H Lehnert

University Medical Center Schleswig-Holstein, Kiel, Schleswig-Holstein, Germany

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Publications (465)1200.05 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: NUCB2/nesfatin and its proteolytically cleaved product nesfatin-1 are recently discovered anorexigenic hypothalamic neuroproteins involved in energy homeostasis. It is expressed both centrally and in peripheral tissues, and appears to have potent metabolic actions. NUCB2/nesfatin neurons are activated in response to stress. Central nesfatin-1 administration elevates circulating ACTH and corticosterone levels. Bilateral adrenalectomy increased NUCB2/nesfatin mRNA levels in rat paraventricular nuclei. To date, studies have not assessed the effects of nesfatin-1 stimulation on human adrenocortical cells. Therefore, we investigated the expression and effects of nesfatin-1 in a human adrenocortical cell model (H295R). Our findings demonstrate that NUCB2 and nesfatin-1 is expressed in human adrenal gland and human adrenocortical cells (H295R). Stimulation with nesfatin-1 inhibits the growth of H295R cells and promotes apoptosis, potentially via the involvement of Bax, BCL-XL and BCL-2 genes as well as ERK1/2, p38 and JNK1/2 signalling cascades. This has implications for understanding the role of NUCB2/nesfatin in adrenal zonal development. NUCB2/nesfatin may also be a therapeutic target for adrenal cancer. However, further studies using in vivo models are needed to clarify these concepts.
    Journal of Endocrinology 04/2015; DOI:10.1530/JOE-14-0496 · 3.59 Impact Factor
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  • Experimental and Clinical Endocrinology & Diabetes 03/2015; 122(03). DOI:10.1055/s-0035-1547657 · 1.76 Impact Factor
  • Experimental and Clinical Endocrinology & Diabetes 03/2015; 122(03). DOI:10.1055/s-0035-1549071 · 1.76 Impact Factor
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    ABSTRACT: Preparing high quality discharge summaries is difficult for first year residents. For 5 years we have been training fourth year students how to write discharge summaries. Our goal is to facilitate the students' start into clinical work. Moreover, we intend to provide the students with a scheme to better memorize patients' histories. Two years after the tutorial the graduates were asked to evaluate the tutorial and to comment on its learning effects. A total of 1228 fourth year students wrote a discharge summary on a patient in whose care the specific student was involved during his or her training in internal medicine. All summaries were read, commented on and graded by a consultant. Two years after the tutorial 310 graduates were invited to complete an online survey on this tutorial. 106 (34 %) of all invited graduates completed the survey. The opinions on the tutorial greatly differed. In principal the students agreed that the tutorial was an important part of medical training and helped to better structure patients' medical data. The majority of the surveyed graduates, however, were not convinced of its practical usefulness for daily work. The students with the poorer grading found their grade less appropriate than the students with the better grading. Though our main goal could not be achieved in the view of the graduates, the overall opinion was rather positive. Problems with this kind of tutorial lay in the enormous effort of correction and in the discouraging effect of grading on the students with difficulties in the task.
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    ABSTRACT: Adrenal insufficiency (AI) is a rare disease caused by destruction of the adrenal glands or dysfunction of the pituitary gland or the hypothalamus. Treatment usually requires lifelong replacement therapy with glucocorticoids. Correct use of glucocorticoids and early dose adjustments are essential to cover the increased glucocorticoid demand in stress. Repeated education of patients and their partners is the best strategy to avoid life-threatening emergencies. However, there is a debate whether physicians' knowledge regarding AI is sufficient, in part due to the rareness of this endocrine disorder. To determine the present specific knowledge of physicians in a large University Department of Internal Medicine with a clinically and scientifically active Division of Endocrinology, all interns, residents / fellows, specialists or senior physicians / consultants were asked to complete a questionnaire with various possible answers on the subject of AI (n=69, median age 30 years, range 23-49 years). The present data suggest that in the investigated University Hospital setting current physicians' knowledge of medical replacement strategies in AI may be insufficient depending on the level of education and experience. Even physicians with training in endocrinology in part demonstrated extensive knowledge gaps. There might be a need for additional structured information and training on AI, even in specialized hospitals.
