Reichardt, Sybille D.

[["dc.bibliographiccitation.firstpage","2921"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.affiliation","Reichardt, Sybille D.; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.affiliation","Amouret, Agathe; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.affiliation","Muzzi, Chiara; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.affiliation","Vettorazzi, Sabine; 2Institute of Comparative Molecular Endocrinology, Ulm University, 89081 Ulm, Germany; sabine.vettorazzi@uni-ulm.de (S.V.); jan.tuckermann@uni-ulm.de (J.P.T.)"],["dc.contributor.affiliation","Tuckermann, Jan P.; 2Institute of Comparative Molecular Endocrinology, Ulm University, 89081 Ulm, Germany; sabine.vettorazzi@uni-ulm.de (S.V.); jan.tuckermann@uni-ulm.de (J.P.T.)"],["dc.contributor.affiliation","Lühder, Fred; 3Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, 37075 Göttingen, Germany; fred.luehder@med.uni-goettingen.de"],["dc.contributor.affiliation","Reichardt, Holger M.; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Amouret, Agathe"],["dc.contributor.author","Muzzi, Chiara"],["dc.contributor.author","Vettorazzi, Sabine"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2022-01-11T14:07:51Z"],["dc.date.available","2022-01-11T14:07:51Z"],["dc.date.issued","2021"],["dc.date.updated","2022-02-09T13:20:27Z"],["dc.description.abstract","For more than 70 years, glucocorticoids (GCs) have been a powerful and affordable treatment option for inflammatory diseases. However, their benefits do not come without a cost, since GCs also cause side effects. Therefore, strong efforts are being made to improve their therapeutic index. In this review, we illustrate the mechanisms and target cells of GCs in the pathogenesis and treatment of some of the most frequent inflammatory disorders affecting the central nervous system, the gastrointestinal tract, the lung, and the joints, as well as graft-versus-host disease, which often develops after hematopoietic stem cell transplantation. In addition, an overview is provided of novel approaches aimed at improving GC therapy based on chemical modifications or GC delivery using nanoformulations. GCs remain a topic of highly active scientific research despite being one of the oldest class of drugs in medical use."],["dc.description.abstract","For more than 70 years, glucocorticoids (GCs) have been a powerful and affordable treatment option for inflammatory diseases. However, their benefits do not come without a cost, since GCs also cause side effects. Therefore, strong efforts are being made to improve their therapeutic index. In this review, we illustrate the mechanisms and target cells of GCs in the pathogenesis and treatment of some of the most frequent inflammatory disorders affecting the central nervous system, the gastrointestinal tract, the lung, and the joints, as well as graft-versus-host disease, which often develops after hematopoietic stem cell transplantation. In addition, an overview is provided of novel approaches aimed at improving GC therapy based on chemical modifications or GC delivery using nanoformulations. GCs remain a topic of highly active scientific research despite being one of the oldest class of drugs in medical use."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/cells10112921"],["dc.identifier.eissn","2073-4409"],["dc.identifier.pii","cells10112921"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97878"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","2073-4409"],["dc.relation.orgunit","Institut für Zelluläre und Molekulare Immunologie"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","The Role of Glucocorticoids in Inflammatory Diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","174"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroendocrinology"],["dc.bibliographiccitation.lastpage","182"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Schweingruber, Nils"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T09:15:58Z"],["dc.date.available","2018-11-07T09:15:58Z"],["dc.date.issued","2012"],["dc.description.abstract","Glucocorticoids (GCs) are widely used to treat inflammatory diseases such as multiple sclerosis (MS). They predominantly act through the GC receptor, a member of the nuclear receptor superfamily that controls transcription by several different mechanisms. Owing to its ubiquitous expression, there are a variety of cell types that could serve as GC targets in the pathogenesis and treatment of MS. This brings about a great diversity of mechanisms potentially involved in the modulation of neuroinflammation by GCs, including the induction of apoptosis, repression of pro-inflammatory mediators and the expansion of myeloid-derived suppressor cells. Nevertheless, it is not well understood which of these mechanisms are essential for therapeutic efficacy. In this review, we summarise findings made concerning the actions of GCs in MS and its animal model experimental autoimmune encephalomyelitis, and also elucidate current concepts and developments that pertain to this clinically highly relevant treatment regimen."],["dc.identifier.doi","10.1111/j.1365-2826.2011.02161.x"],["dc.identifier.isi","000298601800016"],["dc.identifier.pmid","21615563"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27832"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0953-8194"],["dc.title","Mechanisms of Glucocorticoids in the Control of Neuroinflammation"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0190846"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Meers, Garrit K."