johannes Hebebrand - Academia.edu (original) (raw)
Papers by johannes Hebebrand
Molecular Psychiatry, 2014
We conducted a genome-wide association study (GWAS) of anorexia nervosa (AN) using a stringently ... more We conducted a genome-wide association study (GWAS) of anorexia nervosa (AN) using a stringently defined phenotype. Analysis of phenotypic variability led to the identification of a specific genetic risk factor that approached genome-wide significance (rs929626 in EBF1 (Early B-Cell Factor 1); P = 2.04 × 10 −7 ; OR = 0.7; 95% confidence interval (CI) = 0.61-0.8) with independent replication (P = 0.04), suggesting a variant-mediated dysregulation of leptin signaling may play a role in AN. Multiple SNPs in LD with the variant support the nominal association. This demonstrates that although the clinical and etiologic heterogeneity of AN is universally recognized, further careful sub-typing of cases may provide more precise genomic signals. In this study, through a refinement of the phenotype spectrum of AN, we present a replicable GWAS signal that is nominally associated with AN, highlighting a potentially important candidate locus for further investigation. Anorexia nervosa (AN) is a complex and often chronic eating disorder characterized by inability to maintain a normal healthy body weight and a persistent fear of weight gain, resulting in extreme emaciation and even death in some cases 1. Previous genetic and epidemiological studies have indicated a multifactorial etiology, where both genetic and environmental factors contribute to disease risk 2-7. As sample sizes have increased, genome-wide association studies (GWASs) of AN have begun to identify risk variants 8-10. To further elucidate the genetic architecture of AN, we performed a GWAS using data from our previously published study 8 consisting of 1,033 AN cases by excluding 212 patients with AN who experienced diagnostic crossover during the course of their illness. Specifically, we excluded patients who migrated from or to binge-eating disorder (BED) or bulimia nervosa (BN) as assessed with the Structured Interview for Anorexic and Bulimic Disorders 11). Although a previous study indicated women with BN were rarely to cross over to AN 12 , we observed ~43% of AN/BN crossover cases falls into this category in our cohort, suggestive of a confounding factor. We hypothesized that this reduction in phenotypic heterogeneity, despite the fact that AN and BN may share some genetic risk factors 13 , would enhance gene discovery. Results Our discovery cohort included a total of 692 female AN cases of non-Hispanic European (NHE) descent. Cases were included if they were diagnosed with restricting type and binge eating/purging type of AN as defined by
Obesity Facts, 2012
Objective: The common single nucleotide polymorphism (SNP) rs9939609 in the fat mass and obesity-... more Objective: The common single nucleotide polymorphism (SNP) rs9939609 in the fat mass and obesity-associated gene ( FTO ) is associated with obesity. As genetic variants associated with weight regulation might also be implicated in the etiology of eating disorders, we evaluated whether SNP rs9939609 is associated with bulimia nervosa (BN) and anorexia nervosa (AN). Methods: Association of rs9939609 with BN and AN was assessed in 689 patients with AN, 477 patients with BN, 984 healthy non-population-based controls, and 3,951 populationbased controls (KORA-S4). Based on the familial and premorbid occurrence of obesity in patients with BN, we hypothesized an association of the obesity risk A-allele with BN. Results: In accordance with our hypothesis, we observed evidence for association of the rs9939609 A-allele with BN when compared to the non-population-based controls (unadjusted odds ratio (OR) = 1.142, one-sided 95% confidence interval (CI) 1.001-G ; one-sided p = 0.049) and a trend in the population-based controls (OR = 1.124, one-sided 95% CI 0.932-G ; one-sided p = 0.056). Interestingly, compared to both control groups, we further detected a nominal association of the rs9939609 A-allele to AN (OR = 1.181, 95% CI 1.027-1.359, two-sided p = 0.020 or OR = 1.673, 95% CI 1.101-2.541, two-sided p = 0.015,). Conclusion: Our data suggest that the obesity-predisposing FTO allele might be relevant in both AN and BN. (N = 232); or at the Fondazione Centro San Raffaelle del Monte Tabor, Milan, Italy (N = 272). Anthropometric data of the study subjects are listed in table 1 .
