Lymphoepithelial cyst in the pancreas: A case report

A case of lymphoepithelial cyst in the pancreas was reported. A 64-year-old man without any specific compalints was found to have a cystic lesion in the anterior portion of the pancreas, as revealed by ultrasonography of the abdomen at an annual medical examination in 1988. This was dissected easily from the pancreas. Histologically, it was diagnosed to be a benign lymphoepithelial cyst in the pancreas. Cysts of this type are rare, and their histogenesis is also not well understood.     

Motility of the Sphincter of Oddi and Pancreatic Main Ductal Pressure in Patients with Alcoholic, Gallstone-Associated, and Idiopathic Chronic Pancreatitis

We endoscopically measured pressures of the pancreatic duct (PP) and the sphincter of Oddi (SO) in patients with alcoholic (ALCP, n = 10), gallstone-associated (GSCP, n = 7), and idiopathic chronic pancreatitis (ICP, n = 21), and in 20 controls. The PP was significantly higher in the patients with ALCP (55.7 +/- 28.9 mm Hg), GSCP (33.6 +/- 16.2 mm Hg), or ICP (44.5 +/- 25.8 mm Hg) than in the controls (16.2 +/- 8.7 mm Hg), but there was no significant difference between ALCP, GSCP, and ICP. There was no significant difference between control subjects and ICP in the motility of SO. In ICP, there was no correlation between the PP and the motility of SO. In ALCP and GSCP, the frequencies of the papillary sphincter waves were significantly higher than in normal subjects, and there were correlations between the PP and the motility of SO. These data suggest that increased pancreatic ductal pressure in GSCP with papillitis or ALCP may be due in part to papillary dysfunction, but not in ICP.     

Mycobacteria in the Intestine of Japanese Patients with Inflammatory Bowel Disease

Objectives : It is still controversial whether or not a mycobacterial infection may be a cause of Crohn's disease. Mycobaclerium paratuberculosis may be very difficult to detect using routine culture techniques. To clarify this, we delected mycobacterial DNA in patients with inflammatory bowel disease. Methods : IS900 sequences highly specific to M. paratuberculosis and groEL gene encoding a conserved mycobacterial antigen were studied in colonic mucosa using polymerase chain reaction (PCR). PCR products were analyzed by Southern blot hybridization. Results : IS900 sequences were detected in all (100%)of 10 patients with Crohan's disease, in 11 (61.1%) of 18 patients with ulcerative colitis, and in 14 (87.5%) of 16 control patients with noninflammatory bowel disease. All IS900 positive samples had groEL PCR products. Conclusions : Our results, on the basis of the prevalence, do not support the hypothesis that M. paratuberculosis is involved in the pathogenesis of Crohn's disease.     

Identification of the optimal structure required for a Shiga toxin neutralizer with oriented carbohydrates to function in the circulation

Shiga toxin (Stx) is a major virulence factor of Stx-producing Escherichia coli. Recently, we developed a therapeutic Stx neutralizer with 6 trisaccharides of globotriaosyl ceramide, a receptor for Stx, in its dendrimer structure (referred to as "SUPER TWIG [1]6") to function in the circulation. Here, we determined the optimal structure of SUPER TWIG for it to function in the circulation and identified a SUPER TWIG with 18 trisaccharides, SUPER TWIG (2)18, as another potent Stx neutralizer. SUPER TWIGs (1)6 and (2)18 shared a structural similarity, a dumbbell shape in which 2 clusters of trisaccharides were connected via a linkage with a hydrophobic chain. The dumbbell shape was found to be required for formation of a complex with Stx that enables efficient uptake and degradation of Stx by macrophages and, consequently, for potent Stx-neutralizing activity in the circulation. We also determined the binding site of the SUPER TWIGs on Stx.     

Sensitization against pancreatic antigen in Sj?gren's syndrome and chronic pancreatitis. Preliminary communication.

