Solution of Creep-Damage Problems for Beams and Rectangular Plates Using the Ritz and the Finite Element Method

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Historychne związki pomiędzy polskimi i bułgarskimi rewolucjonistami w II pol. XIX w.: przeciwieństwa i wspołpraca

Kolarow, G. Historical Relationships Between Polish and Bulgarian Revolutionaries in the Second Pol. 19th century: opposites and collaboratio

On the accuracy of creep-damage predictions in thinwalled structures using the finite element method

The constitutive model with a single damage parameter describing creep-damage behaviour of metals with respect to the different sensitivity of the damage process due to tension and compression is incorporated into the ANSYS finite element code by modifying the user defined creep material subroutine. The procedure is verified by comparison with solutions for beams and rectangular plates in bending based on the Ritz method. Various numerical tests show the sensitivity of long-term predictions to the mesh sizes and element types available for the creep analysis of thinwalled structures

Anwendung semianalytischer FEM-Lösungen in der Elastizitätstheorie

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Loss of MeCP2 disrupts cell autonomous and autocrine BDNF signaling in mouse glutamatergic neurons

Mutations in the MECP2 gene cause the neurodevelopmental disorder Rett syndrome (RTT). Previous studies have shown that altered MeCP2 levels result in aberrant neurite outgrowth and glutamatergic synapse formation. However, causal molecular mechanisms are not well understood since MeCP2 is known to regulate transcription of a wide range of target genes. Here, we describe a key role for a constitutive BDNF feed forward signaling pathway in regulating synaptic response, general growth and differentiation of glutamatergic neurons. Chronic block of TrkB receptors mimics the MeCP2 deficiency in wildtype glutamatergic neurons, while re-expression of BDNF quantitatively rescues MeCP2 deficiency. We show that BDNF acts cell autonomous and autocrine, as wildtype neurons are not capable of rescuing growth deficits in neighboring MeCP2 deficient neurons in vitro and in vivo. These findings are relevant for understanding RTT pathophysiology, wherein wildtype and mutant neurons are intermixed throughout the nervous system