Explore the vast range of titles available.

Based on tunable diode laser absorption spectroscopy (TDLAS), a water isotopes detection system was developed to detect the isotopic abundance of water vapor in the atmosphere. A single 1483.79 cm−1 quantum cascade laser (QCL) and a 3120 cm optical path multi-pass cell (MPC) were adopted in the detection system. The selected spectral range, as well as the laser technology used, is particularly interesting for the real-time monitoring of water vapor isotopes in the atmosphere. In this study, a single laser can be used to perform high-sensitivity, rapid investigations of H2O, H218O, H217O, and HDO absorption lines. Finally, we measured the abundance values of three isotopes of water vapor in the atmosphere and compared them with data from the Global Network of Isotopes in Precipitation (GNIP) website, dedicated to exploring the possibility of in situ monitoring of H₂O isotopes in the atmosphere.

Conclusions The developed Chang’E 7 LSWMA prototype demonstrates high precision in measuring water content and isotope values, which are the most important part of the measurement process, and the experimental results offer valuable guidance for in-situ measurement and data inversion. The LSWMA will perform the measurements after obtaining drilling (up to 1 m deep) or surface samples on the Moon. The estimated water content has also been affected by the processes of sampling, transportation and heating in addition to TDLAS. Therefore, the overall errors need to be analyzed and corrected. For isotopes measurement, the repetitions of experiments on the Moon’s PSR are limited due to power and temperature constraints. The memory effect error correction algorithm should be introduced to improve accuracy.

High-vigor seeds could show superiority in field production because seed vitality is essentially a comprehensive concept composed of germination rate, germination potential, and vitality index. Seed vitality was a traditional method of measurement, albeit a time-consuming and laborious one accompanied by errors caused by human factors. Optical technology had developed rapidly in the agricultural field, making it possible to detect seeds with high precision, high frequency, and high efficiency. In this article, the basic principles, advantages, and limitations of different optical techniques for obtaining seed vigor estimates are introduced and reviewed, and the key technology of non-destructive optical detection of single seeds will be discussed. In addition, the current situation of optical detection nondestructive technology in single seed detection will be discussed and analyzed, and the three directions of optical principle (seed characteristic spectrum database, intelligent sorting, and grading equipment) will be explored, providing a reference for the research methods using optical technology applied to seed detection.

Fibroblast-to-myofibroblast differentiation is the main cytopathologic characteristic of pulmonary fibrosis. However, its underlying molecular mechanism remains poorly understood. This study elucidated that the nuclear export of lncNONMMUT062668.2 (lnc668) exacerbated pulmonary fibrosis by activating fibroblast-to-myofibroblast differentiation. Mechanistic research revealed that histone H3K9 lactylation in the promoter region of the N6-methyladenosine (m 6 A) writer METTL3 was enriched to enhance METTL3 transcription, leading to the lnc668 m 6 A modification. Meanwhile, the m 6 A reader YTHDC1 recognized m 6 A-modified lnc668 and elevated the METTL3-mediated lnc668 modification. Subsequently, phase-separating YTHDC1 promoted the nuclear export of m 6 A-modified lnc668. In this process, the phase-separating YTHDC1 formed a nuclear pore complex with serine/arginine-rich splicing factor 3, Aly/REF export factor, and exportin-5 to assist the translocation of m 6 A-modified lnc668 from nucleus to cytoplasm. After nuclear export, lnc668 facilitated the translation and stability of its host gene phosphatidylinositol-binding clathrin assembly protein to activate fibroblast-to-myofibroblast differentiation, leading to the aggravation of pulmonary fibrosis, which also depended on YTHDC1 phase separation. This study first clarified that YTHDC1 phase separation is crucial for the m 6 A modification, nuclear export, and profibrotic role of lnc668 in exacerbating pulmonary fibrosis. These findings provide new insights into the nuclear export of cytoplasmic lncRNAs and identified potential targets for pulmonary fibrosis therapy.

Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease with few effective treatment options. While metabolic reprogramming has been associated with IPF, the precise mechanisms connecting mitochondrial metabolic dysfunction to epigenetically driven fibrogenesis remain unclear. In this study, we identify a pathogenic pathway focused on the mitochondrial enzyme pyruvate dehydrogenase E1 alpha subunit (PDHA1). In fibrosis model, downregulation of the deacetylase sirtuin3 (SIRT3) leads to hyperacetylation of PDHA1 at Lys-83. This modification inhibits pyruvate dehydrogenase (PDH) activity, causing a metabolic shift toward glycolysis and increased lactate production. Lactate, in turn, serves as a precursor for the lactylation of histone H4 at K12 (H4K12la), which activates super-enhancer (SE) at the NUAK2 gene locus, significantly enhancing NUAK2 expression. Both genetic and pharmacological inhibition of NUAK2 confirm its role in driving myofibroblast activation and fibrotic progression. Critically, the pro-fibrotic effects of PDHA1 K83 acetylation (K83ac) were reversed by NUAK2 knockdown. Our findings uncover a novel PDHA1 K83ac-H4K12la-NUAK2 pathway that integrates metabolic and epigenetic signals to promote fibrosis, suggesting that targeting PDHA1 deacetylation and inhibiting NUAK2 could be promising therapeutic strategies.

Orychophragmus violaceus (O. violaceus) is a kind of edible wild herb in north China and its seeds have medical potential, however, the effect of O. violaceus seeds on liver injury and the mechanism of action remains poorly understood. Thus, the purpose of the present study is to investigate the effect of O. violaceus seeds on liver injury and further explore the molecular mechanism of the beneficial effects using aqueous extract from the seeds of O. violaceus (AEOV). Mice were orally administrated with saline, AEOV, and biphenyldicarboxylate for 4 days, and were then injected subcutaneously with 0.1% carbon tetrachloride (CCl4) dissolved in corn oil. Sixteen hours later, mice were sacrificed and blood samples were collected. Then, the serum was separated and used for biochemical assay. Livers were excised and were routinely processed for histological examinations. Enzyme activities and protein levels in liver homogenates were detected using commercial kits or by western blot analysis. Additionally, the hepatoprotective effect of AEOV in vitro was evaluated using epigoitrin, the major alkaloid compound isolated from AEOV. We found that AEOV attenuated liver injury induced by CCl4 as evidenced by decreased levels of alanine aminotransferase (ALT) and aminotransferase (AST) in serum, improvement of liver histopathological changes, and substantial attenuation of oxidative stress and inflammation via regulation of nuclear factor-erythroid 2-related factor-2 (Nrf2) and nuclear factor κB (NFκB) pathways. These effects of AEOV were comparable to that of biphenyldicarboxylate which was commonly used as a hepatoprotective reference. Moreover, pretreatment of HepG2 cells with epigoitrin improved cell viability, decreased lactate dehydrogenase (LDH) and malondialdehyde (MDA) levels, increased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity, attenuated the NFκB pathway, and elevated the Nrf2 pathway after exposure to H2O2. These results suggest that AEOV could effectively prevent CCl4-induced liver injury in mice via regulating the Nrf2 and NFκB pathways, and reveal the cytoprotective effects of epigoitrin against H2O2-induced oxidative stress in HepG2 cells.

Fibroblast-to-myofibroblast differentiation is the main cytopathologic characteristic of pulmonary fibrosis. However, its underlying molecular mechanism remains poorly understood. This study elucidated that the nuclear export of lncNONMMUT062668.2 (lnc668) exacerbated pulmonary fibrosis by activating fibroblast-to-myofibroblast differentiation. Mechanistic research revealed that histone H3K9 lactylation in the promoter region of the N6-methyladenosine (m A) writer METTL3 was enriched to enhance METTL3 transcription, leading to the lnc668 m A modification. Meanwhile, the m A reader YTHDC1 recognized m A-modified lnc668 and elevated the METTL3-mediated lnc668 modification. Subsequently, phase-separating YTHDC1 promoted the nuclear export of m A-modified lnc668. In this process, the phase-separating YTHDC1 formed a nuclear pore complex with serine/arginine-rich splicing factor 3, Aly/REF export factor, and exportin-5 to assist the translocation of m A-modified lnc668 from nucleus to cytoplasm. After nuclear export, lnc668 facilitated the translation and stability of its host gene phosphatidylinositol-binding clathrin assembly protein to activate fibroblast-to-myofibroblast differentiation, leading to the aggravation of pulmonary fibrosis, which also depended on YTHDC1 phase separation. This study first clarified that YTHDC1 phase separation is crucial for the m A modification, nuclear export, and profibrotic role of lnc668 in exacerbating pulmonary fibrosis. These findings provide new insights into the nuclear export of cytoplasmic lncRNAs and identified potential targets for pulmonary fibrosis therapy.