Microfluidic Reactors for Plasmonic Photocatalysis Using Gold Nanoparticles.

This work reports a microfluidic reactor that utilizes gold nanoparticles (AuNPs) for the highly efficient photocatalytic degradation of organic pollutants under visible light. The bottom of microchamber has a TiO2 film covering a layer of AuNPs (namely, TiO2/AuNP film) deposited on the F-doped SnO2 (FTO) substrate. The rough surface of FTO helps to increase the surface area and the AuNPs enables the strong absorption of visible light to excite electron/hole pairs, which are then transferred to the TiO2 film for photodegradation. The TiO2 film also isolates the AuNPs from the solution to avoid detachment and photocorrosion. Experiments show that the TiO2/AuNP film has a strong absorption over 400-800 nm and enhances the reaction rate constant by 13 times with respect to the bare TiO2 film for the photodegradation of methylene blue. In addition, the TiO2/AuNP microreactor exhibits a negligible reduction of photoactivity after five cycles of repeated tests, which verifies the protective function of the TiO2 layer. This plasmonic photocatalytic microreactor draws the strengths of microfluidics and plasmonics, and may find potential applications in continuous photocatalytic water treatment and photosynthesis. The fabrication of the microreactor uses manual operation and requires no photolithography, making it simple, easy, and of low cost for real laboratory and field tests.

Silencing of TRPM8 inhibits aggressive tumor phenotypes and enhances gemcitabine sensitivity in pancreatic cancer.

The transient receptor potential TRPM8 ion channel is required for cellular proliferation in pancreatic epithelia and adenocarcinoma. To elucidate the mechanism that mediates the function of TRPM8, we examined its role in the proliferation and invasion of pancreatic cancer (PC) cells. TRPM8 expression increased in both the PC tissues and cell lines; a high TRPM8 expression was correlated with poorer prognosis in patients with PC. In PC cell lines, PACN-1 and BxPC-3, Ca2+ influxes could be evoked by TRPM8; the sensitivity of PC cells to gemcitabine was increased, while the proliferation and invasion of PC cells were suppressed after RNA interference-mediated silencing of TRPM8. The mechanism of TRPM8 in gemcitabine-based chemotherapy was then investigated. The expression and activity of multidrug resistance-associated proteins, P-gp, MRP-2, LRP, was significantly reduced in response to TRPM8 silence. Moreover, TRPM8 knockdown significantly increased hENT1 protein levels and the ratio of Bax/Bcl-2 while decreased the protein levels of RRM1. Thus, TRPM8 is required for PC cell proliferation and invasion and was closely related to the gemcitabine sensitivity of PC. The modulation of TRPM8 expression may help improve treatment response of PC by combining with traditional chemotherapy.