Papillary serous carcinoma of the peritoneum (PSCP) is a primary neoplasm of peritoneal origin, and is histologically difficult to differentiate from papillary serous carcinoma of the ovary (PSCO). PSCP is frequently accompanied by many peritoneal tumors, and has been managed as a disseminated disease. In previous reports, however, the clonality of the tumors has not been fully discussed. Recently, the significant roles of the p53 and BRCA1 genes in PSCP have been reported. In this study, we investigated immunohistochemical staining for p53 proteins, and investigated p53 gene mutations, using DNA sequencing analysis, to clarify the clonality of PSCP tumors. Immunohistochemically, all the tumor samples demonstrated nuclear overexpression of p53 proteins, and the DNA sequencing analysis of the p53 gene showed diverse point mutations at codons 167 and 192 in two of four anatomically different tumors. In conclusion, the possibility of polyclonality of PSCP tumors is suggested.

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In our previous studies, TPI were found to be the molecules responsible for contact-killing of C. neoformans by S. aureus cells. Since TPI is a glycolytic protein that functions in the cytoplasm, evidence that TPI is present on the surface of S. aureus was required. In the present study, the presence of TPI on the cell surface of S. aureus was demonstrated by agglutination test and scanning immunoelectron microscopy. Furthermore, TPI was found to be present at a lower density than protein A/G molecules on the surface of S. aureus. Interaction between microbes colonizing mucosal membranes is known to occur. Recently, we discovered that the bacterium S. aureus, found in the nasopharynx of a large proportion of healthy human subjects (1, 2), kills C. neoformans and fragments its DNA, suggesting that S. aureus in human nasal cavities may prevent the entry of C. neoformans (3). Since this killing required contact between the cells, it seemed unlikely that soluble substances, such as bacteriocin or killer toxins, were involved. Key wordsTo investigate the molecules responsible for contactmediated killing, we attempted to identify the candidate adhesion molecules. TPI and α-(1→3)-mannooligosaccharide (larger than triose) in the backbone of GXM, the main component of the cryptococcal capsule, were identified on S. aureus and C. neoformans, respectively (4). Binding between TPI and mannotriose has previously been confirmed by using purified TPI iso- lated from S. aureus (5). Since TPI is a glycolytic protein that functions in the cytoplasm, evidence for the presence on the surface of S. aureus of the molecules recognizing GXM was required.Here, we visualized by scanning immunoelectron microscopy the localization of TPI, the molecules responsible for contact-mediated killing of C. neoformans, on the surface of S. aureus.For the agglutination test, S. aureus ATCC6538P was cultured in trypticase soy broth at 37• C for 18 hr. The cells were harvested by centrifugation at 1700 g for 10 min and washed with PBS three times. The cell suspension was treated with GXM prepared from C. neoformans B-3501 (6) at a concentration of 0.5 mg/ml, and incubated overnight with shaking. After washing twice with PBS, the suspensions (of about McFarland no.10 turbidity) were subjected to a slide agglutination test. On a slide glass, 368

Enteropathy-associated T-cell lymphoma (ETCL) is a primary extranodal T-cell lymphoma arising in the gastrointestinal tract, and is known as a rare and highly aggressive disease with a poor prognosis. The diagnosis of ETCL is usually established by histological examination using resected tumors or biopsy specimens during endoscopic studies. If tumor specimens for histopathological investigation are not available, then such a case might be difficult to accurately diagnose. We report here a case of ETCL which was diagnosed by cytopathology and flow cytometric immunophenotyping using paracentesis fluid without tumor specimens. Immunophenotyping by flow cytometry (FCM) of the ascitic fluid (AF) was invaluable in the final diagnosis of ETCL. Moreover, genetic alterations in the current case were also demonstrated. We emphasize the usefulness of effusion cytology for the expeditious diagnosis of ETCL. In particular, even in cases without tumor specimens, immunophenotyping by FCM using AF can play an important role in the diagnosis of ETCL, and simultaneous genome analysis may be useful to elucidate the biological characteristics of ETCL.

A case of Basedow's disease, that developed after successful treatment of ulcerative colitis with a total colectomy, is presented, along with a review of the Japanese literature on the coexistence of hyperthyroidism and ulcerative colitis. A 26-year-old man was referred to our department, complaining of general fatigue, appetite loss, and palpitation. At age 14, blood was discovered in his stool and a diagnosis of ulcerative colitis was made. Since then, he has been treated with salazosulfapyridine and prednisolone. On examination, mild exophthalmos and thyroid swelling were observed. Both serum free T3 and T4 levels were increased along with a positive TSHreceptor antibody, while TSH was decreased. Scintigraphic and ultrasonographic examinations of the thyroid gland showed diffuse enlargement. Treatment with thiamazole relieved the symptomsand normalized the thyroid function. Although a high incidence of autoimmunethyroid diseases in association with ulcerative colitis has been suggested, only 6 cases of hyperthyroidism coexisting with ulcerative colitis have been reported in Japan. A common immunological process has been suggested to be implicated in the pathogenesis of this association, however, the exact mechanismremains unclear. (Internal Medicine 40: 44-47, 2001)