The cumulative experience from three European countries suggest that rotavirus is an important cause of diarrhea in Central Europe, but significant local differences clearly demonstrate the need for obtaining national data as a reliable basis for control and prevention of the disease.

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Recently, a novel mechanism introducing genetic instability, termed aberrant somatic hypermutation (ASHM), has been described in diffuse large B-cell lymphoma. To further investigate whether ASHM also occurs in mucosa-associated lymphoid tissue type (MALT) lymphoma, we studied the mutation profile of PIM1, IntroductionExtranodal marginal zone B-cell lymphoma of the mucosaassociated lymphoid tissue type (MALT lymphoma) preferentially arises in the gastrointestinal tract, especially the stomach where it is closely linked to a Helicobacter pylori-induced chronic gastritis. 1,2 In general, MALT lymphoma may affect virtually every organ in the body. 3,4 Because of the interaction between lymphoma cells and mucosal adhesion molecules, 5 MALT lymphomas display an indolent clinical behavior; however, transformation in diffuse large B-cell lymphoma (DLBCL) occurs but, according to the WHO criteria, is considered as a separate entity. 6 Foci of extranodal DLBCL may be seen in MALT lymphoma, termed transformed MALT lymphoma, suggestive of transformation from one to the other entity.MALT lymphomas demonstrate a number of distinct cytogenetic alterations, 7 but a molecular mechanism inducing genetic instability has not been described. In DLBCL somatic hypermutation aberrantly targets the 5Ј sequences of several protooncogenes relevant to lymphomagenesis, including PIM1, PAX5, RhoH/TTF, and cMYC. This phenomenon, termed aberrant somatic hypermutation (ASHM) occurs in over 50% of DLBCL but is rare in indolent lymphomas. 8 Although the molecular mechanism of the SHM is still unknown, studies identified the activation-induced cytidine deaminase (AID) as an absolute requirement for the SHM. 9 The present study was aimed at investigating the role of the aberrant somatic hypermutation in MALT lymphomas and in MALT lymphomas transformed to extranodal DLBCL and to elucidate the role of AID in this process. Materials and methods Materials, diagnoses, and DNA extractionDNA extraction (DNA Mini Kit; Qiagen, Valencia, CA) was performed from formalin-fixed and paraffin-embedded macrodissected tissue containing at least 90% malignant cells. Seventeen MALT lymphoma specimens, 6 of gastric origin and 11 of extragastric origin (2 orbita, 7 parotid gland, 1 thyroid, and 1 soft tissue), and 17 samples of extranodal DLBCL, 10 of gastric origin and 7 of extragastric origin (2 thyroid and 5 parotid gland), and 6 normal controls, including 5 surrounding nonneoplastic tissues samples and one of peripheral blood mononuclear cells were included. All lymphomas were classified according to the WHO classification of lymphoid neoplasms. 6 Attention was made that cases of extranodal DLBCL comprised at least one focus of a low-grade lymphoma component considering these lymphomas as "transformed MALT lymphomas." 10 Immunohistochemistry was performed using monoclonal antibodies to The online version of this article contains a data supplement.The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate ...

Chemokine receptors mediate migration and activation of lymphocytes through binding of their ligands. Recent studies have revealed important contributions of chemokine receptors to the development, progression, and dissemination of haematopoietic neoplasms. Because the chemokine receptor expression profile in extragastric MALT lymphoma is unknown, we performed a comprehensive study on tissue samples of parotid glands, parotid glands affected by Sjögren syndrome, extragastric MALT lymphoma, and extranodal diffuse large B-cell lymphoma (eDLBCL) originating from MALT lymphoma (transformed MALT lymphoma). By investigating the expression of 19 chemokine receptors by real-time PCR using a semi-quantitative approach and of four chemokine receptors (CCR1, CCR5, CXCR6, and XCR1) by immunohistochemistry, we show that the chemokine receptor expression profiles of extragastric MALT lymphomas differ substantially from those of extranodal DBLCL, with lower expression of CCR1, CCR8, and CXCR3, and the absence of expression of CX3CR1 and XCR1 in eDLBCL. Expression of CCR6, CCR7, CXCR3, CXCR4, and CXCR5, responsible for B-cell homing to secondary lymphoid tissue, was detected in both B-cell malignancies. Expression of CCR4 was just detected in trisomy 3-positive MALT lymphoma cases. Comparing gastric with extragastric MALT lymphomas, up-regulation of CXCR1 and CXCR2 accompanied by down-regulation of CCR8 and CX3CR1 and loss of XCR1 expression in extragastric MALT lymphomas appear to be key determinants for the site of origin of MALT lymphomagenesis. Our results support a model of stepwise progression of extragastric MALT lymphoma from a non-neoplastic event to Sjögren syndrome, to MALT lymphoma, and finally to overt eDLBCL, guided by differentially expressed B-cell homeostatic and activation-dependent chemokine receptors and their ligands.

