No abstract

Electrolytes play a critical role in enabling the stable cycling of rechargeable lithium (Li) metal batteries. While carbonate-based and ether-based electrolytes are widely investigated with notably improved electrochemical performances in Li metal batteries, few works have been conducted for systematical understanding and comparison of these two systems. Here, we side-by-side investigated carbonate-based (dimethyl carbonate, DMC) and ether-based (1,2-dimethoxyethane, DME) electrolyte systems in terms of cathodic chemical/electrochemical stabilities, anodic stability, transport properties, Li morphology, Coulombic efficiency, and full cell performances. The experimental results indicate that ether-based electrolyte systems exhibit all-around superior compatibilities with Li metal anode, although the carbonate-based systems can be significantly improved from the commercial baseline by introducing fluorinated co-solvent. The ether-based systems, even at low concentrations, demonstrate acceptable anodic stability when charged to a reasonable cut-off voltage in practical applications. This work sheds light on advanced electrolyte development toward practical Li metal batteries.

This cross-sectional study investigated the associations of psychosocial factors relevant to recovery from substance use disorders with monocyte activation and HIV persistence in a sample of 84 HIV-positive, methamphetamine-using sexual minority men with undetectable HIV viral load (<40 copies/mL). We examined if psychosocial factors were associated with decreased soluble CD14 (sCD14) and lower proviral HIV DNA. Multiple linear regression models adjusted for age, anti-retroviral therapy regimen, and CD4+ T-cell count. Time on ART was also included in models examining proviral HIV DNA. Greater self-efficacy for managing methamphetamine triggers and higher social support for abstinence were independently associated with lower sCD14. Greater social support for abstinence was also independently associated with lower proviral HIV DNA. Psychosocial factors relevant to recovery from substance use disorders are associated with lower monocyte activation and decreased proviral HIV DNA. Findings underscore the need for longitudinal research to identify plausible mechanisms linking psychosocial factors and substance use with biological processes relevant to HIV pathogenesis.

Background: This longitudinal study examined whether co-occurring stimulant use and HIV disease processes predicted greater risk for depression via dysregulated metabolism of amino acid precursors for neurotransmitters. Methods: In total, 110 sexual minority men (ie, gay, bisexual, and other men who have sex with men) living with HIV who had biologically confirmed recent methamphetamine use were enrolled in a randomized controlled trial. The kynurenine/tryptophan (K/T) and phenylalanine/tyrosine (P/T) ratios were measured over 15 months to index dysregulated metabolism of amino acid precursors for serotonin and catecholamines. Markers of gut-immune dysregulation such as lipopolysaccharide binding protein and soluble CD14 (sCD14), HIV persistence in immune cells (ie, proviral HIV DNA), and stimulant use were examined as predictors. These bio-behavioral measures, including the K/T and P/T ratios, were also examined as predictors of greater risk for depression over 15 months. Results: Higher time-varying sCD14 levels (β = 0.13; P = 0.04) and time-varying detectable viral loads (β = 0.71; P < 0.001) were independent predictors of a higher K/T ratio. Time-varying reactive urine toxicology results for stimulants (β = 0.53; P < 0.001) and greater proviral HIV DNA at baseline (β = 0.34; P < 0.001) independently predicted an increased P/T ratio. Greater time-varying, self-reported methamphetamine use uniquely predicted higher odds of screening positive for depression (Adjusted Odds Ratio = 1.08; 95% confidence interval: 1.01 to 1.17). Conclusions: Ongoing stimulant use and HIV persistence independently predict dysregulated metabolism of amino acid precursors for catecholamines, but this did not explain amplified risk for depression.