Discovery and functional investigation of BMP4 as a new causative gene for human congenital heart disease.

OBJECTIVE: Aggregating evidence highlights the strong genetic basis underpinning congenital heart disease (CHD). Here BMP4 was chosen as a prime candidate gene causative of human CHD predominantly because BMP4 was amply expressed in the embryonic hearts and knockout of Bmp4 in mice led to embryonic demise mainly from multiple cardiovascular developmental malformations. The aim of this retrospective investigation was to discover a novel BMP4 mutation underlying human CHD and explore its functional impact. METHODS: A sequencing examination of BMP4 was implemented in 212 index patients suffering from CHD and 236 unrelated non-CHD individuals as well as the family members available from the proband carrying a discovered BMP4 mutation. The impacts of the discovered CHD-causing mutation on the expression of NKX2-5 and TBX20 induced by BMP4 were measured by employing a dual-luciferase analysis system. RESULTS: A new heterozygous BMP4 mutation, NM_001202.6:c.318T>G;p.(Tyr106*), was found in a female proband affected with familial CHD. Genetic research of the mutation carrier's relatives unveiled that the truncating mutation was in co-segregation with CHD in the pedigree. The nonsense mutation was absent from 236 unrelated non-CHD control persons. Quantitative biologic measurement revealed that Tyr106*-mutant BMP4 failed to induce the expression of NKX2-5 and TBX20, two genes whose expression is lost in CHD. CONCLUSION: The current findings indicate BMP4 as a new gene predisposing to human CHD, allowing for improved prenatal genetic counseling along with personalized treatment of CHD patients.

Self-Catalyzed, Visible-Light-Induced Selective C3-H Aroylation of Quinoxalin-2(1H)-ones with Arylaldehydes by Air as an Oxidant.

A self-catalyzed, visible-light-induced, directly selective C3-H aroylation of quinoxalin-2(1H)-ones via energy transfer and hydrogen atom transfer (HAT) catalysis has been developed. The method is highly atom-economical, eco-friendly, and easy to handle. Notably, the reaction proceeded efficiently with ambient air as the sole oxidant at room temperature.

Discovery of BMP10 as a new gene underpinning congenital heart defects.

OBJECTIVE: Aggregating evidence convincingly establishes the predominant genetic basis underlying congenital heart defects (CHD), though the heritable determinants contributing to CHD in the majority of cases remain elusive. In the current investigation, BMP10 was selected as a prime candidate gene for human CHD mainly due to cardiovascular developmental abnormalities in Bmp10-knockout animals. The objective of this retrospective study was to identify a new BMP10 mutation responsible for CHD and characterize the functional effect of the identified CHD-causing BMP10 mutation. METHODS: Sequencing assay of BMP10 was fulfilled in a cohort of 276 probands with various CHD and a total of 288 non-CHD volunteers. The available family members from the proband harboring an identified BMP10 mutation were also BMP10-genotyped. The effect of the identified CHD-causative BMP10 mutation on the transactivation of TBX20 and NKX2.5 by BMP10 was quantitatively analyzed in maintained HeLa cells utilizing a dual-luciferase reporter assay system. RESULTS: A novel heterozygous BMP10 mutation, NM_014482.3:c.247G>T;p.(Glu83*), was identified in one proband with patent ductus arteriosus (PDA), which was confirmed to co-segregate with the PDA phenotype in the mutation carrier's family. The nonsense mutation was not observed in 288 non-CHD volunteers. Functional analysis unveiled that Glu83*-mutant BMP10 had no transactivation on its two representative target genes TBX20 and NKX2.5, which were both reported to cause CHD. CONCLUSION: These findings provide strong evidence indicating that genetically compromised BMP10 predisposes human beings to CHD, which sheds light on the new molecular mechanism that underlies CHD and allows for antenatal genetic counseling and individualized precise management of CHD.

Efficient pollutant degradation by peroxymonosulfate activated by a Co/Mn metal-organic framework.

In this work, a three-dimensional bimetallic metal-organic framework (BMOF), BUC-101 (Co/Mn-H6chhc, H6chhc = cis-1,2,3,4,5,6-cyclohexane-hexacarboxylic acid, BUC = Beijing University of Civil Engineering and Architecture) was synthesized by a one-pot solvothermal method and characterized in detail by single crystal X-ray diffraction (SCXRD), Fourier transform infrared spectroscopy (FTIR), X-ray photoelectron spectroscopy (XPS) and scanning electron microscopy (SEM) element mapping analysis. BUC-101 showed excellent catalytic peroxymonosulfate (PMS) activation performance to degrade rhodamine B (RhB) without energy input. In addition, BUC-101 can maintain good stability and recyclability during the PMS activation processes, in which 99.9% RhB degradation efficiencies could be accomplished in 5 operational runs. The possible PMS activation and RhB degradation mechanisms of the BUC-101/PMS system were proposed and affirmed.

