>Cremona</s2>
<s3>ITA</s3>
<sZ>15 aut.</sZ>
</fA14>
<fA14 i1="06">
<s1>Consorzio per la Ricerca sul Trapianto d'Organi, CORIT</s1>
<s2>Padua</s2>
<s3>ITA</s3>
<sZ>16 aut.</sZ>
</fA14>
<fA20>
<s1>3426-3430</s1>
</fA20>
<fA21>
<s1>2011</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
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<s0>0000</s0>
<s1>© 2012 INIST-CNRS. All rights reserved.</s1>
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<s0>12-0017503</s0>
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<fA60>
<s1>P</s1>
<s2>C</s2>
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<fA61>
<s0>A</s0>
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<fA64 i1="01" i2="1">
<s0>Transplantation proceedings</s0>
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<fA66 i1="01">
<s0>NLD</s0>
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<s0>Galactosyl-transferase knockout (GT-KO) pigs represent the latest major progress to reduce immune reactions in xenotransplantation. However, their organs are still subject to rapid humoral rejection involving complement activation requiring the ongoing development of further genetic modifications in the pig. In a pig-to-baboon renal transplantation setting, we have used donor pigs that are not only GT-KO, but also transgenic for human CD55 (hCD55), hCD59, hCD39, and fucosyl-transferase (hHT). We studied kidney xenograft survival, physiological and immunologic parameters, xenogeneic rejection characteristics, as well as viral transmission aspects among two groups of baboons: control animals (n = 2), versus those (n = 4) treated with a cocktail of cyclophosphamide, tacrolimus, mycophenolate mofetil, steroids, and a recombinant human C1 inhibitor. Whereas control animals showed clear acute humoral rejection at around day 4, the treated animals showed moderately improved graft survival with rejection at around 2 weeks posttransplantation. Biopsies showed signs of acute vascular rejection (interstitial hemorrhage, glomerular thrombi, and acute tubular necrosis) as well as immunoglobulin (Ig)M and complement deposition in the glomerular and peritubular capillaries. The low level of preformed non-Gal-α1.3Gal IgM detected prior to transplantation increased at 6 days posttransplantation, whereas induced IgG appeared after day 6. No porcine endogenous retrovirus (PERV) transmission was detected in any transplanted baboon. Thus, surprisingly, organs from the GT-KO, hCD55, hCD59, hCD39, and hHT transgenic donors did not appear to convey significant protection against baboon anti-pig antibodies and complement activation, which obviously continue to be significant factors under a suboptimal immunosuppression regimen. The association, timing, and doses of immunosuppressive drugs remain critical. They will have to be optimized to achieve longer graft survivals.</s0>
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<s0>002B25</s0>
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<fC02 i1="02" i2="X">
<s0>002A06F</s0>
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<s0>Hétérotransplantation</s0>
<s5>01</s5>
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<fC03 i1="01" i2="X" l="ENG">
<s0>Heterotransplantation</s0>
<s5>01</s5>
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<s0>Heterotrasplante</s0>
<s5>01</s5>
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<fC03 i1="02" i2="X" l="FRE">
<s0>Transferases</s0>
<s2>FE</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Transferases</s0>
<s2>FE</s2>
<s5>02</s5>
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<fC03 i1="02" i2="X" l="SPA">
<s0>Transferases</s0>
<s2>FE</s2>
<s5>02</s5>
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<s0>Gène</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Gene</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Gen</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Mutation</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Mutation</s0>
<s5>05</s5>
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<s0>Mutación</s0>
<s5>05</s5>
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<s0>Facteur accélérateur dissociation</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Decay accelerating factor</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Factor acelerador disociación</s0>
