Macrophages in the infarcted heart acquire a fibrogenic phenotype, expressing matricellular proteins, but do not undergo fibroblast conversion.

Although some studies have suggested that macrophages may secrete structural collagens, and convert to fibroblast-like cells, macrophage to fibroblast transdifferentiation in infarcted and remodeling hearts remains controversial. Our study uses linage tracing approaches and single cell transcriptomics to examine whether macrophages undergo fibroblast conversion, and to characterize the extracellular matrix expression profile of myeloid cells in myocardial infarction. To examine whether infarct macrophages undergo fibroblast conversion, we identified macrophage-derived progeny using the inducible CX3CR1CreER mice crossed with the PDGFRαEGFP reporter line for reliable fibroblast identification. The abundant fibroblasts that infiltrated the infarcted myocardium after 7 and 28 days of coronary occlusion were not derived from CX3CR1+ macrophages. Infarct macrophages retained myeloid cell characteristics and did not undergo conversion to myofibroblasts, endothelial or vascular mural cells. Single cell RNA-seq of CSF1R+ myeloid cells harvested from control and infarcted hearts showed no significant expression of fibroblast identity genes by myeloid cell clusters. Moreover, infarct macrophages did not express significant levels of genes encoding structural collagens. However, infarct macrophage and monocyte clusters were the predominant source of the fibrogenic growth factors Tgfb1 and Pdgfb, and of the matricellular proteins Spp1/Osteopontin, Thbs1/Thrombospondin-1, Emilin2, and Fn1/fibronectin, while expressing significant amounts of several other matrix genes, including Vcan/versican, Ecm1 and Sparc. ScRNA-seq data suggested similar patterns of matrix gene expression in human myocardial infarction. In conclusion, infarct macrophages do not undergo fibroblast or myofibroblast conversion and do not exhibit upregulation of structural collagens but may contribute to fibrotic remodeling by producing several fibrogenic matricellular proteins.

High-Efficiency Carbon-based CsPbI2 Br Perovskite Solar Cells from Dual Direction Thermal Diffusion Treatment with Cadmium Halides.

In recent years, carbon-based CsPbI2 Br perovskite solar cells (PSCs) have attracted more attention due to their low cost and good stability. However, the power conversion efficiency (PCE) of carbon-based CsPbI2 Br PSCs is still no more than 16%, because of the defects in CsPbI2 Br or at the interface with the electron transport layer (ETL), as well as the energy level mismatch, which lead to the loss of energy, thus limiting PCE values. Herein, a series of cadmium halides are introduced, including CdCl2 , CdBr2 and CdI2 for dual direction thermal diffusion treatment. Some Cd2+ ions thermally diffuse downward to passivate the defects inside or on the surface of SnO2 ETL. Meanwhile, the energy level structure of SnO2 ETL is adjusted, which is in favor of the transfer of electron carriers and blocking holes. On the other hand, part of Cd2+ and Cl- ions thermally diffuse upward into the CsPbI2 Br lattice to passivate crystal defects. Through dual direction thermal diffusion treatment by CdCl2 , CdI2 and CdBr2 , the performance of devices has been significantly improved, and their PCE has been increased from 13.01% of the original device to 14.47%, 14.31%, and 13.46%, respectively. According to existing reports, 14.47% is one of the highest PCE of carbon-based CsPbI2 Br PSCs with SnO2 ETLs.

The role of endogenous Smad7 in regulating macrophage phenotype following myocardial infarction.

