National Cheng Kung University

About: National Cheng Kung University is a education organization based out in Tainan City, Taiwan. It is known for research contribution in the topics: Population & Thin film. The organization has 49723 authors who have published 69799 publications receiving 1437420 citations. The organization is also known as: NCKU.

Simplified Model for Wall Deflection and Ground-Surface Settlement Caused by Braced Excavation in Clays

Abstract: Accurate prediction of ground-surface settlement adjacent to an excavation is often difficult to achieve without using accurate representation of small-strain nonlinearity in a soil model within finite-element analyses. In this paper a simplified semiempirical model is proposed for predicting maximum wall deflection, maximum surface settlement, and surface-settlement profile due to excavations in soft to medium clays. A large number of artificial data are generated through finite-element analyses using a well-calibrated, small-strain soil model. These data, consisting of wall displacements and ground-surface settlements in simulated excavations in soft to medium clays, provide the basis for developing the proposed semiempirical model. The proposed model is verified using case histories not used in the development of the model. The study shows that the developed model can accurately predict maximum wall deflection and ground-surface settlement caused by braced excavations in soft to medium clays.

Presynaptic mechanisms underlying cannabinoid inhibition of excitatory synaptic transmission in rat striatal neurons

Abstract: The striatum is a crucial site of action for the motor effects of cannabinoids (CBs). However, the electrophysiological consequences of activation of CB receptors on the striatal neurons have not been established. Here we report for the first time that the cannabimimetic aminoalkylindole WIN 55,212-2 and the endogenous cannabinoid anandamide substantially depress corticostriatal glutamatergic synaptic transmission onto striatal neurons in the brain slice preparation. The selective CB1 receptor antagonist SR 141716 effectively reversed this inhibition. WIN 55,212-2 significantly increased the paired-pulse facilitation of synaptically evoked EPSCs, while having no effect on the sensitivity of postsynaptic neurons to [alpha]-amino-3-hydroxy-5-methylisoxazole-4-propionic acid. WIN 55,212-2 also reduced the frequency of spontaneous, action potential-dependent EPSCs (sEPSCs) without altering their amplitude distribution. Superfusion of WIN 55,212-2 elicited a membrane hyperpolarization accompanied by a decrease in input resistance. Both effects were blocked by intracellular caesium. In contrast, intracellular caesium failed to affect WIN 55,212-2-mediated synaptic inhibition. The WIN 55,212-2-mediated synaptic inhibition was blocked by the Gi/o protein inhibitor pertussis toxin (PTX), but not by the GABA(A) receptor antagonist bicuculline or GABA(B) receptor antagonist SCH 50911. Pretreatment with the N-type Ca2+ channel antagonist [omega]-conotoxin GVIA selectively abolished the WIN-55,212-2-mediated synaptic inhibition. These results suggest that cannabinoids depress the corticostriatal glutamatergic synaptic transmission through the activation of presynaptic CB1 receptors to inhibit N-type Ca2+ channel activity, which in turn reduces glutamate release. The presynaptic action of cannabinoids is mediated by a PTX-sensitive Gi/o protein-coupled signalling pathway.