Breast cancer is the second leading cause of death for women all over the world. Since the cause of the disease remains unknown, early detection and diagnosis is the key for breast cancer control, and it can increase the success of treatment, save lives and reduce cost. Ultrasound imaging is one of the most frequently used diagnosis tools to detect and classify abnormalities of the breast. In order to eliminate the operator dependency and improve the diagnostic accuracy, computer-aided diagnosis (CAD) system is a valuable and beneficial means for breast cancer detection and classification. Generally, a CAD system consists of four stages: preprocessing, segmentation, feature extraction and selection, and classification. In this paper, the approaches used in these stages are summarized and their advantages and disadvantages are discussed. The performance evaluation of CAD system is investigated as well.

In addition to their hemostatic function, platelets play an important role in regulating the inflammatory response. The platelet NLRP3 inflammasome not only promotes interleukin-1β secretion, but was also found to be upregulated during platelet activation and thrombus formation in vitro. However, the role of NLRP3 in platelet function and thrombus formation in vivo remains unclear. In this study, we aimed to investigate the role of NLRP3 in platelet integrin αIIbβ3 signaling transduction. Using NLRP3−/− mice, we showed that NLRP3-deficient platelets do not have significant differences in expression of the platelet-specific adhesive receptors αIIbβ3 integrin, GPIba or GPVI; however, NLRP3−/− platelets transfused into wild-type mice resulted in prolonged tail-bleeding time and delayed arterial thrombus formation, as well as exhibiting impaired spreading on immobilized fibrinogen and defective clot retraction, concomitant with decreased phosphorylation of c-Src, Syk and PLCγ2 in response to thrombin stimulation. Interestingly, addition of exogenous recombinant interleukin-1β reversed the defect in NLRP3−/− platelet spreading and clot retraction, and restored thrombin-induced phosphorylation of c-Src/Syk/PLCγ2, whereas an anti-interleukin-1β antibody blocked spreading and clot retraction mediated by wild-type platelets. Using the direct NLRP3 inhibitor, CY-09, we demonstrated significantly reduced human platelet aggregation in response to threshold concentrations of collagen and ADP, as well as impaired clot retraction in CY-09-treated human platelets, supporting a role for NLRP3 also in regulating human platelet αIIbβ3 outside-in signaling. This study identifies a novel role for NLRP3 and interleukin-1β in platelet function, and provides a new potential link between thrombosis and inflammation, suggesting that therapies targeting NLRP3 or interleukin-1β might be beneficial for treating inflammation-associated thrombosis.

The kidney renal papillary cell carcinoma (KIRP) is a relatively rare type of kidney cancer. There has been no investigation to find a robust signature to predict the survival outcome of KIRP patients in the aspect of tumor immunology. In this study, 285 KIRP samples from The Cancer Genome Atlas (TCGA) were randomly divided into training and testing set. A total of 1534 immune‐related genes from The Immunology Database and Analysis Portal (ImmPort) were used as candidates to construct the signature. Using univariate Cox analysis, we evaluated the relationship between overall survival and immune‐related genes expression and found 272 immune‐related genes with predicting prognostic ability. In order to construct an efficient predictive model, the Cox proportional hazards model with an elastic‐net penalty was used and identified 23 groups after 1000 iterations. As a result, 15‐genes model showing more stable than other gene groups was chosen to construct our immune‐related risk signature. In line with our expectations, the signature can independently predict the survival outcome of KIRP patients. Patients with high‐immune risk were found correlated with advanced stage. We also found that the high‐immune risk patients with higher PBRM1 and SETD2 mutations, increasing chromosomal instability, together with the gene set enrichment analysis (GSEA) results showing intensive connection of our signature with immune pathways. In conclusion, our study constructs a robust 15‐gene signature for predicting KIRP patients’ survival outcome on the basis of tumor immune environment and may provide possible relationship between prognosis and immune‐related biological function.

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