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Abstract The positive electrode|electrolyte interface plays an important role in all-solid-state Li batteries (ASSLBs) based on garnet-type solid-state electrolytes (SSEs) like Li6.4La3Zr1.4Ta0.6O12 (LLZTO). However, the trade-off between solid-solid contact and chemical stability leads to a poor positive electrode|electrolyte interface and cycle performance. In this study, we achieve thermodynamic compatibility and adequate physical contact between high-entropy cationic disordered rock salt positive electrodes (HE-DRXs) and LLZTO through ultrafast high-temperature sintering (UHS). This approach constructs a highly stable positive electrode|electrolyte interface, reducing the interface resistance to 31.6 Ω·cm2 at 25 °C, making a 700 times reduction compared to the LiCoO2 | LLZTO interface. Moreover, the conformal and tight HE-DRX | LLZTO solid-state interface avoids the transition metal migration issue observed with HE-DRX in liquid electrolytes. At 150 °C, HE-DRXs in ASSLBs (Li|LLZTO | HE-DRXs) exhibit an average specific capacity of 239.7 ± 2 mAh/g at 25 mA/g, with a capacity retention of 95% after 100 cycles relative to the initial cycle—a stark contrast to the 76% retention after 20 cycles at 25 °C in conventional liquid batteries. Our strategy, which considers the principles of thermodynamics and kinetics, may open avenues for tackling the positive electrode|electrolyte interface issue in ASSLBs based on garnet-type SSEs.

Abstract While preventing vertical HIV transmission has been very successful, HIV-exposed uninfected infants (iHEU) experience an elevated risk to infections compared to HIV-unexposed and uninfected infants (iHUU). Here we present a longitudinal multimodal analysis of infant immune ontogeny that highlights the impact of HIV/ARV exposure. Using mass cytometry, we show alterations in T cell memory differentiation between iHEU and iHUU being significant from week 15 of life. The altered memory T cell differentiation in iHEU was preceded by lower TCR Vβ clonotypic diversity and linked to TCR clonal depletion within the naïve T cell compartment. Compared to iHUU, iHEU had elevated CD56loCD16loPerforin+CD38+CD45RA+FcεRIγ+ NK cells at 1 month postpartum and whose abundance pre-vaccination were predictive of vaccine-induced pertussis and rotavirus antibody responses post 3 months of life. Collectively, HIV/ARV exposure disrupted the trajectory of innate and adaptive immunity from birth which may underlie relative vulnerability to infections in iHEU.

The quality of immune response to SARS-CoV-2 is thought to wane over time, but it is unclear how long it can persist. Here the authors show persistent immune responses in a large number of patients over the course of a 1-year follow-up from the time of recovery from COVID-19.

The Southern Ocean plays a key role in glacial-interglacial transitions and today, Weddell Sea derived Antarctic Bottom Water is one of the most important deep water masses. New records show that in contrast to today, no Weddell Sea water was exported during the last two glacial maxima, providing new insights towards the condition of Antarctic Bottom Water formation in extreme climate states.

T cells from narcolepsy patients were recently reported to recognize hypocretin, a wakefulness-promoting neurohormone, suggesting autoimmune origin of the disease. Here the authors show that hypocretin-specific T cells expand both in healthy controls and in narcolepsy patients, and identify preliminary features that may distinguish them.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Individuals with narcolepsy suffer from abnormal sleep patterns due to loss of neurons that uniquely supply hypocretin (HCRT). Previous studies found associations of narcolepsy with the human leukocyte antigen (HLA)-DQ6 allele and T-cell receptor α (TRA) J24 gene segment and also suggested that in vitro-stimulated T cells can target HCRT. Here, we present evidence of in vivo expansion of DQ6-HCRT tetramer+/TRAJ24+/CD4+ T cells in DQ6+ individuals with and without narcolepsy. We identify related TRAJ24+ TCRαβ clonotypes encoded by identical α/β gene regions from two patients and two controls. TRAJ24-G allele+ clonotypes only expand in the two patients, whereas a TRAJ24-C allele+ clonotype expands in a control. A representative tetramer+/G-allele+ TCR shows signaling reactivity to the epitope HCRT87–97. Clonally expanded G-allele+ T cells exhibit an unconventional effector phenotype. Our analysis of in vivo expansion of HCRT-reactive TRAJ24+ cells opens an avenue for further investigation of the autoimmune contribution to narcolepsy development. T cells from narcolepsy patients were recently reported to recognize hypocretin, a wakefulness-promoting neurohormone, suggesting autoimmune origin of the disease. Here the authors show that hypocretin-specific T cells expand both in healthy controls and in narcolepsy patients, and identify preliminary features that may distinguish them. [ABSTRACT FROM AUTHOR]