James F. George

Molecular and cellular mechanisms of donor cell-induced tolerance.

Aortic graft transplantation in mice.

Donor PAI-1 expression inhibits the intimal response of early allograft vascular disease.

Allogeneic bone marrow inhibits T-cell activation and clonal expansion in vitro.

Multi-organ transplantation: is there a protective effect against acute and chronic rejection?

Of mice and men: mouse models and the molecular mechanisms of post-transplant coronary artery disease.

Xenotransplantation: an ethical dilemma.

Role for CD4(+)CD25(+) T cells in inhibition of graft rejection by extracorporeal photopheresis.

Suppression by CD4+CD25+ regulatory T cells is dependent on expression of heme oxygenase-1 in antigen-presenting cells.

Mechanical circulatory device thrombosis: a new paradigm linking hypercoagulation and hypofibrinolysis.

IL-10 and IL-4 in skin allograft survival induced by T-cell depletion plus deoxyspergualin.

Patient with hypofibrinolysis-mediated thromboembolism converted to a hypercoagulable/hyperfibrinolytic state via ventricular assist device placement.

Carbon monoxide releasing molecule-2 increases the velocity of thrombus growth and strength in human plasma.

Carbon monoxide rescues heme oxygenase-1-deficient mice from arterial thrombosis in allogeneic aortic transplantation.

Carbon monoxide-releasing molecule-2 decreases fibrinolysis in human plasma.

Carbon monoxide releasing molecule-2 decreases thick diameter fibrin fibre formation in normal and Factor XIII deficient plasmas.

Carbon monoxide releasing molecule-2 increases the velocity of thrombus growth and strength in hemophilia A, hemophilia B and factor VII-deficient plasmas.

Hydrogen: another gas with therapeutic potential.

DCE-MRI detects early vascular response in breast tumor xenografts following anti-DR5 therapy.

Heme oxygenase-1 expression in murine dendritic cell subpopulations: effect on CD8+ dendritic cell differentiation in vivo.

Carbon monoxide releasing molecule-2 enhances coagulation and diminishes fibrinolytic vulnerability in subjects exposed to warfarin.

Carbon monoxide releasing molecule-2 increases fibrinogen-dependent coagulation kinetics but does not enhance prothrombin activity.

Balancing rejection and infection with respect to age, race, and gender: clues acquired from 17 years of cardiac transplantation data.

Carbon monoxide-releasing molecule-2 enhances coagulation and diminishes fibrinolytic vulnerability in diluted plasma in vitro.

On solid-phase antibody assays.

Minimizing infection and rejection death: clues acquired from 19 years of multi-institutional cardiac transplantation data.

Use of gated cardiac computed tomography angiography in the assessment of left ventricular assist device dysfunction.

Carbon monoxide releasing molecule-2 enhances coagulation and diminishes fibrinolytic vulnerability in plasma exposed to heparin or argatroban.

Data quality in the study of the mechanisms of extracorporeal photochemotherapy.

Pathologic features of dilated cardiomyopathy with localized noncompaction in a child with deletion 1p36 syndrome.

Early therapy evaluation of combined cetuximab and irinotecan in orthotopic pancreatic tumor xenografts by dynamic contrast-enhanced magnetic resonance imaging.

Improvement in 2-year survival for ventricular assist device patients after implementation of an intensive surveillance protocol.

The role of fibrinolytic genes and proteins in the development of allograft vascular disease.

Allosensitization and outcomes in pediatric heart transplantation.

Ganciclovir transiently attenuates murine cytomegalovirus-associated renal allograft inflammation.

Total lymphoid irradiation in heart transplantation: long-term efficacy and survival--an 18-year experience.

Comparison of observed survival after ventricular assist device placement versus predicted survival without assist device using the Seattle heart failure model.

In vivo regulation of the heme oxygenase-1 gene in humanized transgenic mice.

Opportunities for improvement in heart transplantation outcomes for young adults 18 to 35 years of age.

A reproducible mouse model of chronic allograft nephropathy with vasculopathy.