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313 results on '"Kullak-Ublick, G."'

1. Roadmap to DILI research in Europe. A proposal from COST action ProEuroDILINet

Author

Instituto de Salud Carlos III, Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Fundação para a Ciência e a Tecnologia (Portugal), Lucena, M. Isabel, Villanueva-Paz, M., Álvarez-Álvarez, I., Aithal, G. P., Björnsson, E. S., Cakan-Akdogan, G., Cubero, Francisco Javier, Esteves, F., Falcón-Pérez, Juan M., Fromenty, B., Garcia-Ruiz, Carmen, Grove, J. I., Konu, O., Kranendonk, M., Kullak-Ublick, G. A., Miranda, Joana, Remesal-Doblado, A., Sancho-Bru, P., Nelson, L., Andrade, Raúl J., Daly, A. K., Fernández-Checa, José C., Instituto de Salud Carlos III, Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Fundação para a Ciência e a Tecnologia (Portugal), Lucena, M. Isabel, Villanueva-Paz, M., Álvarez-Álvarez, I., Aithal, G. P., Björnsson, E. S., Cakan-Akdogan, G., Cubero, Francisco Javier, Esteves, F., Falcón-Pérez, Juan M., Fromenty, B., Garcia-Ruiz, Carmen, Grove, J. I., Konu, O., Kranendonk, M., Kullak-Ublick, G. A., Miranda, Joana, Remesal-Doblado, A., Sancho-Bru, P., Nelson, L., Andrade, Raúl J., Daly, A. K., and Fernández-Checa, José C.

Abstract

In the current article the aims for a constructive way forward in Drug-Induced Liver Injury (DILI) are to highlight the most important priorities in research and clinical science, therefore supporting a more informed, focused, and better funded future for European DILI research. This Roadmap aims to identify key challenges, define a shared vision across all stakeholders for the opportunities to overcome these challenges and propose a high-quality research program to achieve progress on the prediction, prevention, diagnosis and management of this condition and impact on healthcare practice in the field of DILI. This will involve 1. Creation of a database encompassing optimised case report form for prospectively identified DILI cases with well-characterised controls with competing diagnoses, biological samples, and imaging data; 2. Establishing of preclinical models to improve the assessment and prediction of hepatotoxicity in humans to guide future drug safety testing; 3. Emphasis on implementation science and 4. Enhanced collaboration between drug-developers, clinicians and regulatory scientists. This proposed operational framework will advance DILI research and may bring together basic, applied, translational and clinical research in DILI.

Published
2024

2. Roadmap to DILI research in Europe. A proposal from COST action ProEuroDILINet

Author

Lucena, M I, Villanueva-Paz, M, Alvarez-Alvarez, I, Aithal, G P, Björnsson, E S, Cakan-Akdogan, G, Cubero, F J, Esteves, F, Falcon-Perez, J M, Fromenty, B, Garcia-Ruiz, C, Grove, J I, Konu, O, Kranendonk, M, Kullak-Ublick, G A, Miranda, J P, Remesal-Doblado, A, Sancho-Bru, P, Nelson, L, Andrade, R J, Daly, A K, Fernandez-Checa, J C, Lucena, M I, Villanueva-Paz, M, Alvarez-Alvarez, I, Aithal, G P, Björnsson, E S, Cakan-Akdogan, G, Cubero, F J, Esteves, F, Falcon-Perez, J M, Fromenty, B, Garcia-Ruiz, C, Grove, J I, Konu, O, Kranendonk, M, Kullak-Ublick, G A, Miranda, J P, Remesal-Doblado, A, Sancho-Bru, P, Nelson, L, Andrade, R J, Daly, A K, and Fernandez-Checa, J C

