This study investigated the drop-spreading dynamics of pseudo-plastic and dilatant fluids. Experimental results indicated that the spreading law for both fluids is related to rheological characteristics or power exponent n. For the completely wetting system, the evolution of the wetting radius over time can be expressed by the power law R = atm, where the spreading exponent m of the dilatant fluids is >0.1 and the spreading exponent m of pseudo-plastic fluids is <0.1. The strength of non-Newtonian effects is positively correlated to the extent of deviation from the theoretical value 0.1 of m for Newtonian fluids. For the partially wetting system, the power law on the time dependence of the wetting radius no longer holds; therefore, an exponential power law, R = Req(1-exp(-at(m)/Req)), is proposed, where Req denotes the equilibrium radius of drop and a is a coefficient. Comparing experimental data with the exponential power law revealed that both are in good agreement.

The impact of CYP3A5*3, a CYP3A5 nonexpresser genotype, on inhibitory effects of diltiazem on tacrolimus metabolism has not been assessed. In retrospective study, when coadministered with diltiazem, mean increments in dose-adjusted C 0D7 , C max and AUC 0-12 h for tacrolimus were larger in CYP3A5 expressers than in CYP3A5 nonexpressers (48.7 vs 3.7%, 31.7 vs 17.2% and 38.2 vs 18.5%, respectively). Subsequently, a prospective study was carried out, patients were randomized to algorithm-predicted dosing or standard dosing. For CYP3A5 expressers, an algorithm guided by CYP3A5 and diltiazem significantly reduced tacrolimus maintenance dosage (P ¼ 0.009) and improved the accuracy of tacrolimus initial dose, resulting in reduction in out-of-range C 0 after initial dose (P ¼ 0.002) and dose adjustments (P ¼ 0.004). However, for CYP3A5 nonexpressers, primary end points were not achieved, and tacrolimus-sparing effect of diltiazem was not remarkable. Our study results show that CYP3A5 genotype-guided tacrolimus-diltiazem combination is a promising therapy in renal transplant recipients in the early postoperative stage.

Nectin-3, a cell adhesion molecule enriched in hippocampal neurons, has been implicated in stress-related cognitive disorders. Nectin-3 is expressed by granule cells in the dentate gyrus (DG), but it remains unclear whether nectin-3 in DG modulates the structural plasticity of dentate granule cells and hippocampus-dependent memory. In this study, we found that DG nectin-3 expression levels were developmentally regulated and reduced by early postnatal stress exposure in adult mice. Most importantly, knockdown of nectin-3 levels in all DG neuron populations by adeno-associated virus (AAV) mimicked the cognitive effects of early-life stress, and impaired long-term spatial memory and temporal order memory. Moreover, AAV-mediated DG nectin-3 knockdown increased the density of doublecortin-immunoreactive differentiating cells under proliferation and calretinin-immunoreactive immature neurons, but markedly decreased calbindin immunoreactivity, indicating that nectin-3 modulates the differentiation and maturation of adult-born DG granule cells. Using retrovirus to target newly generated DG neurons, we found that selective nectin-3 knockdown in new DG neurons also impaired long-term spatial memory. In addition, suppressing nectin-3 expression in new DG neurons evoked a reduction of dendritic spines, especially thin spines. Our data indicate that nectin-3 expressed in DG neurons may modulate adult neurogenesis, dendritic spine plasticity and the cognitive effects of early-life stress.

Trigeminal ganglionic Nav 1.7 has an important function in the hyperalgesia of the inflamed TMJ, which is dependent on the communication with the satellite glials.