The nanosized effects of short-range multimagnon excitation behavior and short-circuit diffusion in NiO nanowalls synthesized using the Ni grid thermal treatment method were observed. The energy dispersive spectroscopy mapping technique was used to characterize the growth mechanism, and confocal Raman scattering was used to probe the antiferromagnetic exchange energy J2 between next-nearest-neighboring Ni ions in NiO nanowalls at various growth temperatures below the Neel temperature. This study shows that short spin correlation leads to an exponential dependence of the growth temperatures and the existence of nickel vacancies during the magnon excitation. Four-magnon configurations were determined from the scattering factor, revealing a lowest state and monotonic change with the growth temperature.PACS: 75.47.Lx; 61.82.Rx; 75.50.Tt; 74.25.nd; 72.10.Di
Estrogen receptor a (ERA) is a DNA-binding transcription factor that plays an important role in the regulation of cell growth. Previous studies indicated that the expression of ERa in cell lines and tumors derived from oral squamous cell carcinoma (OSCC). The aim of this study was to examine the activity and function of ERa in OSCC cells and the mechanism underlying ERa activation. Immunochemical analyses in benign (nZ11) and malignant (nZ21) lesions of the oral cavity showed that ERa immunoreactivity was observed in 43% (9/21) of malignant lesions, whereas none of benign lesions showed ERa immunoreactivity. The ERa expression was also found in three OSCC cell lines and its transcriptional activity was correlated with cell growth. Addition of estradiol stimulated cell growth, whereas treatment of tamoxifen or knockdown of ERa expression caused reduced cell growth. Interestingly, the expression and activity of focal adhesion kinase (FAK) were associated with the phosphorylation of ERa at serine 118 in OSCC cells. Elevated expression of FAK in the slow-growing SCC25 cells caused increases in ERa phosphorylation, transcriptional activity, and cell growth rate, whereas knockdown of FAK expression in the rapid-growing OECM-1 cells led to reduced ERa phosphorylation and activity and retarded cell growth. Inhibition of the activity of protein kinase B (AKT), but not ERK, abolished FAK-promoted ERa phosphorylation. These results suggest that OSCC cells expressed functional ERa, whose activity can be enhanced by FAK/AKT signaling, and this was critical for promoting cell growth. Thus, FAK and ERa can serve as the therapeutic targets for the treatment of OSCC.
Key Words" oral squamous cell carcinoma " estrogen receptor a " focal adhesion kinase
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