RESUMEN
The laser-induced breakdown spectroscopy (LIBS) experimental platform was applied to obtain LIBS spectral the data of 10 CL60 wheel steel samples. The principle component analysis (PCA) was used to preliminarily analyze the macroscopic characteristics of LIBS spectral data. With the spectral intensity and spectral intensity combined with spectral intensity ratio as variables, three spectral correction methods including median filtering, baseline correction and multiple scattering correction (MSC) were used for pretreatment. And the support vector machine (SVM) qualitative model was established to determine the metallographic structure. It was found that the SVM model established by using the pre-processed data of MSC as the input variable has the best effect. The accuracy rate of calibration set is 100%, and the accuracy rate of prediction set is 98.4%. The research has shown that LIBS combined with SVM model can be used for discriminant analysis of different metallographic structures of train wheel steel.
RESUMEN
Stathmin has been investigated as a tumor biomarker because it appear to be associated with tumorigenesis; however, the effect of stathmin in lung adenocarcinoma (LAC) remains poorly understood. The purpose of this study was to examine the expression of stathmin in lung adenocarcinoma, and to disclose the relationship between them. The expression of stathmin was examined by RT-PCR, IHC and Western blot. Furthermore, small interfering RNA (shRNA)-mediated silencing of stathmin was employed in LAC cells to investigate cell proliferation, invasion and apoptosis. In this study, we showed that overexpression of stathmin was significantly associated with poorly differentiated, lymph node metastasis and advance TNM stages of lung adenocarcinoma. And silencing of stathmin expression inhibited the proliferation, migration and invasion of lung adenocarcinoma PC-9 cells, and retarded the growth of PC-9 cells xenografts in nude mice. Additionally, the anticarcinogenic efficacy of stathmin silencing might be involved in P38 and MMP2 signaling pathways. In conclusion, these results showed that stathmin expression was significantly up-regulated in LAC, which may act as a biomarker for LAC. Furthermore, silence of stathmin inhibiting LAC cell growth indicated that stathmin may be a promising molecular target for LAC therapy.