RESUMO
Serious edge effects of potassium dihydrogen phosphate (${{\rm KH}_2}{{\rm PO}_4}$KH2PO4, KDP) manufactured using single-point diamond turning (SPDT) often result in disqualification of the transmittance wavefront for high-power laser systems. In this paper, based on the theoretical analysis of sucker hole configuration and the pressure distribution law under the vacuum chuck condition of crystal elements, the influence of sucker hole configuration on the transmittance wavefront root-mean-square gradient (GRMS) is verified through fly-cutting experiments. By adopting the newly designed vacuum chuck, the vacuum-chucking quality is effectively improved, and the edge effect is accordingly suppressed in the SPDT. Moreover, the accuracy of the transmittance wavefront GRMS has an improvement of about 25% under the same processing parameters.
RESUMO
OBJECTIVE: Identify the molecular mechanism of inflammatory stimuli induced pancreatic cancer progression. METHODS: RNA-seq, microarray assay and bioinformatics analyses were used to identify differentially expressed genes. Immunohistochemical staining was performed to evaluate CD68, CD163, ß-catenin, CD103, CCL3 markers. Quantitative real-time polymerase chain reaction (qRT-PCR), luciferase reporter assay, apoptosis assay, wound healing assay and immunofluorescence were performed to study the relationship of inflammatory stimuli and WNT/ß-catenin pathway. RESULTS: Differentially expressed genes of macrophage-conditioned medium-treated pancreatic cancer cells were related with WNT/ß-catenin pathway. Inflammatory stimuli could activate WNT/ß-catenin signaling pathway. In 106 pancreatic cancer patients, nuclear ß-catenin expression of CD68-high group was much higher than CD68-low group (P < 0.05), as same as CD163 (P < 0.05). Inflammatory stimuli downregulated the expression of CCL3 via WNT/ß-catenin pathway and inhibited the chemotaxis of CD103 dendritic cells. Six pancreatic cancer prognosis associating genes were upregulated by inflammatory stimuli via WNT/ß-catenin pathway. Transforming growth factor-ß promoted malignant biological behavior of pancreatic cancer cells through WNT/ß-catenin pathway-dependent mechanism. CONCLUSIONS: Our present study provided a novel mechanism involved in the inflammation-driven cancer progression through tumor immune escape and downstream gene regulation of WNT/ß-catenin pathway-dependent manner.