Nonsteroidal anti-inflammatory drug-induced colonic stricture: case report.

Nonsteroidal anti-inflammatory drug-induced colonic strictures are uncommon and usually occur in the proximal ascending colon. We describe the progressive findings of nonsteroidal anti-inflammatory drug-induced strictures in the ascending colon and at the ileocecal valve with subsequent bowel obstruction secondary to intussusception.

Apoptosis in circulating PMN: increased susceptibility in L-selectin-deficient PMN.

Previous work from our laboratory has shown that polymorphonuclear leukocytes (PMN) lose L-selectin as they age in the circulation. The present study was designed to examine the relationship between PMN age and susceptibility to apoptosis in the circulation using L-selectin as a marker of PMN age in rabbits. L-selectin-deficient leukocytes were separated from a mixed population of PMN in leukocyte-rich plasma using magnetic beads. Apoptosis was measured both with both morphological criteria and by determining the level of DNA fragmentation. The L-selectin-deficient cells separated in vitro showed morphological features of apoptosis (P < 0.01) and had higher levels of DNA fragmentation (P < 0.01) than the mixed population of PMN from which they were obtained. To determine if aging had a similar effect in vivo, PMN were labeled in the bone marrow with 5'-bromo-2'-deoxyuridine (BrdU) and L-selectin levels (immunocytochemistry) and DNA fragmentation (sandwich enzyme-linked immunosorbent assay) were measured in BrdU-labeled PMN in peripheral blood. The results showed that the peak release of BrdU-labeled PMN from the bone marrow into peripheral blood was associated with high levels of L-selectin expression, and these PMN had the lowest levels of DNA fragmentation. These results confirm that the level of L-selectin expression can be used as a marker of cell age and extend this observation by showing that aging in the circulation is associated with an increased susceptibility to apoptosis.

In situ hybridization for the Y chromosome reveals a donor origin for a posttransplant lymphoproliferative disorder in a sex-mismatched hepatic allograft.

We report a case of posttransplant lymphoproliferative disorder diagnosed within 4 weeks of orthotopic liver transplantation from a male donor to a female recipient. To determine whether the posttransplant lymphoproliferative disorder was of donor or recipient origin, nonisotopic in situ hybridization for the human Y chromosome was performed on formalin-fixed, paraffin-embedded sections of the donor liver using a digoxigenin-labeled probe. The lymphoid cells hybridized with the Y chromosome probe, indicative of a male genotype consistent with posttransplant lymphoproliferative disorder of donor origin. This case illustrates that nonisotopic in situ hybridization for the Y chromosome can discriminate between donor and recipient cells in sex-mismatched organ transplants.