Novel Oridonin Analog CYD0682 Inhibits Hepatic Stellate Cell Activation via the Heat Shock Protein 90-Dependent STAT3 Pathway.

Introduction: Activated hepatic stellate cells (HSCs) are the primary effector cells in hepatic fibrosis, over depositing extracellular matrix (ECM) proteins. Our previous work found oridonin analog CYD0682 attenuates proliferation, Transforming Growth Factor β (TGFβ)-induced signaling, and ECM production in immortalized HSCs. The underlying mechanism behind these reductions is unclear.

A Rare Case of Erosive Esophagitis Due to Sarcina Ventriculi Infection.

is a Gram-positive anaerobic found in soil that is a rare cause of inflammatory infections of the GI tract. This bacterium has a propensity for causing gastritis in patients with delayed gastric emptying. Of the 66 reported cases in the literature, 10 involved the esophagus.

PARP1 Inhibition and Effect on Burn Injury-Induced Inflammatory Response and Cardiac Function.

Background: Burn injury induces multiple signaling pathways leading to a significant inflammatory storm that adversely affects multiple organs, including the heart. Poly (ADP-ribose) polymerase inhibitor 1 (PARP1) inhibition, with specific agents such as N-(5,6-Dihydro-6-oxo-2-phenanthridinyl)-2-acetamide (PJ34), is effective in reducing oxidative stress and cytokine expression in the heart. We hypothesized that PARP1 inhibition would reduce inflammatory signaling and protect against burn injury-induced cardiac dysfunction.

Cytokine Pathways in Cardiac Dysfunction following Burn Injury and Changes in Genome Expression.

In 2016, an estimated 486,000 individuals sustained burn injuries requiring medical attention. Severe burn injuries lead to a persistent, hyperinflammatory response that may last up to 2 years. The persistent release of inflammatory mediators contributes to end-organ dysfunction and changes in genome expression.