In this study, a new dual‐ion battery (DIB) concept based on an aqueous/non‐aqueous electrolyte is reported, combining high safety in the form of a nonflammable water‐in‐salt electrolyte, a high cathodic stability by forming a protective interphase on the negative electrode (non‐aqueous solvent), and improved sustainability by using a graphite‐based positive electrode material. Far beyond the anodic stability limit of water, the formation of a stage‐2 acceptor‐type graphite intercalation compound (GIC) of bis(trifluoromethanesulfonyl) imide (TFSI) anions from an aqueous‐based electrolyte is achieved for the first time, as confirmed by ex‐situ X‐ray diffraction. The choice of negative electrode material shows a huge impact on the performance of the DIB cell chemistry, i.e., discharge capacities up to 40 mAh g−1 are achieved even at a high specific current of 200 mA g−1. In particular, lithium titanium phosphate (LiTi2(PO4)3; LTP) and lithium titanium oxide (Li4Ti5O12; LTO) are evaluated as negative electrodes, exhibiting specific advantages for this DIB setup. In this work, a new DIB storage concept combining an environmentally friendly, transition‐metal‐free, abundant graphite positive electrode material, and a nonflammable water‐based electrolyte is established, thus paving the path toward a sustainable and safe alternative energy storage technology.

In the treatment of adult attention-deficit/hyperactivity disorder (ADHD) the importance of psychological interventions in combination with pharmacotherapy is widely accepted in contemporary clinical routine. The natural course of the disorder seems to justify additional psychological interventions because even in patients who are highly compliant to pharmacotherapy full remission is not always achieved. The aim of the present study was to analyze the contribution of psychotherapy to the treatment of adult ADHD patients. In a randomized controlled study, the efficacy of a combined treatment of psychotherapy with pharmacotherapy is compared to pharmacological intervention alone. After initiation and stabilization of treatment with methylphenidate (MPH) in all subjects randomization to the two different treatment conditions was done. Afterwards both groups underwent treatment for about 10–12 weeks, the experimental group receiving sessions of cognitive-behavioral therapy (CBT) whereas the control group only received medication and standard clinical management (SCM). ADHD symptoms differed statistically during time but not between the two different treatment conditions. This result was the same for the single ADHD symptoms—inattention, hyperactivity, impulsivity, and emotional symptoms—and also for impairment. Individual standardized ADHD specific CBT program was not able to outperform SCM.

A characteristic of lamina propria lymphocytes (LPL) is their low proliferative response to stimuli of the CD3 pathway. β1 integrins were expressed on LPL; however, their functionis unknown. Therefore, we determined whether β1 integrins contribute to T cell responses by providing costimulatory signals. Integrins on CD4+ LPL of controls and patients with inflammatory bowel disease were characterized by flow cytometry. Cells were stimulated by anti‐CD3 or anti‐CD2 antibodies either alone or in combination with a stimulatory β1 integrinantibody (12G10). Proliferation and apoptosis were measured by [3H]thymidine pulsing or flow cytometry. Cytokine mRNA and apoptosis‐related transcripts were quantified by reverse transcriptase‐PCR. We demonstrated that β1 integrin costimulation restored CD3‐induced proliferation of CD4+ LPL and reduced activation‐induced apoptosis. Activation of β1 integrins by addition of 12G10 antibody to CD3‐stimulated cells restored their capacity to express proinflammatory cytokine transcripts. Further, expression of the activated form of β1 integrins was significantly elevated on LPL from inflamed mucosa. These studies demonstrate that β1 integrin costimulation modulates the response of LPL after TCR stimulation. An increased expression of activated β1 integrins on LPL in intestinal inflammation may abolish their unresponsiveness to antigens and perpetuate the inflammatory process.

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