Daniel G. Sheahan
Yale University
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Featured researches published by Daniel G. Sheahan.
Journal of Clinical Gastroenterology | 1979
Jan M. Novak; James T. Collins; Mark Donowitz; Jack Farman; Daniel G. Sheahan; Howard M. Spiro
Radiation therapy directed at the abdomen may damage the digestive tract, the type and extent of injury depending on the dose of the radiation and the radiation sensitivity of the gut. Characteristic early changes are manifest in the mucosa of the gut: for later ulceration, changes in the collagen tissues and particularly in the vascular channels occur. This paper describes and characterizes injuries to the esophagus, stomach, small intestine and colon. It emphasizes the importance of recognizing radiation-induced damage to the gut which may occur early or late after radiation.
Digestive Diseases and Sciences | 1971
Daniel G. Sheahan; Stanislav A. Horowitz; Norman Zamcheck
A, B and H isoantigens, demonstrable in human gastric and small intestinal mucosae, using the mixed cell agglutination reaction, were diminished or absent in eight of nine gastric epithelial malignancies. In all metastases, there was complete absence of isoantigenic activity, even though in three of the corresponding primary gastric tumors, there was some residual activity. The loss of isoantigenicity noted in tumors paralleled that seen in the intestinalized metaplastic epithelium accompanying such tumors. In 2 patients with pernicious anemia, there was partial retention of such isoantigenicity in tumor tissue. Although it is not known whether they cause or result from malignant change, these findings suggest that an alteration of blood-group substance synthesis occurs in malignant epithelium. It is conceivable that such alterations may contribute to the potential of malignant cells to metastasize.
Journal of Clinical Gastroenterology | 1986
Daniel G. Sheahan; Michael A. Berman
A 62-year-old man with carcinoma of the tongue had two separate asymptomatic carcinomas of the esophagus, one squamous and the other adenocarcinoma arising from Barretts mucosa. We review the multicentric origin and synchronous occurrence of tumors in the oropharyngoesophageal area with and without Barretts mucosa to emphasize the importance of complete evaluation of the esophagus in patients with oropharyngeal malignancy.
Digestive Diseases and Sciences | 1983
Fred S. Gorelick; Vincent A. DeLuca; Daniel G. Sheahan; Pierluigi Marignani; Robert S. Goldblatt; Jerry Winnan; Elliot M. Livstone
To evaluate the relationship between duodenal ulcer disease and duodenitis, duodenal epithelial cell renewal was measured in mucosal biopsies by the incorporation of [3H]thymidine. When 14 patients with duodenal ulcer were compared to 13 control subjects or 7 with endoscopic duodenitis alone, the crypt size was the same in all groups. Similar to other inflammatory processes of the gastrointestinal tract, patients with endoscopic duodenitis showed increased proliferative indices including a greater number of cells incorporating [3H]thymidine. In contrast, the proliferative indices from the duodenal mucosa of patients with duodenal ulcers did not differ from a control group. In a group of 6 patients with both endoscopic duodenitis and duodenal ulcer, the [3H]thymidine incorporation was intermediate between control subjects or patients with duodenal ulcer alone and those with endoscopic duodenitis alone. When subjects were divided according to the histologic appearance of the duodenal mucosa, those having chronic duodenitis demonstrated enhanced [3H]thymidine incorporation in comparison to a control group or patients with chronic active duodenitis (polymorphonuclear leukocytes present). Although there are many possible explanations of these findings, one may speculate that duodenal ulceration does not stimulate duodenal epithelial proliferation.
Gastrointestinal Endoscopy | 1973
Arthur D. Shiff; Daniel G. Sheahan; Solomon S. Schwartz
Nodular lymphoid hyperplasia was found in a defunctionalized colon following ileostomy performed because of localized regional ileitis. With no evidence of dysgammaglobulinemia, ileocolic continuity was re-established with apparent success.
Clinical Genetics | 2008
Lalit M. Ambani; Thomas D. Gelehrter; Daniel G. Sheahan
A pair of monozygotic twins with the Marfan syndrome with variable expression is presented. One of the twins, in addition to more severe musculoskeletal and ocular manifestations, had coarctation of the aorta as the cardiovascular manifestation of this syndrome. Analysis of red cell antigens, serum proteins and dermatoglyphic examination suggests a high probability of monozygosity. Accordingly, the variation in expression of this autosomal dominant disorder between the twins is most likely due to the modifying influences of environmental factors. Also noteworthy is the fact that the resected coarctation tissue domonstrated the histopathologic changes characteristic of cystic medial necrosis, and thus served as an additional piece of evidence supporting the diagnosis of the Marfan syndrome. This was of particular importance in view of the absence of any family history of this syndrome and the absence of ectopia lentis or the more typical cardiovascular manifestations in either twin.
Pediatric Research | 1978
Yvette Piovanetti; Samuel A. Kocoshis; Daniel G. Sheahan; Joyce D. Gryboski
Clinical and histological effects of Cromolyn (DSCG) were studied in 12 patients with inflammatory bowel disease (IFBD) (5 Crohns and 7 UC). Patients had refractory disease for at least 1 year. Treatment varied from 6-18 months and was not associated with adverse effects. Granulated mast cells were estimated in the lamina propria of normal control specimens (22) and others with IFBD. Biopsies were classified as normal, healed or chronic active. Index of disease activity was recorded for each patient. Results were in mast cells/mm2: Normal-343; UC-323 and Crohns-304. During DSCG treatment: in Crohns disease 3 of 5 (60%) improved clinically and 2 had progressive disease. Those who improved showed a mean increase of 105 mast cells/mm2 (from 267 to 372). In UC, 6 of 7 improved clinically (85%). Four of these showed a mean increase of 148 mast cells/mm2 (from 239 to 387/mm2). Two who improved clinically but had no increase in mast cells had active histologic disease pre and post-treatment. Overall, those who responded best to drug both by clinical and histologic criteria showed an increase in mast cells. DSCG is of value in the therapy of IFBD, and its effects may be directly related to its action on mast cells.
Digestive Diseases and Sciences | 1975
Joung Wye Rhee; Joyce D. Gryboski; Daniel G. Sheahan; F Thomas DolanJr.; John M. Dwyer
Diarrhea is common in children with severe combined immunodeficiency (1) but is a rare symptom in patients with infantile X-linked agammaglobulinemia (2-4). Diarrhea in infantile X-linked agammaglobulinemia with abnormalities in the small intestinal mucosa due to giardiasis has been reported (3) and als0 ascribed to isolated lactase deficiency with normal intestinal histology (5). This report describes a child with infantile X-linked agammaglobulinemia who had severe diarrhea associated with intestinal villous atrophy and intramucosal bacteria without evidence of giardiasis or lactase deficiency. In addition to the reduction in peripheral B lymphocytes frequently associated with this disease, a transient but marked reduction in the number and function of thymus-derived lymphocytes in the peripheral blood was also observed during the time when his diarrhea was most severe, usually an indication of a deficiency in cell-mediated immunity.
Human Pathology | 1988
Michael A. Berman; Judith A. Burnham; Daniel G. Sheahan
Journal of Clinical Gastroenterology | 1981
Vincent A. DeLuca; Winnan Gg; Daniel G. Sheahan; Sanders Fj; Greenlaw R; Marignani P; Fred S. Gorelick; Bhalotra R; Goldblatt Rs