Smad7 restrains TGF-ß responses, and has been suggested to exert both pro- and anti-inflammatory actions that may involve effects on macrophages. Myocardial infarction triggers a macrophage-driven inflammatory response that not only plays a central role in cardiac repair, but also contributes to adverse remodeling and fibrosis. We hypothesized that macrophage Smad7 expression may regulate inflammation and fibrosis in the infarcted heart through suppression of TGF-ß responses, or via TGF-independent actions. In a mouse model of myocardial infarction, infiltration with Smad7+ macrophages peaked 7 days after coronary occlusion. Myeloid cell-specific Smad7 loss in mice had no effects on homeostatic functions and did not affect baseline macrophage gene expression. RNA-seq predicted that Smad7 may promote TREM1-mediated inflammation in infarct macrophages. However, these alterations in the transcriptional profile of macrophages were associated with a modest and transient reduction in infarct myofibroblast infiltration, and did not affect dysfunction, chamber dilation, scar remodeling, collagen deposition, and macrophage recruitment. In vitro, RNA-seq and PCR arrays showed that TGF-ß has profound effects on macrophage profile, attenuating pro-inflammatory cytokine/chemokine expression, modulating synthesis of matrix remodeling genes, inducing genes associated with sphingosine-1 phosphate activation and integrin signaling, and inhibiting cholesterol biosynthesis genes. However, Smad7 loss did not significantly affect TGF-ß-mediated macrophage responses, modulating synthesis of only a small fraction of TGF-ß-induced genes, including Itga5, Olfml3, and Fabp7. Our findings suggest a limited role for macrophage Smad7 in regulation of post-infarction inflammation and repair, and demonstrate that the anti-inflammatory effects of TGF-ß in macrophages are not restrained by endogenous Smad7 induction.

Deciphering phase evolution in complex metal oxide thin films via high-throughput materials synthesis and characterization.

Discovery of structure-property relationships in thin film alloys of complex metal oxides enabled by high-throughput materials synthesis and characterization facilities is demonstrated here with a case-study. Thin films of binary transition metal oxides (Ti-Zn) are prepared by pulsed laser deposition with continuously varying Ti:Zn ratio, creating combinatorial samples for exploration of the properties of this material family. The atomic structure and electronic properties are probed by spatially resolved techniques including x-ray absorption near edge structures (XANES) and x-ray fluorescence (XRF) at the Ti and Zn K-edge, x-ray diffraction, and spectroscopic ellipsometry. The observed properties as a function of Ti:Zn ratio are resolved into mixtures of five distinguishable phases by deploying multivariate curve resolution analysis on the XANES spectral series, under constraints set by results from the other characterization techniques. First-principles computations based on density function theory connect the observed properties of each distinct phase with structural and spectral characteristics of crystalline polymorphs of Ti-Zn oxide. Continuous tuning of the optical absorption edge as a function of Ti:Zn ratio, including the unusual observation of negative optical bowing, exemplifies a functional property of the film correlated to the phase evolution.

Association between sun-protective behaviors and hypertension: a cross-sectional study from National Health and Nutrition Examination Survey 2009 to 2014.

BACKGROUND: In previous studies, sun-protective behaviors increased cardiovascular incidence. Our present article is to further analyze the potential relationship between sun-protective behaviors (staying in the shade, wearing long-sleeved clothing, and applying sunscreen) and hypertension. METHOD: The present cross-sectional study evaluated 8,613 participants (aged 20-60 years) from the National Health and Nutrition Examination Survey (NHANES) obtained between 2009 and 2014. We performed multiple logistic regression analysis to examine the relationship between sun-protective behaviors and hypertension. Subgroup analysis was then performed. Multiple linear regression analysis was utilized to examine the relationship of sun-protective behaviors and each sun-protective behavior with systolic and diastolic blood pressure, stratified by sex and race. RESULTS: A total of 8,613 participants (weighted n = 127,909,475) were applied in our study, including 1,694 hypertensive subjects. Our study demonstrated that sun-protective behaviors of the 2-3 category were associated with increased risk of hypertension, but not with higher systolic and diastolic blood pressure. In subgroup analysis, men, Mexican American, and 25 < BMI ≤ 30 who reported sun-protective behaviors (2-3) were prone to hypertension. Multiple linear regression models showed that non-Hispanic white men with sun-protective behaviors (2-3) were positively associated with systolic and diastolic blood pressure. The association between other-Hispanic men with frequent wearing long-sleeved clothing and diastolic blood pressure was positively correlated. CONCLUSION: Sun-protective behaviors of the 2-3 category could increase the incidence of hypertension, but not increase systolic and diastolic blood pressure. We only found that non-Hispanic white men who reported sun-protective behaviors (2-3) were positively associated with systolic and diastolic blood pressure. These findings suggested that excessive sun-protective behaviors should be avoided.

Integrins in cardiac fibrosis.

