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Background: In our earlier studies both corticosterone and cortisol had antioxidant effect in vitro. Objectives: Our aim was to clarify whether corticosterone and cortisol oral administration results in beneficial antioxidant changes in Sprague-Dawley adult male rats in vivo. Methods: Experimental animals were fed a lipid rich diet and treated with corticosterone or cortisol in the drinking fluid. Control group was fed only lipid rich diet with untreated drinking water. The untreated group was fed a normal diet with untreated water. Total scavenger capacity (TSC) was measured before and after 4 weeks of treatment in blood samples using a chemiluminometric assay. Results: Both corticosterone and cortisol treatment caused increased TSC. The control group and the untreated group showed no significant changes in TSC. Conclusion: Our results support the hypothesis that corticosterone and cortisol administration can improve the antioxidant status not only in vitro but also in vivo.

Neutrophil granulocytes form the biggest free radical producing system of the human body. The importance of this system in atherosclerotic plaque formation and other free radical mediated disorders is confirmed by both in vivo and in vitro studies. Estrogen’s effect on free radical production involves multiple estrogen receptors and occurs both on transcriptional and on protein phosphorylational level. Estrogen decreases the superoxide production of neutrophil granulocytes in such a short time frame it is unlikely to be mediated by transcription regulation. We investigated the underlying mechanism through which the mentioned estrogen effect takes place using an immunabsorption-based method. Phosphorylation data of 43 different messenger proteins were used for pathway analysis. The newly identified pathway involved largely second messengers from previously described non-genomic estrogen effects and affected superoxide production via Rac1 – an important regulator of free radical production and chemotaxis. Selective inhibition of the participating second messengers altered superoxide production in the predicted direction confirming that this pathway is at least partly responsible for the effect of 17-β-estradiol on chemoattractant induced superoxide production.

The high cost of infliximab inhibits the regular retreatment of all patients in Hungary with Crohn's disease (CD) after beneficial induction therapy. This study is set out to evaluate the medium-term efficacy of induction therapy with infliximab without retreatment in CD patients with chronic activity and/or fistulae refractory to conventional therapy.A retrospective 1-year review was undertaken of all CD patients with successfully induced remission or fistula closure with 3 infusions of infliximab. Infliximab was administered in a dose of 5 mg/kg 3 times, in weeks 0, 2 and 6. Clinical remission was defined as symptom resolution and an estimated Crohn's Disease Activity Index (CDAI)150 and complete fistula closure. We evaluated the clinical response, the estimated CDAI, the number of draining fistulae, the dosages of steroid and immunosuppressive drugs at 6 and 12 months after the last infusion, and the needs for hospitalization and surgical intervention during this period. Breslow (Generalized Wilcoxon) test was used as the statistical method.The data of the 50 patients (19 luminal, 31 fistulizing disease; average age 29. 3 [13-59] years, disease localization: 23 colon, 13 ileum, 13 ileocolon, 1 duodenum) were suitable for analysis. Infliximab induction therapy without retreatment resulted in a beneficial effect lasting for at least 1 year in 22 of the 50 patients (44%). 11 of the 19 patients (57.9%) with luminal disease remained in steroid-free complete remission, while the fistulae persisted closed in only 11 of the 31 patients (35.5%) (p0.05).Infliximab induction therapy alone may result in sustained remission mainly in patients with luminal disease. These results suggest the need for maintenance therapy with infliximab after successful therapy induction in patients with fistulae, while luminal CD patients could possibly participate in regular retreatment only if needed. If these data are confirmed, this modification of the therapeutic procedure could well increase the cost-effectiveness of infliximab.

