Selective Electrochemical Halogenation of Functionalized Quinolone.

This work describes an effective C3-H halogenation of quinoline-4(1H)-ones under electrochemical conditions, in which potassium halides serve as both halogenating agents and electrolytes. The protocol provides expedient access to different halogenated quinoline-4(1H)-ones with unique regioselectivity, broad substrate scope, and gram-scale synthesis employing convenient, environmentally friendly electrolysis, in an undivided cell. Mechanism studies have shown that halogen radicals can promote the activation of N-H bonds in quinolones.

ETS2 alleviates acute-on-chronic liver failure by suppressing excessive inflammation.

Hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is a syndrome with high short-term mortality. The mechanism of the transcription factor ETS2 in ACLF remains unclear. This study aimed to clarify the molecular basis of ETS2 in ACLF pathogenesis. Peripheral blood mononuclear cells from patients with HBV-ACLF (n = 50) were subjected to RNA sequencing. Transcriptome analysis showed that ETS2 expression was significantly higher in ACLF patients than in patients with chronic liver diseases and healthy subjects (all p < 0.001). Area-under-ROC analysis of ETS2 demonstrated high values for the prediction of 28-/90-day mortality in ACLF patients (0.908/0.773). Significantly upregulated signatures of the innate immune response (monocytes/neutrophils/inflammation-related pathways) were observed in ACLF patients with high ETS2 expression. Myeloid-specific ETS2 deficiency in liver failure mice resulted in deterioration of biofunctions and increased expression of pro-inflammatory cytokines (IL-6/IL-1ß/TNF-α). Knockout of ETS2 in macrophages confirmed the downregulation of IL-6 and IL-1ß caused by both HMGB1 and lipopolysaccharide, and an NF-κB inhibitor reversed the suppressive effect of ETS2. ETS2 is a potential prognostic biomarker of ACLF patients that alleviates liver failure by downregulating the HMGB1-/lipopolysaccharide-triggered inflammatory response and may serve as a therapeutic target for ACLF.

Electrochemically Driven Selective Removal of the S═N Bond-Directing Group Using Cyclohexanone Oxime as the Mediator.

An inexpensive electrochemical induction system was used for the efficient reductive defunctionalization of sulfoximines through a radical pathway. This practical and robust strategy could be used for the removal of the S═N bond-directing group from various sulfoximines. The practicability of this method was demonstrated by its mild conditions, simple operation, one-pot procedure, gram-scale synthesis, and the undivided cell. Furthermore, preliminary mechanistic studies suggested that the reaction might proceed via a homocoupling reaction and a denitrification procedure.

Copper-Catalyzed Sulfonylation Reaction of NH-Sulfoximines with Aryldiazonium Tetrafluoroborates and Sulfur Dioxide: Formation of N-Sulfonyl Sulfoximines.

An efficient and practical SO2 insertion protocol of NH-sulfoximines with aryldiazonium tetrafluoroborates and DABSO toward N-sulfonyl sulfoximines has been developed under mildly basic conditions. This transformation features easy operation, readily available substrates, and mild conditions. A tentative mechanism is proposed, which indicates that the aryldiazonium tetrafluoroborates would be radical donors under standard reaction conditions. The aryl radical produced in situ from diazonium salts would be trapped by SO2 to generate an arylsulfonyl radical and then undergo further transformation to generate the final N-sulfonyl sulfoximines.