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    ABSTRACT: Neuroendocrine neoplasia (NEN) with unknown primary site (NEN-CUP tumors) may have a poor prognosis. We evaluated the clinical presentation, therapy, outcome, and risk factors for adverse outcomes in patients who had these tumors. In 243 patients who had NEN, a retrospective review was performed in 38 patients who had NEN-CUP tumors. The 38 patients who had NEN-CUP tumors were evaluated in three groups: group 1 (surgery; primary tumor detected; ten patients); group 2 (surgery; no primary tumor detected; ten patients); and group 3 (no surgery; 18 patients). Risk factors were evaluated with univariate and multivariate analyses. Most patients who had NEN-CUP tumors [32 patients (84 %)] had World Health Organization (WHO) performance score of 0 or 1, and most tumors [24 patients (63 %)] were well differentiated (WHO grade, G1 or G2; Ki-67 index, ≤20 %). Univariate analysis showed that greater survival was significantly associated with lower patient age, lower WHO performance score, lower WHO grade, lower number of metastatic sites, treatment with surgery, and no treatment with chemotherapy. Multivariate analysis showed that low WHO performance score (hazard ratio 7.63, 95 % confidence interval (CI) 2.63-22.19) and treatment with surgery (hazard ratio 0.10, CI 0.028-0.381) were significant independent predictors of improved survival. In patients with NEN-CUP tumors, surgical treatment is an independent predictor of better survival. Therefore, surgical treatment may be indicated in patients with good general health status and well-differentiated NEN-CUP tumors.
    World Journal of Surgery 02/2015; DOI:10.1007/s00268-015-2963-2 · 2.35 Impact Factor
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    ABSTRACT: Hypokalaemic hypertension is the classical presentation of primary hyperaldosteronism but may also result from other mineralocorticoid activity, such as liquorice ingestion. Onset of hypertension as well as serum renin and aldosterone levels are central for the diagnosis. Liquorice ingestion has been reported to induce hypertension, hypokalaemia and metabolic alkalosis due to inhibition of the enzyme 11-β-hydroxy steroiddehydrogenase 2. Here, we report the case of a hypertensive emergency with acute visual impairment due to hypertensive retinopathy in clear conjunction with a considerable consumption of liquorice.
    The Netherlands Journal of Medicine 02/2015; 73(2):82-5. · 2.21 Impact Factor
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    ABSTRACT: The incidence of obesity in the western world has increased dramatically during recent decades. Epidemiological data suggest that obesity is associated with an increased risk of several but not all types of cancers, with clear sex-specific differences. The underlying mechanisms are still a matter of debate. This review focuses on the potential factors linking obesity to cancer. Current experimental evidence suggests that insulin resistance and a chronic, subclinical inflammation in the visceral fat are the major metabolic events causing alterations in the levels of insulin, glucose, free fatty acids, insulin-like growth factor 1 (IGF-1) and 2, adipose tissue-derived proinflammatory cytokines and other bioactive molecules, such as adipokines (e.g. leptin and adiponectin), vascular endothelial growth factor (VEGF), sex hormones, gut microbiota and secondary bile acids. All these factors may act directly or indirectly on the tumor microenvironment to drive tumor progression via stimulation of cell survival/antiapoptosis, cell proliferation, angiogenesis and invasion/metastasis of the cancer cells. Therapeutic strategies that target dysfunctional or inflamed fat and have been shown to benefit patients include bariatric surgery, while other cell or hormone-directed interventions, such as conversion of visceral fat macrophages to an anti-inflammatory M2 phenotype or the pharmacological modulation of serum adipokine levels are still theoretical and need to be clinically evaluated for their ability to successfully treat or prevent obesity-related cancers.
    Der Internist 02/2015; DOI:10.1007/s00108-014-3536-4 · 0.27 Impact Factor
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    ABSTRACT: Objective: In inflammatory bowel disease (IBD), hepatic disorders are frequently due to nonalcoholic fatty liver disease and drug-induced hepatotoxicity. Immunosuppressive treatment is known to exert hepatotoxic side effects by a still unknown mode. The relevance of liver steatosis for the development of drug-related hepatotoxicity in IBD is unknown. Methods: The charts of 259 patients with IBD under immunosuppression with either azathioprine, 6-mercaptopurine, or methotrexate were reviewed. The prevalence of liver steatosis was assessed by means of ultrasound reports. Aspartate transaminase and alanine transaminase above the normal range were used to indicate liver abnormalities. Results: Liver steatosis on the basis of ultrasound criteria was observed in 73 patients (28.2%). In patients with liver steatosis, the presence of elevated liver enzymes (ELE) was found to be significantly more prevalent (28.8 vs. 14.5%, P=0.0095). The finding of liver steatosis was associated with higher age (44.1 vs. 34.5 years, P<0.0001) and body weight (BMI 26.7 vs. 23.4 kg/m2, P<0.0001). Development of ELE under immunosuppression was seen in 50 patients (19.3%). Of the patients who developed ELE, 44.0% (vs. 24.4%, P=0.0095) showed liver steatosis. Logistic regression analysis revealed that male individuals showed an increased likelihood of developing ELE associated with steatosis (P=0.0118, odds ratio=3.93) and that patients who received steroids less often developed ELE in association with liver steatosis (P=0.0414, odds ratio=0.31). Conclusion: This study suggests that fatty liver represents a risk factor for hepatotoxicity in patients with IBD under immunosuppressive treatment and should be routinely considered in treatment strategies.