Abstract

In the current article the aims for a constructive way forward in Drug-Induced Liver Injury (DILI) are to highlight the most important priorities in research and clinical science, therefore supporting a more informed, focused, and better funded future for European DILI research. This Roadmap aims to identify key challenges, define a shared vision across all stakeholders for the opportunities to overcome these challenges and propose a high-quality research program to achieve progress on the prediction, prevention, diagnosis and management of this condition and impact on healthcare practice in the field of DILI. This will involve 1. Creation of a database encompassing optimised case report form for prospectively identified DILI cases with well-characterised controls with competing diagnoses, biological samples, and imaging data; 2. Establishing of preclinical models to improve the assessment and prediction of hepatotoxicity in humans to guide future drug safety testing; 3. Emphasis on implementation science and 4. Enhanced collaboration between drug-developers, clinicians and regulatory scientists. This proposed operational framework will advance DILI research and may bring together basic, applied, translational and clinical research in DILI.

Published
2023

15. The impact of the rs8005161 polymorphism on G protein-coupled receptor GPR65 (TDAG8) pH-associated activation in intestinal inflammation

Author

Tcymbarevich I, Eloranta J, Spalinger M, Cosin-Roger J, Lang S, Kullak-Ublick G, Wagner C, Seuwen K, Ruiz P, de Valliere C, Abdelrahman K, Ademi G, Aepli P, Thomas A, Anderegg C, Antonino A, Archanioti E, Arrigoni E, de Jong D, Balsiger B, Basturk P, Bauerfeind P, Becocci A, Belli D, Bengoa J, Biedermann L, Binek J, Blattmann M, Boehm S, Boldanova T, Borovicka J, Braegger C, Brand S, Brugger L, Brunner S, Buhr P, Burnand B, Burk S, Burri E, Buyse S, Cao D, Carstens O, Criblez D, Cunningham S, D'Angelo F, de Saussure P, Degen L, Delarive J, Doerig C, Dora B, Drerup S, Egger M, El-Wafa A, Engelmann M, Ezri J, Felley C, Fliegner M, Fournier N, Fraga M, Franc Y, Frei P, Frei R, Fried M, Froehlich F, Furlano R, Garzoni L, Geyer M, Girard L, Girardin M, Golay D, Good I, Bigler U, Gysi B, Haarer J, Halama M, Haldemann J, Heer P, Heimgartner B, Helbling B, Hengstler P, Herzog D, Hess C, Hessler R, Heyland K, Hinterleitner T, Hirschi C, Hruz P, Juillerat P, Khalid-de Bakker C, Kayser S, Keller C, Knellwolf-Grieger C, Knoblauch C, Kohler H, Koller R, Krieger-Grubel C, Kunzler P, Kusche R, Lehmann F, Macpherson A, Maillard M, Manz M, Marot A, Meier R, Meyenberger C, Meyer P, Michetti P, Misselwitz B, Mosler P, Mottet C, Muller C, Mullhaupt B, Musso L, Neagu M, Nichita C, Niess J, Nydegger A, Obialo N, Ollo D, Oropesa C, Peter U, Peternac D, Petit L, Pittet V, Pohl D, Porzner M, Preissler C, Raschle N, Rentsch R, Restellini A, Restellini S, Richterich J, Ris F, Risti B, Ritz M, Rogler G, Rohrich N, Rossel J, Rueger V, Rusticeanu M, Sagmeister M, Saner G, Sauter B, Sawatzki M, Scharl M, Schelling M, Schibli S, Schlauri H, Schluckebier D, Schmid D, Schmid-Uebelhart S, Schnegg J, Schoepfer A, Seematter V, Seibold F, Seirafi M, Semadeni G, Senning A, Sokollik C, Sommer J, Spalinger J, Spangenberger H, Stadler P, Staub P, Staudenmann D, Stenz V, Steuerwald M, Straumann A, Strebel B, Stulz A, Sulz M, Tatu A, Tempia-Caliera M, Thorens J, Truninger K, Tutuian R, Urfer P, Vavricka S, Viani F, Vogtlin J, Von Kanel R, Vouillamoz D, Vulliamy R, Wiesel P, Wiest R, Wohrle S, Zamora S, Zander S, Wylie T, Zeitz J, Zimmermann D, and Swiss IBD Cohort Study Grp