Human molecular genetics, Jan 17, 2015
Polymorphisms rs6232 and rs6234/rs6235 in PCSK1 have been associated with extreme obesity (e.g. b... more Polymorphisms rs6232 and rs6234/rs6235 in PCSK1 have been associated with extreme obesity (e.g. body mass index [BMI]≥40 kg/m(2)), but their contribution to common obesity (BMI≥30 kg/m(2)) and BMI variation in a multi-ethnic context is unclear. To fill this gap, we collected phenotypic and genetic data in up to 331,175 individuals from diverse ethnic groups. This process involved a systematic review of the literature in PubMed, Web of Science, Embase and the NIH GWAS catalog complemented by data extraction from pre-existing GWAS or custom-arrays in consortia and single studies. We employed recently developed global meta-analytic random-effects methods to calculate summary odds ratios (OR) and 95% confidence intervals (CI) or beta estimates and standard errors (SE) for the obesity status and BMI analyses, respectively. Significant associations were found with binary obesity status for rs6232 (OR=1.15, 95% CI 1.06-1.24, P=6.08x10(-6)) and rs6234/rs6235 (OR=1.07, 95% CI 1.04-1.10, P=3.00x10(-7)). Similarly, significant associations were found with continuous BMI for rs6232 (beta=0.03, 95% CI 0.00-0.07; P=0.047) and rs6234/rs6235 (beta=0.02, 95% CI 0.00-0.03; P=5.57x10(-4)). Ethnicity, age and study ascertainment significantly modulated the association of PCSK1 polymorphisms with obesity. In summary, we demonstrate evidence that common gene variation in PCSK1 contributes to BMI variation and susceptibility to common obesity in the largest known meta-analysis published to date in genetic epidemiology.
Child and adolescent psychiatric clinics of North America, 2009
Child and adolescent psychiatric clinics of North America, 2009
Current opinion in psychiatry, 2010
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2013
MMW Fortschritte der Medizin, Jan 15, 2006
European Child & Adolescent Psychiatry, 2014
Journal of Neural Transmission, 2003
The authors explored the binge eating symptomatology in 74 patients receiving clozapine (N = 57) ... more The authors explored the binge eating symptomatology in 74 patients receiving clozapine (N = 57) or olanzapine (N = 17), and compared body mass index (BMI, kg/m2) and weight gain in patients with and without binge eating symptomatology. Subjects who screened positively for binge eating were interviewed using a modified version of the Questionnaire on Eating and Weight Patterns (QEWP). Current BMIs were assessed cross-sectionally, BMIs at initiation of clozapine/olanzapine treatment retrospectively. Thirty-seven subjects (50%) screened positively. Taking clozapine and olanzapine together, 6/27 (22.2%) females and 3/47 (6.4%) males fulfilled criteria for binge eating disorder, 3/27 (11.1%) females and 2/47 (4.3%) males for bulimia nervosa. Patients who screened positively showed higher current BMIs (26.8 ± 3.9 vs. 24.7 ± 3.7 kg/m2) and higher BMI increments during clozapine/olanzapine treatment (3.9 ± 3.1 vs. 2.6 ± 3.4 kg/m2) than patients who screened negatively. We conclude that clozapine/olanzapine may induce binge eating and full blown eating disorders which may have predictive value for weight gain. For future research in this field we suggest a novel DSM-IV research classification “Medication-induced eating disorders”.
European Child & Adolescent Psychiatry, 2014
Prenatal alcohol exposure (PAE) is one of the most prevalent and modifiable risk factors for soma... more Prenatal alcohol exposure (PAE) is one of the most prevalent and modifiable risk factors for somatic, behavioral, and neurological abnormalities. Affected individuals exhibit a wide range of such features referred to as fetal alcohol spectrum disorders (FASD). These are characterized by a more or less specific pattern of minor facial dysmorphic features, growth deficiency and central nervous system symptoms. Nevertheless, whereas the diagnosis of the full-blown fetal alcohol syndrome does not pose a major challenge, only a tentative diagnosis of FASD can be reached if only mild features are present and/or maternal alcohol consumption during pregnancy cannot be verified. The respective disorders have lifelong implications. The teratogenic mechanisms induced by PAE can lead to various additional somatic findings and structural abnormalities of cerebrum and cerebellum. At the functional level, cognition, motor coordination, attention, language development, executive functions, memory, social perception and emotion processing are impaired to a variable extent. The long-term development is characterized by disruption and failure in many domains; an age-adequate independency is frequently not achieved. In addition to primary prevention, individual therapeutic interventions and tertiary prevention are warranted; provision of extensive education to affected subjects and their caregivers is crucial. Protective environments are often required to prevent negative consequences such as delinquency, indebtedness or experience of physical/sexual abuse.
