ABSTRACT
Atomic sawtooth surfaces have emerged as a versatile platform for growth of single-crystal van der Waals layered materials. However, the mechanism governing the formation of single-crystal atomic sawtooth metal (copper or gold) films on hard substrates (tungsten or molybdenum) remains a puzzle. In this study, we aim to elucidate the formation mechanism of atomic sawtooth metal films during melting-solidification process. Utilizing molecular dynamics, we unveil that the solidification of the liquid copper initiates at a high-index tungsten facet with higher interfacial energy. Subsequent tungsten facets follow energetically favourable pathways of forming single-crystal atomic sawtooth copper film during the solidification process near melting temperature. Formation of atomic sawtooth copper film is guaranteed with a film thickness exceeding the grain size of polycrystalline tungsten substrate. We further demonstrate the successful growth of centimeter-scale single-crystal monolayer hexagonal boron nitride films on atomic sawtooth copper films and explore their potential as efficient oxygen barrier.
ABSTRACT
The properties of transition metal dichalcogenides (TMDCs) are critically dependent on the dielectric constant of substrates, which significantly limits their application. To address this issue, we used a perfluorinated polyether (PFPE) self-assembled monolayer (SAM) with low surface energy to increase the van der Waals (vdW) gap between TMDCs and the substrate, thereby reducing the interaction between them. This resulted in a reduction in the subthreshold swing value, an increase in the photoluminescence intensity of excitons, and a decrease in the doping effect by the substrate. This work will provide a new way to control the TMDC/dielectric interface and contribute to expanding the applicability of TMDCs.
ABSTRACT
Microglia-driven neuroinflammation plays an important role in the development of Alzheimer's disease (AD). Microglia activation is accompanied by the formation and chronic maintenance of TLR4 inflammarafts, defined as enlarged and cholesterol-rich lipid rafts serving as an assembly platform for TLR4 dimers and complexes of other inflammatory receptors. The secreted apoA-I binding protein (APOA1BP or AIBP) binds TLR4 and selectively targets cholesterol depletion machinery to TLR4 inflammaraft expressing inflammatory, but not homeostatic microglia. Here we demonstrated that amyloid-beta (Aß) induced formation of TLR4 inflammarafts in microglia in vitro and in the brain of APP/PS1 mice. Mitochondria in Apoa1bp-/- APP/PS1 microglia were hyperbranched and cupped, which was accompanied by increased ROS and the dilated ER. The size and number of Aß plaques and neuronal cell death were significantly increased, and the animal survival was decreased in Apoa1bp-/- APP/PS1 compared to APP/PS1 female mice. These results suggest that AIBP exerts control of TLR4 inflammarafts and mitochondrial dynamics in microglia and plays a protective role in AD associated oxidative stress and neurodegeneration.
ABSTRACT
Glaucoma is a group of ocular diseases that cause irreversible blindness. It is characterized by multifactorial degeneration of the optic nerve axons and retinal ganglion cells (RGCs), resulting in the loss of vision. Major components of glaucoma pathogenesis include glia-driven neuroinflammation and impairment of mitochondrial dynamics and bioenergetics, leading to retinal neurodegeneration. In this review article, we summarize current evidence for the emerging role of apolipoprotein A-I binding protein (AIBP) as an important anti-inflammatory and neuroprotective factor in the retina. Due to its association with toll-like receptor 4 (TLR4), extracellular AIBP selectively removes excess cholesterol from the plasma membrane of inflammatory and activated cells. This results in the reduced expression of TLR4-associated, cholesterol-rich lipid rafts and the inhibition of downstream inflammatory signaling. Intracellular AIBP is localized to mitochondria and modulates mitophagy through the ubiquitination of mitofusins 1 and 2. Importantly, elevated intraocular pressure induces AIBP deficiency in mouse models and in human glaucomatous retina. AIBP deficiency leads to the activation of TLR4 in Müller glia, triggering mitochondrial dysfunction in both RGCs and Müller glia, and compromising visual function in a mouse model. Conversely, restoring AIBP expression in the retina reduces neuroinflammation, prevents RGCs death, and protects visual function. These results provide new insight into the mechanism of AIBP function in the retina and suggest a therapeutic potential for restoring retinal AIBP expression in the treatment of glaucoma.
