image_1_Myeloperoxidase Negatively Regulates Neutrophil–Endothelial Cell Interactions by Impairing αMβ2 Integrin Function in Sterile Inflammation.tif

<p>Interactions of neutrophils with endothelial cells (ECs) and platelets contribute to tissue damage and vascular occlusion under sterile inflammatory conditions. However, the molecular mechanisms regulating the cell–cell interactions remain poorly understood. Previous studies suggest that reactive oxygen species, such as hydrogen peroxide (H₂O₂), produced from NADPH oxidase 2 play a critical role in platelet–neutrophil interactions by regulating the function of neutrophil αMβ2 integrin during sterile inflammation. In this study, we further demonstrate a crucial role for myeloperoxidase (MPO) in regulating the adhesive function of neutrophils through αMβ2 integrin. Using real-time fluorescence intravital microscopy and in vitro assays, we showed that loss of MPO promoted neutrophil–EC interactions and neutrophil emigration but did not affect neutrophil–platelet interactions under inflammatory conditions. Using genetic and pharmacologic approaches, we found that following agonist stimulation, MPO knockout (KO) neutrophils exhibited a significant increase in extracellular H₂O₂ and surface level of αMβ2 integrin and that these effects were dependent on MPO activity. Our in vivo studies using an ischemia/reperfusion-induced hepatic inflammation model revealed that compared to wild-type mice, neutrophils from MPO KO mice—displayed a pro-migratory phenotype while ameliorating tissue damage. These results suggest that MPO plays a negative role in the adhesive and migratory function of neutrophils by impairing αMβ2 integrin function under sterile inflammatory conditions.</p

image_2_Myeloperoxidase Negatively Regulates Neutrophil–Endothelial Cell Interactions by Impairing αMβ2 Integrin Function in Sterile Inflammation.tif

<p>Interactions of neutrophils with endothelial cells (ECs) and platelets contribute to tissue damage and vascular occlusion under sterile inflammatory conditions. However, the molecular mechanisms regulating the cell–cell interactions remain poorly understood. Previous studies suggest that reactive oxygen species, such as hydrogen peroxide (H₂O₂), produced from NADPH oxidase 2 play a critical role in platelet–neutrophil interactions by regulating the function of neutrophil αMβ2 integrin during sterile inflammation. In this study, we further demonstrate a crucial role for myeloperoxidase (MPO) in regulating the adhesive function of neutrophils through αMβ2 integrin. Using real-time fluorescence intravital microscopy and in vitro assays, we showed that loss of MPO promoted neutrophil–EC interactions and neutrophil emigration but did not affect neutrophil–platelet interactions under inflammatory conditions. Using genetic and pharmacologic approaches, we found that following agonist stimulation, MPO knockout (KO) neutrophils exhibited a significant increase in extracellular H₂O₂ and surface level of αMβ2 integrin and that these effects were dependent on MPO activity. Our in vivo studies using an ischemia/reperfusion-induced hepatic inflammation model revealed that compared to wild-type mice, neutrophils from MPO KO mice—displayed a pro-migratory phenotype while ameliorating tissue damage. These results suggest that MPO plays a negative role in the adhesive and migratory function of neutrophils by impairing αMβ2 integrin function under sterile inflammatory conditions.</p

video_2_Myeloperoxidase Negatively Regulates Neutrophil–Endothelial Cell Interactions by Impairing αMβ2 Integrin Function in Sterile Inflammation.wmv

