The Impact on Medical Students of the 9/11 Attacks on New York's World Trade Center.

Phenomenon: Little is known about how participation in disaster relief impacts medical students. During the terror attacks of September 11, 2001, New York Medical College School of Medicine students witnessed the attacks and then became members of emergency treatment teams at St. Vincent's Hospital, the trauma center nearest to the World Trade Center. To date, only two reports describe how 9/11 influenced the lives of medical students. This study was designed to characterize the short- and long-term effects on NYMC students and to compare those effects between students assigned to St Vincent's Hospital and classmates assigned to rotations at facilities more remote from the attack site. We hypothesized that participation in direct relief efforts by students assigned to the St. Vincent's site might have long-lasting effects on their lives and these effects might vary when compared to classmates assigned elsewhere. Approach: This was a retrospective, survey-based, unmatched cohort study. Participants included all school of medicine graduates who were St. Vincent's rotators on 9/11 (N = 22) and classmates (N = 24) assigned to other sites who could be contacted and agreed to participate. Our primary measure was whether the 9/11 experience affected the participant's life, defined as an affirmative response to the item which asked whether the 9/11 experience affected the participant's "life thereafter, career choice, attitudes toward life or attitudes toward practice." Secondary measures included self-reported effects on career, life, attitudes, health, resilience, personal growth, personality features, and the temporal relationship between the attack and stress symptoms. Findings: Completed surveys were received from 16/22 (73%) St. Vincent's and 18/24 (75%) non-Saint Vincent's participants: 62% male, 82% had children, 74% identified as Caucasian/white and 76% employed full-time. Overall, slightly more than half (58%) of respondents reported an effect of 9/11 on their life, with a greater but non-significant proportion of St. Vincent's rotators reporting life impact (67% versus 50% for St. Vincent's versus other locations, respectively). High post-9/11 stress levels, current marriage, and ability to make and keep family and social relationships were associated with an effect on life which approached statistical significance. Participants reported positive or no post 9/11 effects on empathy and altruism (50%), resilience (47%), attitudes toward medical practice and career (32%), and charitable giving (24%), while positive, negative, or no effects were reported for attitude toward life, family and social relations, physical health, and conscientiousness. Mental health was the only domain in which all participants reported unchanged or negative effects. Two St. Vincent's rotators but no students assigned elsewhere believed they experienced 9/11-related post-traumatic stress disorder. Insights: Just over half of New York Medical College School of Medicine students rotating at St. Vincent's Hospital on 9/11 or elsewhere reported significant life-effects as a result of direct/indirect experiences related to the attack. Perceived stress may have been a more important driver of this life-change than other factors such as geographic proximity to the disaster site and/or direct participation in relief efforts. Further study of medical school interventions focused on stress reduction among students who participate in disaster relief is warranted.

Downhill esophageal varices: a therapeutic dilemma.

Esophageal varices can cause life-threatening complications and are most often a sequela of liver disease. Although a rare cause of gastrointestinal bleeding, downhill variceal bleeding secondary to superior vena cava (SVC) obstruction should be considered in the differential diagnosis for patients with upper gastrointestinal hemorrhage. We discuss two such cases of downhill esophageal varices presenting with hematemesis in patients with end stage renal disease and no history of cirrhosis. These varices were thought to be secondary to SVC occlusion caused by complications from previous dialysis catheters. However, their difficult anatomy posed a significant challenge to the therapeutic interventions.

Highly selective intraportal transplantation of pancreatic islets.

