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Results: 5

1.
FIG. 2.

FIG. 2. From: Clinical Islet Xenotransplantation.

Histology of the pancreas of a GTKO/hCD46/hTFPIIns/pCTLA4-IgIns/hCD39Ins pig. hCD46 is expressed throughout the pancreas (green fluorescence). Insulin, hTFPI, pCTLA4-Ig, and hCD39 are expressed exclusively in the islets of Langerhans (green fluorescence). (A high-quality digital representation of this figure is available in the online issue.)

Dirk J. van der Windt, et al. Diabetes. 2012 December;61(12):3046-3055.
2.
FIG. 4.

FIG. 4. From: Clinical Islet Xenotransplantation.

Fasting blood glucose and C-peptide levels in humans, cynomolgus monkeys (cyno), and pigs. Data are presented as mean Ā± SE. Adapted from Casu et al. (48).

Dirk J. van der Windt, et al. Diabetes. 2012 December;61(12):3046-3055.
3.
FIG. 5.

FIG. 5. From: Clinical Islet Xenotransplantation.

A: Absence of islet amyloid polypeptide deposition in pig islets >1 year after transplantation into the liver of a cynomolgus monkey. B:Native islets from a deceased, nondiabetic adult human in which there is significant amyloid deposition (red immunofluorescence). Blue, cell nuclei; green, insulin. (A high-quality digital representation of this figure is available in the online issue.)

Dirk J. van der Windt, et al. Diabetes. 2012 December;61(12):3046-3055.
4.
FIG. 1.

FIG. 1. From: Clinical Islet Xenotransplantation.

Schematic overview of the instant blood-mediated inflammatory response. Tissue factor expression and antibody binding to non-Gal antigens (as well as to Gal on neonatal pig islets) activate coagulation and complement cascades, leading to clotting, direct cellular membrane damage through the membrane attack complex (MAC), and recruitment of macrophages and monocytes through the chemoattractants C3a and C5a. TF, tissue factor.

Dirk J. van der Windt, et al. Diabetes. 2012 December;61(12):3046-3055.
5.
FIG. 3.

FIG. 3. From: Clinical Islet Xenotransplantation.

A: Functional survival of pig islets with a single genetic modification, that is, the transgenic expression of a human complement regulatory protein (hCD46), after transplantation in a cohort of five diabetic cynomolgus monkey recipients. Immunosuppression consisted of induction with antithymocyte globulin and was maintained with an anti-CD154 mAb and mycophenolate mofetil. All experiments were electively terminated; all monkeys were healthy when they were killed. Partial graft function (white bars) and full graft function (insulin independence) (black bars) are shown. Arrowheads indicate retransplantation. B: Serum acute C-peptide responses (ACR) of monkey C-peptide (white bars) and pig C-peptide (black bars) in nanograms per milliliter after a metabolic challenge with intravenous glucose (glu) during follow-up of case 5. The ACR was calculated as the mean of postchallenge C-peptide values obtained at 5 and 15 min minus the corresponding prechallenge value. Pre, the acute monkey C-peptide response before diabetes induction; post, the average of acute monkey C-peptide responses during follow-up after transplantation, monitored until day 372. C: Blood glucose values and insulin requirements in a monkey transplanted with pig islets carrying four genetic modificationsā€”GTKO/hCD46/hTFPIIns/pCTLA4-IgIns. The monkey is currently insulin independent for >150 days. Immunosuppression is identical to the regimen in A.

Dirk J. van der Windt, et al. Diabetes. 2012 December;61(12):3046-3055.

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