The influence of organ acceptance criteria on long-term graft survival: outcomes of a kidney transplant program.

Background: In an effort to improve our transplant program's dead-donor kidney acceptance criteria, we compared 2 different consecutive time periods in our transplant program. Period I, in which the program used more-restrictive criteria in accepting dead-donor kidneys for our patients, and period II, when the program used less-restrictive criteria for the dead-donor kidneys that were accepted. The less-restrictive criteria resulted in an increase in the number of renal transplants performed.

Long-term comparative outcomes between 2 common ureteroneocystostomy techniques for renal transplantation.

Purpose: We compared the incidence of ureteral complications between the classic (Lich-Gregoir) technique and the recently popularized single stitch (Shanfield) technique in renal transplantation.

Materials And Methods: The charts of 721 consecutive transplant recipients from May 1999 to July 2002 were retrospectively reviewed. Ureteral and nonureteral complications were reviewed at 3 to 5-year followup.

Generation of human islets through expansion and differentiation of non-islet pancreatic cells discarded (pancreatic discard) after islet isolation.

Objectives: Islet transplantation is hampered by the shortage of donor tissues. Our objective was to generate islet-like cell clusters (ICCs) from cultures of non-islet pancreatic cells.

Methods: The starting cultured cells came from the non-islet fractions of human pancreases after enzymatic digestion and purification for the purpose of islet isolation.

Inhibition of p38 pathway suppresses human islet production of pro-inflammatory cytokines and improves islet graft function.

Nonspecific inflammation is associated with primary graft nonfunction (PNF). Inflammatory islet damage is mediated at least partially by pro-inflammatory cytokines, such as interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) produced by resident islet macrophages. The p38 pathway is known to be involved in cytokine production in the cells of the monocyte-macrophage lineage.

Silymarin protects pancreatic beta-cells against cytokine-mediated toxicity: implication of c-Jun NH2-terminal kinase and janus kinase/signal transducer and activator of transcription pathways.

Silymarin is a polyphenolic flavonoid that has a strong antioxidant activity and exhibits anticarcinogenic, antiinflammatory, and cytoprotective effects. Although its hepatoprotective effect has been well documented, the effect of silymarin on pancreatic beta-cells is largely unknown. In this study, the effect of silymarin on IL-1beta and/or interferon (IFN)-gamma-induced beta-cell damage was investigated using RINm5F cells and human islets.

Advances in islet cell biology: from stem cell differentiation to clinical transplantation: conference report.

The 3rd Annual Rachmiel Levine Symposium entitled "Advances in Islet Cell Biology-From Stem Cell Differentiation to Clinical Transplantation" was organized by the Department of Diabetes, Endocrinology and Metabolism at the City of Hope National Medical Center, with the support of the Southern California Islet Cell Resources Center, American Diabetes Association-David Shapiro Research Fund, Ross Foundation, the National Center for Research Resources (NCRR), and the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health. The symposium was held at the Hilton Anaheim Hotel in Anaheim, CA, in October 2002, and was attended by nearly 400 participants from 23 countries and 30 U.S.

Kidney transplantation at UCLA.

The demand for renal transplantation continues to increase. Combined organ transplantation currently accounts for approximately 10% of the kidney transplants at UCLA. As the demand for renal transplantation has increased, living kidney donation has become more common and achieves excellent results.

Prevention of primary nonfunction of canine islet autografts by treatment with pravastatin.

Background: Nonspecific inflammation is the primary cause of early islet graft loss. We have shown in mice that pravastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, prevents primary nonfunction of islet isografts by reducing inflammatory reactions at the graft site. This study was designed to test the effectiveness of this agent in a large animal model, dogs, by transplanting autologous islets.