This paper analyses the performance of the experimental setups to assess the punching strength of slab-column connections in continuous flat slabs under vertical and horizontal loading. In the last years, several experimental campaigns have been performed to investigate the punching strength of slabcolumn connections, but most of the experimental tests concerned isolated slab-column connections. Among the few setups aimed at reproducing the eccentric punching failure in continuous flat slabs, the setup developed at the NOVA School of Science and Technology in Lisbon is considered in this paper. The performance of the Lisbon setup is assessed through nonlinear finite element analyses, calibrated on experimental data, by comparison with numerical results of a theoretical continuous setup. Then, the performance of the isolated setups, used in many researches and at the base of some international codes, is also evaluated through the same finite element model. Numerical analyses highlight that the setup developed in Lisbon could provide reliable ultimate rotations of continuous flat slab connections, but it underestimates the punching strength. Despite isolated setups lead to similar results when compared
The present work was undertaken to investigate the effects of acute forced swimming (FS) on the levels of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor B (trkB) proteins in: the ventral tegmental area (VTA); the nucleus accumbens (Acb) shell and core compartments; and the anterior cingulate (ACg), prelimbic (PL) and infralimbic (IL) territories of the prefrontal cortex of genetic models of vulnerability (RLA, Roman low-avoidance rats) and resistance (RHA, Roman high-avoidance rats) to stress-induced depression. We report for the first time that FS induced very rapid and distinct changes in the levels of BDNF and trkB proteins in different areas of the mesocorticolimbic system of RHA and RLA rats. Thus, (1) in the VTA and Acb core, FS elicited a significant increase of both BDNF- and trkB-LI in RHA but not RLA rats, whereas in the Acb shell no significant changes in BDNF- and trkB-LI across the line and treatment were observed; (2) in RLA rats, the basal levels of BDNF-LI in the IL/PL cortex and of trkB-LI in the ACg cortex were markedly lower than those of RHA rats; moreover, BDNF- and trkB-LI in the IL/PL and ACg cortex were increased by FS in RLA rats but decreased in their RHA counterparts. These results provide compelling evidence that the genetic background influences the effects of stress on BDNF/trkB signaling and support the view that the same stressor may impact differently on the expression of BDNF in discrete brain areas.
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