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Reichardt, Sybille D."],["dc.date.accessioned","2019-07-09T11:45:08Z"],["dc.date.available","2019-07-09T11:45:08Z"],["dc.date.issued","2018"],["dc.description.abstract","Inflammatory bowel disease (IBD) is a highly prevalent intestinal disorder for which no cure exists. Currently, the standard first-line treatment of IBD consists of systemic glucocorticoid (GC) application, even though therapy can be complicated by unresponsiveness or adverse effects. In view of the importance of macrophages and neutrophils for the pathogenesis of IBD we set out to define the relevance of these cell types as targets of GC using the mouse model of DSS-induced colitis. We found that the disease did not resolve in GRlysM mice lacking the GC receptor (GR) in myeloid cells after removal of the chemical insult. While clinical symptoms and tissue damage in the colon ameliorated again in GRflox mice, the disease further aggravated in GRlysM littermates. The observed difference coincided with an increased abundance of macrophages in inflammatory infiltrates in the colon of mutant mice whereas neutrophil and T cell numbers were similar. Concomitantly, systemic IL-6 secretion and mRNA levels of pro-inflammatory cytokines in the colon were elevated in GRlysM mice and gene expression of scavenger receptors and IL-10 was diminished. Taken together, our results reveal an important role of myeloid cells as targets of GC in DSS-induced colitis and probably in IBD in humans as well."],["dc.identifier.doi","10.1371/journal.pone.0190846"],["dc.identifier.pmid","29324769"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59164"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Colitis"],["dc.subject.mesh","Colon"],["dc.subject.mesh","Dextran Sulfate"],["dc.subject.mesh","Disease Models, Animal"],["dc.subject.mesh","Interleukin-10"],["dc.subject.mesh","Interleukin-6"],["dc.subject.mesh","Intestinal Mucosa"],["dc.subject.mesh","Mice, Inbred C57BL"],["dc.subject.mesh","Mice, Transgenic"],["dc.subject.mesh","Myeloid Cells"],["dc.subject.mesh","RNA, Messenger"],["dc.subject.mesh","Receptors, Glucocorticoid"],["dc.title","Impaired resolution of DSS-induced colitis in mice lacking the glucocorticoid receptor in myeloid cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","646"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","655"],["dc.bibliographiccitation.volume","235"],["dc.contributor.author","Theiss-Suennemann, Jennifer"],["dc.contributor.author","Joerss, Katharina"],["dc.contributor.author","Messmann, Joanna J."],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Montes-Cobos, Elena"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Groene, Hermann-Josef"],["dc.contributor.author","Strauss, Gudrun"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T10:00:41Z"],["dc.date.available","2018-11-07T10:00:41Z"],["dc.date.issued","2015"],["dc.description.abstract","Glucocorticoids (GCs) are released from the adrenal gland during inflammation and help to keep immune responses at bay. Owing to their potent anti-inflammatory activity, GCs also play a key role in controlling acute graft-versus-host disease (aGvHD). Here we demonstrate that mice lacking the glucocorticoid receptor (GR) in T cells develop fulminant disease after allogeneic bone marrow transplantation. In a fully MHC-mismatched model, transfer of GR-deficient T cells resulted in severe aGvHD symptoms and strongly decreased survival times. Histopathological features were aggravated and infiltration of CD8(+) T cells into the jejunum was increased when the GR was not expressed. Furthermore, serum levels of IL-2, IFN, and IL-17 were elevated and the cytotoxicity of CD8(+) T cells was enhanced after transfer of GR-deficient T cells. Short-term treatment with dexamethasone reduced cytokine secretion but neither impacted disease severity nor the CTLs' cytolytic capacity. Importantly, in an aGvHD model in which disease development exclusively depends on the presence of CD8(+) T cells in the transplant, transfer of GR-deficient T cells aggravated clinical symptoms and reduced survival times as well. Taken together, our findings highlight that suppression of CD8(+) T-cell function is a crucial mechanism in the control of aGvHD by endogenous GCs. Copyright (c) 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/path.4475"],["dc.identifier.isi","000349677700011"],["dc.identifier.pmid","25358639"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37861"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1096-9896"],["dc.relation.issn","0022-3417"],["dc.title","Glucocorticoids attenuate acute graft-versus-host disease by suppressing the cytotoxic capacity of CD8(+) T cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","105485"],["dc.bibliographiccitation.journal","The Journal of Steroid Biochemistry and Molecular Biology"],["dc.bibliographiccitation.volume","195"],["dc.contributor.author","Li, Hu"],["dc.contributor.author","Kaiser, Tina K."],["dc.contributor.author","Borschiwer, Marina"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Meijsing, Sebastiaan H."],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2020-12-10T14:25:26Z"],["dc.date.available","2020-12-10T14:25:26Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.jsbmb.2019.105485"],["dc.identifier.issn","0960-0760"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72552"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Glucocorticoid resistance of allogeneic T cells alters the gene expression profile in the inflamed small intestine of mice suffering from acute graft-versus-host disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4509"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","4516"],["dc.bibliographiccitation.volume","187"],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Theiss, Jennifer"],["dc.contributor.author","Karabinskaya, Anna"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Karow, Ulrike"],["dc.contributor.author","Herold, Marco J."],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Utermoehlen, Olaf"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T08:50:13Z"],["dc.date.available","2018-11-07T08:50:13Z"],["dc.date.issued","2011"],["dc.description.abstract","The activity of acid sphingomyelinase (aSMase) was previously reported to be involved in glucocorticoid-induced cell death (GICD) of T lymphocytes. This mechanism in turn is believed to contribute to the therapeutic efficacy of glucocorticoids (GCs) in the treatment of inflammatory diseases. In this study, we reassessed the role of aSMase in GICD by using aSMase knockout mice. The absence of aSMase largely abolished the partial protection that effector memory CD4(+) T cells in wild-type mice possess against GICD. Reduced IL-2 secretion by aSMase-deficient CD4(+) T cells suggested that a lack of this important survival factor might be the cause of these cells' enhanced susceptibility to GICD. Indeed, addition of IL-2 restored the protection against GICD, whereas neutralization of IL-2 abrogated the otherwise protective effect seen in wild-type effector memory CD4(+) T cells. The therapeutic implications of the altered sensitivity of aSMase-deficient T cells to GICD were assessed in models of inflammatory disorders; namely, experimental autoimmune encephalomyelitis and acute graft-versus-host disease. Surprisingly, GC treatment was equally efficient in both models in terms of ameliorating the diseases, regardless of the genotype of the T cells. Thus, our data reveal a hitherto unrecognized contribution of aSMase to the sensitivity of effector memory CD4(+) T cells to GICD and call into question the traditionally attributed importance of GICD of T cells to the treatment of inflammatory diseases by GCs. The Journal of Immunology, 2011, 187: 4509-4516."],["dc.identifier.doi","10.4049/jimmunol.1100911"],["dc.identifier.isi","000296496000017"],["dc.identifier.pmid","21948986"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21648"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Immunologists"],["dc.relation.issn","0022-1767"],["dc.title","Acid Sphingomyelinase Is Required for Protection of Effector Memory T Cells against Glucocorticoid-Induced Cell Death"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","157"],["dc.bibliographiccitation.journal","Journal of Controlled Release"],["dc.bibliographiccitation.lastpage","169"],["dc.bibliographiccitation.volume","245"],["dc.contributor.author","Montes-Cobos, Elena"],["dc.contributor.author","Ring, Sarah"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Heck, Joachim G."],["dc.contributor.author","Strauss, Judith"],["dc.contributor.author","Schwaninger, Markus"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Feldmann, Claus"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T10:28:25Z"],["dc.date.available","2018-11-07T10:28:25Z"],["dc.date.issued","2017"],["dc.description.abstract","Glucocorticoids (GC) are widely used to treat acute relapses in multiple sclerosis (MS) patients, but their application is accompanied by side effects due to their broad spectrum of action. Here, we report on the therapeutic option to apply GC via inorganic-organic hybrid nanoparticles (IOH-NP) with