@article{27134, author = {{Muckelbauer, R. and Libuda, Lars and Clausen, K. and Kersting, M.}}, issn = {{0305-1862}}, journal = {{Child: Care, Health and Development}}, pages = {{851--857}}, title = {{{Long-term process evaluation of a school-based programme for overweight prevention}}}, doi = {{10.1111/j.1365-2214.2009.00993.x}}, year = {{2009}}, } @article{27135, author = {{Muckelbauer, Rebecca and Libuda, Lars and Clausen, Kerstin and Reinehr, Thomas and Kersting, Mathilde}}, issn = {{1662-4033}}, journal = {{Obesity Facts}}, pages = {{282--285}}, title = {{{A Simple Dietary Intervention in the School Setting Decreased Incidence of Overweight in Children}}}, doi = {{10.1159/000229783}}, year = {{2009}}, } @article{27136, author = {{Muckelbauer, R. and Libuda, Lars and Clausen, K. and Toschke, A. M. and Reinehr, T. and Kersting, M.}}, issn = {{0031-4005}}, journal = {{PEDIATRICS}}, pages = {{e661--e667}}, title = {{{Promotion and Provision of Drinking Water in Schools for Overweight Prevention: Randomized, Controlled Cluster Trial}}}, doi = {{10.1542/peds.2008-2186}}, year = {{2009}}, } @article{27525, author = {{Libuda, Lars and Kersting, Mathilde}}, issn = {{1363-1950}}, journal = {{Current Opinion in Clinical Nutrition and Metabolic Care}}, pages = {{596--600}}, title = {{{Soft drinks and body weight development in childhood: is there a relationship?}}}, doi = {{10.1097/mco.0b013e32833189f6}}, year = {{2009}}, } @article{27583, author = {{Libuda, Lars and Muckelbauer, R. and Kersting, M.}}, journal = {{Journal für Ernährungsmedizin}}, pages = {{23}}, title = {{{Getränkeverzehr und Übergewicht bei Kindern}}}, volume = {{11}}, year = {{2009}}, } @article{27584, author = {{Libuda, Lars}}, journal = {{Ernährungsumschau}}, number = {{8}}, pages = {{480--481}}, title = {{{Einfluss des Konsums von Erfrischungsgetränken auf den Ernährungs- und Gesundheits¬status von Kindern}}}, volume = {{56}}, year = {{2009}}, } @article{27585, author = {{Libuda, Lars and Remer, Thomas and Kersting, M.}}, journal = {{Ernährungsumschau}}, number = {{3}}, pages = {{137}}, title = {{{DONALD News: Zusammenhang zwischen dem Verzehr von Erfrischungsgetränken und dem Knochenstatus von Kindern und Jugendlichen. }}}, volume = {{56}}, year = {{2009}}, } @article{27707, author = {{Toeller, M. and Buyken, Anette and Heitkamp, G. and Scherbaum, W.A. and Krans, H.M.J and Fuller, J.H.}}, issn = {{0947-7349}}, journal = {{Experimental and Clinical Endocrinology & Diabetes}}, pages = {{512--521}}, title = {{{Associations of fat and cholesterol intake with serum lipid levels and cardiovascular disease: The EURODIAB IDDM Complications Study*}}}, doi = {{10.1055/s-0029-1232560}}, year = {{2009}}, } @article{27716, abstract = {{AbstractObjectiveThe present paper describes the systematic development of an FFQ to assess the intake of fatty acids and antioxidants in school-aged children. In addition, a validation study applying 24 h dietary recalls was performed.DesignUsing the variance-based Max_r method, a list of eighty-two foods was compiled from data obtained by 3 d weighed dietary records. The foods were used to design an FFQ, the comprehensibility of which was evaluated in a feasibility study. In addition, the FFQ was validated in a subset of 101 children from the German Infant Nutritional Intervention Study (GINI PLUS) against one 24 h dietary recall.ResultsThe feasibility study attested a good acceptance of the FFQ. Mean intake of foods compared well between the FFQ and the 24 h dietary recall, although intake data generated from the FFQ tended to be higher. This difference became less apparent at the nutrient level, although the estimated average consumption of arachidonic acid and EPA using the FFQ still exceeded values recorded with the 24 h recall method by 45 % and 29 %, respectively.ConclusionsOn the basis of the systematic selection process of the food list, the established practicability of the FFQ and the overall plausibility of the results, the use of this FFQ is justified in future epidemiological studies.