K Mann

Central Institute of Mental Health, Mannheim, Baden-Württemberg, Germany

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Publications (540)1501.29 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Measurement of sex steroids is required to evaluate gonadal function, but normative data are lacking (especially for estimates of physiologically active testosterone). Using modern immunoassays, this study established sex-specific reference ranges (2.5% and 97.5% percentiles) for total testosterone (TOT), bioactive testosterone Vermeulen (BTV), free androgen index (FAI), free testosterone Sartorius (FTS), free testosterone Vermeulen (FTV), and sex hormone binding globulin (SHBG). In the comparative study, subjects were grouped by age (18-30; 31-50; >50 years), BMI (<25; 25-30; >30 kg/m(2)), and sex. Study participants were selected in such a way that each group comprised 12 subjects (e. g., 12 males between 18 and 30 years with a BMI of <25 kg/m(2), and so on), resulting in a total of 216 controls (108 males, 108 females; age: 40.3±1.0; BMI: 27.8±0.4). Multiple stepwise regression analyses were performed (covariates: age, BMI, sex), and sex-specific reference ranges were applied to 50 males (age: 46.1±2.3; BMI: 27.4±0.7) with suspected hypogonadism. Regression analysis identified the strongest predictor of each parameter apart from sex, resulting in age-specific (males: FAI, SHBG, BTV, FTV; females: TOT, FTS, SHBG), BMI-specific (males: TOT, FTS; females: FAI, BTV, FTV) and overall cutoffs for both sexes. In male patients, overall agreement between the results derived from the estimates (i. e., BTV, FTS, FTV) was high (with discordant results in only 4%). In summary, if both the endocrine workup and the clinical presentation were taken into account, the newly established reference ranges allowed reliable identification of hypogonadal males. © Georg Thieme Verlag KG Stuttgart · New York.
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    ABSTRACT: The thyrotropin receptor-cAMP pathway is central in growth regulation of thyroid cells and thyroid tumorigenesis, and it regulates expression of thyroid specific genes. Recently, 2 new protein kinase A-independent cAMP effectors named EPAC1 and 2 were described that activate additional intracellular pathways. The aim of our study was to investigate the role of EPAC proteins in growth regulation of thyroid cells and thyroid carcinomas. EPAC1 expression was investigated immunohistochemically in tissues of various thyroid tumors. Utilizing MTT assay, the effect of EPAC stimulation on proliferation in thyroid carcinoma cells and in non-transformed rat FRTL5 cells was investigated. The activation of intracellular signaling pathways was examined by RAP pull-down assay and Western blots. EPAC1 expression was strong in non-oxyphilic follicular thyroid adenomas and carcinomas and in follicular papillary thyroid carcinomas. It was moderate in oxyphilic follicular tumors and classical and tall cell papillary carcinomas. In contrast, EPAC1 expression was low in poorly differentiated carcinomas and very low in anaplastic carcinomas. Thyroid carcinoma cell lines showed no or very weak EPAC1 expression and exhibited no growth-promoting effect after EPAC stimulation. Non-transformed rat FRTL5 cells were growth-stimulated by an EPAC-specific cAMP-analogue and showed EPAC-dependent activation of RAP, ERK, and p70S6 kinase. EPAC1 expression and cellular response to EPAC activation in rat FRTL5 cells reflect cellular responses to cAMP and TSH stimulation in non-transformed thyroid cells. In undifferentiated thyroid carcinomas, loss of EPAC1 expression may be in accordance with the loss of thyroid-specific functions and the loss of responsiveness of the TSHR-cAMP pathway.
