A facile and controllable strategy, which combines solvothermal treatment with ex situ nitrogen doping by using urea saturated alcohol solution or monoethanolamine as nitrogen source, is used to prepare flexible, freestanding, and compact nitrogen‐doped delaminated Ti3C2 (abbreviated N‐Ti3C2) film electrodes for symmetric electrochemical capacitors (ECs). Compared with the N sites from in situ N solid solution doping, those of ex situ N solvothermal doping enable larger contributions to the capacitance through regulating nitrogen species and content. As a result, the urea‐assisted N‐Ti3C2 (UN‐Ti3C2) film exhibits an ultrahigh volumetric capacitance of 2836 F cm−3 (927 F g−1) at 5 mV s−1 in 3 m H2SO4 solution. This value surpasses the all previously reported volumetric performance of MXenes. A large capacitance of 2643 F cm−3 (786 F g−1) is also obtained for the monoethanolamine‐assisted N‐Ti3C2 film. In addition, the symmetric electrochemical capacitor fabricated from the binder‐free UN‐Ti3C2 film exhibits a high volumetric energy density of 76 Wh L−1, which is the highest value achieved compared to those of MXenes so far. This work presents the effects of nitrogen species and solvothermal treatment on the electrochemical performance of MXene, and opens up an exciting opportunity for fabricating highly flexible and integrated ECs.

Reduced DNA methylation and abnormal expression of methylation-related genes in CD4+ T cells are associated with SLE and SSc.

No abstract

Autoimmune diseases are usually complex and multifactorial, characterized by aberrant production of autoreactive immune cells and/or autoantibodies against healthy cells and tissues. However, the pathogenesis of autoimmune diseases has not been clearly elucidated. The activation, differentiation, and development of CD8+ T cells can be affected by numerous inflammatory cytokines, transcription factors, and chemokines. In recent years, epigenetic modifications have been shown to play an important role in the fate of CD8+ T cells. The discovery of these modifications that contribute to the activation or suppression of CD8+ cells has been concurrent with the increasing evidence that CD8+ T cells play a role in autoimmunity. These relationships have been studied in various autoimmune diseases, including multiple sclerosis (MS), systemic sclerosis (SSc), type 1 diabetes (T1D), Grave's disease (GD), systemic lupus erythematosus (SLE), aplastic anemia (AA), and vitiligo. In each of these diseases, genes that play a role in the proliferation or activation of CD8+ T cells have been found to be affected by epigenetic modifications. Various cytokines, transcription factors, and other regulatory molecules have been found to be differentially methylated in CD8+ T cells in autoimmune diseases. These genes are involved in T cell regulation, including interferons, interleukin (IL),tumor necrosis factor (TNF), as well as linker for activation of T cells (LAT), cytotoxic T-lymphocyte–associated antigen 4 (CTLA4), and adapter proteins. MiRNAs also play a role in the pathogenesis of these diseases and several known miRNAs that are involved in these diseases have also been shown to play a role in CD8+ regulation.