RESUMO
Thermally induced magnetization switching (TIMS) relying solely on a single laser without any applied magnetic field is a key research direction of current spintronics. Most studies on TIMS so far have focused on GdFeCo with Gd concentration above 20%. In this work, we observe the TIMS at low Gd concentration excited by picosecond laser through atomic spin simulations. The results show that the maximum pulse duration for switching can be increased by an appropriate pulse fluence at the intrinsic damping in low Gd concentrations. At the appropriate pulse fluence, TIMS with pulse duration longer than one picosecond is possible for Gd concentration of only 12%. Our simulation results provide new insights for the exploration of the physical mechanism of ultrafast TIMS.
RESUMO
BACKGROUND Calcium-activated chloride channel A4 (CLCA4) is known as a tumor suppressor which contributes to the progression of a number of types of malignant tumors. However, little is known about the functional roles of CLCA4 in colorectal cancer (CRC). MATERIAL AND METHODS In this study, the expression patterns and dysregulation of mRNAs in CRC tissues were profiled by analyzing GSE21510 datasets from Gene Expression Omnibus database which contains 104 primary hepatocellular carcinoma tissues and 24 normal liver tissues, and by performing Kaplan-Meier analysis of TCGA data. Additionally, immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR) were performed using clinical tissues collected at our institute. In order to explore the functional role of CLCA4, gain-of-function cell models were constructed in SW620 and LoVo cells. Wound healing assay and Transwell assay were carried out to access the cell migration and invasion ability. RESULTS It was found that CLCA4 was an independent predictor for overall survival and lymph node metastasis. Additionally, immunohistochemistry and qRT-PCR results of the clinical tissues collected as part of our study further confirmed this correlation. In vitro experiments demonstrated that over-expression of CLCA4 could inhibit cell migration and invasion by suppressing epithelial-mesenchymal transition (EMT) via PI3K/ATK signaling and change the expression patterns of EMT markers in CLCA4-gain-of-function cell models. CONCLUSIONS CLCA4 inhibits migration and invasion by suppressing EMT via PI3K/ATK signaling and predicts favorable prognosis of CRC which may help to distinguish potential risk of lymph node metastasis in CRC.