    Hormone and Metabolic Research 11/2014; · 2.04 Impact Factor
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    ABSTRACT: Thyroid dysfunction may impair fertility, course of pregnancy and fetal development. Physiological alterations of thyroid function parameters, that occur during pregnancy need to be distinguished from pathophysiological states of hypo- and hyperthyroidism. We performed a literature search (PubMed 1990-2013) and review relevant publications as well as consensus and practice guidelines of international thyroid/endocrine societies. Interpretation of thyroid function values in pregnancy must be based on trimester-specific TSH and T4 ranges. Alterations in thyroid function are present in up to 15% of pregnancies (0.4% overt hypothyroidism, 0.1-0.4% hyperthyroidism) and may lead to preventable complications in the pregnant woman and the fetus. Hypothyroidism is associated with an increased risk for abortion, premature delivery and stillbirth, besides impairment of neurocognitive development. The latter has also been shown in situations of grave iodine deficiency. In addition to new-born screening directed at early recognition of congenital hypothyroidism (incidence 0.03%), universal screening of all pregnant women should be implemented in health care guidelines. Newly diagnosed overt hypothyroidism in a pregnant woman requires immediate levothyroxine substitution at adequate doses. In subclinical hypothyroidism thyroid hormone replacement should be considered. Iodine supplementation is strongly recommended in all pregnant and breast-feeding women. Pregnancy causes a number of, that need to be of thyroid dysfunction. Both hypothyroidism and thyrotoxicosis may impair the course of pregnancy and may negatively affect the fetus. In particular, maternal hypothyroidism may lead to irreparable and detrimental deficits in the neurocognitive development of the fetus. Autoimmune thyroid disease is the most common cause of thyroid dysfunction in pregnancy. Hashimoto's thyroiditis is associated with impaired fertility and miscarriage, and may first manifest in pregnancy due to the increased thyroid hormone requirement. Graves' disease often shows a characteristic course in pregnancy with amelioration of thyrotoxicosis in the second half of pregnancy and exacerbation after delivery. In addition transplacental passage of maternal TSH receptor antibodies may lead to thyrotoxicosis in the fetus and/or newborn.
    Deutsche medizinische Wochenschrift (1946). 10/2014; 139(42):2148-2152.
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    ABSTRACT: Human brain anatomy is strikingly diverse and highly inheritable: genetic factors may explain up to 80% of its variability. Prior studies have tried to detect genetic variants with a large effect on neuroanatomical diversity, but those currently identified account for <5% of the variance. Here, based on our analyses of neuroimaging and whole-genome genotyping data from 1765 subjects, we show that up to 54% of this heritability is captured by large numbers of single-nucleotide polymorphisms of small-effect spread throughout the genome, especially within genes and close regulatory regions. The genetic bases of neuroanatomical diversity appear to be relatively independent of those of body size (height), but shared with those of verbal intelligence scores. The study of this genomic architecture should help us better understand brain evolution and disease.Molecular Psychiatry advance online publication, 16 September 2014; doi:10.1038/mp.2014.99.
    Molecular Psychiatry 09/2014; · 15.15 Impact Factor
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    ABSTRACT: Preceding studies have indicated that aberrant expression levels rather than genetic changes of GADD45γ, MEG3, and p8 gene might play a role in the pathogenesis of pituitary adenomas. We analysed their expression in various normal human tissues and in different pituitary tumour types, and investigated GADD45γ mutations in a subset of adenomas. Absolute quantification by real-time RT-PCR was performed in 24 normal tissues as well as in 34 nonfunctioning, 24 somatotroph, 12 corticotroph adenomas, 4 prolactinomas, 1 FSHoma, and in 6 normal pituitaries. Furthermore, we investigated the relationship between clinical data and gene expression. A subset was screened for GADD45γ mutations by single strand conformation polymorphism analysis (SSCP) and sequencing. All normal human tissues expressed GADD45γ, MEG3, and p8 mRNA. For GADD45γ, significantly lower expression levels were found in nonfunctioning adenomas compared with normal pituitary and somatotroph adenomas. P8 and MEG3 mRNA levels were significantly lower in nonfunctioning and corticotroph adenomas compared with normal pituitary. Expression of GADD45γ was significantly higher in pituitary adenomas of female patients. No mutation was found in the GADD45γ gene. GADD45γ, MEG3, and p8 appear to have physiological functions in a variety of human tissues. GADD45γ, MEG3, and P8 may be involved in the pathogenesis of nonfunctioning and corticotroph pituitary tumours. Female gender seems to predispose to slightly higher GADD45γ expression in pituitary adenomas. Mutations of the GADD45γ are unlikely to be involved in the pathogenesis of pituitary adenomas.
