S R Bornstein

King's College London, Londinium, England, United Kingdom

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Publications (378)1251.46 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Obesity is characterized by increased adipocyte number and size as well as white adipose tissue (WAT) inflammation, which is fundamental for the development of insulin resistance and type-2 diabetes. These processes, regulated by various endocrine, paracrine and autocrine factors, are extensively studied with the hope to interfere and to inhibit weight gain and related complications in obese patients. Recent data suggest an important role of bone morphogenic protein 4 (BMP4) in the regulation of adipogenesis and development of obesity. BMP4 is a growth factor of the transforming growth factor-β superfamily. Initially, BMPs were identified as inducers of ectopic bone formation. It is now apparent, however, that these proteins have different pleiotropic developmental actions and including playing a role in white adipogenesis. Methods and results: Here, we demonstrate that the expression of BMP4 in human WAT is negatively correlated to body mass index and to the expression of pro-inflammatory cytokines. In vitro, BMP4 expression in cultured human adipocytes is upregulated after induction of differentiation. Cells treated with exogenous BMP4 increased peroxisome proliferator-activated receptor γ (PPARγ) expression and significantly reduced the expression of pro-inflammatory cytokines including tumor necrosis factor α (TNF-α) and monocyte chemoattractant protein 1. TNF-α treatment of fully differentiated adipocytes resulted in downregulation of the expression of adipogenic genes and elevated expression of pro-inflammatory cytokines. Exogenous BMP4 addition significantly reduced the negative effect of TNF-α on the expression profile of adipocytes. Finally, treatment of human adipocytes with exogenous BMP4 reduced the adipocytes' chemoattractant potential and the migration of monocytes toward adipocyte-conditioned medium. Conclusions: These results indicate that BMP4 is an important anti-inflammatory molecule, which may act through PPARγ and reduces TNF-α-mediated pro-inflammatory cytokine production in human adipocytes. Through its anti-inflammatory potential, BMP4 may serve as a protective factor for inflammation-related diseases such as insulin-tolerance or type-2 diabetes.International Journal of Obesity advance online publication, 25 August 2015; doi:10.1038/ijo.2015.141.
    International journal of obesity (2005) 07/2015; DOI:10.1038/ijo.2015.141 · 5.00 Impact Factor
  • A Barthel · S R Bornstein
    Hormone and Metabolic Research 06/2015; 47(6):470-1. DOI:10.1055/s-0035-1548874 · 2.12 Impact Factor
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    ABSTRACT: Iron deficiency (ID) and iron deficiency anemia (IDA) are common findings in patients undergoing lipoprotein apheresis (LA). Different intravenous (iv) formulations are used to treat ID in LA patients, however guidelines and data on ID/IDA management in LA patients are lacking. We therefore performed a prospective observational multi-center cohort study of ID/IDA in LA patients, comparing two approved i.v. iron formulations, ferric gluconate (FG) and ferric carboxymaltose (FCM). Inclusion criteria were a) serum ferritin <100 μg/L or b) serum ferritin <300 μg/L and transferrin saturation <20%. Patients received either FG (62.5 mg weekly) or FCM (500 mg once in ID or up to 1000 mg if IDA was present) i.v. until iron deficiency was resolved. Efficacy and safety were determined by repeated laboratory and clinical assessment. Iron parameters pre and post apheresis were measured to better understand the pathogenesis of ID/IDA in LA patients. 80% of LA patients treated at the three participating centers presented with ID/IDA; 129 patients were included in the study. Serum ferritin and transferrin levels were reduced following apheresis (by 18% (p < 0.0001) and by 13% (p < 0.0001) respectively). Both FG and FCM were effective and well tolerated in the treatment of ID/IDA in LA patients. FCM led to a quicker repletion of iron stores (p < 0.05), while improvement of ID/IDA symptoms was not different. Number and severity of adverse events did not differ between FG and FCM, no severe adverse events occurred. Our results suggest that FG and FCM are equally safe, well-tolerated and effective in treating ID/IDA in LA patients. These data form the basis for follow-up randomized controlled trials to establish clinical guidelines. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    Atherosclerosis. Supplements 05/2015; 18. DOI:10.1016/j.atherosclerosissup.2015.02.030 · 2.29 Impact Factor
  • Barbara Ludwig · Stefan Bornstein
    Diabetes aktuell 05/2015; 13(02):81-82. DOI:10.1055/s-0035-1552951
