cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.3394639.v44
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO-incompatible red cells, which from a HLA-compatible donor are transfused to a blood group O(H) recipient and undergo immediate destruction, a nucleated, metabolic active tissue that from the same donor is transplanted to the same recipient may,<i> </i>taking into account the effect of all therapeutic measures, occasionally show extreme long survival times. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO-incompatible, metabolically active tissue potentially uses its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the differentiating B-cell surfaces of a HLA-compatible recipient. <br>
DOI: 10.6084/m9.figshare.3394639.v45
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO-incompatible red cells, which from a HLA-compatible donor are transfused to a blood group O(H) recipient and undergo immediate destruction, a nucleated, metabolic active tissue that from the same donor is transplanted to the same recipient may,<i> </i>taking into account the effect of all therapeutic measures, occasionally show extreme long survival times. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO-incompatible, metabolically active tissue potentially uses its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the differentiating B-cell surfaces of a HLA-compatible recipient. <br>
DOI: 10.6084/m9.figshare.3394639.v46
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO-incompatible red cells, which from a HLA-compatible donor are transfused to a blood group O(H) recipient and undergo immediate destruction, a nucleated, metabolic active tissue that from the same donor is transplanted to the same recipient may,<i> </i>taking into account the effect of all therapeutic measures, occasionally show extreme long survival times. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO-incompatible, metabolically active tissue potentially uses its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the differentiating B-cell surfaces of a HLA-compatible recipient. <br>
DOI: 10.6084/m9.figshare.3394639.v47
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO-incompatible red cells, which from a HLA-compatible donor are transfused to a blood group O(H) recipient and undergo immediate destruction, a nucleated, metabolic active tissue that from the same donor is transplanted to the same recipient may,<i> </i>taking into account the effect of all therapeutic measures, occasionally show extreme long survival times. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO-incompatible, metabolically active tissue potentially uses its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the differentiating B-cell surfaces of a HLA-compatible recipient. <br>
DOI: 10.6084/m9.figshare.3394639.v48
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO-incompatible red cells, which from a HLA-compatible donor are transfused to a blood group O(H) recipient and undergo immediate destruction, a nucleated, metabolic active tissue that from the same donor is transplanted to the same recipient may,<i> </i>taking into account the effect of all therapeutic measures, occasionally show extreme long survival times. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO-incompatible, metabolically active tissue potentially uses its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the differentiating B-cell surfaces of a HLA-compatible recipient. <br>
DOI: 10.6084/m9.figshare.3394639.v49
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO-incompatible red cells, which from a HLA-compatible donor are transfused to a blood group O(H) recipient and undergo immediate destruction, a nucleated, metabolic active tissue that from the same donor is transplanted to the same recipient may,<i> </i>taking into account the effect of all therapeutic measures, occasionally show extreme long survival times. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO-incompatible, metabolically active tissue potentially uses its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the differentiating B-cell surfaces of a HLA-compatible recipient. <br>
DOI: 10.6084/m9.figshare.3394639.v50
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO-incompatible red cells, which from a HLA-compatible donor are transfused to a blood group O(H) recipient and undergo immediate destruction, a nucleated, metabolic active tissue that from the same donor is transplanted to the same recipient may,<i> </i>taking into account the effect of all therapeutic measures, occasionally show extreme long survival times. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO-incompatible, metabolically active tissue potentially uses its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the differentiating B-cell surfaces of a HLA-compatible recipient. <br>
DOI: 10.6084/m9.figshare.3394639.v51
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO-incompatible red cells, which from a HLA-compatible donor are transfused to a blood group O(H) recipient and undergo immediate destruction, a nucleated, metabolic active tissue that from the same donor is transplanted to the same recipient may,<i> </i>taking into account the effect of all therapeutic measures, occasionally show extreme long survival times. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO-incompatible, metabolically active tissue potentially uses its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the differentiating B-cell surfaces of a HLA-compatible recipient. <br>
DOI: 10.6084/m9.figshare.3394639.v52
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO-incompatible red cells, which from a HLA-compatible donor are transfused to a blood group O(H) recipient and undergo immediate destruction, a nucleated, metabolic active tissue that from the same donor is transplanted to the same recipient may,<i> </i>taking into account the effect of all therapeutic measures, occasionally show extreme long survival times. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO-incompatible, metabolically active tissue potentially uses its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the differentiating B-cell surfaces of a HLA-compatible recipient. <br>