    Hormone and Metabolic Research 08/2014; 46(9):644-50. · 2.04 Impact Factor
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    ABSTRACT: We present a case of a patient suffering from metastatic differentiated thyroid carcinoma (DTC) and insufficient endogenous TSH production suspicious of secondary hypothyroidism. The use of recombinant human TSH (rhTSH) enabled us to administer a therapeutic activity of radioactive iodine (RAI) under maximal TSH-stimulation, achieving a marked decrease in thyroglobulin accompanied by a clinical improvement.
    Journal of endocrinological investigation 07/2014; 23(7):473-5. · 1.55 Impact Factor
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    ABSTRACT: Motivation is important for learning and cognition. While dopaminergic (D2) transmission in the ventral striatum (VS) is associated with motivation, learning and cognition are more strongly associated with function of the dorsal striatum, including activation in the caudate nucleus. A recent study found an interaction between intrinsic motivation and the DRD2/ANKK1 polymorphism (rs1800497), suggesting that A-carriers of rs1800497 are significantly more sensitive to motivation in order to improve during working memory (WM) training. Using data from the two large-scale imaging genetic datasets - IMAGEN (n=1080, age 13-15 years) and BrainChild (n~300, age 6-27) - we investigated whether rs1800497 is associated with WM. In the IMAGEN-dataset, we tested whether VS/caudate activation during reward anticipation was associated with WM performance and whether rs1800497 and VS/caudate activation interact to affect WM performance. We found that rs1800497 was associated with WM performance in IMAGEN and BrainChild. Higher VS and caudate activation during reward processing were significantly associated with higher WM performance (p<0.0001). An interaction was found between the DRD2/ANKK1 polymorphism rs1800497 and VS activation during reward anticipation on WM (p<0.01), such that carriers of the minor allele (A) showed a significant correlation between VS activation and WM, while the GG homozygotes did not, suggesting that the effect of VS BOLD on WM is modified by inter-individual genetic differences related to D2 dopaminergic transmission.Neuropsychopharmacology accepted article peview online, 09 April 2014; doi:10.1038/npp.2014.83.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 04/2014; · 8.68 Impact Factor
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    ABSTRACT: Despite the recognition that cortical thickness is heritable and correlates with intellectual ability in children and adolescents, the genes contributing to individual differences in these traits remain unknown. We conducted a large-scale association study in 1583 adolescents to identify genes affecting cortical thickness. Single-nucleotide polymorphisms (SNPs; n=54 837) within genes whose expression changed between stages of growth and differentiation of a human neural stem cell line were selected for association analyses with average cortical thickness. We identified a variant, rs7171755, associating with thinner cortex in the left hemisphere (P=1.12 × 10(-)(7)), particularly in the frontal and temporal lobes. Localized effects of this SNP on cortical thickness differently affected verbal and nonverbal intellectual abilities. The rs7171755 polymorphism acted in cis to affect expression in the human brain of the synaptic cell adhesion glycoprotein-encoding gene NPTN. We also found that cortical thickness and NPTN expression were on average higher in the right hemisphere, suggesting that asymmetric NPTN expression may render the left hemisphere more sensitive to the effects of NPTN mutations, accounting for the lateralized effect of rs7171755 found in our study. Altogether, our findings support a potential role for regional synaptic dysfunctions in forms of intellectual deficits.Molecular Psychiatry advance online publication, 11 February 2014; doi:10.1038/mp.2013.197.
