Low field control of spin switching and continuous magnetic transition in an ErFeO3 single crystal.

The magnetic behavior of a rare-earth orthoferrite ErFeO3 single crystal can be controlled by low magnetic fields from a few to hundreds of Oe. Here we investigated a high-quality ErFeO3 single crystal in the temperature range of 5-120 K, with two types of spin switching in the field-cooled-cooling (FCC) and field-cooled-warming (FCW) processes below the temperature of the spin reorientation (SR) transition from Γ4 to Γ2 at 98-88 K. The magnitude of the applied magnetic fields can regulate two types of spin switching along the a-axis of the ErFeO3 single crystal but does not affect the type and temperature range of the SR transition. An interesting "multi-step" type-II spin switching is observed in FCW under low magnetic fields (H < 18 Oe) just below the SR transition temperature, which is associated with the interaction and the change of magnetic configurations from rare-earth and iron magnetic sublattices. When the magnetic field is lower than 15 Oe, the type-II spin switching in the FCW process gradually changes to a continuous magnetic transition along the a-axis of the ErFeO3 single crystal. As the magnetic field is reduced to less than 17 Oe, the type-I spin switching in the FCW process also transforms into a continuous magnetic transition. Understanding the magnetic reversal effects will help us explore the potential applications of these magnetic materials for future information devices.

Plasma Non-targeted Metabolomics Analysis of Yili Horses Raced on Tracks With Different Surface Hardness.

In this study, the plasma non-targeted metabolomics of Yili horses were characterized before and after exercise on tracks that differed in surface hardness to better understand exercise-related biochemical changes. Blood samples were obtained from eight trained Yili horses before and immediately after exercise. Samples were used for metabolomic analysis by ultra-performance liquid chromatography-Q-EXACTIVE mass spectrometry. In total, 938 significantly different metabolites involving sugar, lipid, and amino acid metabolism were detected in the plasma, with significant increases in glucose, glucoheptanoic acid, lactic acid, malic acid, and methylmalonic acid and significant decreases in creatinine, D-tryptophan, carnitine, and citric acid after exercise. Among these metabolites, acetylcarnitine, tuliposide, vitamin C, and methylmalonic acid showed regular changes in concentration after exercise on tracks that differed in surface hardness, providing new insights into equine exercise physiology. The findings indicated the potential of vitamin C and methylmalonic acid as novel biomarkers of equine locomotor injury.

The anti-fibrotic agent nintedanib protects chondrocytes against tumor necrosis factor-ɑ (TNF-ɑ)-induced extracellular matrix degradation.

Osteoarthritis is an inflammatory disease of the musculoskeletal system characterized by damaged articular cartilage. Nintedanib is an oral triple kinase inhibitor with anti-fibrotic and anti-inflammatory properties. Thus, we hypothesized that nintedanib might exert a protective effect in chondrocytes and it could be meaningful to repurpose the drug for osteoarthritis. In this study, we aimed to investigate the potential effects of nintedanib on TNF-α-induced cellular injury in CHON-001 chondrocytes. The results show that nintedanib ameliorated TNF-α-induced reactive oxygen species (ROS) production and reduced glutathione (GSH) decrease. Nintedanib reduced the production of pro-inflammatory cytokines interleukin-6 (IL-6) and interleukin-1ß (IL-1ß) in TNF-α-induced CHON-001 chondrocytes. Nintedanib restored TNF-α caused decreased expression levels of Col II and sry-type high-mobility-group box-9 (SOX-9) in CHON-001 chondrocytes. Moreover, nintedanib ameliorated the TNF-α-caused impairment of protein kinase A/cAMP-response element-binding protein (PKA/CREB) signaling pathway as revealed by the decreased PKA RI expression and increased p-CREB in CHON-001 cells. Inhibition of PKA by H89 abolished the effects of nintedanib on SOX-9 and Col II expression. Taken together, nintedanib presented protective effects on TNF-α-induced oxidative stress, inflammation, and ECM damage in CHON-001 chondrocytes. Mechanically, the effect of nintedanib is associated with the PKA/CREB pathway. These data imply that the anti-fibrotic agent nintedanib may have a potential therapeutic application for osteoarthritis.

Chloroquine and valproic acid combined treatment in vitro has enhanced cytotoxicity in an osteosarcoma cell line.

Choroquine (CQ) and valproic acid (VPA) have been extensively studied for biological effects. Here, we focused on efficacy of combined CQ and VPA on osteosarcoma cell lines. Viability of osteosarcoma cell lines (U20S and HOS) was analyzed by MTT assay. Apoptotic assays and colony formation assays were also applied. ROS generation and Western Blotting were performed to determine the mechanism of CQ and VPA combination in the process of apoptosis. The viability of different osteosarcoma cell lines significantly decreased after CQ and VPA combination treatment compared with either drug used alone, and apoptosis was increased significantly. ROS generation was triggered leading to expression of apoptosis related genes being increased and of anti- apoptotic related genes being decreased. From our data shown here, CQ and VPA combination treatment in vitro enhanced cytotoxicy to osteosarcoma cells.