Proton pump inhibitor (PPI) co-therapy is considered the best strategy in preventing gastrointestinal complications during non-steroidal anti-inflammatory drug (NSAID) treatment, but there is limited information available on its effect on gastric mucosal cell kinetics. To evaluate the effect of PPI co-therapy on gastric mucosa we investigated epithelial cell proliferation, apoptosis, epithelial growth factor receptor (EGFR) and p53 expression in patients on chronic non-selective NSAID or cyclooxygenase-2 selective inhibitor (COX-2) treatment. Gastric biopsies of the antrum were taken from 10-10 patients on chronic NSAID and COX-2, therapy prior and after 6 months PPI co-therapy, and 10 controls without any treatment. Cell proliferation, apoptosis, EGFR and p53 expression were measured by immunohistochemistry. At least 600 glandular epithel cells were encountered and results were expressed as % of total cells counted. We found increased cell proliferation in patients on chronic COX-2 but not on NSAID therapy. Patients on either NSAID or COX-2 therapy had an increased p53 and decreased EGFR expression. PPI therapy reversed not only the increased cell proliferation and p53 expression, but also the suppressed EGFR expression when administered as co-therapy. The fewer gastrointestinal side effects observed during chronic COX-2 therapy may partially be the result of the higher cell proliferation. This effect is not mediated by the EGFR pathway. PPI co-therapy normalizes the disturbed cell kinetics irrespective of NSAID treatment used.

Helicobacter pylori is an important cause of many gastrointestinal disorders, ranging from chronic gastritis to gastric lymphoma and adenocarcinoma. The deoxyribonucleic acid-based assays have the potential to be a powerful diagnostic tool given its ability to specifically identify H. pylori deoxyribonucleic acid. Markers used to include general H. pylori structures and pathogenetic factors like ureaseA, cagA, vacA, iceA. Deoxyribonucleic acid or bacterial ribonucleic acid for polymerase chain reaction assays can be collected from gastric biopsy, gastric juice, stool, buccal specimens. Polymerase chain reaction can yield quantitative and genotyping results with sensitivity and specificity that approaches 100%. A clear trend in the direction of the determination of quantitative H. pylori infection by real-time polymerase chain reaction can be observed. Fluorescent in situ hybridization is suggested for routine antibiotic resistance determination. To identify the organism, deoxyribonucleic acid structure and its virulence factors may be feasible by using oligonucleotide microarray specifically recognizing and discriminating bacterial deoxyribonucleic acid and various virulence factors. Deoxyribonucleic acid-based H. pylori diagnosis yields higher sensitivity, however, specificity requires sophisticated labour environment and associated with higher costs.

Background and study aims Reporting and machine control based on speech technology can enhance work efficiency in the gastrointestinal endoscopy laboratory. Materials and methods The status and activation of endoscopy laboratory equipment were described as a multivariate parameter and function system. Speech recognition, text evaluation and action definition engines were installed. Special programs were developed for the grammatical analysis of command sentences, and a rule-based expert system for the definition of machine answers. A speech backup engine provides feedback to the user. Techniques were applied based on the "Hidden Markov" model of discrete word, user-independent speech recognition and on phoneme-based speech synthesis. Speech samples were collected from three male low-tone investigators. Results The dictation module and machine control modules were incorporated in a personal computer (PC) simulation program. Altogether 100 unidentified patient records were analyzed. The sentences were grouped according to keywords, which indicate the main topics of a gastrointestinal endoscopy report. They were: "endoscope", "esophagus", "cardia", "fundus", "corpus", "antrum", "pylorus", "bulbus", and "postbulbar section", in addition to the major pathological findings: "erosion", "ulceration", and "malignancy". "Biopsy" and "diagnosis" were also included. We implemented wireless speech communication control commands for equipment including an endoscopy unit, video, monitor, printer, and PC. The recognition rate was 95%. Conclusions Speech technology may soon become an integrated part of our daily routine in the endoscopy laboratory. A central speech and laboratory computer could be the most efficient alternative to having separate speech recognition units in all items of equipment.

