The interrelationships of CSF sTREM2, AD pathology, minimal depressive symptoms, and cognition in non-demented adults.

Background: Microglial activation has been suggested to be involved in the pathogenesis of depression and Alzheimer's disease (AD). Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) is a marker of microglial activation. The purpose of this study was to investigate the interrelationships of cerebrospinal fluid (CSF) sTREM2, AD pathology, as well as minimal depressive symptoms (MDSs), and cognition.

Associations of Vascular Risk with Cognition, Brain Glucose Metabolism, and Clinical Progression in Cognitively Intact Elders.

Background: Increasing evidence supports an important role of vascular risk in cognitive decline and dementia.

Objective: This study aimed to examine whether vascular risk was associated with cognitive decline, cerebral hypometabolism, and clinical progression in cognitively intact elders.

Methods: Vascular risk was assessed by the Framingham Heart Study general Cardiovascular disease (FHS-CVD) risk score.

Efficient and Saturated Red Light-Emitting Electrochemical Cells Based on Cationic Iridium(III) Complexes with EQE up to 9.4 .

Solid-state light-emitting electrochemical cells (LECs) have several advantages, such as low-voltage operation, compatibility with inert metal electrodes, large-area flexible substrates, and simple solution-processable device architectures. However, most of the studies on saturated red LECs show low or moderate device efficiencies (external quantum efficiency (EQE) <3.3 %).

Traumatic brain injury in vivo and in vitro contributes to cerebral vascular dysfunction through impaired gap junction communication between vascular smooth muscle cells.

Gap junctions (GJs) contribute to cerebral vasodilation, vasoconstriction, and, perhaps, to vascular compensatory mechanisms, such as autoregulation. To explore the effects of traumatic brain injury (TBI) on vascular GJ communication, we assessed GJ coupling in A7r5 vascular smooth muscle (VSM) cells subjected to rapid stretch injury (RSI) in vitro and VSM in middle cerebral arteries (MCAs) harvested from rats subjected to fluid percussion TBI in vivo. Intercellular communication was evaluated by measuring fluorescence recovery after photobleaching (FRAP).

Propofol inhibits pressure-stimulated macrophage phagocytosis via the GABAA receptor and dysregulation of p130cas phosphorylation.

Surgical stress and anesthesia result in systemic immunosuppression. Propofol, a commonly used anesthetic agent, alters immune cell functions. Previously, we demonstrated that extracellular pressure increases macrophage phagocytosis.