DOI: 10.6084/m9.figshare.3394639.v53
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO-incompatible red cells, which from a HLA-compatible donor are transfused to a blood group O(H) recipient and undergo immediate destruction, a nucleated, metabolic active tissue that from the same donor is transplanted to the same recipient may,<i> </i>taking into account the effect of all therapeutic measures, occasionally show extreme long survival times. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO-incompatible, metabolically active tissue potentially uses its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the differentiating B-cell surfaces of a HLA-compatible recipient. <br>
DOI: 10.6084/m9.figshare.3394639.v54
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO-incompatible red cells, which from a HLA-compatible donor are transfused to a blood group O(H) recipient and undergo immediate destruction, a nucleated, metabolic active tissue that from the same donor is transplanted to the same recipient may,<i> </i>taking into account the effect of all therapeutic measures, occasionally show extreme long survival times. It appears to be established that tissue transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of “glycosidic exclusion”, a transplanted ABO-incompatible, metabolically active tissue potentially uses its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the differentiating B-cell surfaces of a HLA-compatible recipient. <br>
DOI: 10.6084/m9.figshare.3394639.v55
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In comparison with non-nucleated ABO-incompatible red cells, which undergo immediate destruction when transfused to a blood group O(H) recipient, a nucleated, metabolically active tissue transplanted from that same donor to an HLA-compatible recipient of the same blood group may, taking into account all therapeutic measures, occasionally show long survival times. It appears that transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of glycosidic exclusion, the phenotype determines simultaneous glycosylation of the cell surfaces and immunoglobulins. Thus, it may be assumed that a transplanted ABO-incompatible, metabolically active tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the B-cell surfaces of a HLA-compatible recipient.
DOI: 10.6084/m9.figshare.3394639.v56
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In comparison with non-nucleated ABO-incompatible red cells, which undergo immediate destruction when transfused to a blood group O(H) recipient, a nucleated, metabolically active tissue transplanted from that same donor to an HLA-compatible recipient of the same blood group shows, taking into account all therapeutic measures, relatively long survival. It appears that transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of glycosidic exclusion, the phenotype determines simultaneous glycosylation of the cell surfaces and immunoglobulins. Thus, it may be assumed that a transplanted ABO-incompatible, metabolically active tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the B-cell surfaces of a HLA-compatible recipient.
DOI: 10.6084/m9.figshare.3394639.v57
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In comparison with non-nucleated ABO-incompatible red cells, which undergo immediate destruction when transfused to a blood group O(H) recipient, a nucleated, metabolically active tissue transplanted from that same donor to an HLA-compatible recipient of the same blood group shows, taking into account all therapeutic measures, relatively long survival. It appears that transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of glycosidic exclusion, the phenotype determines simultaneous glycosylation of the cell surfaces and immunoglobulins. Thus, it may be assumed that a transplanted ABO-incompatible, metabolically active tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the B-cell surfaces of a HLA-compatible recipient.
DOI: 10.6084/m9.figshare.3394639.v58
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In comparison with non-nucleated ABO-incompatible red cells, which undergo immediate destruction when transfused to a blood group O(H) recipient, a nucleated, metabolically active tissue transplanted from that same donor to an HLA-compatible recipient of the same blood group shows, taking into account all therapeutic measures, relatively long survival. It appears that transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of glycosidic exclusion, the phenotype determines simultaneous glycosylation of the cell surfaces and immunoglobulins. Thus, it may be assumed that a transplanted ABO-incompatible, metabolically active tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the B-cell surfaces of a HLA-compatible recipient.
DOI: 10.6084/m9.figshare.3394639.v59
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In comparison with non-nucleated ABO-incompatible red cells, which undergo immediate destruction when transfused to a blood group O(H) recipient, a nucleated, metabolically active tissue transplanted from that same donor to an HLA-compatible recipient of the same blood group shows, taking into account all therapeutic measures, relatively long survival. It appears that transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of glycosidic exclusion, the phenotype determines simultaneous glycosylation of the cell surfaces and immunoglobulins. Thus, it may be assumed that a transplanted ABO-incompatible, metabolically active tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the B-cell surfaces of a HLA-compatible recipient.