Cells sense mechanical stress and changes in their matrix environment through the integrins, a family of heterodimeric surface receptors that bind to extracellular matrix ligands and trigger cytoskeletal remodeling, while transducing a wide range of intracellular signals. Integrins have been extensively implicated in regulation of inflammation, repair and fibrosis in many different tissues. This review manuscript discusses the role of integrin-mediated cascades in myocardial fibrosis. In vitro studies have demonstrated that ß1 and αv integrins play an important role in fibrogenic conversion of cardiac fibroblast, acting through direct stimulation of FAK/Src cascades, or via accentuation of growth factor signaling. Fibrogenic actions of αv integrins may be mediated, at least in part, through pericellular activation of latent TGF-ß stores. In vivo evidence supporting the role of integrin heterodimers in fibrotic cardiac remodeling is limited to associative evidence, and to experiments using pharmacologic inhibitors, or global loss-of-function approaches. Studies documenting in vivo actions of integrins on fibroblasts using cell-specific strategies are lacking. Integrin effects on leukocytes may also contribute to the pathogenesis of fibrotic myocardial responses by mediating recruitment and activation of fibrogenic macrophages. The profile and role of integrins in cardiac fibrosis may be dependent on the underlying pathologic condition. Considering their cell surface localization and the availability of small molecule inhibitors, integrins may be attractive therapeutic targets for patients with heart failure associated with prominent fibrotic remodeling.

Differential effects of Smad2 and Smad3 in regulation of macrophage phenotype and function in the infarcted myocardium.

TGF-ßs regulate macrophage responses, by activating Smad2/3. We have previously demonstrated that macrophage-specific Smad3 stimulates phagocytosis and mediates anti-inflammatory macrophage transition in the infarcted heart. However, the role of macrophage Smad2 signaling in myocardial infarction remains unknown. We studied the role of macrophage-specific Smad2 signaling in healing mouse infarcts, and we explored the basis for the distinct effects of Smad2 and Smad3. In infarct macrophages, Smad3 activation preceded Smad2 activation. In contrast to the effects of Smad3 loss, myeloid cell-specific Smad2 disruption had no effects on mortality, ventricular dysfunction and adverse remodeling, after myocardial infarction. Macrophage Smad2 loss modestly, but transiently increased myofibroblast density in the infarct, but did not affect phagocytic removal of dead cells, macrophage infiltration, collagen deposition, and scar remodeling. In isolated macrophages, TGF-ß1, -ß2 and -ß3, activated both Smad2 and Smad3, whereas BMP6 triggered only Smad3 activation. Smad2 and Smad3 had similar patterns of nuclear translocation in response to TGF-ß1. RNA-sequencing showed that Smad3, and not Smad2, was the main mediator of transcriptional effects of TGF-ß on macrophages. Smad3 loss resulted in differential expression of genes associated with RAR/RXR signaling, cholesterol biosynthesis and lipid metabolism. In both isolated bone marrow-derived macrophages and in infarct macrophages, Smad3 mediated synthesis of Nr1d2 and Rara, two genes encoding nuclear receptors, that may be involved in regulation of their phagocytic and anti-inflammatory properties. In conclusion, the in vivo and in vitro effects of TGF-ß on macrophage function involve Smad3, and not Smad2.

Histone hyperacetylation mediates enhanced IL-1ß production in LPS/IFN-γ-stimulated macrophages.

Under the condition of lipopolysaccharide (LPS)/interferon (IFN)-γ activation, macrophage metabolism is converted from oxidative phosphorylation to glycolysis. In the present work, we analysed whether glycolysis could affect interleukin (IL)-1ß expression through altering histone acetylation levels in mouse bone marrow-derived macrophages. Immunocytochemistry and Western blot analysis are used to characterize histone acetylation in macrophages stimulated by LPS/IFN-γ. Real-time polymerase chain reaction and enzyme-linked immunosorbent assay were used to determine IL-1ß production. The metabolism of macrophages was monitored in real-time by the Seahorse test. Our results showed that glycolytic metabolism could enhance histone acetylation and promote IL-1ß production in LPS/IFN-γ-activated macrophages. Moreover, increased production of IL-1ß by glycolysis was mediated through enhanced H3K9 acetylation. Importantly, it was found that a high dose of histone deacetylase inhibitor could also significantly increase the expression of IL-1ß in the absence of glycolytic metabolism. In conclusion, this study demonstrates that glycolytic metabolism could regulate IL-1ß expression by increasing histone acetylation levels in LPS/IFN-γ-stimulated macrophages.

Inhibition of TRPA1 Promotes Cardiac Repair in Mice After Myocardial Infarction.

