7 results on '"Annika Deck"'
Search Results
2. From skeletal to cardiovascular disease in 12 steps—the evolution of sclerostin as a major player in CKD-MBD
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Vincent Brandenburg, Pieter Evenepoel, Patrick C. D'Haese, Djalila Mekahli, Ellen Neven, Björn Meijers, and Annika Deck
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Genetic Markers ,0301 basic medicine ,medicine.medical_specialty ,Osteoporosis ,030209 endocrinology & metabolism ,Bone and Bones ,Bone remodeling ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Cardiovascular calcification ,Bone Density ,Chronic kidney disease-mineral and bone disorder ,Internal medicine ,medicine ,Animals ,Humans ,Renal osteodystrophy ,Renal Insufficiency, Chronic ,Adaptor Proteins, Signal Transducing ,business.industry ,Osteoblast ,medicine.disease ,030104 developmental biology ,medicine.anatomical_structure ,Endocrinology ,chemistry ,Cardiovascular Diseases ,Nephrology ,Bone Morphogenetic Proteins ,Pediatrics, Perinatology and Child Health ,Sclerostin ,Human medicine ,Bone Remodeling ,Bone Diseases ,business ,Signal Transduction ,Calcification - Abstract
Canonical Wnt signaling activity contributes to physiological and adaptive bone mineralization and is an essential player in bone remodeling. Sclerostin is a prototypic soluble canonical Wnt signaling pathway inhibitor that is produced in osteocytes and blocks osteoblast differentiation and function. Therefore, sclerostin is a potent inhibitor of bone formation and mineralization. Accordingly, rodent sclerostin-deficiency models exhibit a strong bone phenotype. Moreover, blocking sclerostin represents a promising treatment perspective against osteoporosis. Beyond the bone field novel data definitely associate Wnt signaling in general and sclerostin in particular with ectopic extraosseous mineralization processes, as is evident in cardiovascular calcification or calciphylaxis. Uremia is characterized by parallel occurrence of disordered bone mineralization and accelerated cardiovascular calcification (chronic kidney disease mineral and bone disorder, CKD-MBD), linking skeletal and cardiovascular diseasethe so-called bone-vascular calcification paradox. In consequence, sclerostin may qualify as an emerging player in CKD-MBD. We present a stepwise review approach regarding the rapidly evolving field sclerostin participation in CKD-MBD. Starting from data originating in the classical bone field we look separately at three major areas of CKD-MBD: disturbed mineral metabolism, renal osteodystrophy, and uremic cardiovascular disease. Our review is intended to help the nephrologist revise the potential importance of sclerostin in CKD by focusing on how sclerostin research is gradually evolving from the classical osteoporosis niche into the area of CKD-MBD. In particular, we integrate the limited amount of available data in the context of pediatric nephrology.
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- 2015
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3. Sclerostin deficiency modifies the development of CKD-MBD in mice
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Patrick C. D'Haese, Ayshe Hyusein, Pieter Evenepoel, Daniel Weis, Michaela Kneissel, Annika Deck, Nikolaus Marx, Ina Kramer, Anne Babler, Rafael Kramann, Geert J. Behets, Anja Verhulst, Nadine Kaesler, Jürgen Floege, Annelies De Maré, and Vincent Brandenburg
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medicine.medical_specialty ,Histology ,Physiology ,Endocrinology, Diabetes and Metabolism ,medicine.medical_treatment ,030232 urology & nephrology ,Parathyroid hormone ,030209 endocrinology & metabolism ,03 medical and health sciences ,chemistry.chemical_compound ,Mice ,0302 clinical medicine ,Internal medicine ,Medicine ,Animals ,Renal osteodystrophy ,Biology ,Adaptor Proteins, Signal Transducing ,Glycoproteins ,Bone mineral ,Chronic Kidney Disease-Mineral and Bone Disorder ,Mice, Knockout ,Hyperparathyroidism ,business.industry ,medicine.disease ,Nephrectomy ,Mice, Inbred C57BL ,Endocrinology ,medicine.anatomical_structure ,chemistry ,Sclerostin ,Intercellular Signaling Peptides and Proteins ,Cortical bone ,Secondary hyperparathyroidism ,Female ,Human medicine ,business - Abstract
