Hyper activation of COX-2 with abnormal prostaglandin generation is considered to contribute to the pathophysiology of endometriosis and disease progression.

Abstract. This is the first study comparing hepatitis E virus (HEV) infection in Bangladesh in fulminant hepatitis (FH) patients presumed to have a viral cause and in the apparently healthy population. Sera from 22 FH patients were analyzed for antibodies to hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C and D viruses, and HEV and for hepatitis B surface antigen (HBsAg). Anti-HEV immunoglobulin M (IgM) was detected in the sera of 63.6% of patients, whereas 35.7% were positive for HBsAg. A high prevalence of HEV infection (83.3%) was noted in the HBV carriers. Serum samples from 273 apparently healthy individuals were tested for antibodies to HAV and HEV. Anti-HEV IgM was detected in 7.3% of the samples. The seroprevalence of HAV differed from that of HEV in the same population because all samples were negative for anti-HAV IgM. These data indicate that HEV infection is highly endemic in Bangladesh.

The differential diagnosis of gastrointestinal submucosal tumors is assisted with endoscopic US.

Summary The overexpression of murine double minute 2 (MDM2) is found in several human tumors, and increased expression of MDM2 inactivates the apoptotic and cell cycle arrest function of p53. Interleukin-16 (IL-16) is a pleiotrophic cytokine and the properties of IL-16 suggest that it involve in the pathophysiological process of chronic inflammatory diseases. In this study, we investigated the expression of MDM2 in intestinal metaplasia and gastric cancer as well as the effect of H. pylori infection and IL-16 on epithelial cell proliferation and MDM2 expression in gastric cells in vitro. The expression of MDM2 on gastric biopsies was studied immunohistochemistry. AGS cells were incubated with a combination of IL-16 and Helicobacter pylori (H. pylori). Gastric epithelial cell proliferation was studied by BrdU uptake and the expressions of MDM2 were studied by ELISA. There was no significant difference on the expression of MDM2 between with and without H. pylori infected chronic gastritis. In H. pylori infected gastric mucosa; the MDM2 expression was higher on intestinal metaplasia and gastric cancer than chronic gastritis. IL-16 administration was increased MDM2 expression and cell proliferation on AGS cells, which was decreased by H. pylori infection. In conclusion, the expression of MDM2 in long-term H. pylori infected gastric mucosa may indicate a risk for carcinogenesis. IL-16 secretion in H. pylori infected mucosa is one of the factors for gastric cancer. The expression of MDM2 on mucosa can be a mediator for gastric cancer.

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We treated a 14-year-old boy with Henoch -Schönlein purpura nephritis (HSPN) who died of an intracranial hemorrhage (ICH). Although ICH is a rare complication of HSPN, the consequence of this complication is sometimes very serious. 1 But there are no reports on the pathology and pathogenesis of ICH occurring in the course of HSPN. We examined the autopsied brain tissue and renal biopsy specimen using in situ hybridization (ISH) and polymerase chain reaction (PCR) of human cytomegalovirus (HCMV). The results indicated that he had had latent HCMV infection on admission to hospital. This suggests that reactivation of latent HCMV infection superimposed on HSPN worsened his vasculitis and resulted in fatal ICH. This is the fi rst report investigating the brain pathology of ICH as a result of severe vasculitis of HSPN. Case reportFive years prior to coming to Surugadai Nihon University Hospital , a 9-year-old boy was admitted to a local hospital for abdominal pain and vomiting. He was diagnosed as having HSPN because purpura had appeared on his legs. He was followed as an outpatient by the hospital and was admitted fi ve times after his fi rst admission due to abdominal colic. The patient had proteinuria and hematuria and was given only dipyridamole during these periods. Two months prior to admission to Surugadai Nihon University Hospital he had pretibial edema, hypertension and abdominal distention with heavy proteinuria. He was referred to Surugadai Nihon University Hospital because of his severe nephritis.On admission he was 6 kg heavier than 1 month previously, and he had hypertension (140/92 mmHg) and anasarca. The laboratory fi ndings on admission were as follows: blood urea nitrogen 25.6 mg/dL, creatinine (Cr) 2.29 mg/dL, total protein (TP) 4.1 g/dL, albumin (Alb) 2.3 g/dL, total cholesterol (T-cho) 272 mg/dL, urine red blood cells >100 per high-power fi eld, and urinary protein 819 mg/dL (3.62 g/day), and creatinine clearance (Ccr) 39.6 mL/min, IgG 338 mg/dL, IgA 233 mg/dL, third component of complement (C3) 97.7 mg/dL, fourth component of complement (C4) 19.2 mg/dL, anti-nucleic antibody, anti ds-DNA antibody, proteinase 3 antineutrophil cytoplasmic antibody (PR3-ANCA) and myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA) were negative.Based on these fi ndings a clinical diagnosis of nephronephritic HSPN was made, and treatment with oral prednisolone (2 mg/kg) was started. A renal biopsy showed diffuse mesangial proliferative glomerulonephritis, which was compatible with the International Study of Kidney Disease in Children (ISKDC) grade Vb. Intravenous methylprednisolone pulse therapy in combination with urokinase (3 days/week) was administered for 3 weeks. 2 After this therapy his serum creatinine decreased to 1.5 mg/dL. We then conducted double fi ltration plasmapheresis for 3 days to remove the IgA immune complex (IgA-IC), 3,4 which reduced IgA-IC from 3 mg/dL to 1 mg/dL. But on day 26 he had a fever and complained of a severe headache and delirium. Brain computed tomography (CT) showed a smal...

In this case, OCT showed needle-shaped deposits perpendicular to the retinal surface. Special staining with Congo red revealed the deposit to be amyloid deposition. Immunohistochemical staining suggested light chain-related amyloidosis. Vascular obstructive lesions and neovascular glaucoma secondary to retinal vascular damage in amyloidosis warrant particular attention.

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