}}, author = {{Stiegler, Petra and Sausenthaler, Stefanie and Buyken, Anette and Rzehak, Peter and Czech, Daniel and Linseisen, Jakob and Kroke, Anja and Gedrich, Kurt and Robertson, Claire and Heinrich, Joachim}}, issn = {{1368-9800}}, journal = {{Public Health Nutrition}}, pages = {{38--46}}, title = {{{A new FFQ designed to measure the intake of fatty acids and antioxidants in children}}}, doi = {{10.1017/s1368980009005813}}, year = {{2009}}, } @article{27722, author = {{Shi, Lijie and Berkemeyer, Shoma and Buyken, Anette and Maser-Gluth, Christiane and Remer, Thomas}}, issn = {{0026-0495}}, journal = {{Metabolism}}, pages = {{134--139}}, title = {{{Glucocorticoids and body fat associated with renal uric acid and oxalate, but not calcium excretion, in healthy children}}}, doi = {{10.1016/j.metabol.2009.06.027}}, year = {{2009}}, } @article{27751, author = {{Buyken, Anette and Günther, Anke LB and Barclay, Alan and Brand-Miller, Jennie and Schulze, Matthias B}}, issn = {{0002-9165}}, journal = {{The American Journal of Clinical Nutrition}}, pages = {{243--244}}, title = {{{Glycemic index in overweight development: distinguishing limited evidence from limits in evidence}}}, doi = {{10.3945/ajcn.2009.27742}}, year = {{2009}}, } @article{36056, author = {{Schlegel-Matthies, Kirsten and Methfessel, Barbara and Quellmalz, Kirsten}}, issn = {{0342-5088}}, journal = {{Haushalt & Bildung}}, number = {{2}}, pages = {{25--27}}, publisher = {{Schneider-Verlag}}, title = {{{Soziale Platzierung: Weder Geld noch Bildung allein entscheiden}}}, volume = {{86}}, year = {{2009}}, } @article{36052, author = {{Schlegel-Matthies, Kirsten and Methfessel, Barbara}}, issn = {{0342-5088}}, journal = {{Haushalt & Bildung}}, number = {{2}}, pages = {{15--20}}, publisher = {{Schneider-Verlag}}, title = {{{Geld – zentraler Schlüssel für gesellschaftliche Teilhabe}}}, volume = {{86}}, year = {{2009}}, } @article{36054, author = {{Schlegel-Matthies, Kirsten and Methfessel, Barbara}}, issn = {{0342-5088}}, journal = {{Haushalt & Bildung}}, number = {{2}}, pages = {{21--24}}, title = {{{Ressourcen – Vielfalt, Zusammenwirken und Lebensqualität}}}, volume = {{86}}, year = {{2009}}, } @article{36044, author = {{Schlegel-Matthies, Kirsten}}, issn = {{0342-5088}}, journal = {{Haushalt & Bildung}}, number = {{2}}, pages = {{2}}, publisher = {{Schneider-Verlag}}, title = {{{Ressourcen – Voraussetzung für Teilhabe- und Gestaltungsmöglichkeiten}}}, volume = {{86}}, year = {{2009}}, } @article{36049, author = {{Schlegel-Matthies, Kirsten and Methfessel, Barbara}}, issn = {{0342-5088}}, journal = {{Haushalt & Bildung}}, number = {{2}}, pages = {{3--4}}, title = {{{Ressourcen im Rahmen des Haushaltshandelns}}}, volume = {{86}}, year = {{2009}}, } @article{54931, abstract = {{Proteinuria and increased renal reabsorption of NaCl characterize the nephrotic syndrome. Here, we show that protein-rich urine from nephrotic rats and from patients with nephrotic syndrome activate the epithelial sodium channel (ENaC) in cultured M-1 mouse collecting duct cells and in Xenopus laevis oocytes heterologously expressing ENaC. The activation depended on urinary serine protease activity. We identified plasmin as a urinary serine protease by matrix-assisted laser desorption/ionization time of-flight mass spectrometry. Purified plasmin activated ENaC currents, and inhibitors of plasmin abolished urinary protease activity and the ability to activate ENaC. In nephrotic syndrome, tubular urokinase-type plasminogen activator likely converts filtered plasminogen to plasmin. Consistent with this, the combined application of urokinase-type plasminogen activator and plasminogen stimulated amiloride-sensitive transepithelial sodium transport in M-1 cells and increased amiloride-sensitive whole-cell currents in Xenopus laevis oocytes heterologously expressing ENaC. Activation of ENaC by plasmin involved cleavage and release of an inhibitory peptide from the ENaC gamma subunit ectodomain. These data suggest that a defective glomerular filtration barrier allows passage of proteolytic enzymes that have the ability to activate ENaC.