Seismic retrofit of a steel-reinforced concrete hospital building using continuous energy-dissipative steel columns

Seismic retrofit of an existing steel-reinforced concrete hospital building that features innovative use of a continuous energy-dissipative steel column (CEDC) system is presented in this paper. The special system has been adopted to provide an efficient solution taking into account the difficulties of applying traditional intervention techniques to minimize the impact on architectural functionality and avoid the loss of building function and evacuation during the retrofit implementation. The lateral stiffness and strength of the CEDC system were defined based on the geometric and mechanical properties of the steel strip dampers. The hysteretic behavior under cyclic loadings was defined using a simplified numerical model. Its effectiveness was validated by comparing the results of full-scale experimental data available from the literature. All the main design considerations of the retrofitting plan are described in detail. The effectiveness of the proposed retrofitting system was demonstrated by nonlinear time-history analyses under different sets of earthquake-strong ground motions. The analysis results show that the CEDC system is effective in controlling the deformation pattern and significantly reducing damage to the existing structure during major earthquakes

Pharmacological modulation of long-term potentiation in animal models of Alzheimer' s disease

The discovery of long-term potentiation (LTP) of hippocampal synaptic transmission, which represents a classical model for learning and memory at the cellular level, has stimulated over the past years substantial progress in the understanding of pathogenic mechanisms underlying cognitive disorders, such as Alzheimer s disease (AD). Multiple lines of evidence indicate synaptic dysfunction not only as a core feature but also a leading cause of AD. Multiple pathways may play a significant role in the execution of synaptic dysfunction and neuronal death triggered by beta-amyloid (Abeta) in AD. Following intensive investigations into LTP in AD models, a variety of compounds have been found to rescue LTP impairment via numerous molecular mechanisms. Yet very few of these findings have been successfully translated into disease-modifying compounds in humans. This review recapitulates the emerging disease-modifying strategies utilized to modulate hippocampal synaptic plasticity with particular attention to approaches targeting ligand-gated ion channels, G-protein-coupled receptors (GPCRs), Receptor Tyrosine Kinases (RTKs) and epigenetic mechanisms. It is hoped that novel multi-targeted drugs capable of regulating spine plasticity might be effective to counteract the progression of AD and related cognitive syndromes