Ultrahigh Sensitivity for Thermographic Human-Machine Interface via Precious Metals Atomic Layer Deposition on V-MXene: Computational and Experimental Exploration.

Global healthcare based on the Internet of Things system is rapidly transforming to measure precise physiological body parameters without visiting hospitals at remote patients and associated symptoms monitoring. 2D materials and the prevailing mood of current ever-expanding MXene-based sensing devices motivate to introduce first the novel iridium (Ir) precious metal incorporated vanadium (V)-MXene via industrially favored emerging atomic layer deposition (ALD) techniques. The current work contributes a precise control and delicate balance of Ir single atomic forms or clusters on the V-MXene to constitute a unique precious metal-MXene embedded heterostructure (Ir-ALD@V-MXene) in practical real-time sensing healthcare applications to thermography with human-machine interface for the first time. Ir-ALD@V-MXene delivers an ultrahigh durability and sensing performance of 2.4% °C-1 than pristine V-MXene (0.42% °C-1), outperforming several conventionally used MXenes, graphene, underscoring the importance of the Ir-ALD innovative process. Aberration-corrected advanced ultra-high-resolution transmission/scanning transmission electron microscopy confirms the presence of Ir atomic clusters on well-aligned 2D-layered V-MXene structure and their advanced heterostructure formation (Ir-ALD@V-MXene), enhanced sensing mechanism is investigated using density functional theory (DFT) computations. A rational design empowering the Ir-ALD process on least explored V-MXene can potentially unfold further precious metals ALD-process developments for next-generation wearable personal healthcare devices.

Amphiregulin normalizes altered circuit connectivity for social dominance of the CRTC3 knockout mouse.

Social hierarchy has a profound impact on social behavior, reward processing, and mental health. Moreover, lower social rank can lead to chronic stress and often more serious problems such as bullying victims of abuse, suicide, or attack to society. However, its underlying mechanisms, particularly their association with glial factors, are largely unknown. In this study, we report that astrocyte-derived amphiregulin plays a critical role in the determination of hierarchical ranks. We found that astrocytes-secreted amphiregulin is directly regulated by cAMP response element-binding (CREB)-regulated transcription coactivator 3 (CRTC3) and CREB. Mice with systemic and astrocyte-specific CRTC3 deficiency exhibited a lower social rank with reduced functional connectivity between the prefrontal cortex, a major social hierarchy center, and the parietal cortex. However, this effect was reversed by astrocyte-specific induction of amphiregulin expression, and the epidermal growth factor domain was critical for this action of amphiregulin. These results provide evidence of the involvement of novel glial factors in the regulation of social dominance and may shed light on the clinical application of amphiregulin in the treatment of various psychiatric disorders.

Why Te Doping Can Break the Traditional n-Type Doping Limit of Silicon.

We report a theoretical investigation of the impact of hyperdoping with chalcogens (Se and Te) and pnictogens (P and As) on free-carrier concentrations of Si, employing density functional theory calculations. Our results illustrate that isolated substitutional chalcogens in moderately doped Si function as deep donors that are difficult to ionize at room temperature, unlike isolated substitutional pnictogens. The pairing of substitutional defects is found to be energetically favorable for every dopant element, implying that the concentration of substitutional pairs can be significant in hyperdoped Si. However, chalcogen-substitutional pairs have the capability to increase the carrier concentration, whereas pnictogen-substitutional pairs serve only as compensators for n-type doping. By evaluating the carrier concentrations for Te- and P-hyperdoped Si, we demonstrate the importance of substitutional Te pairs of Te-hyperdoped Si in breaking the traditional n-type doping limit observed in pnictogen-hyperdoped Si. Our work elucidates the underlying microscopic mechanisms that give rise to substantial carrier densities in chalcogen-hyperdoped Si, which will pave the way for the development of high-performance silicon-based devices.

Native point defects in antiperovskite Ba3SbN: a promising semiconductor for photovoltaics.