}}, author = {{Svenningsen, Per and Bistrup, Claus and Friis, Ulla G. and Bertog, Marko and Haerteis, Silke and Krueger, Bettina and Stubbe, Jane and Jensen, Ole Nørregaard and Thiesson, Helle C. and Uhrenholt, Torben R. and Jespersen, Bente and Jensen, Boye L. and Korbmacher, Christoph and Skøtt, Ole}}, journal = {{Journal of the American Society of Nephrology}}, number = {{2}}, pages = {{299–310}}, publisher = {{Ovid Technologies (Wolters Kluwer Health)}}, title = {{{Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel}}}, doi = {{10.1681/asn.2008040364}}, volume = {{20}}, year = {{2009}}, } @article{54932, abstract = {{Incubation of microvascular endothelial cells with combretastatin A-4 phosphate (CA-4P), a microtubule-destabilizing compound that preferentially targets tumor vessels, altered cell morphology and induced scattering of Golgi stacks. Concomitantly, CA-4P up-regulated connective tissue growth factor (CTGF/CCN2), a pleiotropic factor with antiangiogenic properties. In contrast to the effects of other microtubule-targeting agents such as colchicine or nocodazole, up-regulation of CTGF was only detectable in sparse cells, which were not embedded in a cell monolayer. Furthermore, CA-4P induced CTGF expression in endothelial cells, forming tube-like structures on basement membrane gels. Up-regulation of CTGF by CA-4P was dependent on Rho kinase signaling and was increased when p42/44 mitogen-activated protein kinase was inhibited. Additionally, FoxO transcription factors were identified as potent regulators of CTGF expression in endothelial cells. Activation of FoxO transcription factors by inhibition of phosphatidylinositol 3-kinase/AKT signaling resulted in a synergistic increase in CA-4P-mediated CTGF induction. CA-4P-mediated expression of CTGF was thus potentiated by the inhibition of kinase pathways, which are targets of novel antineoplastic drugs. Up-regulation of CTGF by low concentrations of CA-4P may thus occur in newly formed tumor vessels and contribute to the microvessel destabilization and antiangiogenic effects of CA-4P observed in vivo.}}, author = {{Samarin, Jana and Rehm, Margot and Krueger, Bettina and Waschke, Jens and Goppelt-Struebe, Margarete}}, journal = {{Molecular Cancer Research}}, number = {{2}}, pages = {{180–188}}, publisher = {{American Association for Cancer Research (AACR)}}, title = {{{Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing Agent Combretastatin A-4}}}, doi = {{10.1158/1541-7786.mcr-08-0292}}, volume = {{7}}, year = {{2009}}, } @article{54944, abstract = {{The epithelial sodium channel (ENaC) is probably a heterotrimer with three well characterized subunits (alphabetagamma). In humans an additional delta-subunit (delta-hENaC) exists but little is known about its function. Using the Xenopus laevis oocyte expression system, we compared the functional properties of alphabetagamma- and deltabetagamma-hENaC and investigated whether deltabetagamma-hENaC can be proteolytically activated. The amiloride-sensitive ENaC whole-cell current (DeltaI(ami)) was about 11-fold larger in oocytes expressing deltabetagamma-hENaC than in oocytes expressing alphabetagamma-hENaC. The 2-fold larger single-channel Na(+) conductance of deltabetagamma-hENaC cannot explain this