Subject(s)
Glaucoma , Toll-Like Receptor 4 , Mice , Animals , Humans , Toll-Like Receptor 4/metabolism , Neuroinflammatory Diseases , Glaucoma/metabolism , Retina/metabolism , Cholesterol/metabolismABSTRACT
Monolayered transition-metal dichalcogenides (TMDs) are easily exposed to air, and their crystal quality can often be degraded via oxidation, leading to poor electronic and optical device performance. The degradation becomes more severe in the presence of defects, grain boundaries, and residues. Here, we report crack propagation in pristine TMD monolayers grown by chemical vapor deposition under ambient conditions and light illumination. Under a high relative humidity (RH) of â¼60% and white light illumination, the cracks appear randomly. Photo-oxidative cracks gradually propagated along the grain boundaries of the TMD monolayers. In contrast, under low RH conditions of â¼2%, cracks were scarcely observed. Crack propagation is predominantly attributed to the accumulation of water underneath the TMD monolayers, which is preferentially absorbed by hygroscopic alkali metal-based precursor residues. Crack propagation is further accelerated by the cyclic process of photo-oxidation in a basic medium, leading to localized tensile strain. We also found that such crack propagation is prevented after the removal of alkali metals via the transfer of the sample to other substrates.
ABSTRACT
Beyond-silicon technology demands ultrahigh performance field-effect transistors. Transition metal dichalcogenides provide an ideal material platform, but the device performances such as the contact resistance, on/off ratio and mobility are often limited by the presence of interfacial residues caused by transfer procedures. Here, we show an ideal residue-free transfer approach using polypropylene carbonate with a negligible residue coverage of ~0.08% for monolayer MoS2 at the centimetre scale. By incorporating a bismuth semimetal contact with an atomically clean monolayer MoS2 field-effect transistor on hexagonal boron nitride substrate, we obtain an ultralow Ohmic contact resistance of ~78 Ω µm, approaching the quantum limit, and a record-high on/off ratio of ~1011 at 15 K. Such an ultra-clean fabrication approach could be the ideal platform for high-performance electrical devices using large-area semiconducting transition metal dichalcogenides.
ABSTRACT
Layered 2D transition metal dichalcogenides (TMDs) have been suggested as efficient substitutes for Pt-group metal electrocatalysts in the hydrogen evolution reaction (HER). However, poor catalytic activities in neutral and alkaline electrolytes considerably hinder their practical applications. Furthermore, the weak adhesion between TMDs and electrodes often impedes long-term durability and thus requires a binder. Here, a universal platform is reported for robust dual-atom doped 2D electrocatalysts with superior HER performance over a wide pH range media. V:Co-ReS2 on a wafer scale is directly grown on oxidized Ti foil by a liquid-phase precursor-assisted approach and subsequently used as highly efficient electrocatalysts. The catalytic performance surpasses that of Pt group metals in a high current regime (≥ 100 mA cm-2) at pH ≥ 7, with a high durability of more than 70 h in all media at 200 mA cm-2. First-principles calculations reveal that V:Co dual doping in ReS2 significantly reduces the water dissociation barrier and simultaneously enables the material to achieve the thermoneutral Gibbs free energy for hydrogen adsorption.
ABSTRACT
Glaucoma is a neurodegenerative disease manifested in retinal ganglion cell (RGC) death and irreversible blindness. While lowering intraocular pressure (IOP) is the only proven therapeutic strategy in glaucoma, it is insufficient for preventing disease progression, thus justifying the recent focus on targeting retinal neuroinflammation and preserving RGCs. We have identified apolipoprotein A-I binding protein (AIBP) as the protein regulating several mechanisms of retinal neurodegeneration. AIBP controls excessive cholesterol accumulation via upregulating the cholesterol transporter ATP-binding cassette transporter 1 (ABCA1) and reduces inflammatory signaling via toll-like receptor 4 (TLR4) and mitochondrial dysfunction. ABCA1, TLR4 and oxidative phosphorylation components are genetically linked to primary open-angle glaucoma. Here we demonstrated that AIBP and ABCA1 expression was decreased, while TLR4, interleukin 1 beta (IL-1 beta), and the cholesterol content increased in the retina of patients with glaucoma and in mouse models of glaucoma. Restoring AIBP expression by a single intravitreal injection of adeno-associated virus (AAV)-AIBP protected RGCs in glaucomatous DBA/2J mice, in mice with microbead-induced chronic IOP elevation, and optic nerve crush. In addition, AIBP expression attenuated TLR4 and IL-1 beta expression, localization of TLR4 to lipid rafts, reduced cholesterol accumulation, and ameliorated visual dysfunction. These studies collectively indicate that restoring AIBP expression in the glaucomatous retina reduces neuroinflammation and protects RGCs and Muller glia, suggesting the therapeutic potential of AAV-AIBP in human glaucoma.