    European Journal of Gastroenterology & Hepatology 01/2015; DOI:10.1097/MEG.0000000000000350 · 2.15 Impact Factor
  • Clinical Cancer Research 01/2015; DOI:10.1158/1078-0432.CCR-14-2751 · 8.19 Impact Factor
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    ABSTRACT: To investigate the prognostic role of genomic stability and copy number alterations (CNAs) pancreatic neuroendocrine tumors (PanNETs). A high-resolution array-based comparative genomic hybridization approach was utilized in order to investigate and quantify chromosomal aberrations in a panel of 37 primary PanNET and 11 metastatic samples. DNA samples were extracted from formalin-fixed and paraffin-embedded tumor specimen. Genomic findings were correlated with histopathological and immunohistochemical data. Moreover, the dataset was subjected to employing an unsupervised hierarchical clustering analysis approach utilizing Euclidean distance and average linkage and associations between genomically defined tumor groups and recurrent CNAs or clinicopathological features of the study group were assessed. Numerous chromosomal aberrations were recurrently detected in both, primary tumor samples and metastases. Copy number gains were most frequently observed at 06p22.2-p22.1 (27.1%), 17p13.1 (20.8%), 07p21.3-p21.2 (18.8%), 09q34.11 (18.8%). Genomic losses were significantly less frequent and the only recurrent aberration affected 08q24.3 (6.3%). Moreover, we detected a high degree of genomic heterogeneity between primary tumors and metastatic lesions. Unsupervised hierarchical clustering of loci affected by CNAs in more than 3 primary tumor samples revealed two genetically distinct tumor groups as well as two chromosomal clusters of genomic imbalances indicating a small subset of tumors with common molecular features (13.5%). Aberrations affecting 6p22.2-22.1, 8q24.3, 9q34.11 and 17p13.1 (P = 0.011; 0.003; 0.003; 0.001), were significantly associated with a poorer survival prognosis. This study suggests that several frequent CNAs in numerous candidate regions are involved in the pathogenesis and metastatic progression of PanNET.
    Experimental and Clinical Endocrinology & Diabetes 12/2014; 20(46):17498-506. DOI:10.3748/wjg.v20.i46.17498 · 1.76 Impact Factor
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    ABSTRACT: Context: Primary extranodal diffuse large B-cell lymphomas of the thyroid (ptDLBCL) constitute a rare entity, which until now are not fully explored. Objective: Due to recently published data genetically linking ptDLBCL to a subset of thyroid carcinoma, we assessed the occurrence of oncogenic mutations and copy number alterations (CNAs). Design: A high-resolution array-based comparative genomic hybridization approach (aCGH) was applied to quantify genomic aberrations in a study population of 21 ptDLBCL. Further, we investigated the frequency of mutations involving the BRAF, NRAS and MYD88-genes in correlation with immunohistochemical data. Results: Chromosomal gains were recurrently detected at 6p21.33-p21.31, 6p22.2, 12p13.31, 14q31.1, 14q32.33, 19p13.3 and 22q11.22, numeric losses were most frequently observed at 6p21.3-p21.31, 10q26.3, 19p13.3, 20q13.33 and 21q11.2. Aberrations affecting 6p22.2 and 14q32.33 as well as 22q11.22 differed slightly between GCB- and non-GCB-groups. Statistically significant deviations were detected at 20q13.33 and 21q11.2. These specific alterations do not seem to occur in thyroid carcinomas or other DLBCL, according to previously published literature. Analysis of BRAF and NRAS showed mutation frequencies of 4.8 % and 9.5 %, respectively. No MYD88 mutations could be detected in any of the analyzed cases. Fluorescence in situ hybridization demonstrated breakage events involving the BCL2-, BCL6- and cMYC-locus in 14.3%, 9.5% and 9.5%, respectively. Conclusions: Our study revealed ptDLBCL to be predominantly composed of the GCB-type, harboring no MYD88 mutations and showing infrequent mutations in the BRAF and NRAS genes. Additionally, aCGH showed no overlapping alterations between ptDLBCL and thyroid carcinomas or other nodal or extranodal DLBCL.