We present a theoretical investigation on intrinsic defects of hexagonal antiperovskite Ba3SbN, a promising lead-free semiconductor for photovoltaics. Our hybrid functional calculations reveal that Ba, Sb and N vacancies, and N interstitials become major point defects in Ba3SbN. Conversely, other interstitials and antisites have large formation energies and their concentrations are controllable. Herein, defect levels and configuration coordinate diagrams for the major defects are analyzed, thereby revealing that defect-assisted carrier recombination is ineffective. Thus, Ba3SbN can be a defect-tolerant semiconductor that retains excellent optoelectronic properties despite the presence of point defects. By elucidating the stability of the intrinsic defects of Ba3SbN and their impacts on the carrier capture process, this work will pave the way for the development of a new class of high-performance solar cells based on antiperovskite semiconductors.

Suppression of Brown Adipocyte Autophagy Improves Energy Metabolism by Regulating Mitochondrial Turnover.

The high abundance of mitochondria and the expression of mitochondrial uncoupling protein 1 (UCP1) confer upon brown adipose tissue (BAT) the unique capacity to convert chemical energy into heat at the expense of ATP synthesis. It was long believed that BAT is present only in infants, and so, it was not considered as a potential therapeutic target for metabolic syndrome; however, the discovery of metabolically active BAT in adult humans has re-stimulated interest in the contributions of BAT metabolic regulation and dysfunction to health and disease. Here we demonstrate that brown adipocyte autophagy plays a critical role in the regulation BAT activity and systemic energy metabolism. Mice deficient in brown adipocyte autophagy due to BAT-specific deletion of Atg7-a gene essential for autophagosome generation-maintained higher mitochondrial content due to suppression of mitochondrial clearance and exhibited improved insulin sensitivity and energy metabolism. Autophagy was upregulated in BAT of older mice compared to younger mice, suggesting its involvement in the age-dependent decline of BAT activity and metabolic rate. These findings suggest that brown adipocyte autophagy plays a crucial role in metabolism and that targeting this pathway may be a potential therapeutic strategy for metabolic syndrome.

Molecular cloning, regulation, and functional analysis of two GHS-R genes in zebrafish.

Mammalian ghrelin is derived from stomach and regulates growth hormone release and appetite by modulating GHS-R (Growth hormone secretagogue receptor) activity. Zebrafish has been developed as a forward genetic screening model system and previous screening identified a number of genes involved in multiple signaling pathways. In this system, ghrelin has been identified and its function and regulation have been shown to be highly conserved to that of mammals. Here, we identified three isoforms of zGHS-R1 and one of zGHS-R2 (zGHS-R2a), and characterized their expression, regulation and function. Three isoforms of zGHS-R1, which we named zGHS-R1a, zGHS-R1b, and zGHS-R1c, are generated by alternative splicing. The expression of zGHS-R1 is highly enriched in brain, intestine tissue, and skin tissues. Compared to zGHS-R1, the expression pattern of zGHS-R2a is rather evenly distributed. A 15 day fasting elevated expression of zGHS-R1 and zGHS-R2 transcripts in anterior intestine tissues, but not in brain. Whereas zGHS-R1a, zGHS-R1c, and zGHS-R2a appear to be presented on the plasma membrane, the localization of zGHS-R1b seems to be restricted in the intracellular region. Treatment of ghrelin agonist, L692,585 or goldfish ghrelin peptides but not rat ghrelin, elevated intracellular Ca(2+) level and phosphorylation of ERK in HEK-293 cells expressing zGHS-R1a, but not zGHS-R1b, zGHS-R1c, or zGHS-R2a. It appears that besides core ghrelin peptide sequence of GS/TSF additional amino acids are required for the activation of zGHS-R1a, as rat ghrelin induces neither intracellular Ca(2+) mobilization nor ERK phosphrylation. These results suggest that ghrelin system in zebrafish is highly conserved to that of mammals, and thus is an ideal in vivo model for dissecting ghrelin system.

Panax red ginseng extract regulates energy expenditures by modulating PKA dependent lipid mobilization in adipose tissue.

