8 research outputs found

    Non-Charge-Sheet Analytic Model for Ideal Retrograde Doping MOSFETs

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    This paper presents a physics-based non-charge-sheet analytic model for an ideal retrograde doping MOSFET structure. The model adopts an approach of solving Poisson's equation to the heavily-doped region and lightly-doped region, respectively, and ultimately obtains the analytic expression of potential distribution and the drain current of the retrograde doping MOSFET. This paper compares the analytical model with numerical simulation results, which demonstrates that the current analytic model is applicable to both the weak and strong inversion situations and also to different geometry conditions. In this case, this model provides a foundation to develop a complete retrograde doping MOSFET model involved with advanced physical effects, such as short-channel effect, quantum mechanic effect

    The effect of icotinib or apatinib on the pharmacokinetic profile of oxycodone in rats and the underlying mechanism

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    This study aimed to investigate the interactions between icotinib/apatinib and oxycodone in rats and to unveil the underlying mechanism. An ultra-performance liquid chromatography–tandem mass spectrometry (UPLC-MS/MS) method was developed and validated to determine oxycodone and its demethylated metabolite simultaneously. In vivo, Sprague–Dawley (SD) male rats were administered oxycodone with or without icotinib or apatinib. Blood samples were collected and subjected to UPLC-MS/MS analysis. An enzyme incubation assay was performed to investigate the mechanism of drug–drug interaction using both rat and human liver microsomes (RLM and HLM). The results showed that icotinib markedly increased the AUC(0–t) and AUC(0–∞) of oxycodone but decreased the CLz/F. The Cmax of oxycodone increased significantly upon co-administration of apatinib. In vitro, the Km value of oxycodone metabolism was 101.7 ± 5.40 μM and 529.6 ± 19.60 μM in RLMs and HLMs, respectively. Icotinib and apatinib inhibited the disposition of oxycodone, with a mixed mechanism in RLM (IC50 = 3.29 ± 0.090 μM and 0.95 ± 0.88 μM, respectively) and a competitive and mixed mechanism in HLM (IC50 = 22.34 ± 0.81 μM and 0.48 ± 0.05 μM, respectively). In conclusion, both icotinib and apatinib inhibit the metabolism of oxycodone in vitro and in vivo. Therefore, the dose of oxycodone should be reconsidered when co-administered with icotinib or apatinib
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