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The direct use of conventional photosensitizers in photodynamic therapy (PDT) of cancer cells has been thwarted by their low solubility, poor photostability, and aggregation tendency. Hence, complex and hectic synthetic procedures, such as developing nanomaterials and subsequently loading them with photosensitizers, have become mandatory for the effective use of photosensitizers in PDT. In this study, we have avoided complex procedures and produce hematoporphyrin (HP) photosensitizer-encapsulated carbon quantum dots (CQDs) (HP-CQDs) facilely through a well-controlled one-step microwave reaction by using the HP monomer as one of the precursors. The as-synthesized HP-CQDs retained all intrinsic optical and chemical properties of HP, while displaying excellent solubility in water. Importantly, the excellent reactive oxygen species generation ability of HP-CQDs under the illumination of deep red light favored their applicability in PDT-assisted efficient eradication of human breast cancer cells (MCF-7). Compared to HP, HP-CQDs exhibited very high phototoxicity and low dark toxicity toward MCF-7 cells. Overall, this study offers a proof of concept that photosensitizer-implanted CQDs, having excellence in PDT-assisted cancer treatment, can be easily designed by strategically exploiting the diversity available in the selection of precursors and synthesis conditions to produce CQDs. [ABSTRACT FROM AUTHOR]

We present a wet etching process to fabricate good vertical mesa structures that result in high quality (Q) factors up to 2×104, important for smooth sidewall cavities such as the photonic quantum ring (PQR) laser. Q factor analyses also indicate that it can be improved much more once the internal scattering from the wafer materials is minimized. We use an etching solution of H3PO4:CH3OH:H2O2 with a volume ratio of 3:1:1, and a single-layer photoresist etch mask for etching GaAs/AlGaAs structures of the PQR laser several micrometer deep. As the etching temperature is varied from 20 to 40 °C, the etched surface roughness decreases from 4.690 to 0.703 nm according to scanning electron microscope and atomic force microscopy studies. From the activation energy analysis for the above etching process and the temperature dependence, the etching process is shown to be reaction limited. The PQR lasers with an active diameter of 10 μm, fabricated by the wet etching process, show the spectral linewidth of 0.04 nm. Three-dimensional Rayleigh-Fabry-Perot mode spectra for the PQR laser are also reported for the angle-resolved emission modes. [ABSTRACT FROM AUTHOR]

Background: The BRAFV600E mutation leading to constitutive signaling of MEK-ERK pathways causes papillary thyroid cancer (PTC). Ras association domain family 1A (RASSF1A), which is an important regulator of MST1 tumor suppressor pathways, is inactivated by hypermethylation of its promoter region in 20 to 32% of PTC. However, in PTC without RASSF1A methylation, the regulatory mechanisms of RASSF1A-MST1 pathways remain to be elucidated, and the functional cooperation or cross regulation between BRAFV600E and MST1,which activates Foxo3,has not been investigated. Methodology/Principal Findings: The negative regulators of the cell cycle, p21 and p27, are strongly induced by transcriptional activation of FoxO3 in BRAFV600E positive thyroid cancer cells. The FoxO3 transactivation is augmented by RASSF1A and the MST1 signaling pathway. Interestingly, introduction of BRAFV600Emarkedly abolished FoxO3 transactivation and resulted in the suppression of p21 and p27 expression. The suppression of FoxO3 transactivation by BRAFV600Eis strongly increased by coexpression of MST1 but it is not observed in the cells in which MST1, but not MST2,is silenced. Mechanistically, BRAFV600Ewas able to bind to the C-terminal region of MST1 and resulted in the suppression of MST1 kinase activities. The induction of the G1-checkpoint CDK inhibitors, p21 and p27,by the RASSF1A-MST1-FoxO3 pathway facilitates cellular apoptosis, whereasaddition of BRAFV600E inhibits the apoptotic processes through the inactivation of MST1. Transgenic induction of BRAFV600Ein the thyroid gland results in cancers resembling human papillary thyroid cancers. The development of BRAFV600Etransgenic mice with the MST1 knockout background showed that these mice had abundant foci of poorly differentiated carcinomas and large areas without follicular architecture or colloid formation. Conclusions/Significance: The results of this study revealed that the oncogenic effect of BRAFV600E is associated with the inhibition of MST1 tumor suppressor pathways, and that the activity of RASSF1A-MST1-FoxO3 pathways determines the phenotypes of BRAFV600E tumors. [ABSTRACT FROM AUTHOR]

Trichostatin A (TSA) is an inhibitor of histone deacetylase. cDNA microarray analysis was used to identify genes modulated by TSA. A total of 93 genes were up-regulated and 27 genes down-regulated. The expressions of some of these genes were confirmed by RT-PCR analysis. [ABSTRACT FROM AUTHOR]

Presents a corrected reprint of an article in a 2004 issue of the periodical "Journal of Applied Physics" concerning etching fabrication of photonic quantum ring laser.