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2014
The fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) resulted ... more The fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) resulted in substantial changes with regard to the classification of Eating Disorders. In DSM-5, Feeding and Eating Disorders are for the first time subsumed in a single category. The Binge Eating Disorder (BED) was established as the third classical eating disorder in addition to Anorexia Nervosa (AN) and Bulimia Nervosa (BN). The criteria for AN changed remarkably, whereas there were only minor changes to the BN criteria. The criteria for BED differ only marginally from the DSM-IV research criteria. There are now subtypes of AN, BN, and BED in the new category "Other Specific Feeding and Eating Disorders." The rest category "Eating Disorders Not Otherwise Specified" has been renamed to "Unspecified Feeding or Eating Disorders." The practicability of the DSM-5 criteria for Eating Disorders, and for AN in particular, for both clinical practice and research remains to be seen.
American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2014
Deviations from normal body weight are observed prior to and after the onset of Alzheimer's disea... more Deviations from normal body weight are observed prior to and after the onset of Alzheimer's disease (AD). Midlife obesity confers increased AD risk in later life, whereas late-life obesity is associated with decreased AD risk. The role of underweight and weight loss for AD risk is controversial. Based on the hypothesis of shared genetic variants for both obesity and AD, we analyzed the variants identified for AD or obesity from genome-wide association meta-analyses of the GERAD (AD, cases ¼ 6,688, controls ¼ 13,685) and GIANT (body mass index [BMI] as measure of obesity, n ¼ 123,865) consortia. Our cross-disorder analysis of genome-wide significant 39 obesity SNPs and 23 AD SNPs in these two large data sets revealed that: (1) The AD SNP rs10838725 (p AD ¼ 1.1 Â 10 À08 ) at the locus CELF1 is also genome-wide significant for obesity (p BMI ¼ 7.35 Â 10 À09 ). (2) Four additional AD risk SNPs were nominally associated with obesity (rs17125944 at FERMT2, p BMI ¼ 4.03 Â 10 À05 , p BMI corr ¼ 2.50 Â 10 À03 ; rs3851179 at PICALM; p BMI ¼ 0.002, rs2075650 at TOMM40/APOE, p BMI ¼ 0.024, rs3865444 at CD33, p BMI ¼ 0.024). (3) SNPs at two of the obesity risk loci (rs4836133 downstream of ZNF608; p AD ¼ 0.002 and at rs713586 downstream of RBJ/DNAJC27; p AD ¼ 0.018) were nominally associated with AD risk. Additionally, among the SNPs used for confirmation in both studies the AD risk allele of rs1858973, with an AD association just below genome-wide significance (p AD ¼ 7.20 Â 10 À07 ), was also associated with obesity (SNP at
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2012
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2011
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2009
The provision of good mentors and education to medical students in their residency (PJ students) ... more The provision of good mentors and education to medical students in their residency (PJ students) bears three essential advantages: 1) If the students feel themselves in good hands, they will co-operate effectively, thereby reducing the burden of the medical staff. 2) Contented students are potential advertisers for other interns, clinical trainees, medical students in residency and Ph.D. students. 3) Given the lack of doctors, providing students with good mentors and training is a valuable long-term strategy for the recruitment of doctors; in the event of later employment, former students in residency represent employees who are motivated, well trained, and familiar with hospital routine--a classical win-win situation.
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2010
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2006
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2013
Verhaltenstherapie, 2006
... Jan-Michael Dierk Matthias Conradt Pia Schlumberger Elisabeth Rauh Christina Albohn Anke Hinn... more ... Jan-Michael Dierk Matthias Conradt Pia Schlumberger Elisabeth Rauh Christina Albohn Anke Hinney Johannes Hebebrand Winfried Rief ... genetischer Faktoren hin: in den letzten Jahren konnten Muta-tionen definiert werden, die als Ursache der Adipositas anzu-sehen sind. ...