Subjects
UC, pH-sensing, cAMP, IBD, Acidic pH, RhoA, Inflammatory bowel diseases, CD
Abstract

BackgroundTissue inflammation in inflammatory bowel diseases (IBD) is associated with a decrease in local pH. The gene encoding G-protein-coupled receptor 65 (GPR65) has recently been reported to be a genetic risk factor for IBD. In response to extracellular acidification, proton activation of GPR65 stimulates cAMP and Rho signalling pathways. We aimed to analyse the clinical and functional relevance of the GPR65 associated single nucleotide polymorphism (SNP) rs8005161.Methods1138 individuals from a mixed cohort of IBD patients and healthy volunteers were genotyped for SNPs associated with GPR65 (rs8005161, rs3742704) and galactosylceramidase (rs1805078) by Taqman SNP assays. 2300 patients from the Swiss IBD Cohort Study (SIBDC) were genotyped for rs8005161 by mass spectrometry based SNP genotyping. IBD patients from the SIBDC carrying rs8005161 TT, CT, CC and non-IBD controls (CC) were recruited for functional studies. Human CD14+ cells were isolated from blood samples and subjected to an extracellular acidic pH shift, cAMP accumulation and RhoA activation were measured.ResultsIn our mixed cohort, but not in SIBDC patients, the minor variant rs8005161 was significantly associated with UC. In SIBDC patients, we observed a consistent trend in increased disease severity in patients carrying the rs8005161-TT and rs8005161-CT alleles. No significant differences were observed in the pH associated activation of cAMP production between IBD (TT, CT, WT/CC) and non-IBD (WT/CC) genotype carriers upon an acidic extracellular pH shift. However, we observed significantly impaired RhoA activation after an extracellular acidic pH shift in IBD patients, irrespective of the rs8005161 allele.ConclusionsThe T allele of rs8005161 might confer a more severe disease course in IBD patients. Human monocytes from IBD patients showed impaired pH associated RhoA activation upon an acidic pH shift.

Published
2019

23. Arzneimittelsicherheit

Author

Siepmann, T, Kirch, W, Kullak-Ublick, G A, Siepmann, T ( T ), Kirch, W ( W ), Kullak-Ublick, G A ( G A ), Russmann, S, Weiler, S, Stoller, R, Egbring, M, Siepmann, T, Kirch, W, Kullak-Ublick, G A, Siepmann, T ( T ), Kirch, W ( W ), Kullak-Ublick, G A ( G A ), Russmann, S, Weiler, S, Stoller, R, and Egbring, M

Published
2016

24. Pharmakovigilanz

Author

Kullak-Ublick, G A, Siepmann, T, Kirch, Wilhelm, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( Wilhelm ), Weiler, Stefan, Russmann, Stefan, Stoller, Rudolf, Kullak-Ublick, G A, Siepmann, T, Kirch, Wilhelm, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( Wilhelm ), Weiler, Stefan, Russmann, Stefan, and Stoller, Rudolf

Published
2016

25. Unerwünschte Arzneimittelwirkungen (UAW)

Author

Kullak-Ublick, G A, Siepmann, T, Kirch, Wilhelm, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( Wilhelm ), Weiler, Stefan, Stoller, Rudolf, Russmann, Stefan, Kullak-Ublick, G A, Siepmann, T, Kirch, Wilhelm, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( Wilhelm ), Weiler, Stefan, Stoller, Rudolf, and Russmann, Stefan

Published
2016

29. Arzneimittelsicherheit

Author

Russmann, S, Kullak-Ublick, G A, Weiler, S, Stoller, R, Egbring, M, University of Zurich, Siepmann, T, Kirch, W, and Kullak-Ublick, G A

Subjects
10199 Clinic for Clinical Pharmacology and Toxicology, 610 Medicine & health
Published
2016

30. Thiopurine S -methyltransferase polymorphisms: efficient screening method for patients considering taking thiopurine drugs

Author

Wusk, Barbara, Kullak-Ublick, G., Rammert, C., von Eckardstein, A., Fried, M., Rentsch, K., Wusk, Barbara, Kullak-Ublick, G., Rammert, C., von Eckardstein, A., Fried, M., and Rentsch, K.

