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Aims: When entering a mountain plateau, people are at risk of developing acute mountain sickness (AMS), for which there are limited prophylactic medicines available. This study aimed at exploring the effectiveness of ibuprofen, acetazolamide, and methazolamide in preventing AMS and at providing valuable insights for the future development of related drugs. Methods: A total of 137 mountaineers were recruited for this study and divided into six groups: a control group, an ibuprofen group, an acetazolamide group, a methazolamide group, an ibuprofen/methazolamide combination group, and a high‐dose ibuprofen/methazolamide combination group. After the assigned drug was taken for three days at a lower elevation (300 m), the participants ascended to a plateau environment at 5050 m. The Lake Louise AMS Score (LLS) system was used to diagnose and evaluate the AMS rates of the mountaineers in each group, and the results were compared through statistical analysis. Results: The results show that all the medications tested herein were effective in preventing AMS, but their level of effectiveness varied. The prevalence of AMS was 50.00% in the control group, 14.29% in the ibuprofen group, 5.56% in the acetazolamide group, 27.27% in the methazolamide group, 44.8% in the ibuprofen and methazolamide group, and 22.50% in the high‐dose ibuprofen and methazolamide group. Acetazolamide demonstrated a significant prophylactic effect on symptoms related to AMS diagnosis, and ibuprofen showed the best efficacy for preventing headache. Conclusion: Acetazolamide remains an effective medicine for preventing AMS. Ibuprofen combined with methazolamide is less effective than ibuprofen alone to prevent AMS. Trial Registration: ClinicalTrials.gov identifier: ChiCTR-TRC-12002219 [ABSTRACT FROM AUTHOR]

Objective To investigate the role of SRY-Box transcription factor 6 (SOX6)-suppressor of cytokine signaling 3 (SOCS3) on hypoxia-induced proliferation of human pulmonary artery smooth muscle cells (HPASMCs) and explore the possible mechanism. Methods ① The HPASMCs were treated with 4% O2 for 24 h or 48 h. ② siRNA was used to decrease the expression of SOX6 (si-SOX6-NC, si-SOX6-1, si-SOX6-2, si-SOX6-3) and SOCS3 (si-SOCS3-NC, si-SOCS3-1, si-SOCS3-2) in the cells. ③The HPASMCs with stable SOX6 overexpression induced by transfection with a lentiviral vector were exposed to hypoxia for 48 h, with the cells cultured in normoxia condition, or simple hypoxia condition as control. ④CCK-8 assay was used to testify the proliferation of the above groups of cells. The expression of SOX6, SOCS3, proliferating cell nuclear antigen (PCNA) and phosphorylated-signal transduction and activators of transcription 3 (p-STAT3) at mRNA and protein levels were detected by RT-qPCR and Western blotting, respectively. Results Hypoxia decreased the expression levels of SOX6 and SOCS3 (P

For Lentinula edodes, its characteristic flavor is the key determinant for consumer preferences. However, the tissue-specific volatile flavor variations of the fruiting body have been overlooked. Here, we comprehensively investigated the volatile flavor profiles of different tissues, including the pileus skin, context, gill, and stipe of the fruiting body, of two widely cultivated L. edodes strains (T2 and 0912) using the gas chromatography–mass spectrometry (GC–MS) technique combined with a multivariate analysis. We show that the eight-carbon and sulfur compounds, which represented 43.2–78.0% and 1.4–42.9% of the total volatile emissions for strains 0912 and T2, respectively, dominated their volatile profiles. Compared with strain T2, strain 0912 had a higher total content of eight-carbon compounds but a lower total content of sulfur compounds in the fruiting body. The sulfur compounds represented 32.2% and 42.9% of the total volatile emissions for strains 0912 and T2, respectively. In contrast, they constituted only 1.4% in the stipes of strain 0912 and 9.0% in the skin of strain T2. The proportions of the predominant C8 compounds (1-octen-3-one, 1-octen-3-ol, and 3-octanone) and sulfur compounds (lenthionine, 1,2,4-trithiolane, dimethyl disulfide, and dimethyl trisulfide) changed depending on the tissues and strains. Using machine learning, we show that the prediction accuracy for different strains and tissues using their volatile profiles could reach 100% based on the highly diverse strain- and tissue-derived volatile variations. Our results reveal and highlight for the first time the comprehensive tissue-specific volatile flavor variations of the L. edodes fruiting body. These findings underscore the significance of considering strain and tissue differences as pivotal variables when aiming to develop products with volatile flavor characteristics. [ABSTRACT FROM AUTHOR]

Mycelial ageing is associated with ROS and autophagy in Lentinula edodes. However, the underlying cellular and molecular mechanisms between ROS and autophagy remain obscure. This study induced autophagy in L. edodes mycelia through exogenous H2O2 treatment. Results showed that 100 μM H2O2 treatment for 24 h significantly inhibited mycelial growth. H2O2 caused the depolarisation of MMP and accumulation of TUNEL-positive nuclei, which was similar to the ageing phenotype of L. edodes mycelia. Transcriptome analysis showed that differentially expressed genes were enriched in the mitophagic, autophagic, and MAPK pathways. LeAtg8 and LeHog1 were selected as hub genes. RNA and protein levels of LeATG8 increased in the H2O2-treated mycelia. Using fluorescent labelling, we observed for the first time the classic ring structure of autophagosomes in a mushroom, while 3D imaging suggested that these autophagosomes surrounded the nuclei to degrade them at specific growth stages. Phospho-LeHOG1 protein can translocate from the cytoplasm to the nucleus to regulate mycelial cells, resisting ROS-induced oxidative stress. Furthermore, LeATG8 expression was suppressed when LeHOG1 phosphorylation was inhibited. These results suggest that the LeATG8-dependent autophagy in L. edodes mycelial is closely associated with the activity or even phosphorylation of LeHOG1. [ABSTRACT FROM AUTHOR]

[Figure: see text]. [ABSTRACT FROM AUTHOR]