Biomedical subjects

J E Oscarson

Publications and source records attributed to J E Oscarson.

4 recordsLinked to original sources

PubMed1979

Ileal resection potentiates 1,2-dimethylhydrazine-induced colonic carcinogenesis.

The effect of colonic hyperplasia produced by resection of the distal third of the small bowel (DSBR) on the development of chemical carcinogenesis of the colon by dimethylhydrazine (DMH) was tested in rats. For the most part the amounts of RNA and DNA in the small bowel were the same with the combined treatments as with either one alone; quantities of nucleic acids tended to increase only in transverse and distal colon. After 37 weeks the number of neoplasms per rat was increased six-fold by combining DSBR with DMH. Neoplasms were spread throughout the colon after combined treatment as opposed to the ascending colong after DMH alone. Postresectional hyperplasia appears to increase the incidence and distribution of colon tumors.

Animals↗

PubMed1978

Promotion of azoxymethane-induced colonic neoplasia by resection of the proximal small bowel.

Potential enhancement of intestinal neoplasia by compensatory mucosal hyperplasia was tested in rats subjected to 50% proximal small bowel resection (PSBR) 10 days after the last of 16 weekly injections of azoxymethane. Azoxymethane alone increased jejunal contents of RNA and DNA each by 26% at 17 to 18 weeks (p less than 0.01) before there was macroscopic evidence of neoplasia. Three months after PSBR alone, ileal hyperplasia was characterized by increased amounts of RNA (42 to 76%) and DNA (68 to 95%), taller villi, deeper crypts, and luminal dilation (p less than 0.05 to 0.001); however, the colon showed only patchy hyperplasia. When the combined effects of azoxymethane and PSBR were observed 26 to 30 weeks after the first injection, rats with PSBR had an increased number of colonic tumors per animal (2.9 versus 1.6 for controls; p less than 0.02). Despite the intense ileal hyperplasia produced by PSBR, ileal neoplasia did not occur. Enhanced colonic carcinogenesis followed sequential exposure of the mucosa to the carcinogen (azoxymethane) and to the promoting factor (PSBR).

Adaptation, Physiological↗

PubMed1977

Compensatory postresectional hyperplasia and starvation atrophy in small bowel: dissociation from endogenous gastrin levels.

Because exogenous gastrin has been implicated as a tropic hormone for mucosal cells of the intestinal tract and as a regulator of mucosal growth, we studied the effects on the gut of endogenous 23-fold variations of serum gastrin produced by various gastric operations. These were pyloroplasty, vagotomy and pyloroplasty, antrectomy, and fundectomy. After jejunal resection, RNA content, DNA content, incorporation of [3H]thymidine into DNA, crypt depth, and villus height in midgut and ileum were independent of gastrin levels. Loss of RNA and DNA during starvation was not prevented by high endogenous concentrations of serum gastrin, and DNA specific activity was not affected. Tropic effects distal to the duodenum produced by exogenous gastrin and pentagastrin may be results of supranormal levels.

Animals↗

PubMed1976

Alien cancers of the duodenum.

Invasion of the duodenum by contiguous cancer or an isolated metastasis can manifest itself with the signs and symptoms of primary cancer of the duodenum. Fourteen patients were identified with this type of diagnostic confusion. All of their tumors were in the second or third portion of the duodenum. Although the median length of survival after excision of the tumor or palliative bypass operations in these patients was nine months, considerably longer survival times have also been described. Barium enema examinations and excretory urograms should be considered as diagnostic tests for any patient with a tumor of the duodenum to identify the contiguous carcinomas of the colon and kidney subject to long palliation.

Adult↗