Siggelkow, Heide

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","JBMR Plus"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Wilde, Deborah"],["dc.contributor.author","Wilken, Lara"],["dc.contributor.author","Stamm, Bettina"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Heppner, Christina"],["dc.contributor.author","Chavanon, Mira‐Lynn"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Herrmann‐Lingen, Christoph"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2021-06-01T10:50:47Z"],["dc.date.available","2021-06-01T10:50:47Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/jbm4.10245"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17136"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86788"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2473-4039"],["dc.relation.issn","2473-4039"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The HPQ—Development and First Administration of a Questionnaire for Hypoparathyroid Patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","331"],["dc.bibliographiccitation.issue","5-6"],["dc.bibliographiccitation.journal","Journal of Molecular Histology"],["dc.bibliographiccitation.lastpage","341"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Tezval, Mohammad"],["dc.contributor.author","Tezval, Hossein"],["dc.contributor.author","Dresing, Klaus"],["dc.contributor.author","Stuermer, Ewa Klara"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Stuermer, Klaus Michael"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2018-11-07T11:23:52Z"],["dc.date.available","2018-11-07T11:23:52Z"],["dc.date.issued","2009"],["dc.description.abstract","Urocortin-1 (UCN) a corticotropin releasing-factor (CRF) related peptide, has been found to be expressed in many different tissues like the central nervous system, the cardiovascular system, adipose tissue, and skeletal muscle. The effects of UCN are mediated via stimulation of CRF-receptors 1 and 2 (CRFR1 and 2, CRFR's) with a high affinity for CRFR2. It has been shown that the CRF-related peptides and CRFR's are involved in the regulation of stress-related endocrine, autonomic and behavioural responses. Using immunocytochemistry, immunohistochemistry and RT-PCR, we now can show the differentiation dependent expression of UCN mRNA and peptide in human mesenchymal progenitor cells (MSCs) directed to the osteoblastic phenotype for the first time. UCN expression was down regulated by TGF-beta and BMP-2 in the early proliferation phase of osteoblast development, whereas dexamethasone (dex) minimally induced UCN gene expression during matrix maturation after 24 h stimulation. Stimulation of MSCs for 28 days with ascorbate/beta-glycerophosphate (asc/bGp) induced UCN gene expression at day 14. This effect was prevented when using 1,25-vitamin D3 or dex in addition. There was no obvious correlation to osteocalcin (OCN) gene expression in these experiments. In MSCs from patients with metabolic bone disease (n = 9) UCN gene expression was significantly higher compared to MSCs from normal controls (n = 6). Human MSCs did not express any of the CRFR's during differentiation to osteoblasts. Our results indicate that UCN is produced during the development of MSCs to osteoblasts and differentially regulated during culture as well as by differentiation factors. The expression is maximal between proliferation and matrix maturation phase. However, UCN does not seem to act on the osteoblast itself as shown by the missing CRFR's. Our results suggest new perspectives on the role of urocortin in human skeletal tissue in health and disease."],["dc.identifier.doi","10.1007/s10735-009-9244-z"],["dc.identifier.isi","000275443300002"],["dc.identifier.pmid","19949969"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4160"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56279"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1567-2379"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Differentiation dependent expression of urocortin's mRNA and peptide in human osteoprogenitor cells: influence of BMP-2, TGF-beta-1 and dexamethasone"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Riemann, Annika; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, 37075 Göttingen, Germany; annika.riemann@stud.uni-goettingen.de (A.R.); martina.blaschke@medizin.uni-goettingen.de (M.B.); heide.siggelkow@amedes-group.com (H.S.)"],["dc.contributor.affiliation","Blaschke, Martina; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, 37075 Göttingen, Germany; annika.riemann@stud.uni-goettingen.de (A.R.); martina.blaschke@medizin.uni-goettingen.de (M.B.); heide.siggelkow@amedes-group.com (H.S.)"],["dc.contributor.affiliation","Jauho-Ghadimi, Annukka; 2MVZ Endokrinologikum Göttingen, 37075 Göttingen, Germany; mari.jauho-ghadimi@amedes-group.com"],["dc.contributor.affiliation","Siggelkow, Heide; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, 37075 Göttingen, Germany; annika.riemann@stud.uni-goettingen.de (A.R.); martina.blaschke@medizin.uni-goettingen.de (M.B.); heide.siggelkow@amedes-group.com (H.S.)"],["dc.contributor.affiliation","Gollisch, Katja Susanne Claudia; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, 37075 Göttingen, Germany; annika.riemann@stud.uni-goettingen.de (A.R.); martina.blaschke@medizin.uni-goettingen.de (M.B.); heide.siggelkow@amedes-group.com (H.S.)"],["dc.contributor.author","Riemann, Annika"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Jauho-Ghadimi, Annukka"],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Gollisch, Katja