Regulation of balance between lipid accumulation and energy consumption is a critical step for the maintenance of energy homeostasis. Here, we show that Panax red ginseng extract treatments increased energy expenditures and prevented mice from diet induced obesity. Panax red ginseng extracts strongly activated Hormone Specific Lipase (HSL) via Protein Kinase A (PKA). Since activation of HSL induces lipolysis in WAT and fatty acid oxidation in brown adipose tissue (BAT), these results suggest that Panax red ginseng extracts reduce HFD induced obesity by regulating lipid mobilization.

Disorder-Dependent Li Diffusion in Li6PS5Cl Investigated by Machine-Learning Potential.

Solid-state electrolytes with argyrodite structures, such as Li6PS5Cl, have attracted considerable attention due to their superior safety compared to liquid electrolytes and higher ionic conductivity than other solid electrolytes. Although experimental efforts have been made to enhance conductivity by controlling the degree of disorder, the underlying diffusion mechanism is not yet fully understood. Moreover, existing theoretical analyses based on ab initio molecular dynamics (MD) simulations have limitations in addressing various types of disorder at room temperature. In this study, we directly investigate Li-ion diffusion in Li6PS5Cl at 300 K using large-scale, long-term MD simulations empowered by machine-learning potentials (MLPs). To ensure the convergence of conductivity values within an error range of 10%, we employ a 25 ns simulation using a 5 × 5 × 5 supercell containing 6500 atoms. The computed Li-ion conductivity, activation energies, and equilibrium site occupancies align well with experimental observations. Notably, Li-ion conductivity peaks when Cl ions occupy 25% of the 4c sites rather than at 50% where the disorder is maximized. In addition, Li-ion diffusion shows non-Arrhenius behavior, leading to different activation energies at high temperatures (>400 K). These phenomena are explained by the interplay between inter- and intracage jumps. By elucidation of the key factors affecting Li-ion diffusion in Li6PS5Cl, this work paves the way for optimizing ionic conductivity in the argyrodite family.

Human retinal pigment epithelial cells express the long pentraxin PTX3.

PURPOSE: To determine whether the long pentraxin 3 (PTX3) is expressed in human retinal pigment epithelial cells and is induced by inflammatory cytokines, interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ), expression of PTX3 was investigated in the human retinal pigment epithelial cell line, ARPE-19 cells. METHODS: In ARPE-19 cells, we first analyzed PTX3 production in the presence or absence of inflammatory cytokines, IL-1ß, TNF-α, and IFN-γ, dose- and time-dependently using enzyme-linked immunosorbent assay. Protein and mRNA expression of PTX3 was measured with western blotting analysis and real-time reverse transcription-polymerase chain reaction. Specific inhibitors were used to determine the signaling pathways of inflammatory cytokine-induced PTX3 expression. RESULTS: In this study, production of PTX3 was induced by IL-1ß and TNF-α dose- and time-dependently, but not by IFN-γ in ARPE-19 cells. Protein and mRNA expression of PTX3 was significantly upregulated in the presence of IL-1ß and TNF-α. Furthermore, pretreatment with extracellular signal-regulated kinase1/2 and nuclear factor kappa-light-chain-enhancer of activated B cells specific inhibitor abolished IL-1ß and TNF-α-induced PTX3 production, but the other inhibitors had no effect. CONCLUSIONS: These results suggested that human retinal pigment epithelial cells may be a major source of PTX3 production in the presence of proinflammatory cytokines, IL-1ß and TNF-α, and could be an important mediator for host defense and inflammatory response in the retina. The importance of the mitogen-activated protein kinase/extracellular signal-regulated kinase1/2 and nuclear factor kappa-light-chain-enhancer of activated B cells pathways for regulated PTX3 expression may be a potential target for PTX3 regulation in the retina.

Enhanced thermal stability by short-range ordered ferroelectricity in K0.5Na0.5NbO3-based piezoelectric oxides.