difference. Using a chemiluminescence assay, we demonstrated that an increased channel surface expression is also not the cause. Thus, overall channel activity of deltabetagamma-hENaC must be higher than that of alphabetagamma-hENaC. Experiments exploiting the properties of the known betaS520C mutant ENaC confirmed this conclusion. Moreover, chymotrypsin had a reduced stimulatory effect on deltabetagamma-hENaC whole-cell currents compared with its effect on alphabetagamma-hENaC whole-cell currents (2-fold versus 5-fold). This suggests that the cell surface pool of so-called near-silent channels that can be proteolytically activated is smaller for deltabetagamma-hENaC than for alphabetagamma-hENaC. Proteolytic activation of deltabetagamma-hENaC was associated with the appearance of a delta-hENaC cleavage product at the cell surface. Finally, we demonstrated that a short inhibitory 13-mer peptide corresponding to a region of the extracellular loop of human alpha-ENaC inhibited DeltaI(ami) in oocytes expressing alphabetagamma-hENaC but not in those expressing deltabetagamma-hENaC. We conclude that the delta-subunit of ENaC alters proteolytic channel activation and enhances base-line channel activity.}}, author = {{Haerteis, Silke and Krueger, Bettina and Korbmacher, Christoph and Rauh, Robert}}, journal = {{Journal of Biological Chemistry}}, number = {{42}}, pages = {{29024–29040}}, publisher = {{American Society for Biochemistry and Molecular Biology}}, title = {{{The $\delta$-Subunit of the Epithelial Sodium Channel (ENaC) Enhances Channel Activity and Alters Proteolytic ENaC Activation}}}, doi = {{10.1074/jbc.m109.018945}}, volume = {{284}}, year = {{2009}}, } @article{54938, abstract = {{The lipid environment of the epithelial sodium channel (ENaC) and its possible association with so-called lipid rafts may be relevant to its function. The aim of our study was to confirm the association of ENaC with lipid rafts and to analyze the effect of cholesterol depletion of the plasma membrane by methyl-beta-cyclodextrin (MbetaCD) on channel function and regulation. Using sucrose density gradient centrifugation we demonstrated that a significant portion of ENaC protein distributes to low density fractions thought to be typical lipid raft fractions. Importantly, cholesterol depletion of cell lysate by MbetaCD shifted ENaC to non-raft fractions of higher density. Live cell imaging demonstrated that treatment with MbetaCD largely reduced filipin staining over time, confirming cholesterol depletion of the plasma membrane. For electrophysiological studies intact oocytes were exposed to 20 mM MbetaCD for three hours. MbetaCD treatment had no consistent effect on baseline whole-cell ENaC currents. In addition to the typical single channel conductance of about 5 pS, subconductance states of ENaC were occasionally observed in patches from MbetaCD treated but not from control oocytes. Importantly, in outside-out patch clamp recordings the stimulatory effect of recombinant SGK1 in the pipette solution was essentially abolished in oocytes pretreated with MbetaCD. These results indicate that ENaC activation by cytosolic SGK1 is compromised by removing cholesterol from the plasma membrane. Thus, ENaC activation by SGK1 may require the presence of an intact lipid environment and/or of lipid rafts as signalling platform.}}, author = {{Krueger, Bettina and Haerteis, Silke and Yang, Limin and Hartner, Andrea and Rauh, Robert and Korbmacher, Christoph and Diakov, Alexei}}, journal = {{Cellular Physiology and Biochemistry}}, number = {{5-6}}, pages = {{605–618}}, publisher = {{S. Karger AG}}, title = {{{Cholesterol Depletion of the Plasma Membrane Prevents Activation of the Epithelial Sodium Channel (ENaC) by SGK1}}}, doi = {{10.1159/000257516}}, volume = {{24}}, year = {{2009}}, }