Genistein is effective in inhibiting Orf virus infection in vitro by targeting viral RNA polymerase subunit RPO30 protein.

Orf virus (ORFV), a typical member of the genus Parapoxvirus, Poxvirus family, causes a contagious pustular dermatitis in sheep, goats, and humans. Poxviruses encode a multisubunit DNA-dependent RNA polymerase (vRNAP) that carries out viral gene expression in the host cytoplasm, which is a viral factor essential to poxvirus replication. Due to its vital role in viral life, vRNAP has emerged as one of the potential drug targets. In the present study, we investigated the antiviral effect of genistein against ORFV infection. We provided evidence that genistein exerted antiviral effect through blocking viral genome DNA transcription/replication and viral protein synthesis and reducing viral progeny, which were dosedependently decreased in genistein-treated cells. Furthermore, we identified that genistein interacted with the vRNAP RPO30 protein by CETSA, molecular modeling and Fluorescence quenching, a novel antiviral target for ORFV. By blocking vRNAP RPO30 protein using antibody against RPO30, we confirmed that the inhibitory effect exerted by genistein against ORFV infection is mediated through the interaction with RPO30. In conclusion, we demonstrate that genistein effectively inhibits ORFV transcription in host cells by targeting vRNAP RPO30, which might be a promising drug candidate against poxvirus infection.

Somatic GATA4 mutation contributes to tetralogy of Fallot.

Tetralogy of Fallot (TOF) is the most prevalent cyanotic congenital heart pathology and causes infant morbidity and mortality worldwide. GATA-binding protein 4 (GATA4) serves as a pivotal transcriptional factor for embryonic cardiogenesis and germline GATA4 mutations are causally linked to TOF. However, the effects of somatic GATA4 mutations on the pathogenesis of TOF remain to be ascertained. In the present study, sequencing assay of GATA4 was performed utilizing genomic DNA derived from resected heart tissue specimens as well as matched peripheral blood specimens of 62 patients with non-familial TOF who underwent surgical treatment for TOF. Sequencing of GATA4 was also performed using the heart tissue specimens as well as matched peripheral venous blood samples of 68 sporadic cases who underwent heart valve displacement because of rheumatic heart disorder and the peripheral venous whole blood samples of 216 healthy subjects. The function of the mutant was explored by dual-luciferase activity analysis. Consequently, a new GATA4 mutation, NM_002052.5:c.708T>G;p.(Tyr236*), was found in the heart tissue of one patient with TOF. No mutation was detected in the heart tissue of the 68 cases suffering from rheumatic heart disorder or in the venous blood samples of all 346 individuals. GATA4 mutant failed to transactivate its target gene, myosin heavy chain 6. Additionally, this mutation nullified the synergistic transactivation between GATA4 and T-box transcription factor 5 or NK2 homeobox 5, two genes causative for TOF. Somatic GATA4 mutation predisposes TOF, highlighting the significant contribution of somatic variations to the molecular pathogenesis underpinning TOF.

Can China's vehicular emissions regulation reduce air pollution?-a quasi-natural experiment based on the latest National Vehicular Emissions Standard (stage-VI).

The existing evidence on the environmental effects of vehicular emissions regulation almost comes from developed countries, but the effectiveness of this policy tool in developing countries, especially in China, remains unclear. This study, for the first time, examined the mitigating effects of China's vehicular emissions regulation on air pollution at the prefecture level cities, by using the latest implementation of China's National Vehicular Emissions Standard VI (CHINA-VI) as a quasi-natural experimental process of policy shocks. To this end, monthly data from 2018 to 2020 was applied to construct a difference-in-differences (DID) model. The results showed that pilot cities' air quality index (AQI) significantly decreased by 4.74 compared to non-pilot cities after the implementation of CHINA-VI. Also, the concentration of PM2.5, PM10, and O3 has decreased by 3.6 µg∕m3, 6.4 µg∕m3, and 3.0 µg∕m3, respectively, which means the new China's vehicular emissions regulation has comprehensively improved air quality. The findings are still valid after a series of robustness tests using different estimation methods such as PSM-DID and IV-2SLS. In addition, we also found heterogeneity in the environmental performance of CHINA-VI across cities. Specifically, cities with lower levels of green finance development and public environmental concern showed a greater emissions reduction effect, but smart cities showed a greater emissions reduction effect than non-smart cities.