Molecular Psychiatry, 2014
We conducted a genome-wide association study (GWAS) of anorexia nervosa (AN) using a stringently ... more We conducted a genome-wide association study (GWAS) of anorexia nervosa (AN) using a stringently defined phenotype. Analysis of phenotypic variability led to the identification of a specific genetic risk factor that approached genome-wide significance (rs929626 in EBF1 (Early B-Cell Factor 1); P = 2.04 × 10 −7 ; OR = 0.7; 95% confidence interval (CI) = 0.61-0.8) with independent replication (P = 0.04), suggesting a variant-mediated dysregulation of leptin signaling may play a role in AN. Multiple SNPs in LD with the variant support the nominal association. This demonstrates that although the clinical and etiologic heterogeneity of AN is universally recognized, further careful sub-typing of cases may provide more precise genomic signals. In this study, through a refinement of the phenotype spectrum of AN, we present a replicable GWAS signal that is nominally associated with AN, highlighting a potentially important candidate locus for further investigation. Anorexia nervosa (AN) is a complex and often chronic eating disorder characterized by inability to maintain a normal healthy body weight and a persistent fear of weight gain, resulting in extreme emaciation and even death in some cases 1. Previous genetic and epidemiological studies have indicated a multifactorial etiology, where both genetic and environmental factors contribute to disease risk 2-7. As sample sizes have increased, genome-wide association studies (GWASs) of AN have begun to identify risk variants 8-10. To further elucidate the genetic architecture of AN, we performed a GWAS using data from our previously published study 8 consisting of 1,033 AN cases by excluding 212 patients with AN who experienced diagnostic crossover during the course of their illness. Specifically, we excluded patients who migrated from or to binge-eating disorder (BED) or bulimia nervosa (BN) as assessed with the Structured Interview for Anorexic and Bulimic Disorders 11). Although a previous study indicated women with BN were rarely to cross over to AN 12 , we observed ~43% of AN/BN crossover cases falls into this category in our cohort, suggestive of a confounding factor. We hypothesized that this reduction in phenotypic heterogeneity, despite the fact that AN and BN may share some genetic risk factors 13 , would enhance gene discovery. Results Our discovery cohort included a total of 692 female AN cases of non-Hispanic European (NHE) descent. Cases were included if they were diagnosed with restricting type and binge eating/purging type of AN as defined by
Obesity Facts, 2012
Objective: The common single nucleotide polymorphism (SNP) rs9939609 in the fat mass and obesity-... more Objective: The common single nucleotide polymorphism (SNP) rs9939609 in the fat mass and obesity-associated gene ( FTO ) is associated with obesity. As genetic variants associated with weight regulation might also be implicated in the etiology of eating disorders, we evaluated whether SNP rs9939609 is associated with bulimia nervosa (BN) and anorexia nervosa (AN). Methods: Association of rs9939609 with BN and AN was assessed in 689 patients with AN, 477 patients with BN, 984 healthy non-population-based controls, and 3,951 populationbased controls (KORA-S4). Based on the familial and premorbid occurrence of obesity in patients with BN, we hypothesized an association of the obesity risk A-allele with BN. Results: In accordance with our hypothesis, we observed evidence for association of the rs9939609 A-allele with BN when compared to the non-population-based controls (unadjusted odds ratio (OR) = 1.142, one-sided 95% confidence interval (CI) 1.001-G ; one-sided p = 0.049) and a trend in the population-based controls (OR = 1.124, one-sided 95% CI 0.932-G ; one-sided p = 0.056). Interestingly, compared to both control groups, we further detected a nominal association of the rs9939609 A-allele to AN (OR = 1.181, 95% CI 1.027-1.359, two-sided p = 0.020 or OR = 1.673, 95% CI 1.101-2.541, two-sided p = 0.015,). Conclusion: Our data suggest that the obesity-predisposing FTO allele might be relevant in both AN and BN. (N = 232); or at the Fondazione Centro San Raffaelle del Monte Tabor, Milan, Italy (N = 272). Anthropometric data of the study subjects are listed in table 1 .
