No abstract

No abstract

A protocol was established for simultaneous measurements of zircon U-Pb ages and trace elements by LA-ICP-MS at spot sizes of 16−32 μm. This was accomplished by introducing N 2 into ICP to increase the sensitivity. The obtained U-Pb ages for zircon standards GJ-1, TEMORA and SK10-2 are consistent with the preferred values within about 1% uncertainty (2σ) by simple external calibration against zircon standard 91500. Different data reduction softwares could yield different uncertainties for calculation of U-Pb ages. The commercially available program GLITTER4.4 could apply an improper uncertainty calculation strategy, but it may yield artificial high precisions for single analyses. Our trace element analyses indicate that Si is not an ideal internal standard for zircon when calibrated against the NIST glasses. Calibration against the NIST glasses using Si as an internal standard, a systematic deviation of 10%−30% was found for most trace elements including Zr. However, the trace element compositions of zircon can be accurately measured by calibration against multiple reference materials with natural compositions (e.g., BCR-2G, BHVO-2G and BIR-1G), or calibration against NIST SRM 610 and using Zr as an internal standard. Analyses of two pieces of GJ-1 demonstrate that it is relatively homogenous for most trace elements (except for Ti). Zircon, U-Pb age, trace element, uncertainty, LA-ICP-MS Citation: Liu Y S, Hu Z C, Zong K Q, et al. Reappraisement and refinement of zircon U-Pb isotope and trace element analyses by LA-ICP-MS.

No abstract

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common critical diseases. Bone marrow mesenchymal stem cell (BMSC) transplantation is previously shown to effectively rescue injured lung tissues. The therapeutic mechanism of BMSC-derived exosomes is not fully understood. Here, we investigated the BMSC-derived exosomal microRNAs (miRNAs) on effecting lipopolysaccharide- (LPS-) induced ALI and its mechanism. In vitro, rat alveolar macrophages were treated with or without exosomes in the presence of 10 μg/ml LPS for 24 h. Cell viability was determined with Cell Counting Kit-8 assay. Apoptotic ratio was determined with TUNEL and Annexin V-FITC/PI double staining. The levels of miR-384-5p and autophagy-associated genes were measured by RT-qPCR and western blot. Autophagy was observed by TEM and assessed by means of the mRFP-GFP-LC3 adenovirus transfection assay. In vivo, we constructed LPS-induced ALI rat models. Exosomes were injected into rats via the caudal vein or trachea 4 h later after LPS treatment. The lung histological pathology was determined by H&E staining. Pulmonary vascular permeability was assessed by wet-to-dry weight ratio and Evans blue dye leakage assay, and inflammatory cytokines in serum and BALF were measured by ELISA. Furthermore, the therapeutic mechanism involved in miR-384-5p and Beclin-1 was determined. The results showed that BMSC-derived exosomes were taken up by the alveolar macrophages and attenuated LPS-induced alveolar macrophage viability loss and apoptosis. Exosomes effectively improved the survival rate of ALI rats within 7 days, which was associated with alleviating lung pathological changes and pulmonary vascular permeability and attenuating inflammatory response. Furthermore, this study for the first time found that miR-384-5p was enriched in BMSC-derived exosomes, and exosomal miR-384-5p resulted in relieving LPS-injured autophagy disorder in alveolar macrophages by targeting Beclin-1. Therefore, exosomal miR-384-5p could be demonstrated as a promising therapeutic strategy for ALI/ARDS.