    Molecular Psychiatry 02/2014; · 15.15 Impact Factor
  • Suchttherapie 09/2013; 14(S 01). · 0.28 Impact Factor
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    ABSTRACT: Genetic variation in a genomic region on chromosome 15q25.1, which encodes the alpha5, alpha3, and beta4 subunits of the cholinergic nicotinic receptor genes, confers risk to smoking and nicotine dependence (ND). Neural reward-related responses have previously been identified as important factors in the development of drug dependence involving ND. Applying an imaging genetics approach in two cohorts (N=487; N=478) of healthy non-smoking adolescents we aimed to elucidate the impact of genome-wide significant smoking-associated variants in the CHRNA5-CHRNA3-CHRNB4 gene cluster on reward-related neural responses in central regions such as the striatum, orbitofrontal and anterior cingulate cortex and personality traits related to addiction. In both samples carriers of the rs578776 GG compared with AG/AA genotype showed a significantly lower neural response to reward outcomes in the right ventral and dorsal anterior cingulate cortex but not the striatum or the orbitofrontal cortex. Rs578776 was unrelated to neural reward anticipation or reward magnitude. Significantly higher scores of anxiety sensitivity in GG compared to AG/AA carriers were found only in sample 1. Associations with other personality traits were not observed. Our findings suggest that the rs578776 risk variant influences susceptibility to ND by dampening the response of the anterior cingulate cortex to reward feedback, without recruiting the striatum or orbitofrontal cortex during feedback or anticipation. Thus it seems to have a major role in the processing of and behavioral adaptation to changing reward outcomes.Neuropsychopharmacology accepted article preview online, 21 May 2013; doi:10.1038/npp.2013.131.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 05/2013; · 8.68 Impact Factor
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    ABSTRACT: BACKGROUND:: For patients treated with citalopram, it was recently shown that serum concentrations above 50 ng/mL on day 7 of treatment are associated with an improved therapeutic outcome. The aim of this post hoc analysis was to calculate a potential cost-effectiveness of therapeutic drug monitoring (TDM) considering costs for hospitalization, medication, and drug analysis. METHODS:: The study included patients with major depression. Weekly measurements of serum concentrations and assessments of psychopathology were conducted. RESULTS:: Fifty-five patients were included in this analysis. For patients with high citalopram serum concentrations (>50 ng/mL), the mean duration of hospitalization was 49 ± 20 days, and it was 72 ± 37 days (P = 0.03) in the group with low drug concentrations (<50 ng/mL). Considering daily costs for hospitalization of 250&OV0556;, the potential savings amounted to 5750&OV0556; per patient for the 23 days. Assuming that 11% of the variation of duration of hospitalization per patient were attributed to the serum concentration of the drug, the resulting savings were 633&OV0556; per patient. Considering the officially listed price of 21&OV0556; per TDM assay, total costs for weekly measurements over a period of 10 weeks of hospitalization were 210&OV0556;. In the groups with high and low serum concentrations, daily costs for citalopram medication were 3.00 ± 0.80&OV0556; and 2.42 ± 0.70&OV0556;, respectively (P = 0.002), and the mean number of comedications was nearly identical, that is, 1.87 ± 1.74 and 1.81 ± 1.86 drugs, respectively (P = 0.919). CONCLUSIONS:: The data taken together indicate that TDM-guided dosing of citalopram has the potential to be cost effective by reducing the length of hospitalization.
    Therapeutic drug monitoring 05/2013; · 2.43 Impact Factor
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    ABSTRACT: Für die Entstehung und Aufrechterhaltung von Suchtverhalten kommt dem belohnungsassoziierten Lernen eine zentrale Rolle zu. Die hierbei zugrunde liegenden neurobiologischen Grundlagen und die assoziierten neuropsychologischen Mechanismen werden vorgestellt und Parallelen von Substanzabhängigkeit und Verhaltenssüchten aufgezeigt. Im zweiten Abschnitt des Beitrages werden spezifische Befunde zu Veränderungen neurobiologischer Prozesse bei pathologischem Glücksspielen und Computer- und Internetsucht mittels funktioneller Bildgebung herausgearbeitet. Der Schwerpunkt liegt dabei auf Veränderungen in neurokognitiven Prozessen wie Reiz-Reaktivität, Verarbeitung von Belohnung und Bestrafung sowie Verhaltenskontrolle.
