Publications by authors named "Schandl L"

Following the introduction of mono- and then dual hormone (incretin) receptor agonists into therapy, attention was turned to multiple receptor stimulation, with the additional activation of the glucagon receptor, as a new option for the pharmaceutical treatment of type 2 diabetes and obesity. In addition to its role in carbohydrate metabolism, the article reviews the other important physiological tasks of glucagon, especially its participation in intrainsular paracrine regulation, energy expenditure and the shaping of appetite and food consumption. It covers the potential benefits of the triple combination and briefly touches data on the efficacy and safety of the first triple receptor agonist drug, retatrutide, in preclinical human studies.

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The intestinal microbiome plays an important role in the body's physiological processes. One of its most decisive roles is the production of short-chain fatty acids, which has crucial importance in the maintenance of an intact intestinal barrier and immune homeostasis. Dysbiosis in the microbiome caused by dietary habits, regular medication use, and other factors can result in damage to the barrier function, which triggers the translocation of lipopolysaccharides into the portal circulation.

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Among the two incretins that strongly stimulate insulin secretion and are also involved in its physiological regulation in type 2 diabetes, glucagon-like peptide-1 (GLP1) has been the focus of interest for a long time, due to its retained - although reduced - secretagogue nature also in type 2 diabetes. Its receptor agonists were also included in the antidiabetic treatment toolkit. In the light of more recent studies, however, the "other" incretin, the glucose-dependent insulinotropic polypeptide (GIP) has also come into a different light.

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Diabetes mellitus is a cluster of diseases with heterogeneous etiopathogenesis and clinical nature. The exact classification of certain cases is of decisive importance in terms of the optimal choice of treatment. However, the classification is still not completely resolved, despite the available, ever-expanding tool park and rapidly expanding knowledge.

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Background: Patients with inflammatory bowel disease have lower prevalence of Helicobacter pylori infection, but the exact reason for this is not yet clear.

Aim: To examine whether the antibiotics frequently used in inflammatory bowel disease are responsible for the lower prevalence of H. pylori infection.

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Purpose: The fragile histidine triad (FHIT) gene has recently been proposed as being a tumor suppressor gene. FHIT gene deletions or aberrant transcripts have been identified in a variety of human malignancies, including gastric carcinomas, suggesting that FHIT may play a key role in tumor development. However, the clinical impact of FHIT mutations in gastric carcinogenesis is still debated.

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Background: Recent research has revealed a rapid increase in the number of alterations underlying oncogenesis and the proteins which regulate the cell cycle. p16 is a cell cycle regulatory protein acting as a cyclin-dependent kinase inhibitor (CDKI). Because of its antiproliferative effect, p16 has been suggested to be a tumor suppressor gene.

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The incidence of gastric cancer is decreasing; however, in some parts of the world this malignancy is still the second most common cause of cancer-related deaths and recent epidemiological analysis indicates that approximately 1,000,000 individuals will die from gastric cancer every year. Therefore, finding potent mechanisms of cancer prevention is of great importance, since this disease is commonly diagnosed in advanced stages. This review will provide a short update on the mechanisms of gastric carcinogenesis and will present recent data obtained from first clinical intervention studies aimed at the prevention of gastric cancer by Helicobacter pylori eradication.

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In recent years there has been much progress in understanding the pathogenesis of gastric cancer. The role of individual factors in gastric carcinogenesis continues to be debated and is also subject to further analysis. In addition to the activation of oncogenes and the inactivation of tumor suppressor genes, alteration of adhesion molecules seems to be critical for the development of gastric cancer.

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PTEN is a candidate tumour suppressor gene and frequently mutated in multiple cancers, however, not in pancreatic cancer. Recently, it has been demonstrated that PTEN expression is regulated by TGF-beta1. Using TGF-beta1 transgenic mice (n=7) and wildtype littermates (n=6), as well as pancreatic tissues obtained from organ donors (n=10) and patients with pancreatic cancer (n=10), we assessed the expression of PTEN by means of immunohistochemistry and semiquantitative PCR analysis.

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Chronic pancreatitis is an inflammatory disease of the pancreas, characterized by a progressive destruction of the exocrine and endocrine pancreas, leading both to exocrine and endocrine insufficiency. In recent years, our knowledge of this disease has improved, an epidemiological link between chronic pancreatitis and pancreatic cancer has been established, and the molecular alterations underlying their pathogenesis have been partly revealed. Nevertheless, the differentiation of chronic inflammation of the pancreas from cancer of the pancreas remains a great challenge.

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There are several possible methods to detect H. pylori in the gastric mucosa. The aim of our prospective study was to evaluate the diagnostic value of these tests and to define their place in the clinical practice.

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The efficacy of pirenzepin--of anticholinergic effect--and the H2-receptor blocking cimetidine has been studied in duodenal ulcer with random, double blind fashion. Recurrence examinations were carried out 6 and 12 months following the treatment. 50 patients were given pirenzepin and 50 cimetidine.

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