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Salzburg, Austria

Niederwanger A.,Innsbruck Medical University | Ciardi C.,Innsbruck Medical University | Tatarczyk T.,Innsbruck Medical University | Khan M.I.,Innsbruck Medical University | And 5 more authors.
American Journal of Clinical Nutrition | Year: 2014

Background: Type 2 diabetes is associated with pancreatic α cell dysfunction, characterized by elevated fasting plasma glucagon concentrations and inadequate postprandial glucose- and insulin-induced suppression of glucagon secretion. The cause and the underlying mechanisms of α cell dysfunction are unknown. Objective: Because Western dietary habits cause postprandial lipemia for a major part of a day and, moreover, increase the risk of developing type 2 diabetes, we tested the hypothesis that postprandial lipemia with its characteristic elevation of triglyceride-rich lipoproteins (TGRLs) might cause pancreatic α cell dysfunction. Design: In a crossover study with 7 healthy volunteers, 2 experiments using 2 fat-enriched meals were performed on each volunteer; meal 1 was designed to increase plasma concentrations of both TGRLs and nonesterified fatty acids and meal 2 to increase TGRLs only. Intravenous glucose boli were injected at 0800 after an overnight fast and postprandially at 1300, 3 h after ingestion of a fat-enriched meal. Glucagon concentrations were measured throughout the days of the experiments. In addition to the study in humans, in vitro experiments were performed with mouse pancreatic islets and cultured pancreatic alpha TC 1 clone 9 (αTC1c9) cells, which were incubated with highly purified TGRLs. Results: In humans, postprandial lipemia increased plasma glucagon concentrations and led to an inadequate glucose- and insulin-induced suppression of glucagon. There was no difference between the 2 meal types. In mouse pancreatic islets and cultured pancreatic αTC1c9 cells, purified postprandial TGRLs induced abnormalities in glucagon kinetics comparable with those observed in humans. The TGRL-induced α cell dysfunction was due to reduced γ-aminobutyric acid A receptor activation in pancreatic α cells. Conclusion: We concluded that postprandial lipemia induces pancreatic α cell dysfunction characteristic of type 2 diabetes and, therefore, propose that pancreatic α cell dysfunction could be viewed, at least partly, as a postprandial phenomenon. © 2014 American Society for Nutrition. Source


Setaffy L.,Medical University of Graz | Osuna M.J.M.,University of Malaga | Plieschnegger W.,Hospital of Barmherzige Bruder | Del Pino Florez Rial M.,University of Malaga | And 2 more authors.
Endoscopy | Year: 2014

Multifocal stenosing enteritis, not related to Crohn's disease or drug intake, has been described under two different terms: cryptogenic multifocal ulcerous stenosing enteritis (CMUSE) and neuromuscular and vascular hamartoma (NMVH). We present three new cases of this condition and argue that the two terms reflect the same disease entity. Although etiology and pathogenesis of the disease remain largely unclear, obliterative vascular changes may play an important role. © Georg Thieme Verlag KG Stuttgart · New York. Source


Hager M.,Paracelsus Medical University | Haufe H.,Paracelsus Medical University | Lusuardi L.,Paracelsus Medical University | Schmeller N.,Hospital of Barmherzige Bruder | Kolbitsch C.,Innsbruck Medical University
Cancer Investigation | Year: 2011

The present study evaluated pAKT, pmTOR, and PTEN expression in a tissue microarray of primary renal cell carcinomas (PRCCs), their metastases, and normal renal parenchyma (NRP) (N = 45) by means of immunohistochemistry. Metastases in most subcellular compartments showed comparable and stronger expression for pAKT, pmTOR, and PTEN than PRCC and NRP, which was even more pronounced in patients with high-risk Memorial Sloan-Kettering Cancer Center (MSKCC) score. Furthermore, most subcellular compartments showed no differences between lymphogenous, haematogenous, synchronous, and metachronous metastases, which is interesting with regard to sensitivity to mTOR inhibitor therapy in metastasized RCCs with alterations in the PI3K/AKT pathway. © 2011 Informa Healthcare USA, Inc. Source