the composition [ZrO](2+)[(BMP)(0.9)(FMN)(0.1)](2-) (designated BMP-NP with BMP: betamethasone phosphate; FMN: flavinmononucleotide). We found that these BMP-NP have an increased cell type-specificity compared to free GC while retaining full therapeutic efficacy in a mouse model of MS. BMP-NP were preferentially taken up by phagocytic cells and modulated macrophages in vivo more efficiently than T cells. When GC were applied in the form of BMP-NP, treatment of neuroinflammatory disease in mice exclusively depended on the control of macrophage function whereas effects on T cells and brain endothelial cells were dispensable for therapeutic efficacy. Importantly, BMP-NP were not only active in mice but also showed strong activity towards monocytes isolated from healthy human volunteers. We conclude that application of GC via IOH-NP has the potential to improve MS therapy in the future. (C) 2016 Elsevier B.V. All rights reserved."],["dc.description.sponsorship","German Research Foundation (DFG) [RE 1631/15-1, LU 634/9-1]"],["dc.identifier.doi","10.1016/j.jconrel.2016.12.003"],["dc.identifier.isi","000396474500015"],["dc.identifier.pmid","27919626"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43416"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1873-4995"],["dc.relation.issn","0168-3659"],["dc.title","Targeted delivery of glucocorticoids to macrophages in a mouse model of multiple sclerosis using inorganic-organic hybrid nanoparticles"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","68"],["dc.bibliographiccitation.journal","Immunology Letters"],["dc.bibliographiccitation.lastpage","79"],["dc.bibliographiccitation.volume","233"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Wiegers, G. Jan"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2021-06-01T09:41:20Z"],["dc.date.available","2021-06-01T09:41:20Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.imlet.2021.03.010"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84889"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","0165-2478"],["dc.title","A flow cytometric approach to study glucocorticoid receptor expression in immune cell subpopulations of genetically engineered mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3899"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Endocrinology"],["dc.bibliographiccitation.lastpage","3908"],["dc.bibliographiccitation.volume","155"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Weinhage, Toni"],["dc.contributor.author","Rotte, Anand"],["dc.contributor.author","Foeller, Michael"],["dc.contributor.author","Oppermann, Martin"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Lang, Florian"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T09:34:44Z"],["dc.date.available","2018-11-07T09:34:44Z"],["dc.date.issued","2014"],["dc.description.abstract","Glucocorticoids (GCs) constitute a highly pleiotropic class of drugs predominantly employed in the treatment of inflammatory diseases. In our search for new mechanisms of action, we identified a hitherto unknown effect of GCs in the gastrointestinal tract. We found that oral administration of dexamethasone (Dex) to mice caused an enlargement of the stomach due to the induction of gastroparesis and that this effect was abolished in GR(dim) mice carrying the A458T mutation in the GC receptor (GR). Gastroparesis was unrelated to the enhanced gastric acid secretion observed after Dex treatment, although both effects were mediated by the same molecular mechanism of the GR. Using conditional GR-knockout mice, we could further rule out that GC effects on enterocytes or myeloid cells were involved in the induction of gastroparesis. In contrast, we found that Dex upregulated arginase 2 (Arg2) in the stomach both at the mRNA and protein level. This suggests that GC treatment leads to a depletion of L-arginine thereby impeding the production of nitric oxide (NO), which is required for gastric motility. We tested this hypothesis by supplementing the drinking water of the mice with exogenous L-arginine to compensate for the presumed shortage of this major substrate of NO synthases. Importantly, this measure completely prevented both the enlargement of the stomach and the induction of gastroparesis after Dex treatment. Our findings raise considerations of combining orally applied GCs with L-arginine to improve tolerability of GC treatment and provide a possible explanation for the antiemetic effects of GCs widely exploited in chemotherapy."],["dc.identifier.doi","10.1210/en.2014-1246"],["dc.identifier.isi","000342345000018"],["dc.identifier.pmid","25057793"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32240"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Endocrine Soc"],["dc.relation.issn","1945-7170"],["dc.relation.issn","0013-7227"],["dc.title","Glucocorticoids Induce Gastroparesis in Mice Through Depletion of L-Arginine"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]