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The mechanical properties of granular materials at a low shear rate are frequently viewed as rate-independent, and a rate-independent constitutive relation is used to describe the mechanical behaviors of the granular material. However, time-dependent behaviors (or creeping behaviors) become significant in the long run. In this paper, we conduct triaxial experiments to observe the creep of granular materials under both dynamic and static loading conditions. Three typical creeping behaviors, aging, transitional, and fluidic, have been observed. To describe the time-dependent behaviors, an internal state variable characterizing the fluidity of the granular system is introduced to propose a rate-dependent constitutive relation which we call in this paper, a state evolution model. A characteristic strain is also introduced into the model to account for the influences of historic strain on the current state. The experiments are analyzed using the proposed model and it has been found that our model can well discern the observed three creeping behaviors. A criterion to identify the stability of a granular system is also given out based on the proposed model. Two key factors dominating the stability of the granular system are recognized – shear wave velocity and critical velocity. Our laboratory experiments in combination with the proposed criterion offer a physical explanation of the intrinsic triggering mechanism of system evolution from a stable to fluidic state: decrease in wave velocity or/and critical velocity. [ABSTRACT FROM AUTHOR]

Background and purpose:The study investigated whether eugenosedin-A, a 5-hydroxytryptamine and α/β adrenoceptor antagonist, enhanced delayed-rectifier potassium (KDR)- or large-conductance Ca2+-activated potassium (BKCa)-channel activity in basilar artery myocytes through cyclic AMP/GMP-dependent and -independent protein kinases.Experimental approach:Cerebral smooth muscle cells (SMCs) were enzymatically dissociated from rat basilar arteries. Conventional whole cell, perforated and inside-out patch-clamp electrophysiology was used to monitor K+- and Ca2+-channel activities.Key results:Eugenosedin-A (1 μM) did not affect the KDR current but dramatically augmented BKCa channel activity in a concentration-dependent manner. Increased BKCa current was abolished by charybdotoxin (ChTX, 0.1 μM) or iberiotoxin (IbTX, 0.1 μM), but not affected by a small-conductance KCa blocker (apamin, 100 μM). BKCa current activation by eugenosedin-A was significantly inhibited by an adenylate cyclase inhibitor (SQ 22536, 10 μM), a soluble guanylate cyclase inhibitor (ODQ, 10 μM), competitive antagonists of cAMP and cGMP (Rp-cAMP, 100 μM and Rp-cGMP, 100 μM), and cAMP- and cGMP-dependent protein kinase inhibitors (KT5720, 0.3 μM and KT5823, 0.3 μM). Eugenosedin-A reversed the inhibition of BKCa current induced by the protein kinase C activator, phorbol myristyl acetate (PMA, 0.1 μM). Eugenosedin-A also prevented BKCa current inhibition induced by adding PMA, KT5720 and KT5823. Moreover, eugenosedin-A reduced the amplitude of voltage-dependent L-type Ca2+ current (ICa,L), but without modifying the voltage-dependence of the current.Conclusions and implications:Eugenosedin-A enhanced BKCa currents by stimulating the activity of cyclic nucleotide-dependent protein kinases. Physiologically, this activation would result in the closure of voltage-dependent calcium channels and thereby relax cerebral SMCs.British Journal of Pharmacology (2007) 152, 374–385; doi:10.1038/sj.bjp.0707406; published online 13 August 2007 [ABSTRACT FROM AUTHOR]