Publications by authors named "S Enayati"

Background: Fibrosis is a principal sign of systemic sclerosis (SSc) which can affect several organs including the lung, heart, and dermis. Dermal fibroblasts of SSc patients are characterized by persistent and activated Ras and ERK1/2 signaling which stimulates extreme collagen and extracellular matrix synthesis. Salirasib is a Ras inhibitor that competitively prevents the adherence of GTP-bound Ras to the plasma membrane, that inhibits Ras signaling.

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Background: Systemic sclerosis (SSc) is a connective tissue disorder characterized by excessive fibrosis, where activated fibroblasts play a pivotal role in disease progression. This study aimed to investigate the potential of Talabostat, a small molecule inhibitor of dipeptidyl peptidases, in alleviating fibrosis and inflammation associated with SSc pathogenesis.

Methods: Dermal fibroblasts were obtained from skin biopsies of ten diffuse cutaneous SSc patients and healthy controls.

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Background: Biomedical Relation Extraction (RE) is essential for uncovering complex relationships between biomedical entities within text. However, training RE classifiers is challenging in low-resource biomedical applications with few labeled examples.

Methods: We explore the potential of Shortest Dependency Paths (SDPs) to aid biomedical RE, especially in situations with limited labeled examples.

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Background: Nosocomial infections caused by multidrug-resistant are a considerable public health threat, requiring innovative therapeutic approaches.

Objectives: This study explored preconditioning mesenchymal stem cells (MSCs) with the antimicrobial peptide Nisin to enhance their antibacterial properties while maintaining regenerative capacity.

Methods: Human MSCs were preconditioned with varying concentrations of Nisin (0.

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Systemic sclerosis (SSc) is an autoimmune systemic disease that is characterized by immune dysregulation, inflammation, vasculopathy, and fibrosis. Tissue fibrosis plays an important role in SSc and can affect several organs such as the dermis, lungs, and heart. Dysregulation of interferon (IFN) signaling contributes to the SSc pathogenesis and interferon regulatory factor 1 (IRF1) has been indicated as the main regulator of type I IFN.

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