ABSTRACT
PURPOSE OF REVIEW: Advances in single cell techniques revealed a remarkable diversity in macrophage gene expression profiles in atherosclerosis. However, the diversity of functional processes at the macrophage plasma membrane remains less studied. This review summarizes recent advances in characterization of lipid rafts, where inflammatory receptors assemble, in macrophages that undergo reprogramming in atherosclerotic lesions and in vitro under conditions relevant to the development of atherosclerosis. RECENT FINDINGS: The term inflammarafts refers to enlarged lipid rafts with increased cholesterol content, hosting components of inflammatory receptor complexes assembled in close proximity, including TLR4-TLR4, TLR2-TLR1 and TLR2-CD36 dimers. Macrophages decorated with inflammarafts maintain chronic inflammatory gene expression and are primed to an augmented response to additional inflammatory stimuli. In mouse atherosclerotic lesions, inflammarafts are expressed primarily in nonfoamy macrophages and less in lipid-laden foam cells. This agrees with the reported suppression of inflammatory programs in foam cells. In contrast, nonfoamy macrophages expressing inflammarafts are the major inflammatory population in atherosclerotic lesions. Discussed are emerging reports that help understand formation and persistence of inflammarafts and the potential of inflammarafts as a novel therapeutic target. SUMMARY: Chronic maintenance of inflammarafts in nonfoamy macrophages serves as an effector mechanism of inflammatory macrophage reprogramming in atherosclerosis.
Subject(s)
Atherosclerosis , Plaque, Atherosclerotic , Animals , Mice , Toll-Like Receptor 4/metabolism , Toll-Like Receptor 2/metabolism , Lipoproteins, LDL/metabolism , Macrophages/metabolism , Atherosclerosis/metabolism , Foam Cells/metabolism , Plaque, Atherosclerotic/pathologyABSTRACT
Surface self-reconstruction of oxygen evolution reaction (OER) electrocatalysts generally occurs during the electrochemical activation process. Herein, we study the surface self-reconstruction of a 2D layered Fe-doped Ni-thiophosphate (NixFe1-xPS3) nanosheet. The role of Fe in the surface self-reconstruction of NiPS3 during the OER is investigated by using an in situ Raman analysis. Formation of amorphous metal/non-metal oxide layers on the surface of NixFe1-xPS3 can efficiently act as the ultimate catalytic center for the OER.
ABSTRACT
The generation of high-purity localized trions, dynamic exciton-trion interconversion, and their spatial modulation in two-dimensional (2D) semiconductors are building blocks for the realization of trion-based optoelectronic devices. Here, we present a method for the all-optical control of the exciton-to-trion conversion process and its spatial distributions in a MoS2 monolayer. We induce a nanoscale strain gradient in a 2D crystal transferred on a lateral metal-insulator-metal (MIM) waveguide and exploit propagating surface plasmon polaritons (SPPs) to localize hot electrons. These significantly increase the electrons and efficiently funnel excitons in the lateral MIM waveguide, facilitating complete exciton-to-trion conversion even at ambient conditions. Additionally, we modulate the SPP mode using adaptive wavefront shaping, enabling all-optical control of the exciton-to-trion conversion rate and trion distribution in a reversible manner. Our work provides a platform for harnessing excitonic quasiparticles efficiently in the form of trions at ambient conditions, enabling high-efficiency photoconversion.
ABSTRACT
Glaucoma is a leading cause of irreversible blindness worldwide and is characterized by a slow, progressive, and multifactorial degeneration of retinal ganglion cells (RGCs) and their axons, resulting in vision loss. Despite its high prevalence in individuals 60 years of age and older, the causing factors contributing to glaucoma progression are currently not well characterized. Intraocular pressure (IOP) is the only proven treatable risk factor. However, lowering IOP is insufficient for preventing disease progression. One of the significant interests in glaucoma pathogenesis is understanding the structural and functional impairment of mitochondria in RGCs and their axons and synapses. Glaucomatous risk factors such as IOP elevation, aging, genetic variation, neuroinflammation, neurotrophic factor deprivation, and vascular dysregulation, are potential inducers for mitochondrial dysfunction in glaucoma. Because oxidative phosphorylation stress-mediated mitochondrial dysfunction is associated with structural and functional impairment of mitochondria in glaucomatous RGCs, understanding the underlying mechanisms and relationship between structural and functional alterations in mitochondria would be beneficial to developing mitochondria-related neuroprotection in RGCs and their axons and synapses against glaucomatous neurodegeneration. Here, we review the current studies focusing on mitochondrial dynamics-based structural and functional alterations in the mitochondria of glaucomatous RGCs and therapeutic strategies to protect RGCs against glaucomatous neurodegeneration.