A polyphenol and ε-polylysine functionalized bacterial cellulose/PVA multifunctional hydrogel for wound healing.

Hydrogels for wound dressings have recently attracted considerable attention in the field of biomedical materials. Developing hydrogel dressings with multiple functions, including good antibacterial, mechanical and adhesive properties, to enhance wound regeneration is significant for clinical applications. To this end, a novel hydrogel wound dressing (PB-EPL/TA@BC) was developed, which was prepared by incorporating bacterial cellulose (BC) modified with tannic acid and ε-polylysine (EPL) into a PVA and borax matrix through a simple method without introducing any other chemical reagents. The hydrogel exhibited good adhesion (8.8 ± 0.2 kPa) to porcine skin, and the mechanical properties were significantly improved after adding BC. Meanwhile, it showed good inhibition against Escherichia coli, Staphylococcus aureus and Methicillin-resistant Staphylococcus aureus (84.1 ± 2.6 %, 86.0 ± 2.3 % and 80.7 ± 4.5 %) in vitro and Methicillin-resistant Staphylococcus aureus (MRSA) in vivo without the use of antibiotics, ensuring that the process of wound repair with a sterile environment. The hydrogel also presented good cytocompatibility and biocompatibility and could achieve hemostasis within 120 s. The in vivo experiments indicated that hydrogel could not only instantly complete hemostasis of the injured liver models but also obviously promote wound healing in a full-thickness skin. Furthermore, the hydrogel accelerated wound healing process by reducing inflammation promoting collagen deposition compared with commercial Tegaderm™ films. Therefore, the hydrogel is a promising high-end dressing material for wound hemostasis and repair for to enhance the wound healing.

Enhanced hydrophobic ZSM-5 with high capacity for toluene capture under high-humidity conditions.

Industrial volatile organic compounds (VOCs) have the characteristics of large displacement and high humidity. The problem of water resistance of the adsorbent in treating VOCs by adsorption method under high humidity conditions needs to be solved urgently. Herein, methyl triethoxysilane (CH3Si(C2H5O)3) and methyl trimethoxysilane (CH3Si(CH3O)3) are used for hydrophobic modification of ZSM-5, and its adsorption properties for toluene are studied under high-humidity conditions. Fourier infrared spectroscopy and X-ray photoelectron spectroscopy indicate that the hydrophobic groups -CH3 and -CH2- are successfully grafted onto the surface of the ZSM-5. The adsorption-desorption results of toluene show that the hydrophobicity of the modified ZSM-5 is remarkably improved, and the adsorption capacity for toluene is almost 6.5 times higher than that of original ZSM-5 at 80 % relative humidity. The mechanism of surface hydrophobicity modification of ZSM-5 was further investigated and found that the silicone hydroxyl group on the surface of the material reacted with the modifier to graft the hydrophobic group onto the surface of the material, which improved the hydrophobic property of the material. Moreover, the universality of the hydrophobic modification method has been proved feasible in commercial ZSM-5. Therefore, this work provides an important theory and reference for improving the hydrophobic properties of ZSM-5 molecular sieve.

Construction of Microporous Zincophilic Interface for Stable Zn Anode.

Aqueous zinc ion batteries (AZIBs) are promising electrochemical energy storage devices due to their high theoretical specific capacity, low cost, and environmental friendliness. However, uncontrolled dendrite growth poses a serious threat to the reversibility of Zn plating/stripping, which impacts the stability of batteries. Therefore, controlling the disordered dendrite growth remains a considerable challenge in the development of AZIBs. Herein, a ZIF-8-derived ZnO/C/N composite (ZOCC) interface layer was constructed on the surface of the Zn anode. The homogeneous distribution of zincophilic ZnO and the N element in the ZOCC facilitates directional Zn deposition on the (002) crystal plane. Moreover, the conductive skeleton with a microporous structure accelerates Zn2+ transport kinetics, resulting in a reduction in polarization. As a result, the stability and electrochemical properties of AZIBs are improved. Specifically, the ZOCC@Zn symmetric cell sustains over 1150 h at 0.5 mA cm-2 with 0.25 mA h cm-2, while the ZOCC@Zn half-cell achieves an outstanding Coulombic efficiency of 99.79% over 2000 cycles. This work provides a simple and effective strategy for improving the lifespan of AZIBs.

Room-Temperature Continuous-Wave Microcavity Lasers from Solution-Processed Smooth Quasi-2D Perovskite Films with Low Thresholds.