Industrial application of lead-free piezoelectric ceramics is prevented by intrinsic thermal instability. Herein, we propose a method to achieve outstanding thermal stability of converse piezoelectric constant () in lead-free potassium sodium niobate (KNN)-based ceramics by inducing a synergistic interaction between the grain size and polar configuration. Based on computational methods using phase-field simulations and first-principles calculations, the relationship between the grain size and polar configuration is demonstrated, and the possibility of achieving improved thermal stability in fine grains is suggested. A set of KNN systems is presented with meticulous dopant control near the chemical composition at which the grain size changes abnormally. Comparing the two representative samples with coarse and fine grains, significant enhancement in the thermal stability of is exhibited up to 300 °C in the fine grains. The origin of the thermal superiority in fine-grained ceramics is identified through an extensive study from a microstructural perspective. The thermal stability is realized in a device by successfully demonstrating the temperature dependence of piezoelectricity. It is notable that this is the first time that lead-free piezoelectric ceramics are able to achieve exceptionally stable piezoelectricity up to 300 °C, which actualizes their applicability as piezoelectric devices with high thermal stability.

Transforming growth factor-ß1 suppression of endotoxin-induced heme oxygenase-1 in macrophages involves activation of Smad2 and downregulation of Ets-2.

Heme oxygenase (HO)-1 is a cytoprotective molecule that is induced during the response to injury. An increase in HO-1 is an acute indicator of inflammation, and early induction of HO-1 has been suggested to correlate with severity of injury. While a great deal is known about the induction of HO-1 by inflammatory mediators and bacterial lipopolysaccharide (LPS), much less is known about the effects of anti-inflammatory mediators on HO-1 expression. Transforming growth factor (TGF)-ß is known to play a critical role in suppressing the immune response, and the TGF-ß1 isoform is expressed in inflammatory cells. Thus, we wanted to investigate whether TGF-ß1 could inhibit the expression of HO-1 during exposure to an inflammatory stimulus in macrophages. Here we demonstrate that TGF-ß1 is able to downregulate LPS-induced HO-1 in mouse macrophages, and this reduction in HO-1 occurred through signaling of TGF-ß1 via its type I receptor, and activation of Smad2. This TGF-ß1 response is dependent on an intact Ets-binding site (EBS) located 93 base pairs upstream from the mouse HO-1 transcription start site. This EBS is known to be important for Ets-2 transactivation of HO-1 by LPS stimulation, and we show that TGF-ß1 is able to suppress LPS-induced Ets-2 mRNA and protein levels in macrophages. Moreover, silencing of Smad2 is able to prevent the suppression of both HO-1 and Ets-2 by TGF-ß1 during exposure to LPS. These data suggest that the return of HO-1 to basal levels during the resolution of an inflammatory response may involve its downregulation by anti-inflammatory mediators.

Microscopic origin of universal quasilinear band structures of transparent conducting oxides.

A tight-binding-based microscopic theory is developed that accounts for quasilinear conduction bands appearing commonly in transparent conducting oxides. It is found that the interaction between oxygen p and metal s orbtials plays a critical role in determining the band structure around the conduction-band minimum. Under certain types of short-range orders, the tight-binding model universally leads to a dispersion relation which corresponds to that of the massive Dirac particle. The impact of the graphenelike band structure is demonstrated by evaluating the electron mobility of highly doped n-type ZnO.

Nucleotide-binding oligomerization domain protein 2 deficiency enhances neointimal formation in response to vascular injury.