Abstract

Objective: More than 11% of the Caucasian population are heterozygous or homozygous carriers of thiopurine S-methyltransferase (TPMT) mutants and are at risk for toxic side effects when treated with thiopurine drugs. Therefore, screening for TPMT polymorphisms in a patient prior to prescribing these agents is recommended. The goal of this study was to determine a cut-off concentration of the TPMT activity assay beyond which genotyping of the TPMT gene should be performed. Methods: The TPMT activity of 240 unrelated Caucasian subjects was measured using high-performance liquid chromatography. Genotyping for the most frequent allelic variants, TPMT*2, *3A, *3B, *3C and *7 was performed by LightCycler technology and sequencing. Results: The inter-individual TPMT activity showed a range from 23nmol MTG/g*Hb*h−1 to 97nmol MTG/g*Hb*h−1 with a median of 56nmol MTG/g*Hb*h−1. Using a cut-off concentration of 45.5nmol MTG/g*Hb*h−1, a test sensitivity of 100% and a specificity of 89% were reached for heterozygous carriers of a TPMT mutation. We identified 1 carrier of TPMT*2, 14 carriers of TPMT*3A and 3 carriers of TPMT*3C, resulting in a TPMT heterozygosity prevalence of 7.5%. Conclusions: This study defines the cut-off value for the TPMT phenotyping assay at 45.5nmol/g*Hb*h−1, beyond which additional genotyping elucidates the individual risk for drug therapy. Using this cut-off concentration, the number of genotyping assays could be reduced by about 60%

Published
2018

33. P2494Deleterious role of endothelial lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in ischemia/reperfusion-induced cerebral injury

Author

Akhmedov, A, primary, Bonetti, N R, additional, Reiner, M F, additional, Spescha, R D, additional, Merlini, M, additional, Gaul, D S, additional, Diaz-Canestro, C, additional, Savarese, G, additional, Montecucco, F, additional, Matter, C M, additional, Kullak-Ublick, G A, additional, Luscher, T F, additional, Beer, J H, additional, Liberale, L, additional, and Camici, G, additional

Published
2018
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35. Update Diuretika

Author

Dahmke, H, Kullak-Ublick, G A, and University of Zurich

Subjects
10199 Clinic for Clinical Pharmacology and Toxicology, 610 Medicine & health
Published
2016

37. Hypoxia Positively Regulates the Expression of pH-Sensing G-Protein-Coupled Receptor OGR1 (GPR68)

Author

de Valliere C, Cosin-Roger J, Simmen S, Atrott K, Melhem H, Zeitz J, Madanchi M, Tcymbarevich I, Fried M, Kullak-Ublick G, Vavricka S, Misselwitz B, Seuwen K, Wagner C, Eloranta J, Rogler G, and Rui P

Subjects
Inflammation, TDAG8, Inflammatory Bowel Disease, GRP65, Ovarian Cancer G-Protein-Coupled Receptor
Abstract