<s5>06</s5>
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<s0>Animal transgénique</s0>
<s5>08</s5>
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<fC03 i1="06" i2="X" l="ENG">
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<s5>08</s5>
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<s5>08</s5>
</fC03>
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<s0>Porc</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Pig</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Cerdo</s0>
<s5>09</s5>
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<s0>Rein</s0>
<s5>11</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Kidney</s0>
<s5>11</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Riñón</s0>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Primates</s0>
<s2>NS</s2>
<s5>12</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Primates</s0>
<s2>NS</s2>
<s5>12</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Primates</s0>
<s2>NS</s2>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Singe</s0>
<s5>17</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Monkey</s0>
<s5>17</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Mono</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE">
<s0>Médecine</s0>
<s5>18</s5>
</fC03>
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<s0>Medicine</s0>
<s5>18</s5>
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<s0>Medicina</s0>
<s5>18</s5>
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<s0>Transplantation</s0>
<s5>19</s5>
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<fC03 i1="12" i2="X" l="ENG">
<s0>Transplantation</s0>
<s5>19</s5>
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<s0>Trasplantación</s0>
<s5>19</s5>
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<fC03 i1="13" i2="X" l="FRE">
<s0>Greffe</s0>
<s5>25</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG">
<s0>Graft</s0>
<s5>25</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA">
<s0>Injerto</s0>
<s5>25</s5>
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<s0>Traitement</s0>
<s5>26</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG">
<s0>Treatment</s0>
<s5>26</s5>
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<fC03 i1="14" i2="X" l="SPA">
<s0>Tratamiento</s0>
<s5>26</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE">
<s0>Antigène CD55</s0>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC03 i1="16" i2="X" l="FRE">
<s0>Antigène CD59</s0>
<s4>INC</s4>
<s5>87</s5>
</fC03>
<fC03 i1="17" i2="X" l="FRE">
<s0>Antigène CD39</s0>
<s4>INC</s4>
<s5>88</s5>
</fC03>
<fC03 i1="18" i2="X" l="FRE">
<s0>Babouin</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="18" i2="X" l="ENG">
<s0>Baboon</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Artiodactyla</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Artiodactyla</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Artiodactyla</s0>
<s2>NS</s2>
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<fC07 i1="03" i2="X" l="FRE">
<s0>Ungulata</s0>
<s2>NS</s2>
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<fC07 i1="03" i2="X" l="ENG">
<s0>Ungulata</s0>
<s2>NS</s2>
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<fC07 i1="03" i2="X" l="SPA">
<s0>Ungulata</s0>
<s2>NS</s2>
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<fC07 i1="04" i2="X" l="FRE">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Chirurgie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Surgery</s0>
<s5>37</s5>
</fC07>
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<s0>Cirugía</s0>
<s5>37</s5>
</fC07>
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<s0>Génétique</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Genetics</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Genética</s0>
<s5>38</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Appareil urinaire</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Urinary system</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Aparato urinario</s0>
<s5>39</s5>
</fC07>
<fN21>
<s1>002</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
<pR>
<fA30 i1="01" i2="1" l="ENG">
<s1>The French Speaking Society of Transplantation and Transplantation Sans Frontières. Congrès</s1>
<s3>Geneva CHE</s3>
<s4>2000-12-15</s4>