  • Experimental and Clinical Endocrinology & Diabetes 03/2015; 122(03). DOI:10.1055/s-0035-1547699 · 1.56 Impact Factor
  • Experimental and Clinical Endocrinology & Diabetes 03/2015; 122(03). DOI:10.1055/s-0035-1549081 · 1.56 Impact Factor
  • C Jennewein · N Tran · W Kanczkowski · SR Bornstein · K Zacharowski
    Experimental and Clinical Endocrinology & Diabetes; 03/2015
  • J Gräßler · S Sales · M Bickle · R Al-Atrip · SR Bornstein · A Shevchenko
    Experimental and Clinical Endocrinology & Diabetes 03/2015; 122(03). DOI:10.1055/s-0035-1547686 · 1.56 Impact Factor
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    ABSTRACT: The antiepileptic drug valproic acid (VPA) has been shown to influence the neural differentiation and neurite outgrowth of neural stem cells. Sympathoadrenal progenitor cells share properties with neural stem cells and are considered a potential cell source in the treatment of neurodegenerative diseases. The present study therefore aims at modulating the neural differentiation potential of these cells by treatment with the histone deacetylase inhibitor VPA. We studied the epigenetic effects of VPA in two culture conditions: suspension conditions aimed to expand adrenomedullary sympathoadrenal progenitors within free-floating chromospheres and adherent cell cultures optimized to derive neurons. Treatment of chromospheres with VPA may launch neuronal differentiation mechanisms and improve their neurogenic potential upon transplantation. However, also transplantation of differentiated functional neurons could be beneficial. Treating chromospheres for 7 days with clinically relevant concentrations of VPA (2 mm) revealed a decrease of neural progenitor markers Nestin, Notch2 and Sox10. Furthermore, VPA initiated catecholaminergic neuronal differentiation indicated by upregulation of the neuronal marker β-III-tubulin, the dopaminergic transcription factor Pitx3 and the catecholaminergic enzymes TH and GTPCH. In adherent neural differentiation conditions, VPA treatment improved the differentiation of sympathoadrenal progenitor cells into catecholaminergic neurons with significantly elevated levels of nor- and epinephrine. In conclusion, similar to neural stem cells, VPA launches differentiation mechanisms in sympathoadrenal progenitor cells that result in increased generation of functional neurons. Thus, data from this study will be relevant to the potential use of chromaffin progenitors in transplantation therapies of neurodegenerative diseases.Molecular Psychiatry advance online publication, 24 February 2015; doi:10.1038/mp.2015.3.
    Molecular Psychiatry 02/2015; 20(8). DOI:10.1038/mp.2015.3 · 14.50 Impact Factor
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    ABSTRACT: Background: Adrenocortical cancer (ACC) is a rare malignant endocrine tumor. Previously we found that erlotinib (inhibitor of EGFR) had an additive cytotoxic effect to standard therapy with mitotane in H295R cell line, especially after EGF stimulation. Primary cultures of ACC have been proven to be challenging to establish and maintain for further experiments, especially for assessing their steroid profile. Design: The aim of this study was to test the effect in the use of Erlotinib on primary ACC cultures. We successfully cultured 3 ACCs. In 2 ACC cases radical surgery was a treatment of choice, whereas in the last case - surgery was after neo-adjuvant chemotherapy. Because last tumour was very heterogeneous, we cultured 2 samples from macroscopically different areas. Cell proliferation rate and the effect of the drugs were assessed by AlamarBlue assay. We used LCMS/MS to assess tumour steroids production from primary cultures derived from metastatic ACC cases. Results: Treatment with mitotane resulted in the decrease of cell proliferation (9%±2%) in all cases at 10uM and total death at 50μM. In one of radically operated ACCs, erlotinib (10μM) decreased proliferation by 24%, whereas in another it was not effective. Surprisingly, erlotinib has opposite effect on cell proliferation in two samples from metastatic ACC, however its combination with low dose of mitotane (10μM) was sufficient to induce total death. Furthermore the basal steroid production was different in those samples and it changed in a different manner after treatment with mitotane and/or erlotinib (with or without EGF stimulation). Conclusion: Erlotinib can have an anti-proliferative effect in primary ACC cultures and can reduce mitotane effective concentration. For cases pre-treated with neo-adjuvant therapy, erlotinib may cause opposite responses in different parts of the same tumour; hence its clinical use needs further careful consideration. Different responses in steroidogenesis from different parts of the same ACC tumour has not been previously described underlines ACC heterogeneity.