Continuous-wave (CW) lasing in quasi-two-dimensional (2D) perovskite-based distributed feedback cavities has been achieved at room temperature; however, CW microcavity lasers comprising distributed Bragg reflectors (DBRs) have rarely been prepared using solution-processed quasi-2D perovskite films because the roughness of perovskite films significantly increases intersurface scattering loss in the microcavity. Herein, high-quality spin-coated quasi-2D perovskite gain films were prepared using an antisolvent to reduce roughness. The highly reflective top DBR mirrors were deposited via room-temperature e-beam evaporation to protect the perovskite gain layer. Lasing emission of the prepared quasi-2D perovskite microcavity lasers under CW optical pumping was clearly observed at room temperature, featuring a low threshold of ∼1.4 W cm-2 and beam divergence of ∼3.5°. It was concluded that these lasers originated from weakly coupled excitons. These results elucidate the importance of controlling the roughness of quasi-2D films to achieve CW lasing, thus facilitating the design of electrically pumped perovskite microcavity lasers.

Effects of ambient air pollution on cause-specific hospitalizations in Wuhan during 2017-2019.

BACKGROUND: Few studies have focused on the associations between air pollutants and multiple organ system diseases in the entire hospitalized population. The present study aims to explore the short-term effects of six routinely monitored air pollutants on the broad causes of hospital admissions and estimate the resulting hospital admission burdens. METHODS: Daily hospital admission records from 2017 to 2019 were obtained from the Wuhan Information center of Health and Family Planning. Generalized additive models (GAMs) were employed to evaluate the effects of air pollutants on the percent increase in the cause-specific daily number of hospital admissions. Increased hospital admission numbers, days, and expenses were also estimated. RESULTS: A total of 2636,026 hospital admissions were identified. We found that both PM2.5 and PM10 increased the risk of hospital admissions for most disease categories. Short-term exposure to PM2.5 was positively associated with hospitalizations of several rarely studied disease categories, such as diseases of the eye and adnexa (2.83%, 95%CI: 0.96-4.73%, P < 0.01) and diseases of the musculoskeletal system and connective tissue (2.17%, 95% CI: 0.88-3.47%, P < 0.001). NO2 was observed to have a robust effect on diseases of the respiratory system (1.36%, 95%CI: 0.74-1.98%, P < 0.001). CO was significantly associated with hospital admissions for six disease categories. Furthermore, each 10-µg/m3 increase in PM2.5 was associated with an annual increase of 13,444 hospital admissions (95% CI: 6239-20,649), 124,344 admission days (95% CI: 57,705-190,983), and 166-million-yuan admission expenses (95% CI: 77-255). CONCLUSION: Our study suggested that particulate matter (PM) had a short-term effect on hospital admissions of most major disease categories and resulted in a considerable hospital admission burden. In addition, the health effects of NO2 and CO emissions require more attention in megacities.

Discovery of GJC1 (Cx45) as a New Gene Underlying Congenital Heart Disease and Arrhythmias.

As the most prevalent type of birth malformation, congenital heart disease (CHD) gives rise to substantial mortality and morbidity as well as a socioeconomic burden. Although aggregating investigations highlight the genetic basis for CHD, the genetic determinants underpinning CHD remain largely obscure. In this research, a Chinese family suffering from autosomal dominant CHD (atrial septal defect) and arrhythmias was enrolled. A genome-wide genotyping with microsatellite markers followed by linkage assay as well as sequencing analysis was conducted. The functional effects of the discovered genetic mutation were characterized by dual patch-clamp electrophysiological recordings in N2A cells and propidium iodide uptake assays in HeLa cells. As a result, a novel genetic locus for CHD and arrhythmias was located on chromosome 17q21.31-q21.33, a 4.82-cM (5.12 Mb) region between two markers of D17S1861 and D17S1795. Sequencing assays of the genes at the mapped locus unveiled a novel heterozygous mutation in the GJC1 gene coding for connexin 45 (Cx45), NM_005497.4:c.550A>G;p.R184G, which was in co-segregation with the disease in the whole family and was not observed in 516 unrelated healthy individuals or gnomAD. Electrophysiological analyses revealed that the mutation significantly diminished the coupling conductance in homomeric cell pairs (R184G/R184G) and in cell pairs expressing either R184G/Cx45 or R184G/Cx43. Propidium iodide uptake experiments demonstrated that the Cx45 R184G mutation did not increase the Cx45 hemichannel function. This investigation locates a new genetic locus linked to CHD and arrhythmias on chromosome 17q21.31-q21.33 and indicates GJC1 as a novel gene predisposing to CHD and arrhythmias, implying clinical implications for prognostic risk assessment and personalized management of patients affected with CHD and arrhythmias.

Orf virus induces complete autophagy to promote viral replication via inhibition of AKT/mTOR and activation of the ERK1/2/mTOR signalling pathway in OFTu cells.

