Phosphorus-Doped Activated Coconut Shell Carbon-Anchored Highly Dispersed Pt for the Chemoselective Hydrogenation of Nitrobenzene to -Aminophenol.

Highly dispersed Pt nanoparticles (∼2.5 nm) on phosphorus-doped activated coconut shell carbon (Pt/P-ACC) were synthesized by a two-step impregnation route. Pt/P-ACC showed a high activity, chemoselectivity, and reusability toward the hydrogenation of nitrobenzene to -aminophenol, with hydrogen as the reducing agent in sulfuric acid.

One-Pot Synthesis of Al-P-O Catalysts and Their Catalytic Properties for -Methylation of Catechol and Methanol.

A series of Al-P-O catalysts (Al-P-O) were prepared using a P123-assisted one-pot method at different P/Al molar ratios and used for -methylation of catechol and methanol. The influences of the P/Al molar ratio and P123 addition on catalyst structure and surface acid-base characteristics were investigated in detail. Increasing the P/Al molar ratio more favored crystalline aluminophosphate.

Exosomal miR-9-5p secreted by bone marrow-derived mesenchymal stem cells alleviates osteoarthritis by inhibiting syndecan-1.

Mesenchymal stem cells (MSCs) have been demonstrated to serve as targets for the treatment of osteoarthritis (OA) and exosomes derived from MSCs also display chondroprotective effects. This study aims to investigate the regulatory role of exosomal microRNA-9-5p (miR-9-5p) secreted by bone marrow-derived MSCs (BM-MSCs) on OA in a rat model induced by anterior cruciate ligament/medial collateral ligament transection. Luciferase reporter assay was conducted to verify the putative miR-9-5p binding sites to 3'UTR of syndecan-1 (SDC1).

RETRACTED: Human bone mesenchymal stem cells-derived exosomes overexpressing microRNA-26a-5p alleviate osteoarthritis via down-regulation of PTGS2.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy).

Different epidermal growth factor receptor signaling pathways in neurons and astrocytes activated by extracellular matrix after spinal cord injury.

Spinal cord injury (SCI) is a serious central nervous system (CNS) trauma that results in permanent and severe disability. The extracellular matrix (ECM) can affect the activation of extracellular signal-regulated kinase 1/2 (ERK) by interacting with the ERK integrin subunits. In this study, we built a model of SCI with glial fibrillary acidic protein-green fluorescent protein (GFAP-GFP) and thymus cell antigen 1-yellow fluorescent protein-H (Thy1-YFPH) in mice that express specific transgenes in their astrocytes or neurons.

Protective effect of leptin-mediated caveolin-1 expression on neurons after spinal cord injury.

Spinal cord injury (SCI) causes long-term disability and has no effective clinical treatment. After SCI, extracellular adenosine triphosphate (ATP) leads to an influx of extracellular Ca, and this Ca overload causes neuronal toxicosis and apoptosis. The biological functions of leptin have been widely investigated in the central nervous system.

Lithium Inhibits GSK3β Activity via Two Different Signaling Pathways in Neurons After Spinal Cord Injury.

Spinal cord injury (SCI) is a type of long-term disability with a high morbidity rate in clinical settings for which there is no effective clinical treatment to date. Usually, lithium is used as a popular mood stabilizer. Recently, growing evidence has shown that lithium has clear neuroprotective effects after SCI, and the administration of lithium can effectively improve locomotor recovery.

The ameliorative effect of fluoxetine on neuroinflammation induced by sleep deprivation.

It is well known that sleep disorders are harmful to people's health and performance, and growing evidence suggests that sleep deprivation (SD) can trigger neuroinflammation in the brain. The nucleotide-binding domain and leucine-rich repeat protein-3 (NLRP3) inflammasome is reported to be relevant to the neuroinflammation induced by SD, but the regulatory signaling that governs the NLRP3 inflammasome in SD is still unknown. Meanwhile, whether the regulatory action of antidepressants in astrocytes could affect the neuroinflammation induced by SD also remains obscure.