Publications

BACKGROUND

Applications to cardiothoracic surgery training programs have steadily declined. The application cycle for 2004 marked the first time the number of applicants was lower than the positions offered. This survey reflects on this trend in applications and the perspectives of current and graduating residents.

METHODS

In June 2004, the Thoracic Surgery Residents Association, in conjunction with CTSNet, surveyed residents completing accredited cardiothoracic training or additional subspecialization. Participation was anonymous and voluntary.

RESULTS

Of the 140 graduates, 88 responded. Most were male (92%) and married (72%). Their average age was 35.7 years, and 56% had children. The mean educational debt was less than $50,000. Of the 88 respondents, 69 (78%) had plans to seek jobs whereas 15 (17%) sought additional training. Among job-seeking residents, 12% received no offers. Also, 59% of graduates initially sought a position in academics and 41% in private practice. Nearly one quarter (23%) reported that they would not choose a career in cardiothoracic surgery again, and more than half (52%) would not strongly recommend cardiothoracic surgery to potential trainees. Almost all (90%) of the graduates believed that the number of cardiothoracic training spots should be decreased, and 92% believed that a reduction in training positions should be achieved by closing marginal training programs. Additionally, 91% believed reimbursement for cardiothoracic surgery was inadequate, and 88% thought low reimbursement resulted in restricted patient access and decreased quality of care.

CONCLUSIONS

Cardiothoracic training programs are having difficulty in both applicant recruitment and in suitable job placement. This frustration in the job search coupled with reimbursement and lifestyle issues most likely contributes to the general dissatisfaction conveyed by the graduates. If these trends continue, the field will be faced with a crisis of unfilled residency programs and unemployed graduates.

BACKGROUND

The hurricanes and flooding in New Orleans, Louisiana, in October and November 2005 resulted in damp conditions favorable to the dispersion of bioaerosols such as mold spores and endotoxin.

OBJECTIVE

Our objective in this study was to assess potential human exposure to bioaerosols in New Orleans after the flooding of the city.

METHODS

A team of investigators performed continuous airborne sampling for mold spores and endotoxin outdoors in flooded and nonflooded areas, and inside homes that had undergone various levels of remediation, for periods of 5-24 hr during the 2 months after the flooding.

RESULTS

The estimated 24-hr mold concentrations ranged from 21,000 to 102,000 spores/m3 in outdoor air and from 11,000 to 645,000 spores/m3 in indoor air. The mean outdoor spore concentration in flooded areas was roughly double the concentration in nonflooded areas (66,167 vs. 33,179 spores/m3 ; p < 0.05) . The highest concentrations were inside homes. The most common mold species were from the genera of Cladosporium and Aspergillus/Penicillium ; Stachybotrys was detected in some indoor samples. The airborne endotoxin concentrations ranged from 0.6 to 8.3 EU (endotoxin units) /m3 but did not vary with flooded status or between indoor and outdoor environments.

CONCLUSIONS

The high concentration of mold measured indoors and outdoors in the New Orleans area is likely to be a significant respiratory hazard that should be monitored over time. Workers and returning residents should use appropriate personal protective equipment and exposure mitigation techniques to prevent respiratory morbidity and long-term health effects.

BACKGROUND & AIMS

We recently showed that mice deficient in Toll-like receptor 4 (TLR4) or its adapter molecule MyD88 have increased signs of colitis compared with wild-type (WT) mice after dextran sodium sulfate (DSS)-induced injury. We wished to test the hypothesis that cyclooxygenase 2 (Cox-2)-derived prostaglandin E2 (PGE2) is important in TLR4-related mucosal repair.

METHODS

Cox-2 expression was analyzed by real-time polymerase chain reaction, immunohistochemistry, Western blotting, and luciferase reporter constructs. Small interfering RNA was used to inhibit expression of MyD88. TLR4-/- or WT mice were given 2.5% DSS for 7 days. Proliferation and apoptosis were assessed using bromodeoxyuridine staining and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling assays, respectively. PGE2 was given orally to DSS-treated mice.

RESULTS

Intestinal epithelial cell lines up-regulated Cox-2 expression in a TLR4- and MyD88-dependent fashion. Lipopolysaccharide-mediated stimulation of PGE2 production was blocked by a selective Cox-2 inhibitor or small interfering RNA against MyD88. After DSS injury, Cox-2 expression increased only in WT mice. TLR4-/- mice have significantly reduced proliferation and increased apoptosis after DSS injury compared with WT mice. PGE2 supplementation of TLR4-/- mice resulted in improvement in clinical signs of colitis and restoration of proliferation and apoptosis to WT values. The mechanism for improved epithelial repair may be through PGE2-dependent activation of the epidermal growth factor receptor.

CONCLUSIONS

We describe an important link between TLR4 signaling and Cox-2 expression in the gut. TLR4 and MyD88 signaling are required for optimal proliferation and protection against apoptosis in the injured intestine. Although TLR4 signaling is beneficial in the short term, chronic signaling through TLR4 may lower the threshold for colitis-associated cancer.