OBJECTIVE: Nucleotide-binding oligomerization domain protein 2 (NOD2) stimulates diverse inflammatory responses resulting in differential cellular phenotypes. To identify the role of NOD2 in vascular arterial obstructive diseases, we investigated the expression and pathophysiological role of NOD2 in a vascular injury model of neointimal hyperplasia. METHODS AND RESULTS: We first analyzed for neointimal hyperplasia following femoral artery injury in NOD2(+/+) and NOD2(-/-) mice. NOD2(-/-) mice showed a 2.86-fold increase in neointimal formation that was mainly composed of smooth muscle (SM) α-actin positive cells. NOD2 was expressed in vascular smooth muscle cells (VSMCs) and NOD2(-/-) VSMCs showed increased cell proliferation in response to mitogenic stimuli, platelet-derived growth factor-BB (PDGF-BB), or fetal bovine serum, compared with NOD2(+/+) VSMCs. Furthermore, NOD2 deficiency markedly promoted VSMCs migration in response to PDGF-BB, and this increased cell migration was attenuated by a phosphatidylinositol 3-kinase inhibitor. However, protein kinase C and c-Jun N-terminal kinase inhibitors exerted negligible effects. Moreover, muramyl dipeptide-stimulated NOD2 prevented PDGF-BB-induced VSMCs migration. CONCLUSION: Functional NOD2 was found to be expressed in VSMCs, and NOD2 deficiency promoted VSMCs proliferation, migration, and neointimal formation after vascular injury. These results provide evidence for the involvement of NOD2 in vascular homeostasis and tissue injury, serving as a potential molecular target in the modulation of arteriosclerotic vascular disease.

First-Principles Calculations of Luminescence Spectra of Real-Scale Quantum Dots.

The luminescence line shape is an important feature of semiconductor quantum dots (QDs) and affects performance in various optical applications. Here, we report a first-principles method to predict the luminescence spectrum of thousands of atom QDs. In our approach, neural network potential calculations are combined with density functional theory calculations to describe exciton-phonon coupling (EPC). Using the calculated EPC, the luminescence spectrum is evaluated within the Franck-Condon approximation. Our approach results in the luminescence line shape for an InP/ZnSe core/shell QD (3406 atoms) that exhibits excellent agreement with the experiments. From a detailed analysis of EPC, we reveal that the coupling of both acoustic and optical phonons to an exciton are important in determining the spectral line shapes of core/shell QDs, which is in contrast with previous studies. On the basis of the present simulation results, we provide guidelines for designing high-performance core/shell QDs with ultrasharp emission spectra.

Hydrogen-Doping-Enabled Boosting of the Carrier Mobility and Stability in Amorphous IGZTO Transistors.

This study investigated the effect of hydrogen (H) on the performance of amorphous In-Ga-Zn-Sn oxide (a-In0.29Ga0.35Zn0.11Sn0.25O) thin-film transistors (TFTs). Ample H in plasma-enhanced atomic layer deposition (PEALD)-derived SiO2 can diffuse into the underlying a-IGZTO film during the postdeposition annealing (PDA) process, which affects the electrical properties of the resulting TFTs due to its donor behavior in the a-IGZTO. The a-In0.29Ga0.35Zn0.11Sn0.25O TFTs at the PDA temperature of 400 °C exhibited a remarkably higher field-effect mobility (µFE) of 85.9 cm2/Vs, a subthreshold gate swing (SS) of 0.33 V/decade, a threshold voltage (VTH) of -0.49 V, and an ION/OFF ratio of ∼108; these values are superior compared to those of unpassivated a-In0.29Ga0.35Zn0.11Sn0.25O TFTs (µFE = 23.3 cm2/Vs, SS = 0.36 V/decade, and VTH = -3.33 V). In addition, the passivated a-In0.29Ga0.35Zn0.11Sn0.25O TFTs had good stability against the external gate bias duration. This performance change can be attributed to the substitutional H doping into oxygen sites (HO) leading to a boost in ne and µFE. In contrast, the beneficial HO effect was barely observed for amorphous indium gallium zinc oxide (a-IGZO) TFTs, suggesting that the hydrogen-doping-enabled boosting of a-IGZTO TFTs is strongly related to the existence of Sn cations. Electronic calculations of VO and HO using density functional theory (DFT) were performed to explain this disparity. The introduction of SnO2 in a-IGZO is predicted to cause a conversion from shallow VO to deep VO due to the lower formation energy of deep VO, which is effectively created around Sn cations. The formation of HO by H doping in the IGZTO facilitates the efficient connection of atomic states forming the conduction band more smoothly. This reduces the effective mass and enhances the carrier mobility.

