All-Solid-State Infrared Electrochromic Devices Based on Thin Metal Films.

Infrared electrochromic devices (IR-ECDs) are pivotal for dynamic thermal regulation. However, the quest for all-solid-state IR-ECDs with high stability and a broadly tunable range of emissivity remains a challenge. This study presents the development of an all-solid-state infrared electrochromic device (IR-ECD) with the structure of ITO/HxWO3/Ta2O5/Pd/Mg3Ni based on the hydrogen-induced metal-insulator transition of Mg-Ni alloy films. The emissivity modulation is improved by film stack optimization, with changes of 0.32 and 0.47 in the 3-5 and 7.5-14 µm bands, respectively. The introduction of an ultrathin Ti isolation layer between the catalytic and electrolyte layers enhances the cyclic stability. Our findings offer a novel strategy for the design and fabrication of all-solid-state IR electrochromic devices and highlight the potential of Mg-Ni alloy-based all-solid-state IR-ECDs in advanced energy and information fields.

Malic Enzyme 1 as a Novel Anti-Ferroptotic Regulator in Hepatic Ischemia/Reperfusion Injury.

Ferroptosis has been linked to the pathogenesis of hepatic injury induced by ischemia/reperfusion (I/R). However, the mechanistic basis remains unclear. In this study, by using a mouse model of hepatic I/R injury, it is observed that glutathione (GSH) and cysteine depletion are associated with deficiency of the reducing power of nicotinamide adenine dinucleotide phosphate (NADPH). Genes involved in maintaining NADPH homeostasis are screened, and it is identified that I/R-induced hepatic ferroptosis is significantly associated with reduced expression and activity of NADP+ -dependent malic enzyme 1 (Me1). Mice with hepatocyte-specific Me1 gene deletion exhibit aggravated ferroptosis and liver injury under I/R treatment; while supplementation with L-malate, the substrate of ME1, restores NADPH and GSH levels and eventually inhibits I/R-induced hepatic ferroptosis and injury. A mechanistic study further reveals that downregulation of hepatic Me1 expression is largely mediated by the phosphatase and tensin homologue (PTEN)-dependent suppression of the mechanistic target of rapamycin/sterol regulatory element-binding protein 1 (mTOR/SREBP1) signaling pathway in hepatic I/R model. Finally, PTEN inhibitor, mTOR activator, or SREBP1 over-expression all increase hepatic NADPH, block ferroptosis, and protect liver against I/R injury. Taken together, the findings suggest that targeting ME1 may provide new therapeutic opportunities for I/R injury and other ferroptosis-related hepatic conditions.

Iron homeostasis in the heart: Molecular mechanisms and pharmacological implications.

Iron is necessary for the life of practically all living things, yet it may also harm people toxically. Accordingly, humans and other mammals have evolved an effective and tightly regulatory system to maintain iron homeostasis in healthy tissues, including the heart. Iron deficiency is common in patients with heart failure, and is associated with worse prognosis in this population; while the prevalence of iron overload-related cardiovascular disorders is also increasing. Therefore, enhancing the therapy of patients with cardiovascular disorders requires a thorough understanding of iron homeostasis. Here, we give readers an overview of the fundamental mechanisms governing systemic iron homeostasis as well as the most recent knowledge about the intake, storage, use, and export of iron from the heart. Genetic mouse models used for investigation of iron metabolism in various in vivo scenarios are summarized and highlighted. We also go through different clinical conditions and therapeutic approaches that target cardiac iron dyshomeostasis. Finally, we conclude the review by outlining the present knowledge gaps and important open questions in this field in order to guide future research on cardiac iron metabolism.

Study and Analysis of the Effect of Polyamide Seamless Knitted Fabric with Different Graphene Content on the Blood-Flow Velocity of Human-Skin Microcirculation.

In this paper, four kinds of polyamide yarns with different graphene contents and three kinds of seamless knitting structures were used. The scheme of samples was established according to the comprehensive experimental design method, and 12 pieces of knitted fabric samples were woven on the seamless knitting machine. Through testing and analyzing the influence of each sample on the blood-flow rate of human-surface-skin microcirculation, the research shows that the higher the content of graphene in the veil, the better the promotion effect of the fabric prepared under this process condition on the blood-flow rate of human-surface-skin microcirculation. Sample 11# with the veil type of GP-0.8% and fabric weave of 1+1 simulated ribbed stitch has the strongest effect in this experiment, with a promotion multiple of 1.2189, and the influence of tissue structure is not obvious. The relevant performance test data and experimental research results in this paper provide empirical data support for developing medical or health textiles related to promoting the blood-flow velocity of skin microcirculation.