Contribution of theanine to the temperature-induced changes in aroma profile of Wuyi rock tea.

Theanine is a distinctive amino acid in tea that plays a vital role in tea flavor during the roasting process. Model thermal reactions of total amino acids and sugars with different roasting conditions (low-fire, middle-fire, and high-fire) showed theanine competitively inhibited the formation of indole, skatole, 4-hydroxy-2,5-dimethyl-3(2H)-furanone, and Strecker aldehydes, while greatly stimulated the production of roasty pyrazines. In addition, highest amounts of pyrazines were obtained under high-fire degree. Quantification of these reaction products in Wuyi rock tea (WRT) was realized in different roasted Dahongpao teas by means of sensomics approach. The quantitative data revealed the biggest influence of roasting temperatures on the formation of reaction products among indole, lipid oxidation products, and pyrazines, while other reaction products were only slightly affected. The findings of this study provide a fresh perspective on the impact of theanine on aroma formation during the roasting process, which will help to explore the formation of key odorants during tea production.

Formation of dimethyl sulfide from the decomposition of S-methylmethionine in tea (Camellia sinensis) during manufacturing process and infusion brewing.

Dimethyl sulfide (DMS) is a typical odorant contributing a cooked corn-like odor to tea (Camellia sinensis). In the study, noticeable increases of DMS (>350%) occurred in green, black, yellow, and white tea during brewing. Thermal model and quantitative analysis of S-methylmethionine (SMM) confirmed the thermal decomposition of SMM into DMS (44-80%) in tea infusion. The quantitative analysis on green and black tea manufacturing processes demonstrated thermal decomposition of SMM (12% and 9.0%, respectively) leads to DMS formation during the drying step. Besides, DMS was firstly suggested to be biosynthesed from yet unknown precursors due to high concentrations in fresh leaves (180 and 1700 µg/kg) and increases during rolling (190 and 2800 µg/kg) and fermentation (6400 µg/kg in black tea). The findings provided new insight of DMS formation from the decomposition of SMM in tea during manufacturing process and infusion brewing, which also help exploring its biosynthetic pathway during tea production.

Platinum thiolate complexes supported by PBP and POCOP pincer ligands as efficient catalysts for the hydrosilylation of carbonyl compounds.

Diphosphino-boryl-based PBP pincer platinum thiolate complexes, [Pt(SR){B(NCH2PtBu2)2-1,2-C6H4}] (R = H, 1a; Ph, 1b), and benzene-based bisphosphinite POCOP pincer platinum thiolate complexes, [Pt(SR)(tBu2PO)2-1,3-C6H3] (R = H, 2a; Ph, 2b), were prepared and fully characterized by multinuclear NMR, X-ray crystallography, HRMS and elemental analyses. The application of these complexes in the catalytic hydrosilylation of aldehydes and ketones was investigated. It was found that these platinum thiolate complexes are efficient catalysts for the hydrosilylation of aldehydes and ketones at 65-75 °C. Comparatively, the PBP complexes are more active than the corresponding POCOP complexes. Both phenylsilane and polymethylhydrosiloxane (PMHS) can be used as silyl reagents. The expected alcohols were obtained in good to excellent yields after the basic hydrolysis of the hydrosilylation products and many functional groups were not affected. With turnover frequencies (TOFs) of up to 67 000 h-1, the present catalytic system represents the most effective platinum catalytic system for the hydrosilylation of carbonyl compounds. The reactions were likely catalysed by the in situ generated platinum hydride species.

The Stability of Diphosphino-Boryl PBP Pincer Backbone: PBP to POP Ligand Hydrolysis.