Reversible Manipulation of Photoconductivity Caused by Surface Oxygen Vacancies in Perovskite Stannates with Ultraviolet Light.

Programmable optoelectronic devices call for the reversible control of the photocarrier recombination process by in-gap states in oxide semiconductors. However, previous approaches to produce oxygen vacancies as a source of in-gap states in oxide semiconductors have hampered the reversible formation of oxygen vacancies and their related phenomena. Here, a new strategy to manipulate the 2D photoconductivity from perovskite stannates is demonstrated by exploiting spatially selective photochemical reaction under ultraviolet illumination at room temperature. Remarkably, the ideal trap-free photocurrent of air-illuminated BaSnO3 (≈200 pA) is reversibly switched into three orders of magnitude higher photocurrent of vacuum-illuminated BaSnO3 (≈335 nA) with persistent photoconductivity depending on ambient oxygen pressure under illumination. Multiple characterizations elucidate that ultraviolet illumination of BaSnO3  under low oxygen pressure induces surface oxygen vacancies as a result of surface photolysis combined with the low oxygen-diffusion coefficient of BaSnO3 ; the concentrated oxygen vacancies are likely to induce a two-step transition of photocurrent response by changing the characteristics of in-gap states from the shallow level to the deep level. These results suggest a novel strategy that uses light-matter interaction in a reversible and spatially confined way to manipulate functionalities related to surface defect states, for the emerging applications using newly discovered oxide semiconductors.

Identification of Active Sites for CO2 Reduction on Graphene-Supported Single-Atom Catalysts.

Transition metal- and nitrogen-codoped graphene (referred to as M-N-G, where M is a transition metal) has emerged as an important type of single-atom catalysts with high selectivities and activities for electrochemical CO2 reduction (CO2 R) to CO. However, despite extensive previous studies on the catalytic origin, the active site in M-N-G catalysts remains puzzling. In this study, density functional theory calculations and computational hydrogen electrode model is used to investigate CO2 R reaction energies on Zn-N-G, which exhibits outstanding catalytic performance, and to examine kinetic barriers of reduction reactions by using the climbing image nudged elastic band method. We find that single Zn atoms binding to N and C atoms in divacancy sites of graphene cannot serve as active sites to enable CO production, owing to *OCHO formation (* denotes an adsorbate) at an initial protonation process. This contradicts the widely accepted CO2 R mechanism whereby single metal atoms are considered catalytic sites. In contrast, the C atom that is the nearest neighbor of the single Zn atom (CNN ) is found to be highly active and the Zn atom plays a role as an enhancer of the catalytic activity of the CNN . Detailed analysis of the CO2 R pathway to CO on the CNN site reveals that *COOH is favorably formed at an initial electrochemical step, and every reaction step becomes downhill in energy at small applied potentials of about -0.3 V with respect to reversible hydrogen electrode. Electronic structure analysis is also used to elucidate the origin of the CO2 R activity of the CNN site.

CRTC3, a sensor and key regulator for melanogenesis, as a tunable therapeutic target for pigmentary disorders.