Human molecular genetics, Jan 17, 2015
Polymorphisms rs6232 and rs6234/rs6235 in PCSK1 have been associated with extreme obesity (e.g. b... more Polymorphisms rs6232 and rs6234/rs6235 in PCSK1 have been associated with extreme obesity (e.g. body mass index [BMI]≥40 kg/m(2)), but their contribution to common obesity (BMI≥30 kg/m(2)) and BMI variation in a multi-ethnic context is unclear. To fill this gap, we collected phenotypic and genetic data in up to 331,175 individuals from diverse ethnic groups. This process involved a systematic review of the literature in PubMed, Web of Science, Embase and the NIH GWAS catalog complemented by data extraction from pre-existing GWAS or custom-arrays in consortia and single studies. We employed recently developed global meta-analytic random-effects methods to calculate summary odds ratios (OR) and 95% confidence intervals (CI) or beta estimates and standard errors (SE) for the obesity status and BMI analyses, respectively. Significant associations were found with binary obesity status for rs6232 (OR=1.15, 95% CI 1.06-1.24, P=6.08x10(-6)) and rs6234/rs6235 (OR=1.07, 95% CI 1.04-1.10, P=3.00x10(-7)). Similarly, significant associations were found with continuous BMI for rs6232 (beta=0.03, 95% CI 0.00-0.07; P=0.047) and rs6234/rs6235 (beta=0.02, 95% CI 0.00-0.03; P=5.57x10(-4)). Ethnicity, age and study ascertainment significantly modulated the association of PCSK1 polymorphisms with obesity. In summary, we demonstrate evidence that common gene variation in PCSK1 contributes to BMI variation and susceptibility to common obesity in the largest known meta-analysis published to date in genetic epidemiology.
Child and adolescent psychiatric clinics of North America, 2009
Child and adolescent psychiatric clinics of North America, 2009
Current opinion in psychiatry, 2010
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2013
MMW Fortschritte der Medizin, Jan 15, 2006
European Child & Adolescent Psychiatry, 2014
Journal of Neural Transmission, 2003
The authors explored the binge eating symptomatology in 74 patients receiving clozapine (N = 57) ... more The authors explored the binge eating symptomatology in 74 patients receiving clozapine (N = 57) or olanzapine (N = 17), and compared body mass index (BMI, kg/m2) and weight gain in patients with and without binge eating symptomatology. Subjects who screened positively for binge eating were interviewed using a modified version of the Questionnaire on Eating and Weight Patterns (QEWP). Current BMIs were assessed cross-sectionally, BMIs at initiation of clozapine/olanzapine treatment retrospectively. Thirty-seven subjects (50%) screened positively. Taking clozapine and olanzapine together, 6/27 (22.2%) females and 3/47 (6.4%) males fulfilled criteria for binge eating disorder, 3/27 (11.1%) females and 2/47 (4.3%) males for bulimia nervosa. Patients who screened positively showed higher current BMIs (26.8 ± 3.9 vs. 24.7 ± 3.7 kg/m2) and higher BMI increments during clozapine/olanzapine treatment (3.9 ± 3.1 vs. 2.6 ± 3.4 kg/m2) than patients who screened negatively. We conclude that clozapine/olanzapine may induce binge eating and full blown eating disorders which may have predictive value for weight gain. For future research in this field we suggest a novel DSM-IV research classification “Medication-induced eating disorders”.
European Child & Adolescent Psychiatry, 2014
Prenatal alcohol exposure (PAE) is one of the most prevalent and modifiable risk factors for soma... more Prenatal alcohol exposure (PAE) is one of the most prevalent and modifiable risk factors for somatic, behavioral, and neurological abnormalities. Affected individuals exhibit a wide range of such features referred to as fetal alcohol spectrum disorders (FASD). These are characterized by a more or less specific pattern of minor facial dysmorphic features, growth deficiency and central nervous system symptoms. Nevertheless, whereas the diagnosis of the full-blown fetal alcohol syndrome does not pose a major challenge, only a tentative diagnosis of FASD can be reached if only mild features are present and/or maternal alcohol consumption during pregnancy cannot be verified. The respective disorders have lifelong implications. The teratogenic mechanisms induced by PAE can lead to various additional somatic findings and structural abnormalities of cerebrum and cerebellum. At the functional level, cognition, motor coordination, attention, language development, executive functions, memory, social perception and emotion processing are impaired to a variable extent. The long-term development is characterized by disruption and failure in many domains; an age-adequate independency is frequently not achieved. In addition to primary prevention, individual therapeutic interventions and tertiary prevention are warranted; provision of extensive education to affected subjects and their caregivers is crucial. Protective environments are often required to prevent negative consequences such as delinquency, indebtedness or experience of physical/sexual abuse.
