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Growth inhibition and apoptotic/necrotic phenotype was observed in nanogold particle (AuNP)-treated human chronic myelogenous leukemia cells. To elucidate the underlying cellular mechanisms, proteomic techniques including two-dimensional electrophoresis/mass spectrometry and protein microarrays were utilized to study the differentially expressed proteome and phosphoproteome, respectively. Systems biology analysis of the proteomic data revealed that unfolded protein-associated endoplasmic reticulum (ER) stress response was the predominant event. Concomitant with transcriptomic analysis using mRNA expression, microarrays show ER stress response in the AuNP-treated cells. The ER stress protein markers' expression assay unveiled AuNPs as an efficient cellular ER stress elicitor. Upon ER stress, cellular responses, including reactive oxygen species increase, mitochondrial cytochrome c release, and mitochondria damage, chronologically occurred in the AuNP-treated cells. Conclusively, this study demonstrates that AuNPs cause cell death through induction of unmanageable ER stress.

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A cubic-tetragonal-trigonal sequence of phase transitions in the relaxor ferroelectric Na& &~Bi &~& Ti03 (NBT) has been studied by Brillouin scattering. Pronounced anomalies for both the hypersonic velocity and damping have been found that peak just between two phase transitions in contrast to the ordinary well-known behavior with anomalies in the vicinity of every transition point. The fact that these anomalies are centered in the intertransition region and extend beyond both transitions is attributed to the fluctuations of two coupled order parameters associated with disorder in the Naand Bi-cation distribution in a manner characteristic of relaxor ferroelectrics. Such a phenomenon seems to be typical of relaxor materials and to be the basis of the difFuse phase-transition dynamics.