A Novel RAGE Modulator Induces Soluble RAGE to Reduce BACE1 Expression in Alzheimer's Disease.

β-secretase (BACE1) is instrumental in amyloid-β (Aβ) production, with overexpression noted in Alzheimer's disease (AD) neuropathology. The interaction of Aβ with the receptor for advanced glycation endproducts (RAGE) facilitates cerebral uptake of Aβ and exacerbates its neurotoxicity and neuroinflammation, further augmenting BACE1 expression. Given the limitations of previous BACE1 inhibition efforts, the study explores reducing BACE1 expression to mitigate AD pathology.

Effects of genetic mutations on left ventricular myocardial mechanics and fibrosis patterns in hypertrophic cardiomyopathy.

Myocyte disarray and fibrosis are underlying pathologies of hypertrophic cardiomyopathy (HCM) caused by genetic mutations. However, the extent of their contributions has not been extensively evaluated. In this study, we investigated the effects of genetic mutations on myofiber function and fibrosis patterns in HCM.

CO2-driven Oxygen Vacancy Diffusion and Healing on TiO2(110) at Ambient Pressure.

Understanding how TiO2 interacts with CO2 at the molecular level is crucial in the CO2 reduction toward value-added energy sources. Here, we report in-situ observations of the CO2 activation process on the reduced TiO2(110) surface at room temperature using ambient pressure scanning tunneling microscopy. We found that oxygen vacancies (Vo) diffuse dynamically along the bridging oxygen (Obr) rows of the TiO2(110) surface under ambient CO2(g) environments.

Magnolia kobus DC. suppresses neointimal hyperplasia by regulating ferroptosis and VSMC phenotypic switching in a carotid artery ligation mouse model.

Background: Magnolia kobus DC (MO), as a plant medicine, has been reported to have various physiological activities, including neuroprotective, anti-inflammatory, and anti-diabetic effects. However, vascular protective effects of MO remain incompletely understood. In this study, we evaluated the vascular protective effect of MO against ferroptosis in a carotid artery ligation (CAL)-induced neointimal hyperplasia mouse model and in aortic thoracic smooth muscle A7r5 cells.