Investigations of Femtosecond-nanosecond Dual-beam Laser Ablation of Dielectrics

We have conducted experimental investigations for the micromachining of dielectrics (fused silica) using an integrated femtosecond (is) and nanosecond (ns) dual-beam laser system at different time delays between the fs and ns pulses. We found that the maximum ablation enhancement occurs when the fs pulse is shot near the peak of the ns pulse envelope. Enhancements up to 13.4 times in ablation depth and 50.7 times in the amount of material removal were obtained, as compared to fs laser ablation alone. the fs pulse increases the free electron density and changes the optical properties of fused silica to have metallic characteristics, which increases the absorption of the ns laser energy. This study provides an opportunity for efficient micromachining of dielectrics. © 2010 Optical Society of America

Complement C1q Activates Tumor Suppressor WWOX to Induce Apoptosis in Prostate Cancer Cells

BACKGROUND:Tissue exudates contain low levels of serum complement proteins, and their regulatory effects on prostate cancer progression are largely unknown. We examined specific serum complement components in coordinating the activation of tumor suppressors p53 and WWOX (also named FOR or WOX1) and kinases ERK, JNK1 and STAT3 in human prostate DU145 cells. METHODOLOGY/PRINCIPAL FINDINGS:DU145 cells were cultured overnight in 1% normal human serum, or in human serum depleted of an indicated complement protein. Under complement C1q- or C6-free conditions, WOX1 and ERK were mainly present in the cytoplasm without phosphorylation, whereas phosphorylated JNK1 was greatly accumulated in the nuclei. Exogenous C1q rapidly restored the WOX1 activation (with Tyr33 phosphorylation) in less than 2 hr. Without serum complement C9, p53 became activated, and hyaluronan (HA) reversed the effect. Under C6-free conditions, HA induced activation of STAT3, an enhancer of metastasis. Notably, exogenous C1q significantly induced apoptosis of WOX1-overexpressing DU145 cells, but not vehicle-expressing cells. A dominant negative and Y33R mutant of WOX1 blocked the apoptotic effect. C1q did not enhance p53-mediated apoptosis. By total internal reflection fluorescence (TIRF) microscopy, it was determined that C1q destabilized adherence of WOX1-expressing DU145 cells by partial detaching and inducing formation of clustered microvilli for focal adhesion particularly in between cells. These cells then underwent shrinkage, membrane blebbing and death. Remarkably, as determined by immunostaining, benign prostatic hyperplasia and prostate cancer were shown to have a significantly reduced expression of tissue C1q, compared to age-matched normal prostate tissues. CONCLUSIONS/SIGNIFICANCE:We conclude that complement C1q may induce apoptosis of prostate cancer cells by activating WOX1 and destabilizing cell adhesion. Downregulation of C1q enhances prostate hyperplasia and cancerous formation due to failure of WOX1 activation

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The rendering process of Fig. 4(a)-4(d

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The resulting 4D image for a 10-µm fluorescent bea

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Rendering process of the volumetric images using the 21 TFMI-LFM, TF-MPEM, and point-scanning MPEM image

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The rendering process of Fig. 5(a), 5(b), 5(d), and 5(f

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Brownian motion of a 2-µm florescent bead in water with a volumetric imaging rate of 100 H