Publications by authors named "M L Dewal"

Host protein folding stress responses can play important roles in RNA virus replication and evolution. Prior work suggested a complicated interplay between the cytosolic proteostasis stress response, controlled by the transcriptional master regulator heat shock factor 1 (HSF1), and human immunodeficiency virus-1 (HIV-1). We sought to uncouple HSF1 transcription factor activity from cytotoxic proteostasis stress and thereby better elucidate the proposed role(s) of HSF1 in the HIV-1 lifecycle.

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Classically, the unfolded protein response (UPR) safeguards secretory pathway proteostasis. The most ancient arm of the UPR, the IRE1-activated spliced X-box binding protein 1 (XBP1s)-mediated response, has roles in secretory pathway maturation beyond resolving proteostatic stress. Understanding the consequences of XBP1s activation for cellular processes is critical for elucidating mechanistic connections between XBP1s and development, immunity, and disease.

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The speckle noise is inherent to transthoracic echocardiographic images. A standard noise-free reference echocardiographic image does not exist. The evaluation of filters based on the traditional parameters such as peak signal-to-noise ratio, mean square error, and structural similarity index may not reflect the true filter performance on echocardiographic images.

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Clinically, the severity of valvular regurgitation is assessed by manual tracing of the regurgitant jet in the respective chambers. This work presents a computer-aided diagnostic (CAD) system for the assessment of the severity of mitral regurgitation (MR) based on image processing that does not require the intervention of the radiologist or clinician. Eight different texture feature sets from the regurgitant area (selected through an arbitrary criterion) have been used in the present approach.

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Proteostasis in the cytosol is governed by the heat shock response. The master regulator of the heat shock response, heat shock factor 1 (HSF1), and key chaperones whose levels are HSF1-regulated have emerged as high-profile targets for therapeutic applications ranging from protein misfolding-related disorders to cancer. Nonetheless, a generally applicable methodology to selectively and potently inhibit endogenous HSF1 in a small molecule-dependent manner in disease model systems remains elusive.

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