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Sadeghi, L.

Publications and source records attributed to Sadeghi, L..

2 recordsLinked to original sources

A Dynamic Bottom-Up Saliency Detection Method for Still Images

IntroductionExisting saliency detection algorithms in the literature have ignored the importance of time. They create a static saliency map for the whole recording time. However, bottom-up and top-down attention continuously compete and the salient regions change through time. In this paper, we propose an unsupervised algorithm to predict the dynamic evolution of bottom-up saliency in images. MethodWe compute the variation of low-level features within non-overlapping patches of the input image. A patch with higher variation is considered more salient. We use a threshold to ignore less salient parts and create a map. A weighted sum of this map and its center of mass is calculated to provide the saliency map. The threshold and weights are set dynamically. We use the MIT1003 and DOVES datasets for evaluation and break the recording to multiple 100ms or 500ms-time intervals. A separate ground-truth is created for each interval. Then, the predicted dynamic saliency map is compared to the ground-truth using Normalized Scanpath Saliency, Kullback-Leibler divergence, Similarity, and Linear Correlation Coefficient metrics. ResultsThe proposed method outperformed the competitors on DOVES dataset. It also had an acceptable performance on MIT1003 especially within 0-400ms after stimulus onset. ConclusionThis dynamic algorithm can predict an images salient regions better than the static methods as saliency detection is inherently a dynamic process. This method is biologically-plausible and in-line with the recent findings of the creation of a bottom-up saliency map in the primary visual cortex or superior colliculus.

bioengineering↗

Differential transcriptional reprogramming by wild type and lymphoma-associated mutant MYC proteins as B-cells convert to lymphoma-like cells

The transcription factor MYC regulates the expression of a vast number of genes and is implicated in various human malignancies, for which its deregulation by genomic events such as translocation or amplification can be either disease-defining or associated with poor prognosis. In hematological malignancies MYC is frequently subject to missense mutations and one such hot spot where mutations have led to increased protein stability and elevated transformation activity exists within its transactivation domain. Here we present and characterize a model system for studying the effects of gradually increasing MYC levels as B-cells progress to lymphoma-like cells. Inclusion of two frequent lymphoma-associated MYC mutants (T58A and T58I) allowed for discrimination of changes in the MYC regulatory program according to mutation status. Progressive increase in MYC levels significantly altered the transcript levels of 7569 genes and subsets of these were regulated differently in mutant MYC proteins compared to WT MYC or between the mutant MYC proteins. Functional classification of the differentially regulated genes based on expression levels across different MYC levels confirmed previously found MYC regulated functions such as ribosome biogenesis and purine metabolism while other functional groups such as the downregulation of genes involved in B-cell differentiation and chemotaxis were novel. Gene sets that were differently regulated in cells overexpressing mutant MYC proteins contained an over-representation of genes involved in DNA Replication and transition from the G2 phase to mitosis. The cell model presented here mimics changes seen during lymphoma development in the E-Myc mouse model as well as MYC-dependent events associated with poor prognosis in a wide range of human cancer types and therefore constitutes a relevant cell model for in vitro mechanistic studies of wild type and mutant MYC proteins in relation to lymphoma development.

cancer biology↗