Rotavirus (RV) is the most common cause of diarrheal illness in children. We report three solid-organ-transplanted patients in whom RV infection caused increased trough levels of the immunosuppressive macrolide tacrolimus (TAC) by mechanisms that are still under investigation. The virus was detected for longer in the feces of these patients than in infants not receiving immunosuppressive therapy. In association with short-term monitoring of blood trough levels of TAC, the dosage should be reduced early if symptoms of an acute gastroenteritis are present.

Aims-To examine the disease burden and epidemiology of community acquired rotavirus gastroenteritis in Austrian children treated in a paediatric practice. Methods-Aprospective, population based, multicentre study in four paediatric practices and two children's hospitals (Innsbruck and Leoben). Children < 48 months of age presenting with gastroenteritis during a six month period of rotavirus peak between December 1997 and May 1998 were included. Prospective testing of stool samples for rotavirus was performed using ELISA. Results-A total of 6969 children were enrolled; 171 (2.4%) had community acquired gastroenteritis. Of 144 children who could be included in further analysis, 49 (34%; median age 16.7 months) were rotavirus positive, and 95 (66%; median age 17.0 months) were rotavirus negative. Three of the rotavirus positive children (median age 14.6 months) were hospitalised. The severity of rotavirus positive gastroenteritis was significantly higher than that of rotavirus negative gastroenteritis. The incidence of community acquired gastroenteritis was 4.67 per 100 children per year, and of rotavirus positive gastroenteritis 1.33 per 100 children per year. Conclusion-Rotavirus is a relevant cause of community acquired gastroenteritis in children aged 4 years and younger treated by a paediatrician. The data can be used as a basis for developing strategies to prevent infection. (Arch Dis Child 2001;84:393-397)

This cost-of-illness study clearly demonstrates the great impact of RV acute gastroenteritis, mainly of nosocomially acquired infection, on medical health care costs in Austria. To cut costs efforts in disease prevention should be encouraged.

Objectives: The objective of this study was to assess the dye 2′,7′–dichlorofluorescein (DCF) assay in screening for alterations in polymorphonuclear cell (PMN) and monocyte (MC) oxidative burst of cystic fibrosis (CF) patients. Study design: 56 CF patients aged between 2 and 20 years were investigated. Purified cells were stimulated with phorbolmyristate acetate (PMA) and zymosan (ZX). A range for DCF fluorescence for PMA– and ZX–stimulated and non–stimulated cells was established based on data from 60 healthy controls. Results: PMNs showed both enhancement and impairment. A deficient oxidative burst was detected in a total of 14 CF patients caused by abnormally high mean fluorescence intensity (MFI) of resting cells. Enhanced oxidative burst was seen in 6 CF patients. CF patients responded differently to PMA or ZX stimulation. Pseudomonas aeruginosa colonization significantly enhanced (p<0.005) the MFI of resting PMNs. MCs of CF patients showed a significantly (p<0.05) enhanced oxidative burst after stimulation with PMA compared to healthy controls, but no differences could be observed after stimulation with ZX. Serum concentrations of interleukin–6 were elevated in all CF patients, in particular in those with activation of both PMNs and MCs. Conclusion: The DCF assay shows for the first time the heterogeneity of the oxidative burst reaction in CF patients. In our opinion, the DCF assay is a reliable method for detecting pathological oxidative burst in CF patients.