    Modern Pathology 02/2015; 28(2 (Suppl 2)):133. DOI:10.1038/modpathol.2015.14 · 6.19 Impact Factor
  • S Saha · S R Bornstein · J Graessler · S Kopprasch
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    ABSTRACT: Low-density lipoprotein (LDL) is considered to be a risk factor for atherosclerosis. In the presence of hyperglycemia, LDL undergoes glycoxidative modification and this glycoxidized (glycox) LDL promotes atherosclerosis in type 2 diabetic (T2D) individuals. Moreover, because of its cholesterol content, LDL contributes to aldosterone biosynthesis, which is modulated by angiotensin II (AngII) and has been implicated in cardiovascular complications of T2D. However, the molecular mechanism of the crosstalk between glycoxLDL, AngII, and aldosterone has not been explained clearly. Therefore, this study has been aimed to investigate the impact of in vitro modified glycoxLDL on aldosterone release in an AngII-sensitized adrenocortical carcinoma cell line (NCI H295R). Native LDL (natLDL), isolated from healthy volunteers by sequential density gradient ultracentrifugation, was subjected to d-glucose (200 mmol/l), for glycoxidative modification, at 37°C for 6 days. The AngII-sensitized H295R cells were treated with natLDL and glycoxLDL for 24 h and the supernatant was used for aldosterone measurement. The treated cells were utilized for protein isolation and mRNA quantification. Compared to natLDL, glycoxLDL produced a significantly greater effect on aldosterone release from AngII-sensitized cells. The treatment with specific pharmacological inhibitors suggests that modified LDL recruits ERK1/2 and janus kinase-2 for transcriptional regulation of aldosterone synthase. Moreover, glycoxLDL modulates aldosterone release via cAMP-dependent protein kinase A (PKA) pathway. However, glycoxLDL induces ERK phosphorylation independent of PKA activation and this novel mechanism could be targeted for therapeutic trials. In conclusion, this in vitro study emphasizes a possible causal relationship between LDL glycoxidative modification, AngII-sensitization, and adrenocortical steroid hormone release. © Georg Thieme Verlag KG Stuttgart · New York.
    Hormone and Metabolic Research 01/2015; DOI:10.1055/s-0034-1395568 · 2.12 Impact Factor
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    ABSTRACT: Solid organ and cell transplantation, including pancreatic islets constitute the treatment of choice for chronic terminal diseases. However, the clinical use of allogeneic transplantation is limited by the growing shortage of human organs. This has prompted us to initiate a unique multi-center and multi-team effort to promote translational research in xenotransplantation to bring xenotransplantation to the clinical setting. Supported by the German Research Foundation, an interdisciplinary group of surgeons, internal medicine doctors, diabetologists, material sciences experts, immunologists, cell biologists, virologists, veterinarians, and geneticists have established a collaborative research center (CRC) focusing on the biology of xenogeneic cell, tissue, and organ transplantation. A major strength of this consortium is the inclusion of members of the regulatory bodies, including the Paul-Ehrlich Institute (PEI), infection specialists from the Robert Koch Institute and PEI, veterinarians from the German Primate Center, and representatives of influential ethical and religious institutions. A major goal of this consortium is to promote islet xenotransplantation, based on the extensive expertise and experience of the existing clinical islet transplantation program. Besides comprehensive approaches to understand and prevent inflammation-mediated islet xenotransplant dysfunction [immediate blood-mediated inflammatory reaction (IBMIR)], we also take advantage of the availability of and experience with islet macroencapsulation, with the goal to improve graft survival and function. This consortium harbors a unique group of scientists with complementary expertise under a cohesive program aiming at developing new therapeutic approaches for islet replacement and solid organ xenotransplantation. © Georg Thieme Verlag KG Stuttgart · New York.