DOI: 10.6084/m9.figshare.3394639.v60
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO(H)-incompatible red cells, which undergo destruction within minutes, when transfused to a blood group O(H) recipient, such by predominantly anti-A/B-antibodies caused hyperacute rejection of a highly nucleated, metabolically active, solid organ, transplanted from the same donor to an HLA-compatible recipient of the same blood group, occurs relatively rare, and for obviously unknown reason is extremely rare for liver transplants. It appears that transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of glycosidic exclusion, the phenotype determines simultaneous glycosylation of the cell surfaces and immunoglobulins. Thus, it may be assumed that a transplanted ABO-incompatible, metabolically active tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the B-cell surfaces of a HLA-compatible recipient.
DOI: 10.6084/m9.figshare.3394639.v61
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO(H)-incompatible red cells, which when transfused to a blood group O(H) recipient undergo destruction within minutes, such by mainly anti-A/B-antibodies caused hyperacute rejection occurs relatively rare in transplantations of highly nucleated, metabolically active solid organs, transplanted from the same donor to an HLA-compatible recipient of the same blood group and is, for obviously unknown reason, extremely rare in liver transplantations. It appears that transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of glycosidic exclusion, the phenotype determines simultaneous glycosylation of the cell surfaces and immunoglobulins. Thus, it may be assumed that a transplanted ABO-incompatible, metabolically active tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the B-cell surfaces of a HLA-compatible recipient.
DOI: 10.6084/m9.figshare.3394639.v62
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO(H)-incompatible red cells, which when transfused to a blood group O(H) recipient undergo destruction within minutes, such by mainly anti-A/B-antibodies caused hyperacute rejection occurs relatively rare in transplantations of highly nucleated, metabolically active solid organs, transplanted from the same donor to an HLA-compatible recipient of the same blood group and is, for obviously unknown reason, extremely rare in liver transplantations. It appears that transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of glycosidic exclusion, the phenotype determines simultaneous glycosylation of the cell surfaces and immunoglobulins. Thus, it may be assumed that a transplanted ABO-incompatible, metabolically active tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the B-cell surfaces of a HLA-compatible recipient.
DOI: 10.6084/m9.figshare.3394639.v63
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO(H)-incompatible red cells, which when transfused to an HLA-compatible blood group O(H) recipient undergo destruction within minutes, such humoral, hyperacute rejection caused by anti-A/B-antibodies, occurs relatively rare in transplantations of highly nucleated, metabolically active solid organs, and it is extremely rare or uncommon in liver transplantations. Moreover, a case of selective disappearance of donor-specific antibodies after liver transplantation has been reported. It appears that transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of glycosidic exclusion, the phenotype determines simultaneous glycosylation of the cell surfaces and immunoglobulins. Thus, it may be assumed that a transplanted ABO-incompatible, metabolically active tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the B-cell surfaces of a HLA-compatible recipient.
DOI: 10.6084/m9.figshare.3394639.v64
title: How an ABO-incompatible graft may contribute to its survival by phenotype-specific glycosylation of the host. A hypothesis.

description: In contrast to non-nucleated ABO(H)-incompatible red cells, which when transfused to an HLA-compatible blood group O(H) recipient undergo destruction within minutes, such hyperacute, humoral rejection occurs relatively rare in HLA-incompatible transplantations of highly nucleated, metabolically active solid organs, and is extremely rare in liver transplantations (Adams 1991; Della-Guardia et al. 2008;). Moreover, a case of selective disappearance of preexisting donor-specific HLA-antibodies after HLA-incompatible liver transplantation has been reported by Bastiani (2006), and according to Taner et al. (2014), decreased donor-specific antibody levels are not uncommon after liver transplantation. While this phenomenon represents a metabolic achievement of the graft, respective observations on anti-A/B-isoagglutinins are missing, because these more aggressive antibodies are always removed before transplantation. It appears that transplants always maintain their original, phenotype-specific metabolic properties, and expanding the concept of glycosidic exclusion, the phenotype determines simultaneous glycosylation of the cell surfaces and immunoglobulins. Thus, it may be assumed that a transplanted ABO-incompatible, metabolically active tissue may use its phenotype-specific enzymatic equipment to contribute to a compatible environment by consistent glycosylation of complementary sites of the plasma proteins and the B-cell surfaces of a HLA-compatible recipient.