    Der Nervenarzt 05/2013; 84(5). · 0.86 Impact Factor
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    ABSTRACT: Die Zahl von Betroffenen mit ,,Verhaltenssüchten“ nimmt vor allem bei Jugendlichen und jungen Erwachsenen deutlich zu. Psychiater und Psychotherapeuten erwarten Hinweise zur diagnostischen Einordnung und zum therapeutischen Vorgehen. Wir diskutieren nosologische Aspekte und empfehlen Glücksspiel und exzessiven Computer- und Internetgebrauch als Verhaltenssüchte zu behandeln. In Einzelfällen kann das Suchtmodell auch bei pathologischem Kaufen, exzessivem Sexualverhalten und Adipositas therapeutisch genutzt werden.
    Der Nervenarzt 05/2013; 84(5). · 0.86 Impact Factor
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    ABSTRACT: Abnormalities in white-matter (WM) microstructure, as lower fractional anisotropy (FA), have been reported in adolescent-onset bipolar disorder and in youth at familial risk for bipolarity. We sought to determine whether healthy adolescents with subthreshold bipolar symptoms (SBP) would have early WM microstructural alterations and whether those alterations would be associated with differences in gray-matter (GM) volumes. Forty-two adolescents with three core manic symptoms and no psychiatric diagnosis, and 126 adolescents matched by age and sex, with no psychiatric diagnosis or symptoms, were identified after screening the IMAGEN database of 2223 young adolescents recruited from the general population. After image quality control, voxel-wise statistics were performed on the diffusion parameters using tract-based spatial statistics in 25 SBP adolescents and 77 controls, and on GM and WM images using voxel-based morphometry in 30 SBP adolescents and 106 controls. As compared with healthy controls, adolescents with SBP displayed lower FA values in a number of WM tracts, particularly in the corpus callosum, cingulum, bilateral superior and inferior longitudinal fasciculi, uncinate fasciculi and corticospinal tracts. Radial diffusivity was mainly higher in posterior parts of bilateral superior and inferior longitudinal fasciculi, inferior fronto-occipital fasciculi and right cingulum. As compared with controls, SBP adolescents had lower GM volume in the left anterior cingulate region. This is the first study to investigate WM microstructure and GM morphometric variations in adolescents with SBP. The widespread FA alterations in association and projection tracts, associated with GM changes in regions involved in mood disorders, suggest altered structural connectivity in those adolescents.Molecular Psychiatry advance online publication, 30 April 2013; doi:10.1038/mp.2013.44.
    Molecular Psychiatry 04/2013; · 15.15 Impact Factor
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    ABSTRACT: Reward learning represents a crucial mechanism in the acquisition and maintenance of addictive behavior. The underlying neurobiological foundations and associated neurobiological pathways are identified in this review and similarities between substance abuse and behavioral addictions will be discussed. In the second section current neuroimaging findings on neurobiological mechanisms of pathological gambling and computer and internet addiction are discussed. The main focuses are on changes in neurocognitive processes, such as cue reactivity, reward and punishment processing and behavioral control.