Recent studies have shown that TRPA1, a nonselective cation channel with high permeability to calcium, is expressed in many tissues of the cardiovascular system and is involved in the pathogenesis of many cardiovascular diseases. However, the role of TRPA1 in cardiac repair after myocardial infarction (MI) has not been clearly defined. The aim of this study was to confirm whether inhibition of TRPA1 could attenuate MI-induced cardiac ischemia injury. The C57BL/6 mice were subjected to ligation of the left anterior descending coronary artery and treated with TRPA1-specific inhibitor HC-030031 (HC) for 4 weeks. Echocardiography was performed to assess cardiac function. The results showed that HC significantly attenuated MI-induced cardiac dysfunction 4 weeks after MI. Similarly, HC reduced cardiac fibrosis and cell apoptosis after MI and significantly increased angiogenesis in the border zone of the infarct. In vitro, we found that HC promoted the proliferation and migration of human umbilical vein endothelial cells (HUVECs). Importantly, HC treatment decreased phosphatase and tensin homolog expression and augmented the expression of phosphorylated Akt in the myocardium post MI and HUVECs. However, treatment of HUVECs with a PI3K inhibitor, LY294002, before HC administration almost completely abolished HC-induced migration in HUVECs. In conclusion, we demonstrate that the inhibition of TRPA1 promotes angiogenesis after MI, thereby alleviating myocardial ischemia injury via mechanisms involving inhibition of phosphatase and tensin homolog expression and subsequent activation of the PI3K/Akt signaling.

miR-221-3p inhibits oxidized low-density lipoprotein induced oxidative stress and apoptosis via targeting a disintegrin and metalloprotease-22.

Oxidized low-density lipoprotein (ox-LDL)-induced oxidative stress and apoptosis are considered as a critical contributor to atherosclerosis. MicroRNAs (miRNAs) have been reported versatile functions in all biological processes via directly suppressing target messenger RNA at a posttranscriptional level. Although miRNA-221 has been implied to be involved in the regulation of atherosclerosis, the underlying mechanism remains unclear. Here, we showed that ox-LDL treatment remarkably suppressed the expression of miR-221-3p in a concentration-dependent and time-dependent manner. Transfection of miR-221-3p mimic significantly reduced the foam cell formation and expression of lipid biomarkers, while transfection of the miR-221-3p inhibitor showed completely opposite effects. Moreover, miR-221-3p was also found to inhibit the process of cell apoptosis in macrophages. A disintegrin and metalloprotease-22 (ADAM22) is predicted as a direct target of miR-221-3p, and silencing AMAM22 resulted in a reduced foam cell formation and cell apoptosis. Furthermore, silencing AMAM22 restored the stimulatory effect of the miR-221-3p inhibitor in ox-LDL-induced foam cell formation and apoptosis. These findings suggest that miR-221-3p inhibits ox-LDL and apoptosis via directly targeting ADAM22.

Low-Dose Mildronate-Derived Lipidoids for Efficient mRNA Vaccine Delivery with Minimal Inflammation Side Effects.

mRNA vaccines have been revolutionizing disease prevention and treatment. However, their further application is hindered by inflammatory side effects, primarily caused by delivery systems such as lipid nanoparticles (LNPs). In response to this issue, we prepared cationic lipids (mLPs) derived from mildronate, a small-molecule drug, and subsequently developed the LNP (mLNP-69) comprising a low dose of mLP. Compared with the LNP (sLNP) based on SM-102, a commercially available ionizable lipid, mLNP-69 ensures effective mRNA delivery while significantly reducing local inflammation. In preclinical prophylactic and therapeutic B16-OVA melanoma models, mLNP-69 demonstrated successful mRNA cancer vaccine delivery in vivo, effectively preventing tumor occurrence or impeding tumor progression. The results suggest that the cationic lipids derived from mildronate, which exhibit efficient delivery capabilities and minimal inflammatory side effects, hold great promise for clinical application.

Surpassing millisecond coherence in on chip superconducting quantum memories by optimizing materials and circuit design.