    Hormone and Metabolic Research 12/2014; 47(01). DOI:10.1055/s-0034-1395518 · 2.12 Impact Factor
  • Hormone and Metabolic Research 12/2014; 47(01). DOI:10.1055/s-0034-1394453 · 2.12 Impact Factor
  • M Hanefeld · S R Bornstein · A Barthel
    DMW - Deutsche Medizinische Wochenschrift 12/2014; 139(49):2494-7. DOI:10.1055/s-0034-1387406 · 0.54 Impact Factor
  • V Kamvissi · A Salerno · S R Bornstein · G Mingrone · F Rubino
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    ABSTRACT: The role of incretins in glucose homeostasis is well known. Yet, in recent years, the sustained weight loss and rapid glycemic control following bariatric surgery has challenged our understanding of the intestinal-pancreatic interaction. This in turn led to the introduction of metabolic surgery, an innovative medical discipline in which a surgical manipulation of the gastrointestinal tract (e. g., through a Roux-en-Y gastric bypass, RYGB, or Bilio-Pancreatic-Diversion, BPD) yields a sustained remission of diabetes mellitus. The pathophysiological background of this metabolic effect is, amongst other things, based on the anti-incretin theory. This theory postulates that in addition to the well-known incretin effect, nutrient passage through the GI-tract could also activate negative feedback mechanisms (anti-incretins) to balance the effects of incretins and other postprandial glucose-lowering mechanisms (i. e., suppression of ghrelin, glucagon, and hepatic glucose production via activation of nutrient sensing). This in turn prevents postprandial hyperinsulinemic hypoglycemia. The bypass of the duodenum, the entire jejunum and the first portion of the ileum by BPD induce normalization of peripheral insulin sensitivity, while the bypass of a shorter intestinal tract by RYGB mainly improves the hepatic insulin sensitivity. In addition, RYGB greatly increases insulin secretion. Therefore, metabolic surgery highlights the important role of the small intestine in glucose homeostasis, while until few years ago, it was only the pancreas and the liver that were thought to represent the regulatory organs for glucose disposal.
    Hormone and Metabolic Research 11/2014; 47(01). DOI:10.1055/s-0034-1394374 · 2.12 Impact Factor
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    ABSTRACT: Inflammation in the central nervous system (CNS) and disruption of its immune privilege are major contributors to the pathogenesis of multiple sclerosis (MS) and of its rodent counterpart, experimental autoimmune encephalomyelitis (EAE). We have previously identified developmental endothelial locus-1 (Del-1) as an endogenous anti-inflammatory factor, which inhibits integrin-dependent leukocyte adhesion. Here we show that Del-1 contributes to the immune privilege status of the CNS. Intriguingly, Del-1 expression decreased in chronic-active MS lesions and in the inflamed CNS in the course of EAE. Del-1-deficiency was associated with increased EAE severity, accompanied by increased demyelination and axonal loss. As compared with control mice, Del-1(-/-) mice displayed enhanced disruption of the blood-brain barrier and increased infiltration of neutrophil granulocytes in the spinal cord in the course of EAE, accompanied by elevated levels of inflammatory cytokines, including interleukin-17 (IL-17). The augmented levels of IL-17 in Del-1-deficiency derived predominantly from infiltrated CD8(+) T cells. Increased EAE severity and neutrophil infiltration because of Del-1-deficiency was reversed in mice lacking both Del-1 and IL-17 receptor, indicating a crucial role for the IL-17/neutrophil inflammatory axis in EAE pathogenesis in Del-1(-/-) mice. Strikingly, systemic administration of Del-1-Fc ameliorated clinical relapse in relapsing-remitting EAE. Therefore, Del-1 is an endogenous homeostatic factor in the CNS protecting from neuroinflammation and demyelination. Our findings provide mechanistic underpinnings for the previous implication of Del-1 as a candidate MS susceptibility gene and suggest that Del-1-centered therapeutic approaches may be beneficial in neuroinflammatory and demyelinating disorders.Molecular Psychiatry advance online publication, 11 November 2014; doi:10.1038/mp.2014.146.
