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Marburg an der Lahn, Germany

Kamp-Becker I.,Universitatsklinikum Marburg
Nervenheilkunde | Year: 2013

Objective: Autism disorders are early onset, severe neurodevelopmental disorders. There is considerable heterogeneity in the expression and severity of core and associated symptoms which hampers a clear distinction from other disorders. The present study aims at an answer to the question whether Albert Einstein was suffering from an autistic disorder. Methods: Available biographic information was thoroughly checked looking for valid diagnostic criteria for autism. -Results: There is definitely no evidence for an autistic disorder. A comprehensive discussion tries to explain why such a disorder is attributed to Einstein. Conclusion: The attribution of a diagnosis to famous people creates a high identification potential. In return, however, this means that normality is pathologised in order to normalise pathology. Clinical relevance: Actual autism is a vogue diagnosis, whose differentiation to other disorders gets unrecognizable. © Schattauer 2013. Source

The introduction of total genome sequencing led to the confirmation that tumors show substantial genetic heterogeneity. This phenomenon, which describes the presence of different genetic cell clones within a tumor also complicates the diagnostics of HER2. This article gives a review of new knowledge on polysomy 17 and genetic tumor heterogeneity in connection with HER2 determination of breast cancer. Source

Hu X.,University of Georgia | Yang D.,University of Georgia | Zimmerman M.,University of Georgia | Liu F.,University of Georgia | And 8 more authors.
Cancer Research | Year: 2011

IFN regulatory factor 8 (IRF8) is a key transcription factor for myeloid cell differentiation and its expression is frequently lost in hematopoietic cells of human myeloid leukemia patients. IRF8-deficient mice exhibit uncontrolled clonal expansion of undifferentiated myeloid cells that can progress to a fatal blast crisis, thereby resembling human chronic myelogeneous leukemia (CML). Therefore, IRF8 is a myeloid leukemia suppressor. Whereas the understanding of IRF8 function in CML has recently improved, the molecular mechanisms underlying IRF8 function in CML are still largely unknown. In this study, we identified acid ceramidase (ACDase) as a general transcription target of IRF8. We demonstrated that IRF8 expression is regulated by IRF8 promoter DNA methylation in myeloid leukemia cells. Restoration of IRF8 expression repressed A-CDase expression, resulting in C16 ceramide accumulation and increased sensitivity of CML cells to FasL-induced apoptosis. In myeloid cells derived from IRF8-deficient mice, A-CDase protein level was dramatically increased. Furthermore, we demonstrated that IRF8 directly binds to the A-CDase promoter. At the functional level, inhibition of A-CDase activity, silencing A-CDase expression, or application of exogenous C16 ceramide sensitized CML cells to FasL-induced apoptosis, whereas overexpression of A-CDase decreased CML cells' sensitivity to FasL-induced apoptosis. Consequently, restoration of IRF8 expression suppressed CML development in vivo at least partially through a Fas-dependent mechanism. In summary, our findings determine the mechanism of IRF8 downregulation in CML cells and they determine a primary pathway of resistance to Fasmediated apoptosis and disease progression. © 2011 American Association for Cancer Research. Source

Waldegger S.,Universitatsklinikum Marburg
Intensivmedizin und Notfallmedizin | Year: 2010

Disturbances of phosphate homeostasis are a minor but - in view of potential life-threatening complications - important topic in intensive care medicine. Therapeutic strategies require knowledge of the cause of the disturbed phosphate homeostasis. In both hyper- and hypophosphatemia, the daily intake, the distribution over intra- and extracellular compartments, and the amount of renal elimination have to be considered. This report explains the essential components of normal phosphate homeostasis, describes its most important disturbances, and the most recent therapeutic recommendations. With respect to hyperphosphatemia, particular attention is paid to acute phosphate nephropathy caused by the application of salinic laxatives. Within the causes of hypophosphatemia, redistribution phenomena play a pivotal role, mainly caused by respiratory alkalosis and by insulin. Moreover, consequences of severe hypophosphatemia (e.g., rhabdomyolysis, hemolysis, and respiratory insufficiency) are described together with the recommended therapies. © 2010 Springer-Verlag. Source

Kesting M.-L.,University of Marburg | Bredenpohl M.,University of Marburg | Klenke J.,TU Braunschweig | Westermann S.,Universitatsklinikum Marburg | Lincoln T.M.,University of Hamburg
Journal of Behavior Therapy and Experimental Psychiatry | Year: 2013

Background: Vulnerability-stress models propose that social stress triggers psychotic episodes in high risk individuals. Previous studies found not only stress but also a decrease in self-esteem to precede the formation of delusions. As evidence for causal conclusions has not been provided yet, the present study assessed the direct impact of social stress on paranoid beliefs using an experimental design and considered a decrease in self-esteem as a mediator and the proneness to psychosis and paranoia as moderators of the effect. Methods: A nonclinical population sample (n = 76) was randomly assigned to an experimental (EG) or a control group condition (CG). In the EG, participants were excluded during a virtual ball game (Cyberball) by the other two players and received a negative feedback after performing a test. The CG was included in the game and received a neutral feedback. Before and after the experimental conditions, emotions, self-esteem and paranoid beliefs were assessed using state-adapted questionnaires. Results: After the social stress induction, the EG reported a higher increase in subclinical paranoid beliefs compared to the CG. The impact of social stress on paranoid ideation was mediated by a decrease in self-esteem and moderated by proneness to paranoia. Individuals who felt distressed by paranoid thoughts at baseline were more likely to react with an increase in paranoid ideation under social stress. Limitations: The results need to be confirmed in a patient sample to draw conclusions about the processes involved in the formation of delusions in clinically relevant stages. Conclusions: The impact of social stress on symptom formation and self-esteem is discussed in terms of recent models of symptom formation and interventions in psychosis. © 2012 Elsevier Ltd. All rights reserved. Source

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