The performance of superconducting quantum circuits for quantum computing has advanced tremendously in recent decades; however, a comprehensive understanding of relaxation mechanisms does not yet exist. In this work, we utilize a multimode approach to characterizing energy losses in superconducting quantum circuits, with the goals of predicting device performance and improving coherence through materials, process, and circuit design optimization. Using this approach, we measure significant reductions in surface and bulk dielectric losses by employing a tantalum-based materials platform and annealed sapphire substrates. With this knowledge we predict the relaxation times of aluminum- and tantalum-based transmon qubits, and find that they are consistent with experimental results. We additionally optimize device geometry to maximize coherence within a coaxial tunnel architecture, and realize on-chip quantum memories with single-photon Ramsey times of 2.0 - 2.7 ms, limited by their energy relaxation times of 1.0 - 1.4 ms. These results demonstrate an advancement towards a more modular and compact coaxial circuit architecture for bosonic qubits with reproducibly high coherence.

Ultrathin Magnesium-Based Coating as an Efficient Oxygen Barrier for Superconducting Circuit Materials.

Scaling up superconducting quantum circuits based on transmon qubits necessitates substantial enhancements in qubit coherence time. Over recent years, tantalum (Ta) has emerged as a promising candidate for transmon qubits, surpassing conventional counterparts in terms of coherence time. However, amorphous surface Ta oxide layer may introduce dielectric loss, ultimately placing a limit on the coherence time. In this study, a novel approach for suppressing the formation of tantalum oxide using an ultrathin magnesium (Mg) capping layer is presented. Synchrotron-based X-ray photoelectron spectroscopy studies demonstrate that oxide is confined to an extremely thin region directly beneath the Mg/Ta interface. Additionally, it is demonstrated that the superconducting properties of thin Ta films are improved following the Mg capping, exhibiting sharper and higher-temperature transitions to superconductive and magnetically ordered states. Moreover, an atomic-scale mechanistic understanding of the role of the capping layer in protecting Ta from oxidation is established based on computational modeling. This work provides valuable insights into the formation mechanism and functionality of surface tantalum oxide, as well as a new materials design principle with the potential to reduce dielectric loss in superconducting quantum materials. Ultimately, the findings pave the way for the realization of large-scale, high-performance quantum computing systems.

Association between triglyceride glucose-body mass index and heart failure in subjects with diabetes mellitus or prediabetes mellitus: a cross-sectional study.

Background: The triglyceride glucose-body mass index (TyG-BMI) is a surrogate indicator of insulin resistance. However, the association of TyG-BMI with heart failure (HF) in individuals with diabetes mellitus or prediabetes mellitus is unknown. Methods: This study included 7,472 participants aged 20-80 years old with prediabetes or diabetes from the National Health and Nutrition Examination Survey (2007-2018). The TyG-BMI was calculated as Ln [triglyceride (mg/dL) × fasting blood glucose (mg/dL)/2] × BMI, and individuals were categorized into tertiles based on TyG-BMI levels. The relationship of TyG-BMI with HF was analyzed using multiple logistic regression models. Subgroup analyses were stratified by gender, age, hypertension, and diabetes mellitus status. Results: This cross-sectional study had 7,472 participants (weighted n = 111,808,357), including 329 HF participants. Participants with a high TyG-BMI were prone to HF. The highest tertile group with a fully adjusted model was more likely to have HF compared to the lowest tertile group (odds ratio [OR], 2.645; 95% CI, 1.529-4.576). Restricted cubic spline analysis showed a significant dose-response relationship between TyG-BMI and HF (P < 0.001). In subgroup analyses, similar results were seen in terms of age (≥50 years old), gender, hypertension, and diabetes mellitus status. Conclusion: A high TyG-BMI is significantly associated with HF risk in participants with diabetes mellitus or prediabetes mellitus.

Protective effects of macrophage-specific integrin α5 in myocardial infarction are associated with accentuated angiogenesis.

Macrophages sense changes in the extracellular matrix environment through the integrins and play a central role in regulation of the reparative response after myocardial infarction. Here we show that macrophage integrin α5 protects the infarcted heart from adverse remodeling and that the protective actions are associated with acquisition of an angiogenic macrophage phenotype. We demonstrate that myeloid cell- and macrophage-specific integrin α5 knockout mice have accentuated adverse post-infarction remodeling, accompanied by reduced angiogenesis in the infarct and border zone. Single cell RNA-sequencing identifies an angiogenic infarct macrophage population with high Itga5 expression. The angiogenic effects of integrin α5 in macrophages involve upregulation of Vascular Endothelial Growth Factor A. RNA-sequencing of the macrophage transcriptome in vivo and in vitro followed by bioinformatic analysis identifies several intracellular kinases as potential downstream targets of integrin α5. Neutralization assays demonstrate that the angiogenic actions of integrin α5-stimulated macrophages involve activation of Focal Adhesion Kinase and Phosphoinositide 3 Kinase cascades.