    Journal of Clinical Endocrinology &amp Metabolism 11/2014; 100(2):jc20143250. DOI:10.1210/jc.2014-3250 · 6.31 Impact Factor
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    ABSTRACT: Experiments in rodents suggest that hypothalamic insulin signaling essentially contributes to the acute control of peripheral glucose homeostasis. Against this background, we investigated in healthy humans whether intranasal (IN) insulin, which is known to effectively reach the brain compartment, impacts systemic glucose metabolism. Twenty overnight-fasted healthy, normal-weight men were IN administered 210 and 420 IU (10 and 20 IU every 15 min) of the insulin analogue aspart (ins-asp) and placebo, respectively, during experimental sessions lasting 6 h. The use of ins-asp rather than human insulin enabled us to disentangle exogenous and endogenous insulin kinetics. IN insulin dose-dependently decreased plasma glucose concentrations while reducing C-peptide and attenuating endogenous insulin levels. However, we also observed a slight dose-dependent permeation of ins-asp into the circulation. In control experiments mimicking the systemic but not the central nervous uptake of the IN 210 IU dose via IV infusion of ins-asp at a dose of 0.12 mIU/kg/24h (n=10), we obtained essentially identical effects on fasting plasma glucose concentrations. This pattern indicates that sustained IN insulin administration to the human brain to enhance central nervous insulin signaling does not acutely alter systemic glucose homeostasis beyond effects accounted for by concurrent mild hyperinsulinemia.
    Diabetes 10/2014; DOI:10.2337/db14-0931 · 8.47 Impact Factor
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    ABSTRACT: Primary mediastinal large B-cell lymphoma (PMBL) is a distinct subtype of diffuse large B-cell lymphoma (DLBCL) frequently observed in young patients. High-dose immunochemotherapy constitutes the current therapeutic gold-standard, despite significant toxicity and serious late effects. Several hotspots harboring oncogenic gain-of-function mutations were recently shown to pose vital hallmarks in activated B-cell like (ABC-) (CD79B, CARD11 and MYD88) and germinal center like (GCB-) DLBCL (EZH2), respectively. Several promising targeted-therapy approaches, derived from these findings, are currently under development.
    Anticancer research 10/2014; 34(10):5503-7. · 1.87 Impact Factor
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    ABSTRACT: Objectives The corticotrophin-releasing factor (CRF)/urocortin system is expressed in the adipose tissue of mammals but its functional role in this tissue remains unknown.Methods Pharmacological manipulation of CRF-Receptors, CRF1 and CRF2, activity was performed in 3T3L1 white pre-adipocytes and T37i brown pre-adipocytes during in vitro differentiation. The expression of genes of the CRF/Urocortin system and of markers of white and brown adipocytes was evaluated along with mitochondrial biogenesis and cellular oxygen consumption. Metabolic evaluation of corticosterone-deficient or supplemented Crhr null (Crhr(-/-)) mice and their wild-type controls was performed along with gene expression analysis carried out in white (WAT) and brown (BAT) adipose tissues.ResultsPeptides of the CRF/Urocortin system and their cognate receptors were expressed in both pre-adipocyte cell lines. In vitro pharmacological studies showed an inhibition of the expression of the CRF2 pathway by the constitutive activity of the CRF1 pathway. Pharmacological activation of CRF2 and, to a lesser extent, inhibition of CRF1 signaling induced molecular and functional changes indicating transdifferentiation of white pre-adipocytes and differentiation of brown pre-adipocytes. Crhr(-/-) mice showed increased expression of CRF2 and its agonist Urocortin 2 in adipocytes that was associated to brown conversion of WAT and activation of BAT. Crhr(-/-) mice were resistant to diet-induced obesity and glucose intolerance. Restoring physiological circulating corticosterone levels abrogated molecular changes in adipocytes and the favorable phenotype of Crhr(-/-) mice.Conclusions Our findings suggest the importance of the CRF2 pathway in the control of adipocyte plasticity. Increased CRF2 activity in adipocytes induces browning of WAT, differentiation of BAT and is associated with a favorable metabolic phenotype in mice lacking CRF1. Circulating corticosterone represses CRF2 activity in adipocytes and may thus regulate adipocyte physiology through the modulation of the local CRF/Urocortin system. Targeting CRF-receptor signaling specifically in the adipose tissue may represent a novel approach to tackle obesity.International Journal of Obesity accepted article preview online, 05 September 2014. doi:10.1038/ijo.2014.164.
