Under acidic conditions, the diagnostic fragmentation pattern of the Amadori compound featured consecutive dehydration reactions. At higher values (20 eV) it underwent the α-fission at the carbonyl group and produced a prominent diagnostic ion [AA + H + CH2]+ at m/z 88. The Schiff base was found to preferentially undergo the retro-aldol degradation and produce diagnostic ions at m/z 118 [AA + H + diose]+ and m/z 140 [AA + Na + diose]+, together with their sugar complements at m/z 85 [tetrose + H-2H2O]+ and m/z 143 [tetrose + Na]+. In the case of Heyns compound, several diagnostic ions were also detected, including the ions at m/z 154 [M + H-2H2O-C2H4O2]+, m/z 170 [AA + Na + triose]+ and m/z 142 [AA + H + Furan]+. In recent years, zwitterionic polymers have been frequently reported to modify various surfaces to enhance hydrophilicity, antifouling and antibacterial properties, which show significant potentials particularly in biological systems. This review focuses on the fabrication, properties and various applications of zwitterionic polymer grafted surfaces. The "graft-from" and "graft-to" strategies, surface grafting copolymerization and post zwitterionization methods were adopted to graft lots type of the zwitterionic polymers on different inorganic/organic surfaces. The inherent hydrophilicity and salt affinity of the zwitterionic polymers endow the modified surfaces with antifouling, antibacterial and lubricating properties, thus the obtained zwitterionic surfaces show potential applications in biosystems. The zwitterionic polymer grafted membranes or stationary phases can effectively separate plasma, water/oil, ions, biomolecules and polar substrates. The nanomedicines with zwitterionic polymer shells have "stealth" effect in the delivery of encapsulated drugs, siRNA or therapeutic proteins. Moreover, the zwitterionic surfaces can be utilized as wound dressing, self-healing or oil extraction materials. The zwitterionic surfaces are expected as excellent support materials for biosensors, they are facing the severe challenges in the surface protection of marine facilities, and the dense ion pair layers may take unexpected role in shielding the grafted surfaces from strong electromagnetic field. The assay for transposase-accessible chromatin using sequencing (ATAC-seq) has become the preferred method for mapping chromatin accessibility due to its time and input material efficiency. However, it can be difficult to evaluate data quality and identify sources of technical bias across samples. Here, we present ataqv, a computational toolkit for efficiently measuring, visualizing, and comparing quality control (QC) results across samples and experiments. (R)-2-Hydroxyglutarate mouse We use ataqv to analyze 2,009 public ATAC-seq datasets; their QC metrics display a 10-fold range. Tn5 dosage experiments and statistical modeling show that technical variation in the ratio of Tn5 transposase to nuclei and sequencing flowcell density induces systematic bias in ATAC-seq data by changing the enrichment of reads across functional genomic annotations including promoters, enhancers, and transcription-factor-bound regions, with the notable exception of CTCF. ataqv can be integrated into existing computational pipelines and is freely available at https//github.com/ParkerLab/ataqv/. We compare the "patterns of mutation" in biological and technological networks. Negative selection at central nodes in biological networks has been widely reported; however, we show technological networks have an opposite trend. This suggests a potential contrast biological evolution involves random tinkering, whereas man-made systems change according to rational planning. Many studies have suggested a role for gut-resident microbes (the "gut microbiome") in modulating host health; however, the mechanisms by which they impact systemic physiology remain largely unknown. In this study, metabolomic and transcriptional profiling of germ-free and conventionalized mouse liver revealed an upregulation of the Nrf2 antioxidant and xenobiotic response in microbiome-replete animals. Using a Drosophila-based screening assay, we identified members of the genus Lactobacillus capable of stimulating Nrf2. Indeed, the human commensal Lactobacillus rhamnosus GG (LGG) potently activated Nrf2 in the Drosophila liver analog and the murine liver. This activation was sufficient to protect against two models of oxidative liver injury, acetaminophen overdose and acute ethanol toxicity. Characterization of the portal circulation of LGG-treated mice by tandem mass spectrometry identified a small molecule activator of Nrf2, 5-methoxyindoleacetic acid, produced by LGG. Taken together, these data demonstrate a mechanism by which intestinal microbes modulate hepatic susceptibility to oxidative injury. The differentiation of IL-10-producing regulatory B cells (Bregs) in response to gut-microbiota-derived signals supports the maintenance of tolerance. However, whether microbiota-derived metabolites can modulate Breg suppressive function remains unknown. Here, we demonstrate that rheumatoid arthritis (RA) patients and arthritic mice have a reduction in microbial-derived short-chain fatty acids (SCFAs) compared to healthy controls and that in mice, supplementation with the SCFA butyrate reduces arthritis severity. Butyrate supplementation suppresses arthritis in a Breg-dependent manner by increasing the level of the serotonin-derived metabolite 5-Hydroxyindole-3-acetic acid (5-HIAA), which activates the aryl-hydrocarbon receptor (AhR), a newly discovered transcriptional marker for Breg function. Thus, butyrate supplementation via AhR activation controls a molecular program that supports Breg function while inhibiting germinal center (GC) B cell and plasmablast differentiation. Our study demonstrates that butyrate supplementation may serve as a viable therapy for the amelioration of systemic autoimmune disorders. Regulatory T cells (Tregs) maintain immune homeostasis and prevent autoimmunity. Serine stimulates glutathione (GSH) synthesis and feeds into the one-carbon metabolic network (1CMet) essential for effector T cell (Teff) responses. However, serine's functions, linkage to GSH, and role in stress responses in Tregs are unknown. Here, we show, using mice with Treg-specific ablation of the catalytic subunit of glutamate cysteine ligase (Gclc), that GSH loss in Tregs alters serine import and synthesis and that the integrity of this feedback loop is critical for Treg suppressive capacity. Although Gclc ablation does not impair Treg differentiation, mutant mice exhibit severe autoimmunity and enhanced anti-tumor responses. Gclc-deficient Tregs show increased serine metabolism, mTOR activation, and proliferation but downregulated FoxP3. Limitation of cellular serine in vitro and in vivo restores FoxP3 expression and suppressive capacity of Gclc-deficient Tregs. Our work reveals an unexpected role for GSH in restricting serine availability to preserve Treg functionality.