Since moisture may frequently be present in many solvents, it is important to know the reactivity of a catalyst against water for catalytic reactions. In order to explore the stability and understand the transformation process of diphosphino-boryl-based PBP pincer platform, [PdCl{B(NCH2 Pt Bu2 )2 -o-C6 H4 }] (1) was treated with PdCl2 , HB(NCH2 PPh2 )2 -o-C6 H4 was reacted with [PdCl2 (cod)] (cod=cyclo-octa-1,5-diene) and [Pd2 (dba)3 ] (dba=dibenzylideneacetone), respectively, in the presence of water. Some novel palladium POP complexes, [Pd2 Cl2 (µ-Cl){µ-κ3 -P,O,P-OB(NCH2 Pt Bu2 )2 -o-C6 H4 }] (2 a), [Pd4 (µ-Cl)2 (µ-O)2 {µ-κ3 -P,O,P-OB(NCH2 PPh2 )2 -o-C6 H4 }2 ] (2 b), [Pd2 {µ-κ4 -P,P,P,P-O(B(NCH2 PPh2 )2 -o-C6 H4 )2 }{µ-κ2 -P,P-(NHCH2 PPh2 )2 -o-C6 H4 }] (3), were obtained. It was found that the PBP pincer backbone can easily be converted into a POP backbone in the presence of water. From the crystal structures of the resultant palladium complexes, possible pincer backbone transformation pathways were discussed.

FBXO38 mediates PD-1 ubiquitination and regulates anti-tumour immunity of T cells.

Dysfunctional T cells in the tumour microenvironment have abnormally high expression of PD-1 and antibody inhibitors against PD-1 or its ligand (PD-L1) have become commonly used drugs to treat various types of cancer1-4. The clinical success of these inhibitors highlights the need to study the mechanisms by which PD-1 is regulated. Here we report a mechanism of PD-1 degradation and the importance of this mechanism in anti-tumour immunity in preclinical models. We show that surface PD-1 undergoes internalization, subsequent ubiquitination and proteasome degradation in activated T cells. FBXO38 is an E3 ligase of PD-1 that mediates Lys48-linked poly-ubiquitination and subsequent proteasome degradation. Conditional knockout of Fbxo38 in T cells did not affect T cell receptor and CD28 signalling, but led to faster tumour progression in mice owing to higher levels of PD-1 in tumour-infiltrating T cells. Anti-PD-1 therapy normalized the effect of FBXO38 deficiency on tumour growth in mice, which suggests that PD-1 is the primary target of FBXO38 in T cells. In human tumour tissues and a mouse cancer model, transcriptional levels of FBXO38 and Fbxo38, respectively, were downregulated in tumour-infiltrating T cells. However, IL-2 therapy rescued Fbxo38 transcription and therefore downregulated PD-1 levels in PD-1+ T cells in mice. These data indicate that FBXO38 regulates PD-1 expression and highlight an alternative method to block the PD-1 pathway.

Cholesterol Metabolism in T Cells.

Compartmentalization and spatial control of biochemical reactions is the foundation of cell-based life on earth. The lipid bilayer system employed by eukaryote cells not only keeps them separate from the environment but also provides a platform for key receptors to sense and interact with outside factors. Arguably one of the cell types most reliant on interactions of this kind, immune cells depend on their membrane to keep functioning properly. In this review, the influence of variation in cholesterol levels, a key component of lipid bilayer stability, on T cells will be discussed in detail. In comparison to other cells, T cells must be able to undergo rapid activation followed by proliferation. Furthermore, receptor colocalization is an important mechanism in this activation process. The impact of cholesterol availability on the processes of T cell proliferation and receptor sensitivity, as well as its potential for immunomodulation in disease treatment will be considered.

Dynamic regulation of CD28 conformation and signaling by charged lipids and ions.

CD28 provides an essential costimulatory signal for T cell activation, and its function is critical in antitumor immunity. However, the molecular mechanism of CD28 transmembrane signaling remains elusive. Here we show that the conformation and signaling of CD28 are regulated by two counteractive charged factors, acidic phospholipids and Ca2+ ions. NMR spectroscopy analyses showed that acidic phospholipids can sequester CD28 signaling motifs within the membrane, thereby limiting CD28 basal signaling. T cell receptor (TCR) activation induced an increase in the local Ca2+ concentration around CD28, and Ca2+ directly disrupted CD28-lipid interaction, leading to opening and signaling of CD28. We observed that the TCR, Ca2+, and CD28 together form a dual-positive-feedback circuit that substantially amplifies T cell signaling and thus increases antigen sensitivity. This work unravels a new regulatory mechanism for CD28 signaling and thus contributes to the understanding of the dependence of costimulation signaling on TCR signaling and the high sensitivity of T cells.