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Limit and shakedown theorems are exact theories of classical plasticity for the direct computation of safety factors or of the load carrying capacity under constant and varying loads. Simple versions of limit and shakedown analysis are the basis of all design codes for pressure vessels and pipings. Using Finite Element Methods more realistic modeling can be used for a more rational design. The methods can be extended to yield optimum plastic design. In this paper we present a first implementation in FE of limit and shakedown analyses for perfectly plastic material. Limit and shakedown analyses are done of a pipe–junction and a interaction diagram is calculated. The results are in good correspondence with the analytic solution we give in the appendix.
Kompetenz zur Innovation: Vom Druckbetrieb zum Multimedia-Dienstleister . Staudt, E.; Thielemann, F.
(1997)
Innovationsreport Großhandel
(1997)
HSP III Koordinatenmessgerät
(1997)
Focus Artaud : Textcollage
(1997)
Animal experiments and preliminary results in humans have indicated alterations of hippocampal muscarinic acetylcholine receptors (mAChR) in temporal lobe epilepsy. Patients with temporal lobe epilepsy often present with a reduction in hippocampal volume. The aim of this study was to investigate the influence of hippocampal atrophy on the quantification of mAChR with single photon emission tomography (SPET) in patients with temporal lobe epilepsy. Cerebral uptake of the muscarinic cholinergic antagonist [123I]4-iododexetimide (IDex) was investigated by SPET in patients suffering from temporal lobe epilepsy of unilateral (n=6) or predominantly unilateral (n=1) onset. Regions of interest were drawn on co-registered magnetic resonance images. Hippocampal volume was determined in these regions and was used to correct the SPET results for partial volume effects. A ratio of hippocampal IDex binding on the affected side to that on the unaffected side was used to detect changes in muscarinic cholinergic receptor density. Before partial volume correction a decrease in hippocampal IDex binding on the focus side was found in each patient. After partial volume no convincing differences remained. Our results indicate that the reduction in hippocampal IDex binding in patients with epilepsy is due to a decrease in hippocampal volume rather than to a decrease in receptor concentration.