RESUMO
The world-class Shizhuyuan W-Sn-Mo-Bi deposit is spatially related to the Qianlishan granite complex (QGC) in Hunan Province, China. However, the age and classification of the QGC are still debated, and a better understanding of the temporal genetic relationship between the QGC and the Shizhuyuan deposit is essential. Here, we present chemical compositions the intrusive phases of the QGC and the results of detailed zircon U-Pb dating and muscovite Ar-Ar dating of a mineralized greisen vein. Our new zircon laser ablation inductively coupled plasma mass spectrometry U-Pb age data constrain the emplacement of the QGC to 155-151.7 Ma. According to petrological, geochemical and geochronological data and the inferred redox conditions, the QGC can be classified into four phases: P1, porphyritic biotite granites; P2, porphyritic biotite granites; P3, equigranular biotite granite; and P4, granite porphyry dikes. All phases, and especially P1-P3, have elevated concentrations of ore-forming metals and heat-producing elements (U, Th, K; volume heat-producing rate of 5.89-14.03 µWm-3), supplying the metal and heat for the metalogic process of the Shizhuyuan deposit. The Ar-Ar muscovite age (154.0 ± 1.6 Ma) of the mineralized greisen vein in the Shizhuyuan deposit is consistent with the emplacement time of the QGC, suggesting their temporal genetic relationship.
RESUMO
Taxol (paclitaxel), one of the most active cancer chemotherapeutic agents, can cause programmed cell death (PCD) and cytoplasmic vacuolization. The objective of this study was to analyze the morphological characteristics induced by taxol. Human lung adenocarcinoma (ASTC-a-1) cells were exposed to various concentration of taxol. CCK-8 was used to assay the cell viability. Atomic force microscopy (AFM), plasmid transfection and confocal fluorescence microscopy were performed to image the cells morphological change induced by taxol. Fluorescence resonance energy transfer (FRET) was used to monitor the caspase-3 activation in living cells during taxol-induced cell death. Cells treated with taxol exhibited significant swelling and cytoplasmic vacuolization which may be due to endoplasmic reticulum (ER) vacuolization. Caspase-3 was not activated during taxol-induced cytoplasmic vacuolization and cell death. These findings suggest that taxol induces caspase-3-independent cytoplasmic vacuolization, cell swelling and cell death through ER vacuolization.