Motohiro Ogura

Transdiaphragmatic duodenal duplication in a premature infant

A case of transdiaphragmatic duodenal duplication in a premature infant is presented. Vertebral abnormalities, which have invariably accompanied this disorder in reported cases so far, were characteristically absent. Therefore, the initial tentative diagnosis was right-sided diaphragmatic hernia. Barium examination was helpful in preoperative diagnosis.

AN ELECTRON MICROSCOPIC STUDY ON DIGESTIVE TRACT AMYLOIDOSIS IN FERRIC NITRILOTRIACETATE (Fe‐NTA)‐INDUCED “F1 AMYLOIDOSIS” MICE

The histological distribution and ultrastructural findings were investigated in 52 amyloid‐positive cases obtained from 80 F, mice (32 males and 48 females) receiving 126 to 502 daily intraperitoneal injections of ferric nitrilotriacetic acid (Fe‐NTA) resulting from reciprocal crossing of 20 parental mice receiving daily intraperitoneal injections of Fe‐NTA for 5 months. Of 52 amyloidotic F1 mice 49 (94%) developed a moderate degree of amyloid deposits in the gastrointestinal tract. Moderate amounts of amyloid deposits were sporadically discernible in the lamina propria of the stomach pars glandularis, the duodenal mucosa, and to a lesser extent in that of the rectal mucosa. Electron microscopic observation revealed that macrophages adjacent to amyloid mass were radiating outward abundant bundles of non‐branching amyloid fibrils from the cytoplasmic invaginations. In the cytoplasm of the macrophages there were occasionally acid phosphatase‐positive lysosomes including amyloid fibrils measuring approximately 100 Å in width. Moreover, it is discussed whether fibroblasts or fibroblast‐like interstitial cells are involved in amyloid formation.

AN ELECTRON MICROSCOPICAL AND HISTOCHEMICAL STUDY ON FERRIC NITRILOTRIACETATE‐INDUCED “F, AMYLOIDOSIS”

Of a total of 80 offspring obtained by reciprocal crossing of ICR/JCL strain of mice of both sexes receiving 84–140 injections of Fe‐NTA over 98–163 days before crossing, 52 (65%) showed severe generalized amyloidosis after 93–502 injections of Fe‐NTA over 115–522 days, but not “hemochromatosis”, which was a striking contrast to the findings of “hemochromatosis” without amyloidosis observed in the parent mice. Electron microscopic examinations revealed numerous bundles of non‐branching, well‐oriented amyloid fibrils radiated outward from the surface of cytoplasmic invaginations of the Kupffer cells or splenic reticuloendothelial cells of the F, mice with amyloidosis, and close contact frequently observed between “amyloid‐forming cells” and adjacent lymphocytes in the amyloid‐laden liver and spleen of the F, mice. Since the above findings in the F, mice were not found in the parent mice treated with multiple Fe‐NTA injections, the present authors assumed that the immunological memory for the Fe‐NTA conjugate transmitted via the placenta to the fetus from the mother that received multiple Fe‐NTA injections might be involved in the development of generalized amyloidosis in the F, mice, although the possible mechanism by which Fe‐NTA‐induced “F, amyloidosis” has been developed remains yet undetermined.