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The use of light, which is s a powerful tool for imaging and sensing, has also become one of the most prospective strategies in tumor treatment. Optical microfibers, which have engineerable waveguiding properties, are highly attractive for optical sensing and photothermal therapy on the micro/nanoscale. However, for their real‐world application, the sensitivity limit needs to be addressed, as does the issue of improving the intrinsic photothermal performance of silica microfibers. Herein, a nanointerface consisting of triangular Au@Ag2S nanoplates and VO2 nanoparticles on an optical microfiber is designed to fabricate a structurally resilient hierarchical microfiber sensor with well‐distributed plasmonic hotspot enhancement. The nanointerface enhances the evanescent field with temperature tunability, adding a self‐photothermal modulation function to the sensor. The sensor exhibits a temperature‐tunable sensitivity to alpha‐fetoprotein with a limit of detection of 0.62 × 10−18m. It differentiates hepatoma carcinoma cells from normal cells and provides photothermal therapy aimed at the former. Quantitative evaluation of the sensor indicates that photothermal therapy kills more than 82% of cancer cells using a lower power. This work provides a new opportunity for selective evanescent field modulation for evanescent biosensors as well as a potential approach to the integration of cellular diagnosis and therapy. [ABSTRACT FROM AUTHOR]

ABSTRACT: The novel polycarbonate resin compositions comprising polycarbonate (PC) and acrylic resin were prepared by solution blending and analyzed by differential scanning calorimetry, atomic force microscopy, gel permeation chromatography, and gas chromatography‐mass spectrometry. Furthermore, the optical performance and the thermal and mechanical properties were tested, respectively. The results demonstrate that the blended material which was prepared by 100 parts of PC and 0.05 parts of acrylic resin achieves excellent transparency in blue‐light region (280–400 nm). Meanwhile, it retains excellent high‐heat resistance and mechanical performance of PC. Because of its high transparency in the blue‐light region which is caused by a doping of a tiny amount of acrylic resin, this material takes steps towards solving the optical problem that light becomes yellow when leaving the end of waveguides of PC. © 2018 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2018, 135, 46529. [ABSTRACT FROM AUTHOR]

Background and Purpose: The clinical use of doxorubicin, an effective anticancer drug, is severely hampered by its cardiotoxicity. 23-Hydroxybetulinic acid (23-HBA), isolated from Pulsatilla chinensis, enhances the anticancer effect of doxorubicin while simultaneously reducing its cardiac toxicity, but does not affect the concentration of doxorubicin in the plasma and heart. As the metabolite doxorubicinol is more potent than doxorubicin at inducing cardiac toxicity, in the present study we aimed to clarify the role of doxorubicinol in the protective effect of 23-HBA.Experimental Approach: Doxorubicin was administered to mice for two weeks in the presence or absence of 23-HBA. The heart pathology, function, myocardial enzymes and accumulation of doxorubicin and doxorubicinol were then analysed. A cellular pharmacokinetic study of doxorubicin and doxorubicinol, carbonyl reductase 1 (CBR1) interference and molecular docking was performed in vitro.Key Results: 23-HBA alleviated the doxorubicin-induced cardiotoxicity in mice, and this was accompanied by inhibition of the metabolism of doxorubicin and reduced accumulation of doxorubicinol selectively in hearts. In H9c2 cells, the protective effect of 23-HBA was shown to be closely associated with a decreased rate and extent of accumulation of doxorubicinol in mitochondria and nuclei. siRNA and docking analysis demonstrated that CBR1 has a crucial role in doxorubicin-mediated cardiotoxicity and 23-HBA inhibits this metabolic pathway.Conclusions and Implications: Inhibition of CBR-mediated doxorubicin metabolism might be one of the protective mechanisms of 23-HBA against doxorubicin-induced cardiotoxicity. The present study provides a new research strategy guided by pharmacokinetic theory to elucidate the mechanism of drugs with unknown targets. [ABSTRACT FROM AUTHOR]

Background and Purpose: Intracellular pharmacokinetics of anticancer drugs in multi-drug resistance (MDR) cancer cells is hugely important in the evaluation and improvement of drug efficacy. By using adriamycin as a probe drug in MDR cancer cells, we developed a cellular pharmacokinetic-pharmacodynamic (PK-PD) model to reveal the correlation between cellular pharmacokinetic properties and drug resistance. In addition, the ability of 20(S)-ginsenoside Rh2 (20(S)-Rh2) to reverse MDR was further investigated.Experimental Approach: The cellular pharmacokinetics of adriamycin were analysed visually and quantitatively in human breast cancer cells MCF-7 and in adriamycin-resistant MCF-7 (MCF-7/Adr) cells. Mitochondria membrane potential was assayed to evaluate the apoptotic effect of adriamycin. Subsequently, a PK-PD model was developed via MATLAB.Key Results: Visual and quantitative data of the dynamic subcellular distribution of adriamycin revealed that it accumulated in cells, especially nuclei, to a lesser and slower extent in MCF-7/Adr than in MCF-7 cells. 20(S)-Rh2 increased the rate and amount of adriamycin entering cellular/subcellular compartments in MCF-7/Adr cells through inhibition of P-glycoprotein (P-gp) activity, in turn augmenting adriamycin-induced apoptosis. The integrated PK-PD model mathematically revealed the pharmacokinetic mechanisms of adriamycin resistance in MCF-7/Adr cells and its reversal by 20(S)-Rh2.Conclusions and Implications: P-gp, which is overexpressed and functionally active at cellular/subcellular membranes, influences the cellular pharmacokinetic and pharmacological properties of adriamycin in MCF-7/Adr cells. Inhibition of P-gp activity represents a key mechanism by which 20(S)-Rh2 attenuates adriamycin resistance. Even more importantly, our findings provide a new strategy to explore the in-depth mechanisms of MDR and evaluate the efficacy of MDR modulators. [ABSTRACT FROM AUTHOR]