Our study found that the use of anti-diarrheals and neoadjuvant therapy for rectal cancer were associated with readmission. Our findings imply that the use of anti-diarrheals may be a marker for patients at risk for fluid and electrolyte abnormalities; these patients should be strictly monitored at home. Our study also suggests consideration of avoidance of ileostomy creation or different discharge criteria for at-risk patients. Prospective studies focused on stoma monitoring after discharge may help reduce rehospitalizations for fluid and electrolyte abnormalities after ileostomy creation.

Elective surgery in the elderly is safe. Emergency surgery is accompanied by significant morbidity and mortality.

Our study suggests that 1) after radiation, the gross ulcer cannot be used to determine the sole area of potential residual tumor, 2) cancer cells may be found up to 3 cm distally from the gross ulcer, so the traditional 2-cm margin may not be adequate, and 3) local excision of the ulcer or no excision after apparent complete response appears to be insufficient treatment for rectal cancer.

APC mutations initiate most colorectal cancers (CRCs), but cellular mechanisms linking this to CRC pathology are unclear. We reported that wild-type APC in the colon down-regulates the anti-apoptotic protein survivin, and APC mutation up-regulates it, explaining why most CRCs display survivin overexpression and apoptosis inhibition. However, it does not explain another hallmark of CRC pathologyincreased mitotic figures and cell proliferation. Because survivin activates aurora-B kinase (ABK) in vitro, catalyzing mitosis, we hypothesized that in normal colonic crypts, APC controls ABK activity, while in neoplastic APC-mutant crypts, ABK activity is up-regulated, increasing mitosis. We quantitatively mapped intracryptal distributions of survivin, ABK, and markers of activated downstream signaling and mitosis (INCENP, phospho-histone-H3, phospho-centromere-protein-A). In normal crypts, gradients for these markers, ABK:survivin:INCENP complexes, and ABK activity were highest in the lower crypt (inverse to the APC gradient). In neoplastic crypts that harbor Although several lines of evidence indicate that a mutation at the APC locus initiates most cases of colorectal cancer (CRC), much less is known about the subsequent molecular and cellular mechanisms that link this mutation to the pathophysiology of colon tumorigenesis. Investigating this link by studying the anti-apoptotic protein survivin, we found that wild-type APC down-regulates survivin expression 1 and mutation of APC up-regulates it in mouse 2 and man. 3 While this might explain why most colon tumor cells show increased survivin expression and inhibition of apoptosis, it does not explain the increased mitotic figures and cell proliferation that are also pathological hallmarks of tumors. Since experiments using cultured cells have shown that survivin activates ABK, 4,5 which catalyzes mitosis, and since several lines of evidence suggest that ABK is involved in tumorigenesis, 6 -10 we hypothesized that: (i) in normal human colonic crypts wild-type APC down-regulates ABK

Students are generally accepted in outpatient colorectal clinics (81 percent). Reasons for acceptance of students included being able to contribute to the teaching of future doctors. Reasons for refusal included perceived increased length of the office visit and patient privacy. We noticed significant differences in compliance by gender, race, and severity of disease, but not age, patient level of income, or education.