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The degree of withering significantly affected the formation of tea quality. This study analyzed the effects of light withering (LW), moderate withering (MW) and heavy withering (HW) on tea quality jointly by transcriptome and metabolomics. It was found that LW was more beneficial in increasing gene expression of the ko00500, ko00511, ko00940, ko00944, ko00941, ko00740 and ko02010 pathways in tea leaves, thereby increasing the content of quinones, phenolic acids, lignans and coumarins, and flavonoids; MW was more beneficial in increasing gene expression of ko00500, ko00511, ko00130, ko00380 and ko00520 pathways, thereby increasing the content of terpenoids, organic acids and lipids. The aroma intensity was highest in moderately withering tea leaves and bitterness intensity was highest in lightly withering tea leaves, while the intensity of mellowness, fresh and brisk taste was significantly higher in MW and LW than in HW. This study provides an important basis for guiding the processing of Wuyi rock tea with different flavors. • The degree of withering can significantly change the taste of tea. • Light withering mainly enhanced gene expression of 7 metabolic pathways. • Light withering mainly increased the content of 4 categories metabolites. • Aroma intensity was strongest in tea leaves with moderate withering. • Bitterness intensity was strongest in tea leaves with light withering. [ABSTRACT FROM AUTHOR]

[Display omitted] Traumatic brain injury (TBI) is a brain injury resulting from blunt mechanical external forces, which is a crucial public health and socioeconomic problem worldwide. TBI is one of the leading causes of death or disability. The primary injury of TBI is generally irreversible. Secondary injury caused by neuroinflammation could result in exacerbation of patients, which indicated that anti-inflammation and immunomodulatory were necessary for the treatment of TBI. Accumulated evidence reveals that the transplantation of umbilical cord mesenchymal stem cells (UCMSCs) could regulate the microenvironment in vivo and keep a balance of helper T 17(Th17)/ regulatory T cell (Treg). Therefore, it is reasonable to hypothesize that the UCMSCs could repair neurological impairment by maintaining the balance of Th17/Treg after TBI. In the study, we observed the phenomenon of trans-differentiation of T lymphocytes into Th17 cells after TBI. Rats were divided into Sham, TBI, and TBI + UCMSCs groups to explore the effects of the UCMSCs. The results manifested that trans-differentiation of Th17 into Treg was facilitated by UCMSCs, which was followed by promotion of neurological recovery and improvement of learning and memory in TBI rats. Furthermore, UCMSCs decreased the phosphorylation of nuclear factor-kappa B (NF-κB) and increased the expression of mothers against decapentaplegic homolog 3 (Smad3) in vivo and vitro experiments. In conclusion, UCMSCs maintained Th17/Treg balance via the transforming growth factor-β (TGF-β)/ Smad3/ NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]