BACKGROUND & AIMS: A novel family of proton-sensing G-protein-coupled receptors, including ovarian cancer G-protein-coupled receptor 1 (OGR1) (GPR68) has been identified to play a role in pH homeostasis. Hypoxia is known to change tissue pH as a result of anaerobic glucose metabolism through the stabilization of hypoxia-inducible factor-1 alpha. We investigated how hypoxia regulates the expression of OGR1 in the intestinal mucosa and associated cells. METHODS: OGR1 expression in murine tumors, human colonic tissue, and myeloid cells was determined by quantitative reverse-transcription polymerase chain reaction. The influence of hypoxia on OGR1 expression was studied in monocytes/macrophages and intestinal mucosa of inflammatory bowel disease (IBD) patients. Changes in OGR1 expression in MonoMac6 (MM6) cells under hypoxia were determined upon stimulation with tumor necrosis factor (TNF), in the presence or absence of nuclear factor-kappa B (NF-kappa B) inhibitors. To study the molecular mechanisms involved, chromatin immunoprecipitation analysis of the OGR1 promoter was performed. RESULTS: OGR1 expression was significantly higher in tumor tissue compared with normal murine colon tissue. Hypoxia positively regulated the expression of OGR1 in MM6 cells, mouse peritoneal macrophages, primary human intestinal macrophages, and colonic tissue from IBD patients. In MM6 cells, hypoxia-enhanced TNF-induced OGR1 expression was reversed by inhibition of NF-kappa B. In addition to the effect of TNF and hypoxia, OGR1 expression was increased further at low pH. Chromatin immunoprecipitation analysis showed that HIF-1 alpha, but not NF-kappa B, binds to the promoter of OGR1 under hypoxia. CONCLUSIONS: The enhancement of TNF- and hypoxia-induced OGR1 expression under low pH points to a positive feed-forward regulation of OGR1 activity in acidic conditions, and supports a role for OGR1 in the pathogenesis of IBD.

Published
2016

38. Pharmakoepidemiologie

Author

Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), Russmann, S, Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), and Russmann, S

Published
2012

39. Clinical decision support systems

Author

Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), Egbring, M, Russmann, S, Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), Egbring, M, and Russmann, S

Published
2012

40. Arzneimittelsicherheit in klinischen Studien

Author

Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), Russmann, S, Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), and Russmann, S

Published
2012

41. Schmerztherapie und Lokalanästhetika

Author

Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), Curkovic, I, Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), and Curkovic, I

Published
2012

42. Intensivmedizinische Arzneitherapie

Author

Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), Corti, N, Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), and Corti, N

Published
2012

43. Arzneimittelsicherheit

Author

Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), Russmann, S, Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), and Russmann, S

Published
2012

44. Arzneitherapie gastrointestinaler Erkrankungen

Author

Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), Müller, E A, Krattinger, R, Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), Müller, E A, and Krattinger, R

Published
2012

45. Unerwünschte Arzneimittelwirkungen

Author

Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), Sift Carter, R, Stoller, R, Russmann, S, Kullak-Ublick, G A, Siepmann, T, Kirch, W, Kullak-Ublick, G A ( G A ), Siepmann, T ( T ), Kirch, W ( W ), Sift Carter, R, Stoller, R, and Russmann, S

Published
2012

48. Arzneimittelsicherheit

Author

Russmann, S, Kullak-Ublick, G A, University of Zurich, Kullak-Ublick, G A, Siepmann, T, and Kirch, W

Subjects
10199 Clinic for Clinical Pharmacology and Toxicology, 610 Medicine & health
Published
2012

49. Schmerztherapie und Lokalanästhetika

Author

Curkovic, I, Kullak-Ublick, G A, University of Zurich, Kullak-Ublick, G A, Siepmann, T, and Kirch, W

Subjects
10199 Clinic for Clinical Pharmacology and Toxicology, 610 Medicine & health
Published
2012

50. Clinical decision support systems

Author

Egbring, M, Russmann, S, Kullak-Ublick, G A, University of Zurich, Kullak-Ublick, G A, Siepmann, T, Kirch, W, and Russmann, S

Subjects
3004 Pharmacology, 10199 Clinic for Clinical Pharmacology and Toxicology, 2736 Pharmacology (medical), 610 Medicine & health
Published
2012

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