<p>Interactions of neutrophils with endothelial cells (ECs) and platelets contribute to tissue damage and vascular occlusion under sterile inflammatory conditions. However, the molecular mechanisms regulating the cell–cell interactions remain poorly understood. Previous studies suggest that reactive oxygen species, such as hydrogen peroxide (H₂O₂), produced from NADPH oxidase 2 play a critical role in platelet–neutrophil interactions by regulating the function of neutrophil αMβ2 integrin during sterile inflammation. In this study, we further demonstrate a crucial role for myeloperoxidase (MPO) in regulating the adhesive function of neutrophils through αMβ2 integrin. Using real-time fluorescence intravital microscopy and in vitro assays, we showed that loss of MPO promoted neutrophil–EC interactions and neutrophil emigration but did not affect neutrophil–platelet interactions under inflammatory conditions. Using genetic and pharmacologic approaches, we found that following agonist stimulation, MPO knockout (KO) neutrophils exhibited a significant increase in extracellular H₂O₂ and surface level of αMβ2 integrin and that these effects were dependent on MPO activity. Our in vivo studies using an ischemia/reperfusion-induced hepatic inflammation model revealed that compared to wild-type mice, neutrophils from MPO KO mice—displayed a pro-migratory phenotype while ameliorating tissue damage. These results suggest that MPO plays a negative role in the adhesive and migratory function of neutrophils by impairing αMβ2 integrin function under sterile inflammatory conditions.</p

image_4_Myeloperoxidase Negatively Regulates Neutrophil–Endothelial Cell Interactions by Impairing αMβ2 Integrin Function in Sterile Inflammation.tif

<p>Interactions of neutrophils with endothelial cells (ECs) and platelets contribute to tissue damage and vascular occlusion under sterile inflammatory conditions. However, the molecular mechanisms regulating the cell–cell interactions remain poorly understood. Previous studies suggest that reactive oxygen species, such as hydrogen peroxide (H₂O₂), produced from NADPH oxidase 2 play a critical role in platelet–neutrophil interactions by regulating the function of neutrophil αMβ2 integrin during sterile inflammation. In this study, we further demonstrate a crucial role for myeloperoxidase (MPO) in regulating the adhesive function of neutrophils through αMβ2 integrin. Using real-time fluorescence intravital microscopy and in vitro assays, we showed that loss of MPO promoted neutrophil–EC interactions and neutrophil emigration but did not affect neutrophil–platelet interactions under inflammatory conditions. Using genetic and pharmacologic approaches, we found that following agonist stimulation, MPO knockout (KO) neutrophils exhibited a significant increase in extracellular H₂O₂ and surface level of αMβ2 integrin and that these effects were dependent on MPO activity. Our in vivo studies using an ischemia/reperfusion-induced hepatic inflammation model revealed that compared to wild-type mice, neutrophils from MPO KO mice—displayed a pro-migratory phenotype while ameliorating tissue damage. These results suggest that MPO plays a negative role in the adhesive and migratory function of neutrophils by impairing αMβ2 integrin function under sterile inflammatory conditions.</p

video_1_Myeloperoxidase Negatively Regulates Neutrophil–Endothelial Cell Interactions by Impairing αMβ2 Integrin Function in Sterile Inflammation.wmv

<p>Interactions of neutrophils with endothelial cells (ECs) and platelets contribute to tissue damage and vascular occlusion under sterile inflammatory conditions. However, the molecular mechanisms regulating the cell–cell interactions remain poorly understood. Previous studies suggest that reactive oxygen species, such as hydrogen peroxide (H₂O₂), produced from NADPH oxidase 2 play a critical role in platelet–neutrophil interactions by regulating the function of neutrophil αMβ2 integrin during sterile inflammation. In this study, we further demonstrate a crucial role for myeloperoxidase (MPO) in regulating the adhesive function of neutrophils through αMβ2 integrin. Using real-time fluorescence intravital microscopy and in vitro assays, we showed that loss of MPO promoted neutrophil–EC interactions and neutrophil emigration but did not affect neutrophil–platelet interactions under inflammatory conditions. Using genetic and pharmacologic approaches, we found that following agonist stimulation, MPO knockout (KO) neutrophils exhibited a significant increase in extracellular H₂O₂ and surface level of αMβ2 integrin and that these effects were dependent on MPO activity. Our in vivo studies using an ischemia/reperfusion-induced hepatic inflammation model revealed that compared to wild-type mice, neutrophils from MPO KO mice—displayed a pro-migratory phenotype while ameliorating tissue damage. These results suggest that MPO plays a negative role in the adhesive and migratory function of neutrophils by impairing αMβ2 integrin function under sterile inflammatory conditions.</p