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2014
The fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) resulted ... more The fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) resulted in substantial changes with regard to the classification of Eating Disorders. In DSM-5, Feeding and Eating Disorders are for the first time subsumed in a single category. The Binge Eating Disorder (BED) was established as the third classical eating disorder in addition to Anorexia Nervosa (AN) and Bulimia Nervosa (BN). The criteria for AN changed remarkably, whereas there were only minor changes to the BN criteria. The criteria for BED differ only marginally from the DSM-IV research criteria. There are now subtypes of AN, BN, and BED in the new category "Other Specific Feeding and Eating Disorders." The rest category "Eating Disorders Not Otherwise Specified" has been renamed to "Unspecified Feeding or Eating Disorders." The practicability of the DSM-5 criteria for Eating Disorders, and for AN in particular, for both clinical practice and research remains to be seen.
American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2014
Deviations from normal body weight are observed prior to and after the onset of Alzheimer's disea... more Deviations from normal body weight are observed prior to and after the onset of Alzheimer's disease (AD). Midlife obesity confers increased AD risk in later life, whereas late-life obesity is associated with decreased AD risk. The role of underweight and weight loss for AD risk is controversial. Based on the hypothesis of shared genetic variants for both obesity and AD, we analyzed the variants identified for AD or obesity from genome-wide association meta-analyses of the GERAD (AD, cases ¼ 6,688, controls ¼ 13,685) and GIANT (body mass index [BMI] as measure of obesity, n ¼ 123,865) consortia. Our cross-disorder analysis of genome-wide significant 39 obesity SNPs and 23 AD SNPs in these two large data sets revealed that: (1) The AD SNP rs10838725 (p AD ¼ 1.1 Â 10 À08 ) at the locus CELF1 is also genome-wide significant for obesity (p BMI ¼ 7.35 Â 10 À09 ). (2) Four additional AD risk SNPs were nominally associated with obesity (rs17125944 at FERMT2, p BMI ¼ 4.03 Â 10 À05 , p BMI corr ¼ 2.50 Â 10 À03 ; rs3851179 at PICALM; p BMI ¼ 0.002, rs2075650 at TOMM40/APOE, p BMI ¼ 0.024, rs3865444 at CD33, p BMI ¼ 0.024). (3) SNPs at two of the obesity risk loci (rs4836133 downstream of ZNF608; p AD ¼ 0.002 and at rs713586 downstream of RBJ/DNAJC27; p AD ¼ 0.018) were nominally associated with AD risk. Additionally, among the SNPs used for confirmation in both studies the AD risk allele of rs1858973, with an AD association just below genome-wide significance (p AD ¼ 7.20 Â 10 À07 ), was also associated with obesity (SNP at
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2012
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2011
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2009
The provision of good mentors and education to medical students in their residency (PJ students) ... more The provision of good mentors and education to medical students in their residency (PJ students) bears three essential advantages: 1) If the students feel themselves in good hands, they will co-operate effectively, thereby reducing the burden of the medical staff. 2) Contented students are potential advertisers for other interns, clinical trainees, medical students in residency and Ph.D. students. 3) Given the lack of doctors, providing students with good mentors and training is a valuable long-term strategy for the recruitment of doctors; in the event of later employment, former students in residency represent employees who are motivated, well trained, and familiar with hospital routine--a classical win-win situation.
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2010
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2006
Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 2013
Verhaltenstherapie, 2006
... Jan-Michael Dierk Matthias Conradt Pia Schlumberger Elisabeth Rauh Christina Albohn Anke Hinn... more ... Jan-Michael Dierk Matthias Conradt Pia Schlumberger Elisabeth Rauh Christina Albohn Anke Hinney Johannes Hebebrand Winfried Rief ... genetischer Faktoren hin: in den letzten Jahren konnten Muta-tionen definiert werden, die als Ursache der Adipositas anzu-sehen sind. ...