BACKGROUND: Histological assessment of intraportally transplanted islets in experimental rodent models is limited by the wide dissemination of islets throughout the liver. We describe a technique of highly selective intraportal islet transplantation, which increases the density of transplanted islets and hence facilitates their histological analysis and validate this model as a means of quantitative histological analysis of islet graft survival. We also compared the number of islets visualized histologically with that of nonabsorbable dextran beads, representing the number of transplanted islets there would have been if there had been no graft loss. MATERIALS AND METHODS: Diabetic Lewis rats or nondiabetic Sprague-Dawley rats were transplanted with 500 or 1000 syngeneic islets or an equivalent number of beads either into the main branch (MB), or selectively into the right branch (RB) of the portal vein. RESULTS: Islet transplantation led to an identical fall in blood glucose levels whichever technique was used. The graft area and number of islets recovered for histological analysis was 3- to 4-fold higher when islets were transplanted using the RB technique. Quantitative histological graft analysis demonstrated that 46% to 61% of intraportally transplanted islets were lost compared with corresponding bead graft sizes. Fewer islets were lost when a greater islet mass was transplanted. CONCLUSIONS: Selective islet transplantation increases the concentration of islets and hence facilitates islet recovery after intraportal transplantation without detrimental effects on transplantation outcome. This technique, when combined with bead transplantation and digital image analysis, provides an accurate method for estimating the number of islets surviving intra-portal transplantation.

Time course of islet loss after intraportal transplantation.

A high percentage of islets fail to survive intraportal transplantation, but the absolute amount and time course of this loss are uncertain. We have devised a technique to directly quantitate the number of surviving islets using simultaneous selective transplantation of islets and inert beads into the posterior lobes of the liver. Islet:bead ratio did not change significantly within the first 2 hours, but fell progressively thereafter, giving calculated islet survival rates of 89, 43, and 66% at days 1, 7 and 28, respectively. This technique provides a baseline from which to develop strategies to improve the survival of intraportally transplanted islets.

The isoprostane 8-iso-PGF2alpha suppresses monocyte adhesion to human microvascular endothelial cells via two independent mechanisms.

Isoprostanes, produced in vivo by non-enzymatic free-radical-induced lipid peroxidation, are markers of oxidative stress. Elevated serum and urine levels of 8-iso-PGF2alpha have been reported in a variety of diseases, many of which are characterized by early perivascular inflammatory infiltrates. It has been suggested that, in addition to being markers of oxidative stress, isoprostanes may have pathogenic functions. In this study, we investigated the potential role of 8-iso-PGF2alpha in inflammation, focusing on its effects on adhesion of monocytes to microvascular endothelial cells, an early event in the inflammatory response. In monocyte adhesion assays, 8-iso-PGF2alpha (>10(-8) M) suppressed both basal and TNF-alpha-induced monocyte adhesion to quiescent or proliferating human dermal (HMEC) and rat renal microvascular endothelial cells. In contrast, 8-iso-PGF2alpha stimulated monocyte adhesion to human umbilical vein endothelial cells (HUVEC) as also reported by others. 8-Iso-PGF2alpha had no effect on the viability (Trypan Blue exclusion) of U937 monocytes or HMEC. 8-Iso-PGF2alpha also had no effect on HMEC surface expression of ICAM-1 or VCAM-1. Exposure of HMEC to 8-iso-PGF2alpha for 1-2 h was sufficient to reduce monocyte adhesion to the cell surface, and this effect was independent of de novo protein synthesis by HMEC. The effect of 8-iso-PGF2alpha was mimicked by a thromboxane receptor (TP) agonist (U46619) and blocked by a TP antagonist (SQ29548), indicating a TP-mediated process. Signal transduction pathway inhibitors (SB203580, curcumin, and PD98059) implicated p38 and JNK, but not ERK, in 8-iso-PGF2alpha-induced suppression of monocyte adhesion. In addition to a direct effect, conditioned medium (CM) transfer experiments suggest that 8-iso-PGF2alpha induces a secondary mediator, which also suppresses monocyte adhesion but via an alternative mechanism initiated between 3-4 h, which is TP-independent, requires new protein synthesis, and is primarily dependent on activation of p38. The data show that 8-iso-PGF2alpha can suppress the attachment of monocytes to HMECs via two independent pathways, indicating a potential anti-inflammatory effect of 8-iso-PGF2alpha in the microvasculature.