Toward High-Performance Lithium–Sulfur Batteries: Upcycling of LDPE Plastic into Sulfonated Carbon Scaffold via Microwave-Promoted Sulfonation

Lithium–sulfur batteries were intensively explored during the last few decades as next-generation batteries owing to their high energy density (2600 Wh kg^–1) and effective cost benefit. However, systemic challenges, mainly associated with polysulfide shuttling effect and low Coulombic efficiency, plague the practical utilization of sulfur cathode electrodes in the battery market. To address the aforementioned issues, many approaches have been investigated by tailoring the surface characteristics and porosities of carbon scaffold. In this study, we first present an effective strategy of preparing porous sulfonated carbon (PSC) from low-density polyethylene (LDPE) plastic via microwave-promoted sulfonation. Microwave process not only boosts the sulfonation reaction of LDPE but also induces huge amounts of pores within the sulfonated LDPE plastic. When a PSC layer was utilized as an interlayer in lithium–sulfur batteries, the sulfur cathode delivered an improved capacity of 776 mAh g^–1 at 0.5C and an excellent cycle retention of 79% over 200 cycles. These are mainly attributed to two materialistic benefits of PSC: (a) porous structure with high surface area and (b) negatively charged conductive scaffold. These two characteristics not only facilitate the improved electrochemical kinetics but also effectively block the diffusion of polysulfides via Coulomb interaction

Tailored Carbon Anodes Derived from Biomass for Sodium-Ion Storage

Sodium-ion batteries are emerging as an alternative energy storage system for lithium-ion batteries because of the abundance and low cost of sodium. Various carbon-based anode materials have been investigated in order to improve sodium battery performance and cycle life. In this study, because of its abundance and high porosity, pistachio shell was selected as the primary carbon source, and carbonization temperatures ranged from 700 to 1500 °C. Pistachio shell carbonized at 1000 °C resulted in a highly amorphous structure with specific surface area 760.9 m² g^–1 and stable cycle performance (225 mA h g^–1 at 10 mA g^–1). Our initial results obtained from carbonized pistachio shell suggest that sufficient electrochemical performance may be obtained from biowaste materials, offering new pathways for sustainable electro-mobility and other battery applications

Uniform Graphene Quantum Dots Patterned from Self-Assembled Silica Nanodots

Graphene dots precisely controlled in size are interesting in nanoelectronics due to their quantum optical and electrical properties. However, most graphene quantum dot (GQD) research so far has been performed based on flake-type graphene reduced from graphene oxides. Consequently, it is extremely difficult to isolate the size effect of GQDs from the measured optical properties. Here, we report the size-controlled fabrication of uniform GQDs using self-assembled block copolymer (BCP) as an etch mask on graphene films grown by chemical vapor deposition (CVD). Electron microscope images show that as-prepared GQDs are composed of mono- or bilayer graphene with diameters of 10 and 20 nm, corresponding to the size of BCP nanospheres. In the measured photoluminescence (PL) spectra, the emission peak of the GQDs on the SiO₂ substrate is shown to be at ∼395 nm. The fabrication of GQDs was supported by the analysis of the Raman spectra and the observation of PL spectra after each fabrication step. Additionally, oxygen content in the GQDs is rationally controlled by additional air plasma treatment, which reveals the effect of oxygen content to the PL property

Self-Assembly-Induced Formation of High-Density Silicon Oxide Memristor Nanostructures on Graphene and Metal Electrodes

We report the direct formation of ordered memristor nanostructures on metal and graphene electrodes by a block copolymer self-assembly process. Optimized surface functionalization provides stacking structures of Si-containing block copolymer thin films to generate uniform memristor device structures. Both the silicon oxide film and nanodot memristors, which were formed by the plasma oxidation of the self-assembled block copolymer thin films, presented unipolar switching behaviors with appropriate set and reset voltages for resistive memory applications. This approach offers a very convenient pathway to fabricate ultrahigh-density resistive memory devices without relying on high-cost lithography and pattern-transfer processes