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R. Murugan

Publications and source records attributed to R. Murugan.

3 recordsLinked to original sources

A Novel Global Context-aware Deep Neural Network for Enhanced Brain Tumor Segmentation using Magnetic Resonance Images

Brain cancer's severity necessitates precise brain tumor segmentation, which is crucial for effective brain tumor diagnosis. Manual identification, burdened by high costs, labor, and error risks, highlights the need for automated methods. In this study, we introduce the Global Context-aware Squeeze and Excite Residual UNet (GCSER-UNet), which facilitates a fusion of spatial and channel-wise attention and thus enhances the model's capacity to capture intricate spatial dependencies and contextual information. GCSER-UNet efficiently extracts tumor segments from multimodal MRI slices, delivering exceptional performance. Evaluations on benchmark databases exhibit its superiority, achieving a notable 94 percent dice score on the TCGA LGG dataset, surpassing the state-of-the-art dice score of 91.8 percent. In the BraTS 2020 dataset, the proposed GCSER-UNet ensemble approach yielded dice scores of 95 percent, 92 percent, and 90 percent for the tumor regions - Whole Tumor (W), Tumor Core (T), and Enhancing Tumor (E), respectively. The current state-of-the-art dice scores were 94 percent, 93 percent, and 88 percent. These compelling outcomes highlight the efficacy of GCSER-UNet in precise brain tumor segmentation and thus can aid neurologists in effective brain cancer management and treatment planning.

cs.CV

Theory on the mechanisms of combinatorial binding of transcription factors with DNA

We develop a theoretical framework on the mechanism of combinatorial binding of transcription factors (TFs) with their specific binding sites on DNA. We consider three possible mechanisms viz. monomer, hetero-oligomer and coordinated recruitment pathways. In the monomer pathway, combinatorial TFs search for their targets in an independent manner and the protein-protein interactions among them will be insignificant. The protein-protein interactions are very strong so that the hetero-oligomer complex of TFs as a whole searches for the cognate sites in case of hetero-oligomer pathway. The TF which arrived first will recruit the adjacent TFs in a sequential manner in the recruitment pathway. The free energy released from the protein-protein interactions among TFs will be in turn utilized to stabilize the TFs-DNA complex. Such coordinated binding of TFs in fact emerges as the cooperative effect. Monomer and hetero-oligomer pathways are efficient only when few TFs are involved in the combinatorial regulation. Detailed random walk simulations suggest that when the number of TFs in a combination increases then the searching efficiency of TFs in these pathways decreases with the increasing number of TFs in a power law manner. The power law exponent associated with the monomer pathway seems to be strongly dependent on the number of TFs, distance between the initial position of TFs from their specific binding sites and the hop size associated with the dynamics of TFs on DNA.

q-bio.SC

Theory on the mechanism of site-specific DNA-protein interactions in the presence of traps

The speed of site-specific binding of transcription factor (TFs) proteins with genomic DNA seems to be strongly retarded by the randomly occurring sequence traps. Traps are those DNA sequences sharing significant similarity with the original specific binding sites. It is an intriguing question how the naturally occurring TFs and their specific binding sites are designed to manage the retarding effects of such randomly occurring traps. We develop a simple random walk model on the site-specific binding of TFs with genomic DNA in the presence of sequence traps. Our dynamical model predicts that (a) the retarding effects of traps will be minimum when the traps are arranged around the specific binding site such that there is a negative correlation between the binding strength of TFs with traps and the distance of traps from the specific binding site and (b) the retarding effects of sequence traps can be appeased by the condensed conformational state of DNA. Our computational analysis results on the distribution of sequence traps around the putative binding sites of various TFs in mouse and human genome clearly agree well the theoretical predictions. We propose that the distribution of traps can be used as an additional metric to efficiently identify the specific binding sites of TFs on genomic DNA.

q-bio.SC