[Effects of phosphorus application rate on distribution of 13C assimilates and spike formation in different til-lers of wheat with supplementary irrigation]. / 补灌条件下施磷量对小麦不同茎蘖13CåŒåŒ–ç‰©åˆ†é åŠå ¶æˆç©—çš„å½±å“.

To clarify the appropriate rate of phosphorus application and physiological mechanism for promoting wheat tillering and efficient utilization of phosphorus fertilizer with supplementary irrigation, we used 'Jimai 22' wheat variety as the test material, to set up three phosphorus application treatments, including low (90 kg P2O5·hm-2, P1), medium (135 kg P2O5·hm-2, P2), and high (180 kg P2O5·hm-2, P3) application rates, with no phosphorus application as the control (P0). We increased the relative soil water content of each treatment at join-ting stage and anthesis stage to 70%, and measured the area of tiller node, the content of endogenous hormones, the number of tillers in each tiller position, photosynthetic parameters, the distribution of 13C assimilates in each stem and tiller, as well as the grain yield and partial productivity of phosphate fertilizer. The results showed that compared with P0 and P1 treatments, P2 significantly increased the area of tiller node and the trans-zeatin (tZ), the photosynthetic parameters of the uppermost expanded leaves of the main stem, the total tillers per plant, and the distribution of 13C assimilates in each tiller. The number of ears per plant was increased by 0.51 and 0.36, and grain yield was increased by 40.3% and 13.2%, respectively. In P3 treatment, the number of tillers increased, but the panicles per plant, and the grain yield and phosphate fertilizer partial productivity decreased. Our results suggested that the moderate phosphorus treatment (135 kg·hm-2) under supplementary irrigation was suitable for high yield and high efficiency of wheat.

TUG1 exacerbates cerebral ischemia-reperfusion injury through miR-340-5p-mediated PTEN.

Long non-coding RNAs (LncRNAs) play a substantial role in the process of cerebral ischemia-reperfusion injury (CIRI). The present work aimed to determine the probable mechanism by which LncRNA TUG1 exacerbates CIRI via the miR-340-5p/phosphatase and tensin homolog (PTEN) pathway. After developing a middle cerebral artery occlusion/reperfusion (MCAO/R) model, pcDNA-TUG1 together with miR-340-5p agomir were administrated in vivo. Furthermore, the neurologic defects in rats were assessed by a modified neurological severity score. Moreover, 2,3,5-Triphenyl-2 H-tetrazolium chloride stain-step was performed to determine the brain's infarct size. In addition, western blotting, immunohistochemistry, and qRT-PCR experiments were utilized for gauging the proteomic/genomic expression-profiles. Luciferase reporter assay validated correlations across TUG1, miR-340-5p, together with PTEN. The results indicated relatively reduced miR-340-5p levels in MCAO/R models, while upregulated TUG1 levels. The pcDNA-TUG1-treated rats indicated increasing neurological dysfunction, whereas the miR-340-5p agomir-treated rats showed improvement. Furthermore, miR-340-5p was determined to be the expected and confirmed TUG1 target. All things considered, the findings suggested that PTEN can serve as the target of miR-340-5p. In addition, TUG1 served as a miR-340-5p ceRNA, which promotes PTEN modulation. Furthermore, TUG1 overexpression decreased miR-340-5p's capacity to fend against CIRI. Conclusively, this work proved that in CIRI, targeting the TUG1/miR-340-5p/PTEN regulatory axis is a viable approach for the treatment of ischemic stroke.