    International journal of obesity (2005) 09/2014; DOI:10.1038/ijo.2014.164 · 5.39 Impact Factor
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    ABSTRACT: Purpose To show a rare case of Cushing’s disease and possible cause of failed transsphenoidal surgery. Method We report on a 50-year-old woman suffering from ACTH-dependent Cushing’s syndrome. Endocrinological work-up including low-dose/high-dose dexamethasone test (Liddle-test) and CRH test were clearly compatible with pituitary origin. Although an MRI showed no pituitary tumor, CRH-stimulated petrosal sinus sampling revealed a significant central-peripheral gradient in ACTH concentrations, rendering Cushing’s disease very likely. The patient underwent transsphenoidal surgery with negative exploration of the pituitary gland. After intraoperative re-evaluation of the preoperative MRI, a “polyp” at the bottom of the sphenoid sinus was identified. The intraoperative microscopic aspect as well as instantaneous sections and cytology of a biopsy confirmed an adenoma, which was then removed. Histological analysis demonstrated an ACTH-producing pituitary adenoma adjacent to respiratory mucous membrane consisting of ciliated epithelium with submucous connective tissue. Postoperatively, ACTH concentrations were decreased and intermittent hydrocortisone substitution treatment was initiated. At the 3-month follow up, Cushing’s stigmata were found to be alleviated and the hydrocortisone dosage could be reduced. Conclusion Ectopic pituitary adenoma tissue causing Cushing’s disease is extremely rare but a potential cause for surgical failure or re-evaluation.
    Pituitary 08/2014; 18(2). DOI:10.1007/s11102-014-0591-8 · 2.22 Impact Factor
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    ABSTRACT: The attenuated counterregulatory response to hypoglycaemia following antecedent hypoglycaemic episodes is associated with an increase in gamma-aminobutyric acid (GABA) signalling. We therefore tested the hypothesis that the pharmacological suppression of GABAergic activity during a repeated hypoglycaemic episode enhances counterregulatory responses. Fourteen healthy men participated in two experimental sessions each comprising three insulin-induced hypoglycaemic episodes. Before the third hypogylcaemia, participants received the GABA-antagonistic drug modafinil (200 mg orally) and placebo, respectively. In the placebo condition, the secretion of norepinephrine, ACTH, cortisol, and growth hormone and the perception of neuroglycopenic symptoms were attenuated during the third as compared to the first hypoglycaemic episode (each P<0.05). Modafinil reversed this effect for the noradrenergic response (P<0.05) while the attenuation of other hormonal responses and the perception of symptoms were not significantly affected (P>0.3). Our findings indicate that increases in GABAergic signalling could contribute to aspects of the attenuated counterregulatory response following recurrent hypoglycaemia in humans.
    Diabetes Obesity and Metabolism 07/2014; 16(12). DOI:10.1111/dom.12358 · 5.46 Impact Factor
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    ABSTRACT: Enteroendocrine cells (EEC) produce neuropeptides, which are crucially involved in the maintenance of the intestinal barrier. Hence, EEC dysfunction is suggested to be involved in the complex pathophysiology of inflammatory bowel disease (IBD), which is characterized by decreased intestinal barrier function. However, the underlying mechanisms for EEC dysfunction are not clear and suitable models for a better understanding are lacking. Here, we demonstrate that Carboxypeptidase E (CPE) is specifically expressed in EEC of the murine colon and ileum and that its deficiency is associated with reduced intestinal levels of Neuropeptide Y (NPY) and Peptide YY (PYY), which are both produced by EEC. Moreover, cpe-/- mice exhibit an aggravated course of DSS-induced chronic colitis compared to wildtype littermates. In addition, we observed elevated mucosal IL-6 and KC transcript levels already at baseline conditions in cpe-/- mice. Moreover, supernatants obtained from isolated intestinal crypts of cpe-/- mice lead to increased IL-6 and KC expression in MODE-K cells in the presence of LPS. This effect was reversible by co-administration of recombinant NPY, suggesting a CPE mediated immunosuppressive effect in the intestines by influencing the processing of specific neuropeptides. In this context, the chemotaxis of bone marrow derived macrophages towards respective supernatants was enhanced. In conclusion, our data point to an anti-inflammatory role of CPE in the intestine by influencing local cytokine levels and thus regulating the migration of myeloid immune cells into the mucosa. These findings highlight the importance of EEC for intestinal homeostasis and propose EEC as potential therapeutic targets in IBD.
