No abstract

Hepatic granulomas were induced in mice by injection of blastospores, cell walls, and glucan of Candida albicans. Granulomatous reactions in liver tissue initially multiplied but later decreased. A dose-response relationship was apparent with up to 3 mg of inoculum. Shortly after injection of C. albicans spores, fungal elements appeared in liver macrophages and were detectable in granuloma and Kupffer cells for 20 days. Gram-stain, periodic acid-Schiff (PAS), and immunofluorescence reactions soon vanished, and the organisms could no longer be seen. Glucan of C. albicans, which lacked PAS and immunofluorescence reactivity, proved active in initiation of granulomas. Degradation of phagocytized spores of C. albicans, reductions of cytoplasm, and cell wall deformation and collapse support the premise that loss of PAS and immunofluorescence reactivity was caused by enzymatic breakdown of candida cell wall mannan in macrophages. We conclude that C. albicans can induce granulomatous reactions in mouse liver when the glucan that forms the cell wall matrix in Candida persists in identifiable residues.

Several mannan-containing fractions were obtained from whole cells, cell walls, and cytoplasm of Candida albicans by means of treatment with hot formamide or precipitation with (NH4)2SO4. The immunological and chemical characteristics of the fractions were compared with those of C. albicans mannan prepared by standard procedures. Antisera to C. albicans from rabbits immunized with whole cells of the organism were found to be primarily directed against the mannan content. With use of such antisera, mannan was localized in both the inner and outer layers of the cell wall, whereas the middle layer was found in all likelihood to represent the glucan polymer. Stepwise removal of mannan from whole cells or cell walls resulted in increasing loss of periodic acid-Schiff staining, immunofluorescence, and peroxidase reactivity. Thus, it appears that mannan is responsible for the ability of cell walls of C. albicans to be stained by periodic acid-Schiff or labeled with fluorescent antibody. The component of the pathogen most resistant to physical or chemical treatment was the glucan, which lacked all immunological reactivity.

No abstract

The results of treatment of early gastric carcinoma were analysed in 65 patients. In 33 patients the operation was performed 5 years ago. The 5-year-survival rate was 70%. Prognosis was predominantly influenced by the histology of the tumour. Signet ring cell and anaplastic early carcinomas (diffuse type) had a worse prognosis than intestinal (differentiated) forms. Carcinomas localised wholly in the mucosa had no better prognosis than those penetrating into the submucosa. There is no choice of surgical method according to prognostic criteria as the diagnosis "early gastric carcinoma" can be made only postoperatively from the resection material. Bioptic proof of carcinomatous gastric mucosal changes requires full observation of the rules of cancer surgery.