    Der Nervenarzt 04/2013; · 0.86 Impact Factor
  • Experimental and Clinical Endocrinology & Diabetes 03/2013; 121(03). · 1.76 Impact Factor
  • C Berg, J Chittamadathil, S Petersenn, M Walensi, M Broecker-Preuss, M Bauer, S Möhlenkamp, U Roggenbuck, N Lehmann, IE Sandalcioglu, U Sure, KH Jöckel, R Erbel, K Mann, D Führer
    Experimental and Clinical Endocrinology & Diabetes 03/2013; 121(03). · 1.76 Impact Factor
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    ABSTRACT: Coronary risk factors in patients with acromegaly after first-line transsphenoidal surgery (TSS) or first-line somatostatine analogue (SSA) treatment have rarely been examined. Aim of this study was an evaluation of cardiovascular risk factors and left ventricular hypertrophy (LVH) in 3 different patient groups with treatment naïve, active (ACT), first-line medically controlled (MED) and first-line surgically treated (SUR) acromegaly and a calculation of the Framingham Weibull Risk Score (FS).Retrospective comparative matched case-control study.40 acromegalic patients (cases aged 45-74 years, 23 men) were matched with respect to age and gender to 200 controls from the general population. 13 patients had treatment-naïve acromegaly (ACT), 12 patients were SSA treated (MED) and 15 patients were operated by TSS (SUR). Coronary risk factors were assessed after 12 months of treatment by interviews and direct laboratory measurements. Only patients normalized for IGF-I in MED and SUR group were included. FS and odds ratios (OR) from multiple conditional logistic regression (matched for age and gender, adjusted for BMI) were calculated.Compared to matched controls ACT patients had higher HbA1c levels (6.9±1.4 vs. 5.5±0.7% (p<0.0001)) and an increased prevalence of left ventricular hypertrophy (LVH) (30.8 vs. 3.2% (p=0.007). MED and SUR groups were similar for gender, age, disease duration and IGF-I levels at diagnosis. Compared to matched controls, MED patients had a significantly increased diastolic blood pressure (89±9 vs. 79±11 mmHg (p=0.001), prevalence of LVH (41.7 vs. 1.7% (p<0.0001), prevalence of diabetes mellitus (33.3 vs. 10.0% (p=0.03)), higher HbA1c levels (6.8±1.3 vs. 5.5±0.7% (p=0.0005)) and a higher FS (21.2±9.7 vs. 12.4±7.7% (p=0.002), OR 1.11 [1.02-1.21] (p=0.01)) while in the SUR group only higher prevalences of LVH (40.0 vs. 4.1% (p<0.0001)) and HbA1c levels (6.4±1.2 vs. 5.5±0.8% (p=0.006)) were found compared to controls.When comparing treatment naive, medically treated and surgically cured patients with acromegaly to age- and gender-matched subjects from the general population, we have found an increased cardiovascular risk in patients at 12 months after first-line SSA treatment but not in patients after first-line surgery.
    Experimental and Clinical Endocrinology & Diabetes 01/2013; · 1.76 Impact Factor
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    ABSTRACT: Background: The American (ATA) and the European Thyroid Association (ETA) recommend a thyroid scintiscan for the detection of a suspected autonomy only when serum thyrotropin (TSH) levels are low or suppressed. If ultrasound reveals a thyroid nodule > 1.0 cm and TSH is normal, a fine-needle biopsy is recommended without a preceding scintiscan as the next step. The aim of this prospective study was to evaluate the incidence of reduced or suppressed TSH in 100 autonomous adenoma > 1.0 cm and to clarify, if normal TSH does substantially exclude a focal autonomy. When the study was conducted no data of German patients were available. Patients and Methods: An unselected group of 496 patients with a nodular goiter was continuously screened by scintiscan in order to detect 100 autonomous adenoma > 1.0 cm for the study. The following investigations were carried out: ultrasound, scintiscan and laboratory tests (fT3, fT4, TSH, TPO-antibodies). The reference range of TSH was 0.4 to 4.0 µU/ml.Results: 21% of patients (100/476) with a nodular goiter had a focal autonomy. 32 % (32/100) of autonomous adenoma revealed a reduced (< 0.4 µU/ml) or completely suppressed TSH, while in 68 % (68/100) normal TSH level were found.Conclusion: In Germany autonomous adenoma are still frequent (21 % of all thyroid nodules). Most of them (68 %) reveal normal TSH levels. Our data demonstrate, that there is no relevant connection between TSH level and autonomous adenoma detected by scintiscan. In most cases, TSH is not able to discriminate, whether a nodule is autonomous or not. Biopsy of undetected autonomous nodules should not be performed, as they often show cytological features of follicular neoplasias. In thyroid nodules > 1.0 cm a scintiscan should routinely be performed in primary diagnostics to avoid unnecessary fine-needle biopsy of autonomous adenoma.