Summary Background : Carbonic anhydrase IX has been linked to cancer development and progression. Aim : To analyse carbonic anhydrase IX expression and anhydrase inhibition in pancreatic cancer and to correlate these findings with p53 expression and microvessel density. Materials and methods : Seventy-seven pancreatic cancers were examined (43 males, 34 females; mean age, 64 years). The anti-carbonic anhydrase IX M75 antibody was used for immunohistochemistry and Western blot analysis. Microvessels were visualized using the anti-CD34 antibody, and p53 expression in cancer cells was assessed with a specific anti-p53 antibody. Quantitative polymerase chain reaction was performed in order to assess carbonic anhydrase IX mRNA levels in the pancreas. Furthermore, pancreatic cancer cell lines were treated with acetazolamide, a carbonic anhydrase inhibitor. Results : In the normal pancreas, carbonic anhydrase IX immunoreactivity was observed at the basolateral membrane of ductal cells in 24 cases (31%). Carbonic anhydrase IX expression was found at the membrane and in the cytoplasm of pancreatic cancer cells in 16 pancreatic cancers (21%). Carbonic anhydrase IX expression was independent of the localization, stage, size, metastases and differentiation of the tumour. p53 expression was significantly more frequent in poorly differentiated cancers (P = 0.0323); however, p53 expression and microvessel density were independent of carbonic anhydrase IX expression. Overall, carbonic anhydrase IX expression was not altered in pancreatic cancers vs. adjacent normal pancreatic tissue as assessed by Western blot and quantitative polymerase chain reaction analysis. However, incubation of pancreatic cancer cell lines with acetazolamide led to a significant inhibition of cell proliferation in AsPC-1 and PANC-1 pancreatic cancer cells. Conclusion : Carbonic anhydrase IX expression is observed in both ductal epithelial and cancer cells of the pancreas. Although the expression of carbonic anhydrase IX in pancreatic cancer is not associated with angiogenesis or advanced disease, it may well be a target for carbo-anhydrase inhibitors in a subset of pancreatic cancers.

s / Pancreatolog S20 Patients & methods: Pubmed, Cochrane library, Ovid and Google Scholar were searched for the terms “pancreatic ductal adenocarcinoma”, “pancreatic cancer”, “survival”, “tumor recurrence” and “perineural invasion” and a systematic review and meta-analysis were performed according PRISMA guidelines. All articles meeting predefined criteria were analyzed on relevance, and meta-analysis pooling univariate and multivariate hazard ratios/HR were performed. Results: A total of 110 studies were identified analyzing the influence of PDAC on OS, Disease-free-survival/DFS and Recurrence-free-survival/RFS. The meta-analyses demonstrate a negative prognostic influence of PN in PDAC. The pooled univariate (1.86; CI 1.67-2.08; p

Ziel: Abklarung, ob die Qualitatsparameter der Koloskopie durch eine Sedierung beeinflusst werden. Methoden: Die Daten von insgesamt 2490 Koloskopien, die in der 2. Inneren Klinik der Semmelweis Universitat im Zeitraum vom 1.9.2011 bis zum 31.8.2012 erhoben wurden, wurden retrospektiv ausgewertet. Abhangig von Geschlecht und der Sedierung der Patienten wurden vier Gruppen gebildet: Die Verteilung der Daten war wie folgt: weibliche Patienten ohne Sedierung (n = 203); weibliche Patienten mit Sedierung (n = 1235); mannliche Patienten ohne Sedierung (n = 326); mannliche Patienten mit Sedierung (n = 726). Folgende Parameter wurden untersucht: Alter der Patienten, Adenomadetektionsrate (ADR), Rate der Adenomadetektion-bei-Coecumintubation (AD-CIR), Coecumintubationsrate (CIR), Ileumintubationsrate (IIR). Es wurde kein Unterschied gemacht, ob es sich bei der Untersuchung um eine Erst- oder Nachfolgeuntersuchung handelte. Ergebnis: Von 2490 Koloskopien wurde in 80,2% (weibliche Patienten in 85,8%, mannliche Patienten in 60,9%) der Falle eine Sedierung angewandt. Dabei wurden altere Patienten weniger oft sediert. Die Sedierung hatte bei beiden Geschlechtern keinen signifikanten Einfluss auf die ADR, unabhangig davon, ob das Coecum erreicht wurde oder nicht. Bei weiblichen Patienten waren die CIR (p 25% mannlich, > 15% weiblich). Auch ist die ADR bei einer kompletten Koloskopie (wenn das Coecum eingesehen werden kann) erwartungsgemas mit 4,5 – 6% hoher. Einzig die sedierten, weiblichen Patienten zeigen kaum einen Zuwachs der ADR bei Coecumintubation.