Subject(s)
Glaucoma , Optic Nerve Diseases , Humans , Retinal Ganglion Cells/pathology , Mitochondrial Dynamics , Intraocular Pressure , Optic Nerve Diseases/etiologyABSTRACT
BACKGROUND: Reprogramming of monocytes and macrophage manifests in hyperinflammatory responses and chronification of inflammation in atherosclerosis. Recent studies focused on epigenetic, transcriptional, and metabolic alterations that characterize trained immunity. However, the underlying effector mechanisms driving the hyperinflammatory response of reprogrammed macrophages remain unclear. We hypothesized that the plasma membrane of atherosclerotic lesion macrophages undergoes reprogramming to maintain inflammarafts, enlarged lipid rafts (LR) serving as a platform for assembly of inflammatory receptor complexes. METHODS: Single-cell suspensions from the aortae of Western diet-fed Ldlr-/- mice were gated for BODIPY-high foamy and BODIPY-low nonfoamy F4/80 macrophages by flow cytometry. Inflammarafts were characterized by increased levels of LR, TLR4 (toll-like receptor-4) localization to LR, TLR4 dimers, and the proximity between TLR2, TLR1, and CD36. In a cellular model of trained immunity, LR, TLR4 dimers, and the inflammatory response were measured in bone marrow-derived macrophages subjected to a 24-hour treatment with LPS (lipopolysaccharide) or OxLDL (oxidized low-density lipoprotein), followed by a 6-day wash-out period. RESULTS: Nonfoamy macrophages, which constituted ≈40% of macrophages in atherosclerotic lesions, expressed significantly higher levels of LR and TLR4 dimers, as well as proximity ligation signals for TLR4-LR, TLR2-CD36, and TLR2-TLR1 complexes, compared with foamy macrophages. These inflammaraft measures associated, to a different degree, with plasma cholesterol and inflammatory cytokines, as well as the size of the atherosclerotic lesions and necrotic cores. The bone marrow-derived macrophages trained with LPS simulated nonfoamy atherosclerotic lesion macrophages and continued to express inflammarafts and inflammatory genes for 6 days after LPS removal and displayed a hyperinflammatory response to Pam3CSK4, a TLR2/TLR1 agonist. OxLDL-exposed, lipid-laden macrophages did not express inflammarafts. CONCLUSIONS: Our data support the hypothesis that persistent inflammarafts in nonfoamy macrophages in atherosclerotic lesions serve as effectors of macrophage reprogramming into a hyperinflammatory phenotype.
Subject(s)
Atherosclerosis , Foam Cells , Mice , Animals , Foam Cells/pathology , Toll-Like Receptor 4/genetics , Toll-Like Receptor 4/metabolism , Lipopolysaccharides , Toll-Like Receptor 2/genetics , Toll-Like Receptor 2/metabolism , Toll-Like Receptor 1/metabolism , Macrophages/metabolism , Atherosclerosis/pathology , Lipoproteins, LDL/metabolism , CD36 Antigens/genetics , CD36 Antigens/metabolismABSTRACT
Millions of people suffer from arthritis worldwide, consistently struggling with daily activities due to debilitating pain evoked by this disease. Perhaps the most intensively investigated type of inflammatory arthritis is rheumatoid arthritis (RA), where, despite considerable advances in research and clinical management, gaps regarding the neuroimmune interactions that guide inflammation and chronic pain in this disease remain to be clarified. The pain and inflammation associated with arthritis are not isolated to the joints, and inflammatory mechanisms induced by different immune and glial cells in other tissues may affect the development of chronic pain that results from the disease. This review aims to provide an overview of the state-of-the-art research on the roles that innate immune, and glial cells play in the onset and maintenance of arthritis-associated pain, reviewing nociceptive pathways from the joint through the dorsal root ganglion, spinal circuits, and different structures in the brain. We will focus on the cellular mechanisms related to neuroinflammation and pain, and treatments targeting these mechanisms from the periphery and the CNS. A comprehensive understanding of the role these cells play in peripheral inflammation and initiation of pain and the central pathways in the spinal cord and brain will facilitate identifying new targets and pathways to aide in developing therapeutic strategies to treat joint pain associated with RA.