    DMW - Deutsche Medizinische Wochenschrift 10/2012; 137(41):2089-92. · 0.65 Impact Factor

Publication Stats

6k Citations
1,501.29 Total Impact Points


  • 2000–2014
    • Central Institute of Mental Health
      • Klinik für Abhängiges Verhalten und Suchtmedizin
      Mannheim, Baden-Württemberg, Germany
  • 1997–2014
    • University Hospital Essen
      • • Institut für Medizinische Informatik, Biometrie und Epidemiologie
      • • Institut für Medizinische Psychologie und Verhaltensimmunbiologie
      • • Klinik für Endokrinologie
      Essen, North Rhine-Westphalia, Germany
  • 2013
    • University of Bonn
      Bonn, North Rhine-Westphalia, Germany
  • 1995–2013
    • University of Duisburg-Essen
      • • Department of Internal and Integrative Medicine
      • • Faculty of Medicine
      Essen, North Rhine-Westphalia, Germany
    • Universitätsklinikum Jena
      Jena, Thuringia, Germany
  • 2009
    • Endokrinologikum Hamburg
      Hamburg, Hamburg, Germany
    • Friedrich-Alexander Universität Erlangen-Nürnberg
      Erlangen, Bavaria, Germany
  • 2003–2009
    • Universität Heidelberg
      • Central Institute of Mental Health
      Heidelberg, Baden-Wuerttemberg, Germany
    • University of Innsbruck
      • Institute of Biochemistry
      Innsbruck, Tyrol, Austria
  • 1994–2009
    • Johannes Gutenberg-Universität Mainz
      • Klinik und Poliklinik für Psychosomatische Medizin und Psychotherapie
      Mainz, Rhineland-Palatinate, Germany
  • 1989–2009
    • University of Tuebingen
      • • Department of Psychiatry and Psychotherapy
      • • Department of Neurology
      Tübingen, Baden-Wuerttemberg, Germany
  • 2008
    • Universität Mannheim
      Mannheim, Baden-Württemberg, Germany
    • Universitätsklinikum Freiburg
      • Department of Psychiatry and Psychotherapy
      Freiburg, Lower Saxony, Germany
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 2007–2008
    • Brigham and Women's Hospital
      • Division of General Internal Medicine and Primary Care
      Boston, MA, United States
    • Technische Universität Dresden
      Dresden, Saxony, Germany
  • 2006
    • Charité Universitätsmedizin Berlin
      • Medical Department, Division of Hepatology and Gastroenterology
      Berlin, Land Berlin, Germany
  • 2005
    • Kliniken Essen-Mitte Knappschafts-Krankenhaus
      Essen, North Rhine-Westphalia, Germany
    • Universität Ulm
      Ulm, Baden-Württemberg, Germany
  • 2002
    • Humboldt-Universität zu Berlin
      • Department of Psychology
      Berlin, Land Berlin, Germany
  • 2001
    • Clinic for Minimally Invasive Surgery
      Berlín, Berlin, Germany
    • Royal Prince Alfred Hospital
      Camperdown, New South Wales, Australia
  • 1992–1999
    • Austrian Academy of Sciences
      • Institut für Biomedizinische Alternsforschung
      Vienna, Vienna, Austria
  • 1990–1996
    • Ludwig-Maximilian-University of Munich
      • Department of Internal Medicine II
      München, Bavaria, Germany
  • 1992–1995
    • Psychiatrische Universitätsklinik Zürich
      Zürich, Zurich, Switzerland
  • 1985–1995
    • Universitätsklinikum Tübingen
      Tübingen, Baden-Württemberg, Germany
  • 1993
    • University of Pennsylvania
      • Department of Psychiatry
      Philadelphia, PA, United States
  • 1988–1993
    • Technische Universität München
      • Medizinische Klinik und Poliklinik III - Hämatologie/Onkologie
      München, Bavaria, Germany
  • 1979–1988
    • University Hospital München
      München, Bavaria, Germany