Hager M.,Paracelsus Medical University | Haufe H.,Paracelsus Medical University | Lusuardi L.,Paracelsus Medical University | Schmeller N.,Hospital of Barmherzige Bruder | Kolbitsch C.,Innsbruck Medical University
Clinical and Experimental Metastasis | Year: 2010

In cancer therapy novel concepts focus on phosphoinositide 3-kinase (PI3K)/activated protein kinase B (p-AKT)/mammalian target of rapamycin (mTOR) inhibitors. In this context, p-AKT overexpression was previously shown to be associated with sensitivity to inhibitors of mTOR. The present study evaluated p-AKT expression in a tissue microarray of primary renal cell carcinomas (PRCCs) (n = 45), their metastases (primary onset n = 45, secondary onset n = 5), and normal renal parenchyma (n = 45) by means of immunohistochemistry. Total p-AKT overexpression was found in 24/45 (53.3%) PRCCs, in 32/45 (71.1%) primary and in 3/5 (60%) secondary onset metastases. Membranous p-AKT overexpression was seen more frequently in PRCCs, namely 11/45 (24.4%), than in primary onset metastases 1/45 (2.2%). Overexpression of total p-AKT solely in metastases without overexpression in PRCC was exclusively demonstrated in primary onset metastases, namely in 28.9%. Patients with total p-AKT overexpression in primary carcinomas showed a trend to longer, and those with total p-AKT overexpression in metastases a tendency to shorter survival. In conclusion, the present study shows total p-AKT overexpression to be more frequent in metastases than in PRCCs. Total p-AKT overexpression in metastases without concomitant overexpression in their primary tumors was found in approximately one-third of primary onset metastases, which is interesting with regard to the association between high p-AKT expression and sensitivity to mTOR inhibitor therapy. © 2010 Springer Science+Business Media B.V. Source


Brunnler T.,Hospital of Barmherzige Bruder | Susewind M.,Hospital of Barmherzige Bruder | Hoffmann U.,Hospital of Barmherzige Bruder | Rockmann F.,Hospital of Barmherzige Bruder | And 3 more authors.
Internal Medicine | Year: 2015

Objective To assess the outcomes in a large cohort of patients suffering from rheumatic diseases admitted to the ICU of a tertiary university medical center. Methods A retrospective chart analysis was performed in 108 patients suffering from various rheumatic diseases and the outcomes, including morbidity and mortality, were assessed in relation to the underlying diseases, treatments and complications. Results Overall, 48 patients with rheumatoid arthritis, five patients with spondyloarthritis, 14 patients with vasculitis, 30 patients with connective tissue diseases and 11 patients suffering from other rheumatologic conditions were admitted to the intensive care unit (ICU). The reasons for ICU admission included infection (30%), cardiovascular complications (22%), gastrointestinal problems (18%), endocrinological disorders (7%), neurological complications (2%) and others (3%). A total of 4% of the admitted patients required close monitoring and 14% suffered from acute exacerbation of the underlying rheumatic disease. The ICU mortality rate was 16%, whereas the overall hospital mortality rate was 20%. Fatal outcomes were related to exacerbation of the rheumatic disease in 14% of the patients, infectious complications in 46% of the patients and other reasons in 41% of the patients. An increased Apache II score, the need for mechanical ventilation, renal replacement therapy, treatment with vasopressor drugs and plasma exchange therapy were identified as risk factors for mortality. Conclusion The overall outcomes of critically ill patients with rheumatic diseases are impaired compared to that observed in other patient groups. However, there were no significant differences in outcomes between the different rheumatic disease groups or based on the use of immunosuppressive therapy in this study. An increased Apache II score, the need for mechanical ventilation, renal replacement therapy, treatment with vasopressor drugs and plasma exchange therapy were identified as risk factors for mortality. © 2015 The Japanese Society of Internal Medicine. Source

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