A young woman was examined for a mild thrombocytopenia which was present for some months. No signs of bleeding had so far occurred. Physical examination was normal except for a moderately enlarged spleen. Laboratory investigations showed a low platelet count. There was no evidence of an autoimmune or hematologic disease. Bone narrow aspirate indicated Gaucher's-like cells raising the suspicion of Gaucher's disease. This was further supported by electron microscopic demonstration of Gaucher's bodies in crista biopsy specimens. However, the definitive diagnosis was obtained by verifying deficient lysosomal glucosylceramide-beta-D-glucosidase activity in peripheral blood leukocytes. Upon the absence of neurologic involvement the patient was typical for the adult-onset or type 1 form of Gaucher's disease.

There is evidence of a disbalance in the inflammatory regulation of patients with inflammatory bowel diseases (IBD). Interleukin-1 beta plays an important role in the pro-inflammatory response. Our aim was to study the influence which IL1B gene polymorphisms may have on the severity and course of these diseases. Ninety-six patients with ulcerative colitis (UC), 98 patients with Crohn's disease (CD), and 132 ethnically matched healty individuals (HC) were typed for the polymorphic sites in the promoter region (position -511) and in exon 5 (position +3953) of the IL1B gene, using polymerase chain reaction (PCR)-based methods. In the CD group a significant association (P = 0.009) was found in this pair of genes. Homozygotes for allele 1 at position +3953 were more often present (69% vs 31%) in the subgroup of patients carrying at least one copy of allele 2 at position -511. This association was significant in patients with non-perforating disease (P = 0.002), but was not present in patients with perforating-fistulizing disease. The distribution of both allelic pairs in the non-fistulizing group proved to be significantly different from HC (P0.05), UC (P0.03), and the fistulizing group (P0.05). There was a similar association in non-operated patients (P = 0.024), whereas no such association was found in surgically treated patients. Among carriers of allele 2 at position -511, UC patients with more severe bleeding symptoms (P = 0.006) were less frequently found. These results suggest that IL1B gene polymorphisms participate in determining the course and severity of inflammatory bowel disease and contribute to explain the heterogeneity of these diseases.

There is growing evidence of the importance of genetic predisposition and the activation of the mucosal immune system in the pathogenesis of inflammatory bowel disease. Thus, genes involved in the regulation of inflammation are receiving increased attention. We have studied whether Crohn's disease (CD) or ulcerative colitis (UC) is associated with certain allelic combinations of IL1B/IL1RA gene polymorphisms in a different European population than the ones studied so far.Ninety-six patients with UC, 97 with CD, and 132 healthy individuals (HC) were typed for the polymorphic regions in exon 5 of the IL1B gene and in intron 2 of the IL1RA gene, using polymerase chain reaction-based methods.In CD homozygotes for allele 1 in IL1B gene polymorphism were more often present (72% versus 28%; P = 0.01) in the subgroup of patients carrying at least one copy of allele 2 in IL1RA gene polymorphism. This association was not found in HC (HC versus CD; P = 0.03) or UC. However, in UC patients with pancolitis a similar trend was observed (75% versus 25%). Several genotype combinations characterized by the presence of allele 2 of the IL1RA gene polymorphism were more common in CD (P = 0.001) and UC (P = 0.049) than in HC.Our data support the concept that CD and severe UC have a genetic disequilibrium in the distribution of IL1B and IL1RA gene polymorphisms. These findings together with functional studies will contribute to the understanding of the pathogenesis of the chronicity of inflammation in these diseases.

Gut-associated lymphoid tissue (GALT) is supposed to play an integral role in the organization of colonic repair mechanisms. Majority of the GALT is composed of isolated and aggregated lymphoid follicles distributed throughout the intestines. These lymphoid follicles, including Peyer’s patches of the small, and isolated lymphoid follicles (ILFs) of both the small and large intestines, are composed of a specialised follicle associated epithelium overlying a subepithelial dome containing numerous dendritic cells, macrophages, T and B cells. Within inflammatory conditions the number, the diameter and the density of ILFs are increasing. Follicles are involved not just in immune surveillance, but their presence is also indispensable for normal colonic mucosal regeneration. Regarding mucosal repair the relation of ILFs to bone marrow derived stem cells, follicular dendritic cells, subepithelial myofibroblasts and crypt formations, and the putative organizer role of ILFs have not been clarified yet.