Ein nichtlineares anisotropes Materialmodell auf der Basis der Hencky-Dehnung und der logarithmischen Rate zur Beschreibung duktiler Schädigung

Ein nichtlineares, dreidimensionales und anisotropes Sehddigungsmodell wird vorgestellt. Basis des Modells ist der Rahmen für finite Elastoplastizität von Xiao, Bruhns & Meyers. Von entscheidender Bedeutung für die Modellierung ist eine doppelte Interpretation des Schädigungsparameters. Für die thermodgnamischen Betrachtungen wird der Schädigungsparameter als eine interne Zustandsuariable betrachtet. Zur Modellierung der schädigungsinduzierten Anisotropie wird er als ein sich mit der  Deformation entwickelnder Struktur- oder Materialtensor interpretiert. Schädigungsmodellierung reduziert sich damit auf die Formulierung von Euolutionsgleichungen, die Festlegung von Versagenskriterien und die Bestimmung von Materialkonstanten

Dialogues:Anthropology and theology

The past five years have witnessed an increased interest in a dialogue between anthropology and theology, evidenced in part by a suite of edited volumes (e.g. Lauterbach & Vähäkangas 2020; Lemons 2018; Tomlinson & Mathews 2018). Analyses informed by this interdisciplinary nexus have demonstrated the utility of theological concepts for anthropological inquiry (e.g. Robbins 2020; Tomlinson 2020; Williams Green 2021). The following series of dialogues between anthropologists and theologians builds on this growing body of work, expanding it at two main points. First, while the above conversations are all focused on Christian theology, mainly as a means of engaging Christian practice, our dialogues move beyond this religion. The following conversations engage the intersection of anthropology and Islamic, Buddhist, Hindu, as well as Christian, theology.1 Second, many of these dialogues foreground particular experiences of scholars in both anthropology and theology who identify in some way with the religious traditions they study. Some of these dialogues took place between scholars who had an established relationship; others involved partners who had not previously met, but who agreed to correspond in view of a shared interest in this interdisciplinary dialogue. As a starting point, participants were given a series of questions to orient their exchanges, such as, ‘How does faith relate to knowledge in both disciplines?’ Conversations mostly took place over email and were later edited with the help of one of the journal editors, Adam Reed, and one of the members of our Editorial Board, Naomi Haynes.Publisher PDFPeer reviewe

Ein finites anisotropes Materialmodell auf der Basis der Hencky-Dehnung und der logarithmischen Rate zur Beschreibung duktiler Schaedigung

SIGLEAvailable from TIB Hannover: RN 4503(127) / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekDEGerman

The Role of Rac1 in Synaptic Plasticity, Learning and Memory

During the process of learning and memory, neuronal synapses undergo changes involving gene expression, protein synthesis, and cytoarchitectural remodeling, referred to as synaptic plasticity. Changes in the morphology of synapses are necessary for learning and memory storage, and require the rearrangement of the actin cytoskeleton at dendrites and actin rich dendritic spines which are the loci excitatory of synaptic transmission in the central nervous system. Rac1, a protein of the Rho subfamily of GTP binding proteins (GTPases), is largely known for its involvement in cytoskeleton remodeling, and has been implicated in neuronal development, participating in the morphological changes required for migration of newborn neurons to characteristic locations, extension of axons and dendrites into proper target regions, and formation of synapses with appropriate partners. However, the functional role of Rac1 in adult neuronal signaling has been relatively unclear. Our laboratory previously demonstrated that that Rac1 is highly expressed in the adult mouse hippocampus, a part of the brain, which is very crucial for memory acquisition. In vitro studies in hippocampal slices indicated that activation of the hippocampal N-methyl-D-aspartate (NMDA) receptor, the receptor that was modified to produce the “smart mouse” results in membrane translocation and activation of Rac1. Moreover, our laboratory has observed that translocation and activation of Rac1 are associated with fear learning in the adult mice. The purpose of this study was to examine whether Rac1 is required for regulation of the cytoskeletal dynamics leading to morphological plasticity observed at neuronal synapses during hippocampal learning and memory. To evaluate the importance of Rac1 in plasticity and learning we generated a mouse bearing a conditional inactivation of the rac1 gene in the hippocampus (referred herein as Rac1 knockouts [KO] or mutants) using the Cre/LoxP system. We showed that the disappearance of Rac1 in the Rac1 knock out (KO) is time dependent, with a 16% significant decrease at two months and 90% at six months as compared to their wild type (WT) littermates. No differences in protein levels were observed between the wild type and heterozygous littermates. Next, we studied neuronal morphology in hippocampal slices using the rapid Golgi-Cox technique to determine whether Rac1 was necessary for the neuroanatomical and cytoarchitectural changes associated with synaptic plasticity in the adult mice. We showed that loss of Rac1 leads to a significant reduction in spine density in Rac1 mutant mice as compared to the wild type controls. In an attempt to correlate this effect with an alteration in the actin dynamics pathway, we performed Western blot analysis, which showed in the Rac1 mutant significant reduction in p-PAK-1, p-LIMK-1 and p-Cofilin-1, all proteins downstream of Rac1 and essential for cytoskeletal rearrangements leading to dendritic spine development. In order to evaluate the involvement of Rac1 in long term synaptic plasticity (LTP and LTD), hippocampal slices from age matched wild type and Rac1 mutant were given high frequency stimulation (HFS) to generate LTP and low frequency stimulation (LFS) to induce LTD. Rac1 deficient mice showed impaired LTP and LTD as compared to their littermate controls. Furthermore, to assess whether Rac1 is associated with, and necessary for hippocampus-dependent learning and memory in the intact animal, Rac1 mutant mice and their littermate controls were examined in a battery of behavioral tests beginning with six control tests namely, the Open Field Activity, Rotating Rod, Pre-pulse Inhibition of Startle Response, Hot Plate test, Light-dark, Elevated Plus Maze, and ending with two learning and memory tests, the Morris Water Maze and Fear conditioning paradigm. Rac1 deficient mice showed the same performance as the wild type and the heterozygotes in control tests, however, they showed impaired learning in the learning and memory tests. Collectively, these data suggest that Rac1 is an important protein required for proper dendritic spine morphogenesis, long-term synaptic plasticity, as well as learning and memory. These phenomena are abnormal in some autistic disorders, making Rac1 an interesting target in the study of these diseases.Pharmacological and Pharmaceutical Sciences, Department o