Sclerostin is a soluble antagonist of canonical Wnt signaling and a strong inhibitor of bone formation. We present experimental data on the role of sclerostin in chronic kidney disease - bone mineral disorder (CKD-MBD). Methods We performed 5/6 nephrectomies in 36-week-old sclerostin-deficient (SOST−/−) B6-mice and in C57BL/6J wildtype (WT) mice. Animals received a high phosphate diet for 11 weeks. The bones were analyzed by high-resolution micro-computed tomography (μCT) and quantitative bone histomorphometry. Aortic tissue was analyzed regarding the extent of vascular calcification. Results All nephrectomized mice had severe renal failure, and parathyroid hormone was highly increased compared to corresponding sham animals. All SOST−/− animals revealed the expected high bone mass phenotype. Overall, the bone compartment in WT and SOST−/− mice responded similarly to nephrectomy. In uremic WT animals, μCT data at both the distal femur and lumbar spine revealed significantly increased trabecular volume compared to non-uremic WTs. In SOST−/− mice, the differences between trabecular bone volume were less pronounced when comparing uremic with sham animals. Cortical thickness and cortical bone density at the distal femur decreased significantly and comparably in both genotypes after 5/6 nephrectomy compared to sham animals (cortical bone density − 18% and cortical thickness − 32%). Overall, 5/6 nephrectomy and concomitant hyperparathyroidism led to a genotype-independent loss of cortical bone volume and density. Overt vascular calcification was not detectable in either of the genotypes. Conclusion Renal osteodystrophy changes were more pronounced in WT mice than in SOST−/− mice. The high bone mass phenotype of sclerostin deficiency was detectable also in the setting of chronic renal failure with severe secondary hyperparathyroidism. Abbreviations α-SMA, alpha smooth muscle actin; AjAR, adjusted apposition rate; B.Ar, bone area; BFR, bone formation rate; cbfa1, core binding factor 1; CKD-MBD, chronic kidney disease and mineral bone disorder; EPm, eroded perimeter; Ntx, nephrectomy; O.Ar, osteoid area; Ob, osteoblast perimeter; Oc, osteoclast perimeter; O.Wi, osteoid width; PTH, parathyroid hormone; s.c., subcutaneous; VSMCs, vascular smooth muscle cells; WT, wildype
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- 2017
4. Mechanism and biological relevance of blue-light (420-453 nm)-induced nonenzymatic nitric oxide generation from photolabile nitric oxide derivates in human skin in vitro and in vivo
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Matthias Born, Frank Anton Van Abeelen, Jörg Liebmann, Christine M. Volkmar, Christoph V. Suschek, Klaus-Dietrich Kröncke, Christian Opländer, Michael Kirsch, Annika Deck, Ernst E. van Faassen, and Joachim Windolf
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Adult ,Male ,Luminescence ,Light ,Nitrite ,Chemie ,Human skin ,Free radicals ,Photochemistry ,Biochemistry ,Nitroso compounds ,Nitric oxide ,law.invention ,030207 dermatology & venereal diseases ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,law ,In vivo ,Physiology (medical) ,Cell Line, Tumor ,Animals ,Humans ,Irradiation ,Cyclic GMP ,Nitrites ,030304 developmental biology ,Chemiluminescence ,Skin ,0303 health sciences ,S-Nitrosothiols ,Serum Albumin, Bovine ,Phototherapy ,Photodecomposition ,In vitro ,3. Good health ,Bioavailability ,Rats ,chemistry ,Biophysics ,Female ,Copper - Abstract
Human skin contains photolabile nitric oxide (NO) derivates such as nitrite and S-nitrosothiols, which upon UVA radiation decompose under high-output NO formation and exert NO-specific biological responses such as increased local blood flow or reduced blood pressure. To avoid the injurious effects of UVA radiation, we here investigated the mechanism and biological relevance of blue-light (420-453 nm)-induced nonenzymatic NO generation from photolabile nitric oxide derivates in human skin in vitro and in vivo. As quantified by chemiluminescence detection (CLD), at physiological pH blue light at 420 or 453 nm induced a significant NO formation from S-nitrosoalbumin and also from aqueous nitrite solutions by a to-date not entirely identified Cu(1+)-dependent mechanism. As detected by electron paramagnetic resonance spectrometry in vitro with human skin specimens, blue light irradiation significantly increased the intradermal levels of free NO. As detected by CLD in vivo in healthy volunteers, irradiation of human skin with blue light induced a significant emanation of NO from the irradiated skin area as well as a significant translocation of NO from the skin surface into the underlying tissue. In parallel, blue light irradiation caused a rapid and significant rise in local cutaneous blood flow as detected noninvasively by using micro-light-guide spectrophotometry. Irradiation of human skin with moderate doses of blue light caused a significant increase in enzyme-independent cutaneous NO formation as well as NO-dependent local biological responses, i.e., increased blood flow. The effects were attributed to blue-light-induced release of NO from cutaneous photolabile NO derivates. Thus, in contrast to UVA, blue-light-induced NO generation might be therapeutically used in the treatment of systemic and local hemodynamic disorders that are based on impaired physiological NO production or bioavailability.