Background: Although CREB phosphorylation is known to be essential in UVB/cAMP-stimulated melanogenesis, CREB null mice did not show identifiable pigmentation phenotypes. Here, we show that CREB-regulated transcription co-activator 3 (CRTC3) quantitatively regulates and orchestrates melanogenesis by directly targeting microphthalmia-associated transcription factor (MITF) and regulating the expression of most key melanogenesis-related genes. Methods: We analyzed CRTC3-null, KRT14-SCF transgenic, and their crossover mice. The molecular basis of CRTC3 effects on pigmentation was investigated by histology, melanin/tyrosinase assay, immunoblotting, shRNA, promoter assay, qRT-PCR, and subcellular localization. These analyses were carried out in primary cultured melanocytes, mouse cell lines, normal human cells, co-cultures, and ex vivo human skin. CRTC/CREB activity screening was performed to identify candidate agents for the regulation of melanogenesis. Results: The coat and skin color of CRTC3-null mice was paler due to a reduction in melanin deposition. Melanogenesis-related genes were reduced in CRTC3-deficient cultured melanocytes and tail skin of CRTC3-null mice. Notably, basal levels of MITF present in CRTC3-null mice were sufficient for melanocytic differentiation/survival. Thus CRTC3-null mice showed a comparable number of epidermal melanocytes compared to control mice. Stem cell factor (SCF) introduction by crossing with KRT14-SCF mice increased epidermal melanocytes and melanin deposition in control and CRTC3-null mice, but the skin color remained still light on the CRTC3-null background. Furthermore, we identified the therapeutic potential of altiratinib to inhibit melanogenesis in human melanocytes and human skin effectively and safely. Conclusion: CRTC3 appears to be a key sensor for melanogenesis and can be used as a reversible and tunable tool for selectively regulating melanogenesis without affecting melanocyte integrity. Thus, CRTC3 can also serve as a screening tool for the discovery of ideal melanogenesis-modulating small molecules.

Regulation of heme oxygenase-1 gene by peptidoglycan involves the interaction of Elk-1 and C/EBPalpha to increase expression.

Heme oxygenase (HO)-1 is a cytoprotective enzyme with anti-inflammatory properties. HO-1 is induced during a systemic inflammatory response, and expression of HO-1 is beneficial during sepsis of a Gram-positive source. Systemic infection from Gram-positive organisms has emerged as an important cause of sepsis, with Staphylococcus aureus as a common etiology. An important mediator of Gram-positive infections is peptidoglycan (PGN), a cell wall component of these organisms. Here, we demonstrate that HO-1 played an important, protective role in vivo, as mice deficient in HO-1 were very sensitive to the lethal effects of PGN derived from S. aureus. PGN induced HO-1 protein and mRNA levels, and this regulation occurred at the level of gene transcription. The PGN-responsive region of the HO-1 promoter (from -117 to -66 bp) contains a functional EBS, and Ets proteins are known to be involved in the regulation of inflammatory responses. We showed previously that Ets factors (activators Ets-2 and Ets-1 and repressor Elk-3) regulate HO-1 expression by Gram-negative endotoxin. However, during exposure to a Gram-positive stimulus in the present study, Elk-1 was a potent activator of HO-1 in conjunction with PGN. The ability of Elk-1 to induce HO-1 promoter activity was independent of direct DNA binding, but rather occurred by interacting with the CCAAT/enhancer-binding protein-alpha (C/EBPalpha), which binds to DNA. Moreover, silencing of C/EBPalpha in macrophages prevented induction of HO-1 promoter activity by either Elk-1 or PGN. These data provide further insight into the regulation and function of HO-1 by a mediator of Gram-positive bacteria.

Antiperovskite Oxides as Promising Candidates for High-Performance Ferroelectric Photovoltaics: First-Principles Investigation on Ba4As2O and Ba4Sb2O.

Owing to polarization-driven efficient charge carrier separation, ferroelectric semiconductors with narrow band gaps (∼1.3 eV) can constitute an ideal active layer for photovoltaics (PVs), as demonstrated in recent studies on lead halide perovskite solar cells. In this study, antiperovskite oxides with a composition of Ba4Pn2O (Pn = As or Sb) are proposed as promising candidates for high-performance ferroelectric PVs. Using density functional theory calculations, it is revealed that Ba4Pn2O exhibits moderate macroscopic polarization enough for charge carrier separation. Moreover, they are predicted to have direct band gaps close to the optimal Shockley-Queisser value. By investigating optical absorption coefficients and resulting short-circuit currents, it is demonstrated that a very thin layer of Ba4Pn2O can yield large photocurrents. The effective masses of charge carriers in Ba4Pn2O are found to be fairly small (<0.2me), implying facile extraction of photocarriers. The favorable simulation results along with the confirmed synthesizability of the materials strongly suggest that Ba4Pn2O will be an active layer suitable for PVs.