</fA30>
</pR>
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<server>
<NO>PASCAL 12-0017503 INIST</NO>
<ET>Xenotransplantation of Galactosyl-Transferase Knockout, CD55, CD59, CD39, and Fucosyl-Transferase Transgenic Pig Kidneys Into Baboons</ET>
<AU>LE BAS-BERNARDET (S.); TILLOU (X.); POIRIER (N.); DILEK (N.); CHATELAIS (M.); DEVALLIERE (J.); CHARREAU (B.); MINAULT (D.); HERVOUET (J.); RENAUDIN (K.); CROSSAN (C.); SCOBIE (L.); COWAN (P. J.); D'APICE (A. J. F.); GALLI (C.); COZZI (E.); SOULILLOU (J. P.); VANHOVE (B.); BLANCHO (G.)</AU>
<AF>Institut de Transplantation-Urologie-Néphrologie, ITUN and INSERM UMR643/Nantes/France (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut., 17 aut., 18 aut., 19 aut.); Pathology Laboratory, CHU-Hôtel Dieu/Nantes/France (10 aut.); Department of Biological and Biomedical Sciences, Glasgow Caledonian University/Glasgow/Royaume-Uni (11 aut., 12 aut.); Immunology Research Centre, St Vicent's Hospital/Victoria/Australie (13 aut., 14 aut.); The Laboratorio di Tecnologie della Riproduzione, LTR/Cremona/Italie (15 aut.); Consorzio per la Ricerca sul Trapianto d'Organi, CORIT/Padua/Italie (16 aut.)</AF>
<DT>Publication en série; Congrès; Niveau analytique</DT>
<SO>Transplantation proceedings; ISSN 0041-1345; Coden TRPPA8; Pays-Bas; Da. 2011; Vol. 43; No. 9; Pp. 3426-3430; Bibl. 14 ref.</SO>
<LA>Anglais</LA>
<EA>Galactosyl-transferase knockout (GT-KO) pigs represent the latest major progress to reduce immune reactions in xenotransplantation. However, their organs are still subject to rapid humoral rejection involving complement activation requiring the ongoing development of further genetic modifications in the pig. In a pig-to-baboon renal transplantation setting, we have used donor pigs that are not only GT-KO, but also transgenic for human CD55 (hCD55), hCD59, hCD39, and fucosyl-transferase (hHT). We studied kidney xenograft survival, physiological and immunologic parameters, xenogeneic rejection characteristics, as well as viral transmission aspects among two groups of baboons: control animals (n = 2), versus those (n = 4) treated with a cocktail of cyclophosphamide, tacrolimus, mycophenolate mofetil, steroids, and a recombinant human C1 inhibitor. Whereas control animals showed clear acute humoral rejection at around day 4, the treated animals showed moderately improved graft survival with rejection at around 2 weeks posttransplantation. Biopsies showed signs of acute vascular rejection (interstitial hemorrhage, glomerular thrombi, and acute tubular necrosis) as well as immunoglobulin (Ig)M and complement deposition in the glomerular and peritubular capillaries. The low level of preformed non-Gal-α1.3Gal IgM detected prior to transplantation increased at 6 days posttransplantation, whereas induced IgG appeared after day 6. No porcine endogenous retrovirus (PERV) transmission was detected in any transplanted baboon. Thus, surprisingly, organs from the GT-KO, hCD55, hCD59, hCD39, and hHT transgenic donors did not appear to convey significant protection against baboon anti-pig antibodies and complement activation, which obviously continue to be significant factors under a suboptimal immunosuppression regimen. The association, timing, and doses of immunosuppressive drugs remain critical. They will have to be optimized to achieve longer graft survivals.</EA>
<CC>002B25; 002A06F</CC>
<FD>Hétérotransplantation; Transferases; Gène; Mutation; Facteur accélérateur dissociation; Animal transgénique; Porc; Rein; Primates; Singe; Médecine; Transplantation; Greffe; Traitement; Antigène CD55; Antigène CD59; Antigène CD39; Babouin</FD>
<FG>Enzyme; Artiodactyla; Ungulata; Mammalia; Vertebrata; Chirurgie; Génétique; Appareil urinaire</FG>
<ED>Heterotransplantation; Transferases; Gene; Mutation; Decay accelerating factor; Transgenic animal; Pig; Kidney; Primates; Monkey; Medicine; Transplantation; Graft; Treatment; Baboon</ED>
<EG>Enzyme; Artiodactyla; Ungulata; Mammalia; Vertebrata; Surgery; Genetics; Urinary system</EG>
<SD>Heterotrasplante; Transferases; Gen; Mutación; Factor acelerador disociación; Animal transgénico; Cerdo; Riñón; Primates; Mono; Medicina; Trasplantación; Injerto; Tratamiento</SD>
<LO>INIST-14765.354000507348890670</LO>
<ID>12-0017503</ID>
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