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A 62-year-old man with epigastralgia was referred to our hospital for the evaluation of an intractable duodenal ulcer, which did not improve following proton pump inhibitor treatment. An upper gastrointestinal endoscopy revealed that the base of the ulcer was gray-white in color with conspicuous fibrosis tissue, unlike the appearance of common ulcers. A contrast-enhanced abdominal CT scan and angiography revealed tortuous and dilated vascular structures in the pancreatic head. This was diagnosed as a pancreatic arteriovenous malformation. We suggest that the intractable duodenal ulcer was caused by the pancreatic arteriovenous malformation. Therefore, we performed a pancreaticoduodenectomy. Pancreatic arteriovenous malformations should be considered as one of the causes of treatment-resistant duodenal ulcers.

Background and Aim White opaque substance (WOS) in gastric neoplasias is a unique finding visualized in magnifying endoscopy (ME) with narrow band imaging (NBI) and it represents intramucosal accumulation of lipid droplets using oil red O staining. Methods Subjects were 26 WOS-positive (13 adenomas and 13 well-differentiated adenocarcinomas) and 27 WOS-negative gastric epithelial neoplasias. We carried out immunohistochemical staining using a monoclonal antibody specific for adipophilin as a marker of lipids. Immunoelectron microscopy was used to evaluate morphology of the lipid droplets. Results Adipophilin was detected in 24 of 25 (96.0%) WOS-positive neoplasias, but it was detected in only two of 27 (7.4%) WOS-negative neoplasias. Lipid droplets were only seen in the surface epithelium in 10 of 11 (91.1%) adenomas, whereas the lipid droplets also existed in the cryptal epithelium in seven of 13 (53.8%) adenocarcinomas. Immunoelectron microscopy revealed numerous lipid droplets mainly existing in the subnuclear cytoplasm of the epithelium. The shape of the lipid droplets in adenomas was round and uniform, whereas that in adenocarcinomas was irregular. Conclusions The present study confirmed that the presence of WOS in gastric neoplasias was dependent upon intramucosal accumulation of lipid droplets using anti-adipophilin staining. Intraepithelial distribution and morphology of the lipid droplets differed between adenoma and adenocarcinoma.

The patient was a 67-year-old man with a 39-mm unilocular pancreatic tumor detected by computed tomography (CT). Further examinations with contrast-enhanced CT, magnetic resonance imaging, endoscopic ultrasonography, and endoscopic retrograde cholangiopancreatography revealed an internal heterogeneous structure attributed to bleeding or necrosis. Consequently, we expected either a pancreatic neuroendocrine tumor or a solid pseudopapillary neoplasm and performed pancreaticoduodenectomy. Pathological examination showed that the tumor had a denatured structure with evidence of internal bleeding and cubic epithelial cysts of various sizes. The final diagnosis was a macrocystic-type serous cystic neoplasm.

Although the appendix is recognized as an inductive site of intestinal inflammation, lymphocyte migration to lymphoid tissues of the appendix has not been characterized. The authors investigated if there are specific features in T-lymphocyte adhesion to microvessels of the appendix compared to mouse Peyer's patches (PPs).T-lymphocyte interaction with postcapillary venules (PCVs) of lymph follicles of the appendix and PPs was observed using an intravital microscope. Antibodies against ICAM-1, MAdCAM-1, or anti-L-selectin were administered prior to lymphocyte administration, and in some experiments CCR7 on T-lymphocytes was desensitized by excess CCL21.The number of adhered T-lymphocytes reached the maximum value earlier in PCVs of PPs than in those of the appendix. T-lymphocyte adherence was significantly inhibited by anti-MAdCAM-1 at either the appendix or PPs, but adherence in the appendix was also significantly inhibited by anti-ICAM-1, suggesting a dependency on ICAM-1 in the appendix. Histologically, there was a significant ICAM-1 expression in the appendix. Desensitization of CCR7 suppressed T-cell adhesion in PCVs of the appendix and PPs to the same extent.ICAM-1 appeared to be more important in T-lymphocyte sticking in PCVs of the appendix compared with intestinal PPs, while MAdCAM-1 and CCR7 were shown to play important roles in T-lymphocyte adherence in all sites.

White opaque substance (WOS) in gastric neoplasias is a unique finding visualized in magnifying endoscopy (ME) with narrow band imaging (NBI) and it represents intramucosal accumulation of lipid droplets using oil red O staining.Subjects were 26 WOS-positive (13 adenomas and 13 well-differentiated adenocarcinomas) and 27 WOS-negative gastric epithelial neoplasias. We carried out immunohistochemical staining using a monoclonal antibody specific for adipophilin as a marker of lipids. Immunoelectron microscopy was used to evaluate morphology of the lipid droplets.Adipophilin was detected in 24 of 25 (96.0%) WOS-positive neoplasias, but it was detected in only two of 27 (7.4%) WOS-negative neoplasias. Lipid droplets were only seen in the surface epithelium in 10 of 11 (91.1%) adenomas, whereas the lipid droplets also existed in the cryptal epithelium in seven of 13 (53.8%) adenocarcinomas. Immunoelectron microscopy revealed numerous lipid droplets mainly existing in the subnuclear cytoplasm of the epithelium. The shape of the lipid droplets in adenomas was round and uniform, whereas that in adenocarcinomas was irregular.The present study confirmed that the presence of WOS in gastric neoplasias was dependent upon intramucosal accumulation of lipid droplets using anti-adipophilin staining. Intraepithelial distribution and morphology of the lipid droplets differed between adenoma and adenocarcinoma.

A 46-year-old man was admitted to our hospital for further evaluation of a hypoechogenic mass in the pancreatic body. He had no history of hypertension, pancreatitis, abdominal trauma, or portal hypertension. He had no abdominal symptoms. A contrast-enhanced CT scan demonstrated a hypodense, round shaped mass. EUS and MRI also showed it to be a pancreatic mass. Because of the tumor size of more than 30mm and the possibility of malignancy, distal pancreatectomy was performed. Microscopic findings showed the mass was the dissection of the proximal splenic artery. The true lumen of the dissecting aneurysm was occluded and the false lumen developed fusiform dilatation. Moreover, microscopic findings revealed the rupture of the false lumen complicated by pseudoaneurysm. We finally diagnosed the lesion simulating a pancreatic tumor as the pseudoaneurysm of the splenic artery.

The appendix was long considered a redundant organ. However, thereafter, analysis of immune components of the appendix revealed that slightly fewer than one third of its cells are T cells and that normal adult appendiceal lymphocyte reactivity is predominated by helper T cells [1]. In addition, the appendix has been reported to be involved in intestinal inflammation. For example,“skip lesions”of the appendix were detected in ulcerative colitis (UC) specimens examined [2], and discontinuous appendiceal involvement was found in patients undergoing proctocolectomy for UC [3]. As regards the mechanisms in appendiceal inflammation, Bittinger et al. demonstrated a different expression of cell adhesion molecules by endothelial (EC) and mesothelial cells (MC) in the various stages of appendicitis, with early Eselectin and intercellular cell adhesion molecule-1 (ICAM-1) expression in EC, followed by vascular cell adhesion molecule (VCAM-1) in EC and MC [4], suggesting that adhesion molecules play pivotal roles in appendiceal inflammation. In addition, recently, potential roles of chemokines and their receptors in lymphocyte migration have been reported. On the other hand, preventive effects of appendectomy for UC have been reported in a clinical setting [5–8]. Moreover, in an experimental model of young T-cell receptor (TCR)-a deficient mice, removal of the appendix inhibited the induction of experimental colitis [9]. In another experimental model