Susanne Claudia"],["dc.date.accessioned","2022-08-03T14:32:55Z"],["dc.date.available","2022-08-03T14:32:55Z"],["dc.date.issued","2022-07-24"],["dc.date.updated","2022-08-03T13:41:59Z"],["dc.description.abstract","Non-alcoholic fatty liver disease (NAFLD) is a common yet little recognized health problem in women with polycystic ovary syndrome (PCOS). In a retrospective setting, we investigated the effects of metformin treatment on the hepatic steatosis index (HSI) as a readily available biomarker panel for NAFLD. HSI values of >36 are considered to be highly suggestive for NAFLD. In our cohort, HSI values indicating NAFLD were found in 60/81 (74.1%) women at baseline. The mean HSI improved significantly after the metformin treatment from 43.2 ± 1.0 to 41.0 ± 1.1. Subgroup analyses of non-obese (body mass index (BMI) < 30 kg/m2), obese (BMI 30–35 kg/m2) and very obese (BMI > 35 kg/m2) women yielded mean baseline HSI values of 35.5 ± 4.5, 41.2 ± 2.7 and 51.2 ± 4.7, respectively. A significant improvement in the HSI of 1.5 ± 2.1 was observed after metformin treatment in non-obese women but not in the obese subgroups. The data suggest a new aspect of metformin treatment in non-obese PCOS patients, namely, a possible improvement in NAFLD. This study highlighted hepatic steatosis as a common comorbidity in PCOS patients that can severely affect their long-term health, and therefore, deserves more attention in the management of PCOS patients."],["dc.identifier.doi","10.3390/jcm11154294"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112604"],["dc.language.iso","en"],["dc.relation.eissn","2077-0383"],["dc.rights","CC BY 4.0"],["dc.title","Metformin Improves the Hepatic Steatosis Index in Non-Obese Patients with Polycystic Ovary Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","JBMR Plus"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Stamm, Bettina"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Wilken, Lara"],["dc.contributor.author","Wilde, Deborah"],["dc.contributor.author","Heppner, Christina"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Herrmann‐Lingen, Christoph"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2022-04-01T10:01:30Z"],["dc.date.available","2022-04-01T10:01:30Z"],["dc.date.issued","2022"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1002/jbm4.10586"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105677"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2473-4039"],["dc.relation.issn","2473-4039"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","The Influence of Conventional Treatment on Symptoms and Complaints in Patients With Chronic Postsurgical Hypoparathyroidism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1483"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Endocrine Connections"],["dc.bibliographiccitation.lastpage","1492"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Kahlert, Elin"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Freiberg, Clemens"],["dc.contributor.author","Janssen, Onno E"],["dc.contributor.author","Stahnke, Nikolaus"],["dc.contributor.author","Strik, Domenika"],["dc.contributor.author","Merkel, Martin"],["dc.contributor.author","Mann, Alexander"],["dc.contributor.author","Liesenkötter, Klaus-Peter"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2020-12-10T18:42:39Z"],["dc.date.available","2020-12-10T18:42:39Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1530/EC-19-0418"],["dc.identifier.eissn","2049-3614"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17040"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78038"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Deficient knowledge in adult Turner syndrome care as an incentive to found Turner centers in Germany"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","JBMR Plus"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Wilde, Deborah"],["dc.contributor.author","Wilken, Lara"],["dc.contributor.author","Stamm, Bettina"],["dc.contributor.author","Heppner, Christina"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Herrmann‐Lingen, Christoph"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2021-06-01T10:50:50Z"],["dc.date.available","2021-06-01T10:50:50Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/jbm4.10368"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17513"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86799"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2473-4039"],["dc.relation.issn","2473-4039"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Quantification of Symptom Load by a Disease‐Specific Questionnaire HPQ 28 and Analysis of Associated Biochemical Parameters in Patients With Postsurgical Hypoparathyroidism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","45"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Advances in Clinical and Experimental Medicine"],["dc.bibliographiccitation.lastpage","56"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Koepp, Regine"],["dc.contributor.author","Cortis, Julia"],["dc.contributor.author","Komrakova, Marina"],["dc.contributor.author","Schieker, Matthias"],["dc.contributor.author","Hempel, Ute"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2020-12-10T18:42:47Z"],["dc.date.available","2020-12-10T18:42:47Z"],["dc.date.issued","2018"],["dc.description.abstract","BACKGROUND: Crohn´s disease (CD) is associated with a higher prevalence of osteoporosis. The pathogenesis of bone affliction remains controversial, especially if inflammatory cytokines or glucocorticoid therapy are