Publications by authors named "Johannes Buerger"

Article Synopsis
  • * Our findings revealed lower levels of formate and fumarate in individuals with AD, along with decreased microbial secretion of formate in personalized metabolic models.
  • * The study highlights that specific genetic reactions linked to AD may affect formate production, suggesting its potential as an early marker and indicating a complex interplay between gut microbiota and AD.
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Objective: Given the severity of eating disorders, effective and easily implementable prevention programs which reduce incidence rates and in addition have health-economic benefits are essential. The majority of research on prevention programs focuses on questionnaire-based efficacy or the reduction of eating disorder symptoms while neglecting the health-economic perspective. By contrast, the present study focuses on both an efficacy analysis considering diagnostic criteria (DSM-5) and on evaluating the cost-benefit of a universal prevention program for eating disorders ("MaiStep").

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Background: Galloway-Mowat syndrome (GAMOS) is characterized by neurodevelopmental defects and a progressive nephropathy, which typically manifests as steroid-resistant nephrotic syndrome. The prognosis of GAMOS is poor, and the majority of children progress to renal failure. The discovery of monogenic causes of GAMOS has uncovered molecular pathways involved in the pathogenesis of disease.

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Eating disorders are difficult to treat and often associated with morbidity and mortality. Universal prevention approaches are increasingly focusing on enhancing skills, but few eating disorder programs are available for under-15-year-olds. This study aimed to develop and examine a school-based universal prevention program ('MaiStep') for adolescent boys and girls.

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Insulin is a central player in the regulation of metabolic as well as non-metabolic cells: inefficient signal transduction (insulin resistance) not only represents the cornerstone in the pathogenesis of type 2 diabetes mellitus, but also drives atherosclerosis through inducing endothelial dysfunction. Last but not least epidermal homeostasis depends on insulin. We summarize the effects of insulin on proliferation and differentiation of human keratinocytes as well as the relevance of cytokine-induced insulin resistance for alterations in epidermal homeostasis characteristic for psoriasis.

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Epidemiologic data document not only a higher prevalence of joint involvement among psoriasis patients than previously thought, but also an association with numerous other diseases, including depression, smoking, alcoholism, Crohn's disease, and metabolic syndrome. The resulting increased cardiovascular mortality is of particular clinical importance, and its pathogenetic link as a complication of the psoriatic inflammation is well recognized. Thus, we need to re-invent the management of psoriasis: Dermatologists are not only the sentinel regarding the early diagnosis of psoriatic arthritis, but also of metabolic complications such as dyslipidemia or diabetes.

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