    PLoS ONE 07/2014; 9(7):e102347. DOI:10.1371/journal.pone.0102347 · 3.53 Impact Factor
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    ABSTRACT: ABSTRACT Epstein-Barr Virus- (EBV) associated diffuse large B-cell lymphoma (DLBCL) of the elderly constitutes a provisional clinicopathological entity in the current WHO Classification and its genomic features remain sparsely characterized. We investigated a cohort of 26 untreated de novo EBV-positive DLBCL of the elderly by high-resolution array-based comparative genomic profiling and FISH. Moreover, we screened for activating mutations affecting nuclear factor (NF)-kappa B pathway signaling and chromatin remodeling (EZH2, CD79B, CARD11 and MYD88) due to their impact of gene expression signatures and postulated upcoming therapeutic targetability. We identified an overlap between genomic aberrations previously described to be exclusive features of plasmablastic lymphoma (PL), post-transplant lymphoprolierative disorders (PTLD) and DLBCL, respectively, indicating a close cytogenetic relation between these entities. Few mutations affecting CD79B and CARD11 and no MYD88 mutations were detectable hinting at an EBV-mediated activation of NF-kappa B as an alternative to pathologically enforced B-cell receptor signaling in this rare entity.
    Leukemia and Lymphoma 07/2014; DOI:10.3109/10428194.2014.944522 · 2.61 Impact Factor

Publication Stats

6k Citations
1,200.05 Total Impact Points

Institutions

  • 2008–2014
    • University Medical Center Schleswig-Holstein
      Kiel, Schleswig-Holstein, Germany
    • Universität zu Lübeck
      • Department of Internal Medicine I
      Lübeck Hansestadt, Schleswig-Holstein, Germany
  • 2007–2014
    • Universitätsklinikum Schleswig - Holstein
      Kiel, Schleswig-Holstein, Germany
    • University Hospitals Coventry and Warwickshire NHS Trust
      Coventry, England, United Kingdom
  • 2006–2014
    • The University of Warwick
      • Warwick Medical School (WMS)
      Coventry, England, United Kingdom
  • 2013
    • National Institutes of Health
      • Branch of Radiation Oncology
      Bethesda, MD, United States
  • 2011
    • Goethe-Universität Frankfurt am Main
      • Zentrum der Inneren Medizin
      Frankfurt am Main, Hesse, Germany
  • 2004–2011
    • Technische Universität Dresden
      • Institut für Klinische Pharmakologie
      Dresden, Saxony, Germany
  • 2010
    • Leiden University Medical Centre
      • Department of Nephrology
      Leyden, South Holland, Netherlands
  • 2009
    • Klinikum Stuttgart
      Stuttgart, Baden-Württemberg, Germany
  • 2005–2008
    • Coventry University
      Coventry, England, United Kingdom
  • 1995–2008
    • Otto-von-Guericke-Universität Magdeburg
      Magdeburg, Saxony-Anhalt, Germany
  • 1994–2006
    • University Hospital Magdeburg
      Magdeburg, Saxony-Anhalt, Germany
  • 2003
    • Max Planck Institute of Psychiatry
      München, Bavaria, Germany
    • Carl Gustav Carus-Institut
      Pforzheim, Baden-Württemberg, Germany
  • 1988–2000
    • Johannes Gutenberg-Universität Mainz
      • • III. Department of Medicine
      • • Abteilung für Retinologie
      Mayence, Rheinland-Pfalz, Germany
  • 1989–1993
    • Universität Trier
      • Department of Clinical Psychophysiology
      Trier, Rheinland-Pfalz, Germany
    • Universitätsklinikum Tübingen
      Tübingen, Baden-Württemberg, Germany
  • 1991
    • Max Planck Institute for Experimental Medicine
      Göttingen, Lower Saxony, Germany
  • 1987
    • Harvard University
      • Department of Nutrition
      Cambridge, Massachusetts, United States
  • 1984
    • Massachusetts Institute of Technology
      • Department of Brain and Cognitive Sciences
      Cambridge, Massachusetts, United States