Chemical Profiles of the Oxides on Tantalum in State of the Art Superconducting Circuits.

Over the past decades, superconducting qubits have emerged as one of the leading hardware platforms for realizing a quantum processor. Consequently, researchers have made significant effort to understand the loss channels that limit the coherence times of superconducting qubits. A major source of loss has been attributed to two level systems that are present at the material interfaces. It is recently shown that replacing the metal in the capacitor of a transmon with tantalum yields record relaxation and coherence times for superconducting qubits, motivating a detailed study of the tantalum surface. In this work, the chemical profile of the surface of tantalum films grown on c-plane sapphire using variable energy X-ray photoelectron spectroscopy (VEXPS) is studied. The different oxidation states of tantalum that are present in the native oxide resulting from exposure to air are identified, and their distribution through the depth of the film is measured. Furthermore, it is shown how the volume and depth distribution of these tantalum oxidation states can be altered by various chemical treatments. Correlating these measurements with detailed measurements of quantum devices may elucidate the underlying microscopic sources of loss.

Identification of macrophages in normal and injured mouse tissues using reporter lines and antibodies.

Reliable tools for macrophage identification in mouse tissues are critical for studies investigating inflammatory and reparative responses. Transgenic reporter mice and anti-macrophage antibodies have been used as "specific pan-macrophage" markers in many studies; however, organ-specific patterns of expression and non-specific labeling of other cell types, such as fibroblasts, may limit their usefulness. Our study provides a systematic comparison of macrophage labeling patterns in normal and injured mouse tissues, using the CX3CR1 and CSF1R macrophage reporter lines and anti-macrophage antibodies. Moreover, we tested the specificity of macrophage antibodies using the fibroblast-specific PDGFR[Formula: see text] reporter line. Mouse macrophages exhibit organ-specific differences in expression of macrophage markers. Hepatic macrophages are labeled for CSF1R, Mac2 and F4/80, but lack CX3CR1 expression, whereas in the lung, the CSF1R+/Mac2+/Mac3+ macrophage population is not labeled with F4/80. In the splenic red pulp, subpopulations of CSF1R+/F4/80+/Mac3+cells were labeled with Mac2, CX3CR1 and lysozyme M. In the kidney, Mac2, Mac3 and lysozyme M labeled a fraction of the CSF1R+ and CX3CR1+ macrophages, but also stained tubular epithelial cells. In normal hearts, the majority of CSF1R+ and CX3CR1+ cells were not detected with anti-macrophage antibodies. Myocardial infarction was associated with marked expansion of the CSF1R+ and CX3CR1+ populations that peaked during the proliferative phase of cardiac repair, and also expressed Mac2, Mac3 and lysozyme M. In normal mouse tissues, a small fraction of cells labeled with anti-macrophage antibodies were identified as PDGFR[Formula: see text]+ fibroblasts, using a reporter system. The population of PDGFR[Formula: see text]+ cells expressing macrophage markers expanded following injury, likely reflecting emergence of cellular phenotypes with both fibroblast and macrophage characteristics. In conclusion, mouse macrophages exhibit remarkable heterogeneity. Selection of the most appropriate markers for identification of macrophages in mouse tissues is dependent on the organ and the pathologic condition studied.

Enhancing efficiency of perovskite solar cells from surface passivation of Co2+ doped CuGaO2 nanocrystals.

