A tutorial guide and detailed summary of CO2 reduction with Cu-based heterogeneous electrocatalysts for newcomers to the field.
Nanotechnology is an important and emerging industry with a projected annual market of around one trillion US dollars by 2011-2015. Concerns about the toxicity of nanomaterials in humans, however, have recently been raised. Although studies of nanoparticle toxicity have focused on lung disease the molecular link between nanoparticle exposure and lung injury remained unclear. In this report, we show that cationic Starburst polyamidoamine dendrimer (PAMAM), a class of nanomaterials that are being widely developed for clinical applications can induce acute lung injury in vivo. PAMAM triggers autophagic cell death by deregulating the Akt-TSC2-mTOR signaling pathway. The autophagy inhibitor 3-methyladenine rescued PAMAM dendrimer-induced cell death and ameliorated acute lung injury caused by PAMAM in mice. Our data provide a molecular explanation for nanoparticle-induced lung injury, and suggest potential remedies to address the growing concerns of nanotechnology safety.
ORCID IDs: 0000-0001-6683-6415 (J.X.); 0000-0002-9910-3119 (J.M.); 0000-0002-4265-7399 (J.L.); 0000-0002-0757-5208 (Q.W.); 0000-0003-2959-6461 (S.Z.)Antimicrobial compounds have critical roles in plant immunity; for example, Arabidopsis thaliana and other crucifers deploy phytoalexins and glucosinolate derivatives in defense against pathogens. The pathogen-responsive MITOGEN-ACTIVATED PROTEIN KINASE3 (MPK3) and MPK6 have essential functions in the induction of camalexin, the major phytoalexin in Arabidopsis. In search of cyanide, a coproduct of ethylene and camalexin biosynthesis, we found that MPK3 and MPK6 also affect the accumulation of extracellular thiocyanate ion derived from the indole glucosinolate (IGS) pathway. Botrytis cinerea infection activates MPK3/MPK6, which promote indole-3-yl-methylglucosinolate (I3G) biosynthesis and its conversion to 4-methoxyindole-3-yl-methylglucosinolate (4MI3G). Gain-and loss-of-function analyses demonstrated that MPK3/MPK6 regulate the expression of MYB51 and MYB122, two key regulators of IGS biosynthesis, as well as CYP81F2 and IGMT1/ IGMT2, which encode enzymes in the conversion of I3G to 4MI3G, through ETHYLENE RESPONSE FACTOR6 (ERF6), a substrate of MPK3/MPK6. Under the action of PENETRATION2 (PEN2), an atypical myrosinase, and PEN3, an ATP binding cassette transporter, 4MI3G is converted to extracellular unstable antimicrobial compounds, possibly isothiocyanates that can react with nucleophiles and release the stable thiocyanate ion. Recent studies demonstrated the importance of PEN2/ PEN3-dependent IGS derivatives in plant immunity. Here, we report that MPK3/MPK6 and their substrate ERF6 promote the biosynthesis of IGSs and the conversion of I3G to 4MI3G, a target of PEN2/PEN3-dependent chemical defenses in plant immunity.
Graphene fiber-based supercapacitors (GFSCs) hold high power density, fast charge-discharge rate, ultralong cycling life, exceptional mechanical/electrical properties, and safe operation conditions, making them very promising to power small wearable electronics. However, the electrochemical performance is still limited by the severe stacking of graphene sheets, hydrophobicity of graphene fibers, and complex preparation process. In this work, we develop a facile but robust strategy to easily enhance electrochemical properties of all-solid-state GFSCs by simple plasma treatment. We find that 1 min plasma treatment under an ambient condition results in 33.1% enhancement of areal specific capacitance (36.25 mF/cm) in comparison to the as-prepared GFSC. The energy density reaches 0.80 μW h/cm in polyvinyl alcohol/HSO gel electrolyte and 18.12 μW h/cm in poly(vinylidene difluoride)/ethyl-3-methylimidazolium tetrafluoroborate electrolyte, which are 22 times of that of as-prepared ones. The plasma-treated GFSCs also exhibit ultrahigh rate capability (69.13% for 40 s plasma-treated ones) and superior cycle stability (96.14% capacitance retention after 20 000 cycles for 1 min plasma-treated ones). This plasma strategy can be extended to mass-manufacture high-performance carbonaceous fiber-based supercapacitors, such as graphene and carbon nanotube-based ones.
During normal aging, innate immunity progresses to a chronic state. However, how oxidative stress and chronic neuroinflammation arise during aging remains unclear. In this study, we found that genetic ablation of cathepsin B (CatB) in mice significantly reduced the generation of reactive oxygen species (ROS) and neuroinflammation and improved cognitive impairment during aging. In cultured microglia, pharmacological inhibition of CatB significantly reduced the generation of mitochondria‐derived ROS and proinflammatory mediators induced by L‐leucyl‐L‐leucine methyl ester (LLOMe), a lysosome‐destabilizing agent. In the CatB‐overexpressing microglia after treatment with LLOMe, which mimicked the aged microglia, CatB leaked in the cytosol is responsible for the degradation of the mitochondrial transcription factor A (TFAM), resulting in the increased generation of mitochondria‐derived ROS and proinflammatory mediators through impaired mtDNA biosynthesis. Furthermore, intralateral ventricle injection of LLOMe‐treated CatB‐overexpressing microglia induced cognitive impairment in middle‐aged mice. These results suggest that the increase and leakage of CatB in microglia during aging are responsible for the increased generation of mitochondria‐derived ROS and proinflammatory mediators, culminating in memory impairment.
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