Determining the origin of poorly differentiated adenocarcinomas remains a challenge for the pathologist. This manuscript reports the use of a panel of specific immunohistochemical stains to determine the primary site of a tumor in the colon. A 45-year-old man had a right hemicolectomy for adenocarcinoma. Immunohistochemical staining documented that the lesion was a metastasis from a primary pancreatic adenocarcinoma--an unusual pattern of spread. The case emphasizes the important use of immunohistochemistry in identifying the primary source of lesions, allowing for appropriate treatment and staging.

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To investigate the characteristics of intestinal ion and fluid secretion induced by the adherent, effacing enteropathogenic Escherichia coli strain RDEC-1, we infected weanling rabbits with 10(7)-10(8) RDEC-1 organisms and then studied cecal ion transport under short-circuit conditions in Ussing chambers. Results in tissues with confluent adherent organisms were compared with those in uninfected ceca and in ceca stimulated with dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP). The short-circuited cecum normally absorbed Na and Cl, secreted bicarbonate (as represented by the residual ion flux), and displayed a high rate of nondiffusional Na and Cl transport. RDEC-1 infection did not alter the short-circuit current (Isc), but it increased the conductance (Gt), decreased the potential difference (PD), abolished net Na absorption, and reversed Cl absorption to secretion. The changes in Na and Cl net fluxes may be explained by inhibition of a Na-Cl linked absorptive process. In contrast, DBcAMP significantly increased the Isc, PD, and Gt, decreased net Na flux, and abolished net Cl absorption by stimulating electrogenic Cl secretion. These results suggest that RDEC-1-induced changes in cecal ion transport are not mediated by cAMP. The reduction in Na-Cl linked absorption is consistent with anatomic changes in the apical surfaces of absorptive epithelial characteristic of effacing enteroadherence, whereas the increased conductance is consistent with tight junction disruption seen with RDEC-1 infection.

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Radiation with doses > 7.5 Gy damages the canine intestinal mucosa, and pretreatment with WR2721 reduces this damage. However, the effects of radiation and of WR2721 on in vivo intestinal transport are unclear. Therefore, we determined canine survival, intestinal transport, and mucosal histology following unilateral abdominal irradiation. Isoperistaltic ileostomies were prepared in 23 dogs under general anesthesia and aseptic conditions. After a three-week recovery period, animals were given either placebo or WR2721, 150 mg/kg intravenously, 30 min prior to 10 Gy cobalt-60 abdominal irradiation. Ileal transport and histology were determined in both groups before exposure and one, four, and seven days after irradiation. Seven-day survival was significantly improved by pretreatment with WR2721 (91% vs 33%, P < 0.02). On day 4, both mucosal integrity and net intestinal absorption were significantly better (P < 0.05) after WR2721 than after placebo. Thus, radiation-induced damage to the ileal mucosa is accompanied by a reduction in net ileal absorption of water and electrolytes in vivo. In addition, pretreatment with WR2721 improves animal survival while reducing ileal damage and improving intestinal absorption.