    Molecular Psychiatry 11/2014; 20(7). DOI:10.1038/mp.2014.146 · 14.50 Impact Factor
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    ABSTRACT: Background: Adipocyte fatty acid-binding protein (FABP4) is a member of a highly conserved family of cytosolic proteins that bind with high affinity to hydrophobic ligands, such as saturated and unsaturated long-chain fatty acids and eicosanoids. Recent evidence has supported a novel role for FABP4 in linking obesity with metabolic and cardiovascular disorders. In this context, we identified FABP4 as a main bioactive factor released from human adipose tissue that directly suppresses heart contraction in vitro. As FABP4 is known to be a transport protein, it cannot be excluded that lipid ligands are involved in the cardiodepressant effect as well, acting in an additional and/or synergistic way. Objective: We investigated a possible involvement of lipid ligands in the negative inotropic effect of adipocyte factors in vitro. Results: We verified that blocking the CYP epoxygenase pathway in adipocytes attenuates the inhibitory effect of adipocyte-conditioned medium (AM) on isolated adult rat cardiomyocytes, thus suggesting the participation of epoxyeicosatrienoic acids (EETs) in the cardiodepressant activity. Analysis of AM for EETs revealed the presence of 5,6-, 8,9-, 11,12- and 14,15-EET, whereas 5,6-EET represented about 45% of the total EET concentration in AM. Incubation of isolated cardiomyocytes with EETs in similar concentrations as found in AM showed that 5,6-EET directly suppresses cardiomyocyte contractility. Furthermore, after addition of 5,6-EET to FABP4, the negative inotropic effect of FABP4 was strongly potentiated in a concentration-dependent manner. Conclusions: These data suggest that adipocytes release 5,6-EET and FABP4 into the extracellular medium and that the interaction of these factors modulates cardiac function. Therefore elevated levels of FABP4 and 5,6-EET in obese patients may contribute to the development of heart dysfunction in these subjects.
    International journal of obesity (2005) 11/2014; 121(3). DOI:10.1038/ijo.2014.193 · 5.00 Impact Factor
  • M Zhao · P Choudhary · P Srinivasan · H Tang · N Heaton · M Fung · A Barthel · S. R. Bornstein · S A Amiel · G C Huang
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    ABSTRACT: Revascularisation of transplanted islets is an essential prerequisite for graft survival and function. However, current islet isolation procedures deprive the islets of endothelial tubulets. This may have a detrimental effect on the revascularisation process of islets following transplantation. We hypothesise that modification of the isolation procedure that preserves islet endothelial vessels may improve the islet revascularisation process following transplantation. Here, we present a modified islet isolation method by which a substantial amount of endothelial cells still attached to the islets could be preserved. The islets with preserved endothelial cells isolated by this method were revascularised within 3 days, not observed in islets isolated by standard methods. Further, we observed that grafts of islets isolated by standard methods had more patches of dead tissue than islet grafts obtained by the modified method, indicating that attached endothelial cells may play an important role in the islet revascularisation process and potentially help to improve the transplantation outcome.
    Hormone and Metabolic Research 11/2014; 47(01). DOI:10.1055/s-0034-1390489 · 2.12 Impact Factor
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    S Rahmig · S R Bornstein · T Chavakis · E Jaeckel · C Waskow
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    ABSTRACT: We comment here on the suitability of available mouse models for type 1 diabetes research including research on therapeutic pancreatic islet transplantation. The major emphasis will be laid on models that require minimal invasive procedures.Most biological processes are too complex for a complete recapitulation in a test tube. The study of innate or even adaptive immune responses involves a number of different cell types and organs making in vitro studies unreliable but also providing extreme challenges for the use of surrogate model organisms. Studying these processes directly in humans is impossible due to ethical and technical constraints. To resolve this problem small animal models such as mice or rats are frequently used to study mechanisms of complex diseases. This has brought much insight into hematopoiesis and immune cell function including type 1 diabetes (T1D); however, 65 million years of evolution introduced striking differences between mice and humans 1. In fact, none of the many suggested therapies arising from studies using mice 2 3 that have promised prevention or even reversion of T1D made it into the clinic yet 4 5 6. The reason for this are major species-specific differences between rodents and humans regarding the immune system and beta cells.