A fractionated pancreatic antigen was prepared using a monoclonal antibody, SP3-1, which reacts with the duct cells of various exocrine organs. The cell-mediated immune response to this antigen was studied by the leukocyte migration inhibition test (LMT) in patients with chronic pancreatitis (CP), Sj?gren's syndrome (SjS), and chronic sialoadenitis (CSA). The migration index (MI) for the LMT was 0.97 +/- 0.07 in normal controls (mean +/- SD, n = 11, range: 0.88-1.08). A positive LMT result (MI less than 0.82 = mean -2 SD in controls) was obtained in 7/8 (88%) SjS patients, 4/22 (18%) CP patients, 2/3 CP patients with SjS, and 0/3 CSA patients. These results indicated sensitization against the pancreatic antigen in most SjS patients and some CP patients, and may suggest that an immune response to a common antigenic determinant of the duct cells of exocrine glands plays a role in the pathophysiology of both diseases.     

Overexpression of src family gene for tyrosine-kinase p59fyn in CD4-CD8- T cells of mice with a lymphoproliferative disorder.

Overexpression of a src family gene, lck, has been associated with differentiation of the murine thymic lymphoma line LSTRA. Recent findings by several groups strongly suggest a functional role for the gene product p56lck protein-tyrosine kinase (PTK) in the activation of normal T cells. A single recessive gene, lpr or gld, induces a lymphoproliferative disorder concomitant with autoimmune disease in mice. In this study, a 10-fold elevated activity of PTK encoded by fyn, another src family gene, was demonstrated in CD4-CD8- T cells in mutant mice. The increased PTK activity was consistent with overexpression of fyn mRNA. The elevated fyn mRNA expression appeared to be a characteristic of CD4-CD8- T cells, since it was not observed in normal T cells at any stage of differentiation. The fact that fyn mRNA expression was markedly induced in normal T cells by mitogenic stimulation with anti-T3 epsilon antiserum supports the possibility that p59fyn PTK is a signal-generating molecule in T cells. Thus, our findings provide insight into the physiological role for a src gene family kinase in T-cell development and contribute to a better understanding of the molecular mechanisms of disease-inducing recessive genes.     

Mutations of the p53 and ras genes in childhood t(1;19)-acute lymphoblastic leukemia

We have investigated the alterations of p53 and ras genes including H-, K-, and N-ras genes in 22 acute lymphoblastic leukemia (ALL) cases and five cell lines carrying t(1;19) by use of polymerase chain reaction (PCR)-single-strand conformation polymorphism (SSCP) analysis and direct sequencing. The mutations of the p53 gene were found in 2 of 20 t(1;19)-ALL cases at diagnosis (10%), all of 4 cases at relapse (100%), and 4 of the 5 cell lines (80%). Four of the five patients who died had missense mutations at codons 49, 177, 179, and 248. In cases examined sequentially, one had the same point mutation at codon 179 at both diagnosis and relapse, and another had the same p53 gene mutation at codon 240 both in leukemic cells at relapse and in a cell line derived at that time. The other case had no mutation at diagnosis but had the mutation at codon 177 at relapse and cell lines derived from blast cells at diagnosis, suggesting that a small number of leukemic cells with the p53 gene mutation at diagnosis might have escaped PCR-SSCP analysis. In cell lines, SCMC-L9 had three point mutations in the p53 gene at codons 175, 248, and 358, whereas SCMC-L10 had frame shift at codons 209-211. One case had a rare polymorphism at codon 11. We found only one mutation of the N-ras gene that was a 2-bp substitution of GGT(Gly) to GTC(Val) at codon 13 among 22 t(1;19)-ALL cases and five cell lines. This case showed no mutation of the p53 gene and has had a good course. These results suggest that in t(1;19)-ALL, mutations of the p53 and ras genes are infrequent at diagnosis and that p53 gene alterations may be associated with relapse phase or progression of t(1;19)-ALL.