Before completely applying inorganic materials as hole transport materials (HTM) for perovskite solar cells (PSCs), modifying devices with inorganic oxides that have the potential as inorganic hole transporters is an effective way to improve device performance and stability. Co2+ doped CuGaO2 nanocrystals (Co-CuGaO2 NCs) with sizes about 20 nm are synthesized by hydrothermal method and used for surface passivation at the interface of perovskite (PVK)/2,2',7,7'-Tetrakis[N,N-di (4-methoxyphenyl) amino]-9,9'-spirobifluorene (spiroOMeTAD). Co-CuGaO2 NCs have a larger bandgap with lower valance band compared with spiroOMeTAD, which is more beneficial to the conduction of holes and the blocking of electrons. Furthermore, the Co-CuGaO2 has a lower valance band energy compared with the original CuGaO2, which reduces the energy gap between Co-CuGaO2 and PVK. Co-CuGaO2 NCs fully cover the upper surface of PVK, which helps prevent direct contact between PVK and oxygen and moisture. The Co-CuGaO2 NCs surface passivation also gives better hole transport as revealed by the ultraviolet photoelectron spectroscopy (UPS), steady-state photoluminescence (PL), and time-resolved photoluminescence (TRPL) data. When the concentration of Co-CuGaO2 NCs solution is set to 7.5 mg mL-1, the device exhibits a best PCE of 20.39% and maintains 84.34% of the initial power conversion efficiency (PCE) after stored 30 days under air atmosphere with 15 ±â€¯5% humidity.

High-efficiency and ultraviolet stable carbon-based CsPbIBr2 solar cells from single crystal three-dimensional anatase titanium dioxide nanoarrays with ultraviolet light shielding function.

TiO2 is commonly used to prepare electron transport layers (ETLs) in perovskite solar cells (PSCs). However, conventional TiO2 ETLs suffer from low electron mobility and charge recombination. Here, we report the direct growth of TiO2 ETLs on fluorine doped conductive (FTO) glasses with titanium tetrafluoride (TiF4) as the reactant by hydrothermal method. The TiO2 ETLs have pure anatase phase, single crystal structure and three-dimensional (3D) nanoarrays morphology. This 3D-TiO2 ETLs mainly consist of thermodynamically stable surfaces {101} and more reactive surfaces {001}. Compared with the conventional TiO2 ETLs, the 3D-TiO2 ETLs can effectively optimize energy level matching and charge transfer dynamics. The special morphology of 3D-TiO2 ETLs can well assist to form high quality CsPbIBr2 with larger crystal grains. The champion CsPbIBr2 PSC with 3D-TiO2 ETL achieves an efficiency as high as 10.65%, which is equal to the one with hole-transport and Au electrode structure (10.79%) and much higher than the pristine one (7.16%) with the conventional TiO2 ETL. Furthermore, the 3D-TiO2 ETLs show ultraviolet (UV) shielding function, which can effectively overcome the UV instability defect of conventional TiO2 ETLs and obviously enhance UV stability of CsPbIBr2 and the corresponding PSCs. Therefore, the 3D-TiO2 ETLs can be good candidates for preparing high-efficiency and UV stable carbon-based CsPbIBr2 PSCs.

Smad7 effects on TGF-ß and ErbB2 restrain myofibroblast activation and protect from postinfarction heart failure.

Repair of the infarcted heart requires TGF-ß/Smad3 signaling in cardiac myofibroblasts. However, TGF-ß-driven myofibroblast activation needs to be tightly regulated in order to prevent excessive fibrosis and adverse remodeling that may precipitate heart failure. We hypothesized that induction of the inhibitory Smad, Smad7, may restrain infarct myofibroblast activation, and we examined the molecular mechanisms of Smad7 actions. In a mouse model of nonreperfused infarction, Smad3 activation triggered Smad7 synthesis in α-SMA+ infarct myofibroblasts, but not in α-SMA-PDGFRα+ fibroblasts. Myofibroblast-specific Smad7 loss increased heart failure-related mortality, worsened dysfunction, and accentuated fibrosis in the infarct border zone and in the papillary muscles. Smad7 attenuated myofibroblast activation and reduced synthesis of structural and matricellular extracellular matrix proteins. Smad7 effects on TGF-ß cascades involved deactivation of Smad2/3 and non-Smad pathways, without any effects on TGF-ß receptor activity. Unbiased transcriptomic and proteomic analysis identified receptor tyrosine kinase signaling as a major target of Smad7. Smad7 interacted with ErbB2 in a TGF-ß-independent manner and restrained ErbB1/ErbB2 activation, suppressing fibroblast expression of fibrogenic proteases, integrins, and CD44. Smad7 induction in myofibroblasts serves as an endogenous TGF-ß-induced negative feedback mechanism that inhibits postinfarction fibrosis by restraining Smad-dependent and Smad-independent TGF-ß responses, and by suppressing TGF-ß-independent fibrogenic actions of ErbB2.