the main contributors. In postmenopausal osteoporosis, bone resorption is induced by IL-6, IL-1β and TNF-α. In contrast, in children with CD, IL-6 exclusively decreased bone formation without affecting bone resorption. OBJECTIVES: The objective of this study was to further clarify the pathophysiology of bone affliction in adult patients with CD with the use of an osteoblast and osteoclast cell model. MATERIAL AND METHODS: Inflammatory cytokines IL-6, IL-1β, and TNF-α were measured in adult CD patients' serum. Mean values of these cytokines were applied with or without dexamethasone to the human cell line SCP-1 (osteoblastic cell model). Also, the effect of cytokines on primary human osteoclast differentiation and activity was determined. RESULTS: The combined cytokine application increased the receptor activator of NF-κB ligand/osteoprotegerin (RANKL/OPG) ratio 2-fold after 2 and 14 days. Additional application of dexamethasone to SCP-1 cells further increased the RANKL/OPG ratio 3-fold, but decreased IL-6 and IL-1β expression to 10% and 50%, respectively. TNF-α expression was maximally suppressed to 16% by dexamethasone in the presence of cytokines. In osteoclasts, the combined cytokine treatment decreased expression of characteristic genes to approx. 30%, while increasing osteoclast resorption activity to 148%. In addition, a cytokine stimulated osteoblast cell culture-generated supernatant stimulated osteoclast resorption activity by 170%. CONCLUSIONS: Our results suggest that IL-6, IL-1β, and TNF-α only in combination induced osteoclaststimulating activity represented by the RANKL/OPG ratio in osteoblasts. Dexamethasone further increased this effect in osteoblasts, while decreasing cytokine expression. The results in osteoclasts support a direct and osteoblast-mediated effect on bone resorption. Our in vitro results differentiate for the first time the effect of cytokines on bone turnover as measured in adult CD patients from the additional dexamethasone effect on osteoblasts as part of the pathophysiology of osteoporosis."],["dc.identifier.doi","10.17219/acem/67561"],["dc.identifier.issn","1899-5276"],["dc.identifier.pmid","29521042"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15197"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78085"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.issn","1899-5276"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","IL-6, IL-1β, and TNF-α only in combination influence the osteoporotic phenotype in Crohn’s patients via bone formation and bone resorption"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","26"],["dc.bibliographiccitation.journal","Journal of Clinical & Translational Endocrinology"],["dc.bibliographiccitation.lastpage","38"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Koepp, Regine"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Kruppa, Jochen"],["dc.contributor.author","Jung, Klaus"],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2019-07-09T11:45:44Z"],["dc.date.available","2019-07-09T11:45:44Z"],["dc.date.issued","2018"],["dc.description.abstract","Background: Crohn's disease (CD) is associated with a higher prevalence of osteoporosis, a complication that is recognized as a significant cause of morbidity. Its pathogenesis is controversial, but the activity of CD is one contributing factor. Methods: We stimulated SCP-1 cells (mesenchymal stem cell line) under osteogenic conditions with serum from adult patients with CD in the symptomatic phase (SP) and in remission (R) and with control sera. Concentrations of IL-6, IL-1 beta, and TNF alpha in the sera were measured. Patients were classified as normal or osteopenic/osteoporotic based on bone mineral density (BMD) T-score measurements. After 14 days in culture, protein expression and gene ontology (GO) annotation analysis was performed. Results: Cytokine concentrations (IL-6, IL-1 beta, TNF alpha) varied within sera groups. None of the cytokines were significantly increased in the symptomatic phase compared to remission. Protein analysis revealed 17 proteins regulated by the SP versus R phase sera of disease. A linear relationship between CDAI (Crohn's disease activity index) and normalized protein expression of APOA1 and 2, TTR, CDKAL1 and TUBB6 could be determined. Eleven proteins were found to be differentially regulated comparing osteoporosis-positive and osteoporosis-negative sera. Gene annotation and further analysis identified these genes as part of heme and erythrocyte metabolism, as well as involved in hypoxia and in endocytosis. A significant linear relationship between bone mineral density and normalized protein expression could be determined for proteins FABP3 and TTR. Conclusion: Our explorative results confirm our hypothesis that factors in serum from patients with CD change the protein expression pattern of human immortalized osteoblast like cells. We suggest, that these short time changes indeed influence factors of bone metabolism."],["dc.identifier.doi","10.1016/j.jcte.2018.06.002"],["dc.identifier.pmid","30003044"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15299"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59299"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2214-6237"],["dc.rights","CC BY-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Crohn's disease patient serum changes protein expression in a human mesenchymal stem cell model in a linear relationship to patients' disease stage and to bone mineral density"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]