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- 2013
5. Validation of commercially available ELISAs for the detection of circulating sclerostin in hemodialysis patients
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Annika Deck, Pieter Evenepoel, Ulf Janssen, Mark Hennies, Sebastian F. Mause, Nadine Kaesler, Vincent Brandenburg, and William A. Boisvert
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Oncology ,medicine.medical_specialty ,business.industry ,medicine.medical_treatment ,medicine.disease ,Article ,chemistry.chemical_compound ,Endocrinology ,chemistry ,Internal medicine ,medicine ,Sclerostin ,Biomarker (medicine) ,Hemodialysis ,business ,Vascular calcification ,Kidney disease - Abstract
Sclerostin is an endocrine regulator in chronic kidney disease - mineral and bone disorder (CKD-MBD). Validation of assay comparability and pre-analytical handling is mandatory for establishment of sclerostin as a biomarker.Blood samples (serum, EDTA, heparin and citrate plasma) were obtained from 12 hemodialysis (HD) patients after the long dialysis interval. Passing-Bablok regression analysis and Bland-Altman difference plots were used to evaluate the agreement between sclerostin levels measured with two commercially available ELISAs from TECOmedical and Biomedica.Independent of the sample type, the agreement of the two assays was poor with a strong proportional but no systematic bias. Compared to the TECOmedical assay, the Biomedica test yielded almost 2-fold higher sclerostin values throughout all sample types. Spike recovery and linear dilution studies revealed a higher accuracy of the TECOmedical assay (97% and 96%) compared to the Biomedica assay (118% and 78%). Sclerostin levels were stable within 4 hours after sample collection, in particular when analyzed in plasma. In contrast to the Biomedica assay, the TECOmedical showed a systematic but no proportional bias between serum and plasma samples with higher values for plasma samples. Among the 3 different plasma samples no systematic error could be documented.Careful consideration of the pre-analytical handling and comparative assay validation are necessary to facilitate a more differentiated interpretation of studies reporting circulating sclerostin levels. The presence of a proportional bias demonstrates that in HD patients the two ELISAs for measuring sclerostin should not be used interchangeably. Furthermore, caution is necessary when comparing sclerostin results obtained from different blood sample types.
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- 2016
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6. Wirkung von Blaulicht auf humane Hautzellen
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Annika Deck, Norbert Pallua, Christoph V. Suschek, Christian Opländer, and Christine M. Volkmar
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Chemistry ,Cell ,Human skin ,610 Medical sciences ,Medicine ,Cell biology ,Chromatin ,Extracellular matrix ,medicine.anatomical_structure ,ddc: 610 ,Apoptosis ,medicine ,Wound healing ,Keratinocyte ,Incubation - Abstract
Einleitung: Im Rahmen der Wundheilung spielen Fibroblasten im Auf- bzw. Umbau der extrazellulären Matrix und im Prozess des Wundverschlusses eine wesentliche Rolle. Eine unzureichende Apoptoserate hyperaktiver Fibroblasten im Wundgeschehen korreliert mit der Entstehung von hypertrophen Narben und[for full text, please go to the a.m. URL], 127. Kongress der Deutschen Gesellschaft für Chirurgie
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- 2010
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7. IntelliCage Automated Behavioral Phenotyping Reveals Behavior Deficits in the 3xTg-AD Mouse Model of Alzheimer’s Disease Associated With Brain Weight
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Wendy Winslow, Ian McDonough, Savannah Tallino, Annika Decker, Austin S. Vural, and Ramon Velazquez
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IntelliCage ,3xTg-AD ,brain weight ,cognition ,amyloidosis ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Transgenic rodent models of Alzheimer’s disease (AD) were designed to study mechanisms of pathogenesis and connect these mechanisms with cognitive decline. Measurements of cognition in rodents can be confounded, however, by human handling and interaction; the IntelliCage was created to circumvent these issues while measuring various facets of cognition in a social environment with water consumption as the primary motivator for task completion. Here, for the first time, we examined the behavioral performance of 3xTg-AD mice in the IntelliCage. Seven- to 9-month-old female 3xTg-AD and non-transgenic (NonTg) mice were tested for 29 days in the IntelliCage to measure prefrontal cortical and hippocampal function. We found that a higher percentage of NonTg mice (86.96%) were able to successfully complete the training (adaptation) phases compared to their 3xTg-AD (57.14%) counterparts. Furthermore, the 3xTg-AD mice showed impairments in attention and working memory. Interestingly, we found that differences in body and brain weight between NonTg and 3xTg-AD mice were associated with whether mice were able to complete the IntelliCage tasks. 3xTg-AD mice that completed IntelliCage tasks had lower cortical insoluble amyloid-β40 fractions than their 3xTg-AD counterparts who failed to complete the tasks. Collectively, these results demonstrate deficits in cognition in the 3xTg-AD mouse and inform scientists of important factors to consider when testing this transgenic model in the IntelliCage.
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- 2021
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