    Hormone and Metabolic Research 11/2014; 47(01). DOI:10.1055/s-0034-1390446 · 2.12 Impact Factor
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    ABSTRACT: Xenotransplantation (xeno-Tx) is considered as an alternative solution to overcome the shortage of human donor organs. However, the success of xeno-Tx is hindered by immune reactions against xenogeneic cells (e. g. of porcine origin). More specifically, activation of innate immune mechanisms such as complement and triggering of the coagulation cascade occur shortly after xeno-Tx, and adhesion of human leukocytes to porcine endothelium is another early critical step mediating the immune attack. To investigate the therapeutic potential of complement inhibition in the context of xenogeneic interactions, we have employed a whole-blood model in the present study. Incubation of human blood with porcine endothelial cells (PAECs) led to activation of complement and coagulation as well as to increased leukocyte adhesion. The observed responses can be attributed to the pig-to-human xenogeneicity, since the presence of human endothelium induced a minor cellular and plasmatic inflammatory response. Importantly, complement inhibition using a potent complement C3 inhibitor, compstatin analogue Cp40, abrogated the adhesion of leukocytes and, more specifically, the attachment of neutrophils to porcine endothelium. Moreover, Cp40 inhibited the activation of PAECs and leukocytes, since the levels of the adhesion molecules E-selectin, ICAM-1, ICAM-2, and VCAM-1 on PAECs and the surface expression of integrin CD11b on neutrophils were significantly decreased. Along the same line, inhibition of CD11b resulted in decreased leukocyte adhesion. Taken together, our findings provide a better understanding of the mechanisms regulating the acute innate immune complications in the context of xeno-Tx and could pave the way for complement-targeting therapeutic interventions.
    Hormone and Metabolic Research 10/2014; 47(01). DOI:10.1055/s-0034-1390452 · 2.12 Impact Factor

Publication Stats

7k Citations
1,251.46 Total Impact Points


  • 2014–2015
    • King's College London
      • Division of Diabetes and Nutritional Sciences
      Londinium, England, United Kingdom
    • ICL
      Londinium, England, United Kingdom
  • 1998–2015
    • Technische Universität Dresden
      • • Center for Internal Medicine
      • • Medical Clinic III
      • • Medical Clinic III, Department General Medicine
      Dresden, Saxony, Germany
  • 1999–2014
    • Carl Gustav Carus-Institut
      Pforzheim, Baden-Württemberg, Germany
    • University of Gothenburg
      Goeteborg, Västra Götaland, Sweden
  • 2012
    • Institut für klinische Pharmakologie
      Stuttgart, Baden-Württemberg, Germany
  • 2011–2012
    • Center for Regenerative Therapies, Dresden
      Dresden, Saxony, Germany
    • University of Texas Health Science Center at San Antonio
      • Division of Diabetes
      San Antonio, TX, United States
  • 2007–2012
    • Universitätsklinikum Dresden
      • Medizinische Klinik und Poliklinik III
      Dresden, Saxony, Germany
    • Universitätsklinikum Düsseldorf
      • Klinik für Endokrinologie und Diabetologie
      Düsseldorf, North Rhine-Westphalia, Germany
    • Universität Regensburg
      • Department of Clinical Chemistry and Laboratory Medicine
      Ratisbon, Bavaria, Germany
  • 1998–2009
    • National Institute of Child Health and Human Development
      Maryland, United States
  • 2008
    • Garki Hospital Abuja
      Abuja, Abuja Federal Capital Territory, Nigeria
  • 2006
    • German Diabetes Center
      Düsseldorf, North Rhine-Westphalia, Germany
  • 2001–2006
    • Heinrich-Heine-Universität Düsseldorf
      Düsseldorf, North Rhine-Westphalia, Germany
  • 2002
    • Evangelic Hospital Bielefeld
      Bielefeld, North Rhine-Westphalia, Germany
    • Graz University of Technology
      • Institut für Medizintechnik
      Graz, Styria, Austria
    • Rambam Medical Center
      • Department of Pediatrics
      H̱efa, Haifa, Israel
  • 1995–2001
    • University of Leipzig
      • Institute of Immunology
      Leipzig, Saxony, Germany
  • 2000
    • Northern Inyo Hospital
      BIH, California, United States
  • 1999–2000
    • Eunice Kennedy Shriver National Institute of Child Health and Human Development
      Роквилл, Maryland, United States
  • 1998–1999
    • National Institutes of Health
      • Section on Reproductive Endocrinology
      베서스다, Maryland, United States
  • 1991–1994
    • Universität Ulm
      • • Clinic of Internal Medicine I
      • • Clinic of Gynecology and Obstetrics
      Ulm, Baden-Wuerttemberg, Germany