Publications by authors named "R C Parmar"

Air-liquid interface (ALI) culture can differentiate airway epithelial cells to recapitulate the respiratory tract in vitro. Here, we present a protocol for isolating and culturing nasal epithelial cells from turbinate tissues for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We describe steps to overcome challenges of imaging fragile cultures, detect the production of mucus, and quantify intracellular virus post-SARS-CoV-2 infection.

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Background: Estimation of long-term risk for cardiovascular events using the SMART (Secondary Manifestations of Arterial Disease) risk score can be potentially valuable in devising risk mitigation strategies.

Objectives: The objective of this study was to apply the SMART risk score to compute the risk for major adverse cardiovascular events (MACE) in the U.S.

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Peptides can operate as therapeutic agents that sit within a privileged space between small molecules and larger biologics. Despite examples of their potential to regulate receptors and modulate disease pathways, the development of peptides with drug-like properties remains a challenge. In the quest to optimize physicochemical parameters and improve target selectivity, unnatural amino acids (UAAs) have emerged as critical tools in peptide- and peptidomimetic-based drugs.

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HLA donor-specific antibodies (DSA) elicit alloimmune responses against the graft vasculature, leading to endothelial cell (EC) activation and monocyte infiltration during antibody-mediated rejection (AMR). AMR promotes chronic inflammation and remodeling, leading to thickening of the arterial intima termed transplant vasculopathy (TV) or cardiac allograft vasculopathy (CAV) in heart transplants. Intragraft-recipient macrophages serve as a diagnostic marker in AMR however, their polarization and function remain unclear.

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Cyclooxygenase-2 (COX-2), a key enzyme in the cyclooxygenase family, is pivotal in producing pro-inflammatory prostaglandins, driving chronic inflammation and related disorders. Targeting COX-2 with selective inhibitors can mitigate these conditions while avoiding the gastrointestinal and hepatotoxic/nephrotoxic side effects of traditional NSAIDs. However, the selectivity towards COX-2 inhibition has been associated with cardiovascular risks, necessitating the discovery of novel molecular scaffolds avoiding CVS side effects.

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