Simultaneously tuning the luminescent color and realizing an optical temperature sensor by negative thermal expansion in Sc2(WO4)3:Tb/Eu phosphors.

At present, many researchers are focusing on trivalent lanthanide (Ln3+)-doped thermally enhanced upconversion luminescent (UCL) materials with negative thermal expansion (NTE) properties. However, selective anti-thermal quenching downshifting emissions of the activator and thermal quenching of the sensitizer in a phosphor with NTE properties are not implemented. Herein, Tb3+/Eu3+ co-doped Sc2(WO4)3 phosphors synthesized by the solid-state method are explored in selectively enhanced red emission (Eu3+:5D0 → 7F2) due to the energy-transfer efficiency from Tb3+ to Eu3+ and the promoted radiative transition probability. The selective thermally quenched green emission (Tb3+:5D4 → 7F5) is owing to the change of energy transfer from Tb3+ to Eu3+ as the temperature increased. Moreover, under ultraviolet 365 nm excitation, the thermally stimulated color emission tuned from yellow to red with the increase in temperature. Based on the radically different thermal response downshifting the luminescence of the activator and sensitizer, the luminescence intensity ratio (LIR) of non-thermally coupled levels (NTCLs) for 5D0 (Eu3+) and 5D4 (Tb3+) is adopted for optical temperature sensing. The optimal relative sensitivity of temperature sensing in the Sc2(WO4)3:25%Tb3+/3%Eu3+ sample could reach 2.94% K-1 at 347 K. All these indicate that this Sc2(WO4)3:Tb3+/Eu3+ material is a promising candidate for high-sensitivity optical temperature sensing.

PRRSV infection activates NLRP3 inflammasome through inducing cytosolic mitochondrial DNA stress.

Porcine reproductive and respiratory syndrome virus (PRRSV) infection causes severe interstitial pneumonia and inflammatory response in piglets and growing pigs. IL-1ß is implicated in PRRSV-mediated inflammatory response and the pathogenesis of PRRSV infection. Mitochondria are critical intracellular organelles which is served as signaling platform for antiviral immunity response to participate in immune response of virus infection. The role of mitochondria in PRRSV-mediated inflammatory response and the pathogenesis of PRRSV infection has not been elucidated. Here, our data suggested that PRRSV infection facilitates mitochondrial dysfunction, which induces cytosolic mitochondrial DNA (mtDNA) stress and ROS accumulation, severally activates the NLRP3 inflammasome and NF-κB signaling pathway, and consequently stimulates IL-1ß production in PAMs. Furthermore, mtDNA degradation by DNase I abrogates the activation of NLRP3 inflammasome and IL-1ß secretion during PRRSV infection. Scavenging ROS significantly inhibits NF-κB signaling activation and the subsequently transcription and secretion of IL-1ß. In conclusion, our results indicate that cytosolic mtDNA stress and ROS accumulation after PRRSV infection-induced mitochondrial dysfunction activate NLRP3 inflammasome and NF-κB signaling pathway to promote IL-1ß production, revealing a new strategy for vaccine and drug development to PRRSV.

The Food Additive ß-Caryophyllene Exerts Its Neuroprotective Effects Through the JAK2-STAT3-BACE1 Pathway.

Despite extensive research on Alzheimer's disease (AD), its diagnosis and treatment remain challenging, and no effective therapies are currently available. Amyloid ß (Aß) extracellular plaques and intracellular neurofibrillary tangles are the histological characteristics of AD that have been directly linked to neuropathological events such as synaptic and neuronal cell loss. In this study, we explored whether the "JAK2-STAT3-BACE1" pathway is involved in neuroprotection conferred by the food flavouring agent ß-caryophyllene (BCP). PC-12 cells with overexpressed amyloid-ß protein precursor (APP) were utilised to construct an AD model in vitro, which was then split into four groups, namely control, empty vector, APP overexpression, and BCP (5, 10, and 20 µM). CCK-8 was used to evaluate cell viability, immunofluorescence was utilised to examine synaptic morphology, and quantitative real-time polymerase chain reaction and western blot were used to examine gene and protein expression levels. The relative expression levels of JAK2, STAT3, and BACE1 mRNA in the transfected PC-12 cells were found to be significantly upregulated. The cell morphology altered dramatically 72 h after transfection, becoming rounder, with a decrease in cell number. BCP exhibited the potential to dramatically increase PC-12 cell viability while protecting cell morphology. BCP inhibited APP, JAK2, STAT3, BACE1 mRNA and BACE1 protein overexpression, as well as JAK2 and STAT3 hyperphosphorylation. Molecular docking simulated the docking of BCP with JAK2, STAT3, BACE1, CB2. And JAK2 was found to be the most stable protein. In conclusion, inhibition of the "JAK2-STAT3-BACE1" signalling pathway may be one of the mechanisms through which BCP protects neurons and antagonises Aß's neurotoxicity.