How Does Resident Participation Alter the Outcome of Surgery for Pectus Excavatum?

BACKGROUND: General surgery resident participation in the operating room is critical in training the next generation of surgeons. As of yet, the impact of resident participation on outcomes of surgery for pectus excavatum and many complex subspecialty operations has not been well studied. METHODS: A multi-institutional retrospective study of patients undergoing operative repair for pectus excavatum was performed. All relevant data were analyzed (IRB 11144). RESULTS: Two hundred and fourteen patients underwent operative correction (195 Nuss, 19 Ravitch). There were 185 males. Average age at repair was 14.7 years with a Haller index of 4.5. Average surgery time was 144 minutes (57-255) for the Nuss procedure and 263 minutes (141-373) for the Ravitch procedure. The presence of a second pediatric surgeon reduced the surgery time from 170 to 135 minutes (p < 0.01) and the presence of residents increased the time from 129 to 155 minutes (p < 0.01) for the Nuss procedure. One hundred and fifty patients had a single bar and 57 patients had 2 bars (28%). Average length of stay was 4.96 days (3-11). Long-term follow-up averaged 1737 days (42-3894). There were few complications and no difference in complication rate or length of stay between groups. Ninety nine percent of patients deemed the repair excellent and no patients required revision. CONCLUSIONS: Resident participation increases operative time, but with no demonstrable effect on hospital stay or long-term outcomes. Complication rates are low regardless of operating team composition. Thus, continuing to allow resident involvement, especially in subspecialty operations such as the Nuss and Ravitch procedures, may be worthwhile for resident education and surgical experience.

CYP2E1 induced by ethanol causes oxidative stress, proteasome inhibition and cytokeratin aggresome (Mallory body-like) formation.

The role of oxidative stress in alcoholic liver disease and cytokeratin aggresome formation is the focus of this in vitro study. HepG2 cells transduced to over express CYP2E1 (E47) and control HepG2 cells (C34) were first treated with arachidonic acid, then Fe-NAT, and finally with ethanol. In the E47 ethanol-treated cells, CYP2E1 was induced and a higher level of reactive oxygen species and carbonyl proteins were generated. The proteasome activity decreased significantly in the E47 ethanol-treated cells. This inhibition was prevented when CYP2E1 was inhibited by DAS. Microarray analysis showed gene expression down regulation of the proteasome subunit, as well as ubiquitin pathway proteins in the E47 ethanol-treated cells. 4-Hydroxynonenal (4-HNE) adducts were increased in the E47 cells treated with ethanol. Furthermore, the immunoprecipitated 4-HNE modified proteins from these cells stained positive with antibodies to the proteasome subunit alpha 6. These results indicate that the ethanol induced CYP2E1 generates oxidative stress that is responsible for the decrease in proteasome activity. Cytokeratin 8 and 18 were induced by ethanol treatment of E47 cells and polyubiquitinated forms of these proteins were found in the polyubiquitin smear upon Western blots analysis. Cytokeratin aggresomes and Mallory body-like inclusions formed in the ethanol-treated E47 cells, indicating that the ubiquitinated cytokeratins accumulated as a result of the inhibition of the proteasome by ethanol treatment when oxidation of ethanol induced oxidative stress. This is the first report where ethanol caused Mallory body-like cytokeratin inclusions in transformed human liver cells in vitro.