ABSTRACT
High pressure or strain is an effective strategy for generating phase transformations in van der Waals (vdW) layered materials without introducing defects, but this approach remains difficult to perform consistently. We present a scalable and facile method for achieving phase transformation in vdW materials, wherein solid vdW materials are subject to internal thermal stress within a molten metal mantle as it undergoes cooling. This internal thermal stress is principally the product of differential thermal expansion between mantle and core and can be tuned by the mantle material and temperature conditions. We validated this approach by achieving phase transformation of red phosphorus to black phosphorus, and metallic 1T'- to semiconducting 2H-MoTe2 crystals. We further demonstrate quantum electronic phase transformation of suppressed charge density wave in TiSe2 by means of electron-phonon coupling using the same system.
ABSTRACT
Two-dimensional (2D) transition metal dichalcogenides (TMDs) and their heterostructures have attracted significant interest in both academia and industry because of their unusual physical and chemical properties. They offer numerous applications, such as electronic, optoelectronic, and spintronic devices, in addition to energy storage and conversion. Atomic and structural modifications of van der Waals layered materials are required to achieve unique and versatile properties for advanced applications. This review presents a discussion on the atomic-scale and structural modifications of 2D TMDs and their heterostructures via post-treatment. Atomic-scale modifications such as vacancy generation, substitutional doping, functionalization and repair of 2D TMDs and structural modifications including phase transitions and construction of heterostructures are discussed. Such modifications on the physical and chemical properties of 2D TMDs enable the development of various advanced applications including electronic and optoelectronic devices, sensing, catalysis, nanogenerators, and memory and neuromorphic devices. Finally, the challenges and prospects of various post-treatment techniques and related future advanced applications are addressed.
ABSTRACT
Integration of distinct materials to form heterostructures enables the proposal of new functional devices based on emergent physical phenomena beyond the properties of the constituent materials. The optical responses and electrical transport characteristics of heterostructures depend on the charge and exciton transfer (CT and ET) at the interfaces, determined by the interfacial energy level alignment. In this work, heterostructures consisting of aggregates of fluorescent molecules (DY1) and 2D semiconductor MoS2 monolayers are fabricated. Photoluminescence spectra of DY1/MoS2 show quenching of the DY1 emission and enhancement of the MoS2 emission, indicating a strong electronic interaction between these two materials. Nanoscopic mappings of the light-induced contact potential difference changes rule out the CT process at the interface. Using femtosecond transient absorption spectroscopy, the rapid interfacial ET process from DY1 aggregates to MoS2 and a fourfold extension of the exciton lifetime in MoS2 are elucidated. These results suggest that the integration of 2D inorganic semiconductors with fluorescent molecules can provide versatile approaches to engineer the physical characteristics of materials for both fundamental studies and novel optoelectronic device applications.
ABSTRACT
Vertical van der Waals heterostructures (vdWhs), which are made by layer-by-layer stacking of two-dimensional (2D) materials, offer great opportunities for the development of extraordinary physics and devices such as topological superconductivity, robust quantum Hall phenomenon, electron-hole pair condensation, Coulomb drag, and tunneling devices. However, the size of vdWhs is still limited to the order of a few micrometers, which restricts the large-scale roll-to-roll processes for industrial applications. Herein, we report the sequential growth of a 14 in. vertical vdWhs on a rollable Al foil via chemical vapor deposition. By supplying chalcogen precursors to liquid transition-metal precursor-coated Al foils, we grew a wide range of individual 2D transition-metal dichalcogenide (TMD) films, including MoS2, VS2, ReS2, WS2, SnS2, WSe2, and vanadium-doped MoS2. Additionally, by repeating the growth process, we successfully achieved the layer-by-layer growth of ReS2/MoS2 and SnS2/ReS2/MoS2 vdWhs. The chemically inert Al native oxide layer inhibits the diffusion of chalcogen and metal atoms into Al foils, allowing for the growth of diverse TMDs and their vdWhs. The conductive Al substrate enables the effective use of vdWhs/Al as a hydrogen evolution reaction electrocatalyst with a transfer-free process. This work provides a robust route for the commercialization of 2D TMDs and their vdWhs at a low cost.