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Drug-induced hypersensitivity syndrome (DIHS)/drug reaction with eosinophilia and systemic symptoms (DRESS) is a severe drug adverse reaction with skin eruption and visceral organ involvement. The characteristic clinical features of DIHS/DRESS are reactivation of human herpesviruses (HHV) and the development of autoimmune diseases, but their pathogenesis and associations are not yet understood. Here, we report a 66-year-old man who presented with fever, generalized erythema, diffuse lymphadenopathy, and diarrhea after 3 weeks of treatment with zonisamide. Reactivation of HHV-6 and cytomegalovirus (CMV) was detected during the clinical course. The patient was diagnosed with DIHS/DRESS and treated with systemic prednisolone, i.v. immunoglobulin therapy, and ganciclovir. However, severe enterocolitis persisted for 6 months. A series of examinations revealed features of both CMV enterocolitis, as indicated by identification of a few CMV-positive cells on immunohistochemical analysis, and graft-versus-host disease (GVHD)-like enterocolitis indicated by orange-peel appearance on endoscopic examination and histopathological loss of goblet cells. Intractable enterocolitis continued and the patient finally died of pneumonia. An autoimmune predisposition in DIHS/DRESS patients in combination with CMV reactivation was considered to trigger the severe enterocolitis of this case that showed GVHD-like features of the gastrointestinal tract. GVHD-like organ damage is a pathological condition rarely observed in DIHS/DRESS but should be recognized as one of the most severe complications of the disease.

Cobalt-free, nickel-rich positive electrode materials are attracting attention because of their high energy density and low cost, and the ultimate material is LiNiO

Co-free Ni-rich (Ni ≥ 80 at%) layered positive electrode materials have been attracting attention for lithium-ion batteries with high energy density and low cost. In this study, LiNixAl1−xO2 (x = 0.92, 0.95), in which Ni and Al are atomically mixed, was synthesized. LiNiO2, LiNi0.95Co0.05O2 and LiNi0.95Co0.03Al0.02O2 with similar particle morphologies were also synthesized to clarify the effects of Al and Co substitution in Ni-rich layered electrode materials. After 500 cycles in full cells under conditions of 45 °C, 2C, and 2.5–4.2 V, LiNi0.95Al0.05O2 and LiNi0.95Co0.05O2 showed a similar capacity retention (54.1%, 56.5%), whereas LiNi0.92Al0.08O2 showed excellent capacity retention (75%). The increase of charge transfer resistance with cycling was remarkably suppressed in LiNixAl1−xO2, compared to LiNiO2 and LiNi0.95Co0.05O2, owing to nano-scale Al-rich layers on the surface of LiNixAl1−xO2 suppressing the side reactions with the electrolytes and thus the surface degradation. Furthermore, though the Co substitution has some effects of preventing particle cracking, the least particle cracking was observed in LiNi0.92Al0.08O2, suggesting that the surface degradation and the bulk degradation were suppressed with the Al substitution to produce the excellent cycle performance. This indicates that LiNixAl1−xO2 synthesized under optimum conditions is a promising Co-free Ni-rich electrode material.

The stratum corneum (SC), the outermost epidermal layer, consists of nonviable anuclear keratinocytes, called corneocytes, which function as a protective barrier. The exact modes of cell death executed by keratinocytes of the upper stratum granulosum (SG1 cells) remain largely unknown. Here, using intravital imaging combined with intracellular Ca(2+)- and pH-responsive fluorescent probes, we aimed to dissect the SG1 death process in vivo. We found that SG1 cell death was preceded by prolonged (∼60 min) Ca(2+) elevation and rapid induction of intracellular acidification. Once such intracellular ionic changes were initiated, they became sustained, irreversibly committing the SG1 cells to corneocyte conversion. Time-lapse imaging of isolated murine SG1 cells revealed that intracellular acidification was essential for the degradation of keratohyalin granules and nuclear DNA, phenomena specific to SC corneocyte formation. Furthermore, intravital imaging showed that the number of SG1 cells exhibiting Ca(2+) elevation and the timing of intracellular acidification were both tightly regulated by the transient receptor potential cation channel V3. The functional activity of this protein was confirmed in isolated SG1 cells using whole-cell patch-clamp analysis. These findings provide a theoretical framework for improved understanding of the unique molecular mechanisms underlying keratinocyte-specific death mode, namely corneoptosis.

To investigate the contribution of lithium-ion diffusibility of lithium tungsten oxides (LWOs) to low interfacial resistance, we fabricate thin-film electrodes of 6 Li-enriched LiCoO 2 ( 6 LCO) modified with various structure-types of 6 Li-enriched LWOs by pulsed laser deposition. The electrodes are subjected to X-ray diffraction (XRD), electrochemical impedance spectroscopy (EIS), and secondary-ion mass spectrometry (SIMS) analyses. XRD reveals that the LWO layers have Li 2 WO 4 structure with rhombohedral and tetragonal symmetries and amorphous states. EIS shows that the lowest interfacial resistance of the positive electrodes is given by the amorphous state, followed in order by the tetragonal and the rhombohedral symmetry, and that the diffusion coefficients of lithium-ions in the electrodes increase in the same order. SIMS demonstrates that the fastest lithium-ion self-diffusibility into the LWOs is found in the amorphous state, followed in order by tetragonal and rhombohedral symmetry. Furthermore, the amorphous state LWO modification shows smooth lithium-ion diffusion between the LWO and LCO layers after the electrochemical test. Conversely, the rhombohedral LWO modification demonstrates congested lithium-ion diffusion between the LWO and LCO layers after the test. Thus, fast lithium-ion self-diffusibility into the LWO-modified LCO contributes to enhancing the diffusion of lithium-ions, resulting in the reduction of interfacial resistance.