Orf virus (ORFV) is the causative agent of contagious ecthyma, which is an important zoonotic pathogen with a widespread distribution affecting sheep, goats and humans. Our previous research showed that autophagy can be induced in host cells by ORFV infection. However, the exact mechanism of ORFV-induced autophagy remains unknown. In this study, we investigated the underlying mechanisms of autophagy induced by ORFV in OFTu cells and the impact of autophagy on ORFV replication. By using specific autophagy inhibitors and activators, Western blotting, immunofluorescence and transmission electron microscopy imaging, we confirmed that ORFV infection triggered intracellular autophagosome accumulation and the activation of autophagic flux. Moreover, ORFV-induced autophagic activity was found to rely on an increase in the phosphorylation of tuberous sclerosis complex 2 (TSC2) and a decrease in the phosphorylation of mammalian target of rapamycin (mTOR), which is mediated by the suppression of the PI3K/AKT/mTOR signalling pathway and activation of the ERK1/2/mTOR signalling pathway. Furthermore, we investigated the role of mTOR-mediated autophagy during ORFV replication using pharmacological agents and demonstrated that ORFV-induced autophagy correlated positively with viral replication. Taken together, our data reveal the pathways of ORFV-induced autophagy and the impact of autophagy on ORFV replication, providing new insights into ORFV pathogenesis.

LINP1 represses unfolded protein response by directly inhibiting eIF2α phosphorylation to promote cutaneous squamous cell carcinoma.

BACKGROUND: Endoplasmic reticulum stress (ER stress) may destroy endoplasmic reticulum homeostasis (ER homeostasis) and leads to programmable cell death. Unfolded protein response (UPR) originally stimulated by ER stress is critical for the survival of tumor cells through trying to re-establish ER homeostasis as an adaption to harsh microenvironment. However, mechanisms involving key regulators in modulating UPR remain underexplored. METHODS: The expression of LINP1 in cutaneous squamous cell carcinoma (cSCC) tissues and cell lines was assessed. Subsequently, LINP1 was knocked out, knocked down or overexpressed in cSCC cells. CCK-8 assays, colony forming assays, transwell migration assays and invasiveness measurement by matrigel-coated transwell were performed to examine the role of LINP1 in cSCC development through gain-of-function and loss-of-function experiments. Transcriptomic sequencing (RNA-Seq) was conducted and indicated the key downstream signaling events regulated by LINP1 including UPR and apoptosis signaling. Furthermore, the direct interaction between LINP1 and eIF2α to modulate UPR and apoptosis was confirmed by RNA pulldown, RNA immunoprecipitation (RIP), ChIP-qPCR and in vitro phosphorylation assays. RESULTS: In this study, LncRNA in non-homologous end joining pathway 1 (LINP1) was identified to be one of the top ten highest-expressed LncRNAs in cSCC, the second most common cancer in the world. Functional studies using in vitro and in vivo models revealed that LINP1 functions as an oncogene to promote cell proliferation, colony formation, migration and invasiveness while inhibiting cell apoptosis in cSCC. Transcriptomic sequencing after knockdown of LINP1 indicated LINP1 negatively regulates UPR-related pathways involving key effectors for activating UPR and the apoptosis following the prolonged UPR. Mechanistic study showed LINP1 physically interacts with eIF2α to inhibit its phosphorylation for avoiding unmitigated UPR. Loss of LINP1 followed by enhanced eIF2α phosphorylation led to overactivated UPR and induced DDIT3 expression, contributing to ER stress-induced apoptosis and suppression of cSCC development. CONCLUSIONS: Our findings demonstrate a novel regulatory hierarchy of UPR by demonstrating LINP1 as a critical modulator for eIF2α phosphorylation and a suppressor of UPR-mediated apoptosis, which suggests a novel therapeutic target for cSCC treatment.

Recent Advances in the Synthesis of 3,n-Fused Tricyclic Indole Skeletons via Palladium-Catalyzed Domino Reactions.

3,n-fused (n = 4-7) tricyclic indoles are pervasive motifs, embedded in a variety of biologically active molecules and natural products. Thus, numerous catalytic methods have been developed for the synthesis of these skeletons over the past few decades. In particular, palladium-catalyzed transformations have received much attention in recent years. This review summarizes recent developments in the synthesis of these tricyclic indoles with palladium-catalyzed domino reactions and their applications in the total synthesis of representative natural products.

The trade-offs and synergies of the ecological-production-living functions of grassland in the Qilian mountains by ecological priority.

Grassland degradation has caused increasingly prominent conflict between ecological environment conservation and socioeconomic development in the Qilian Mountains, China. How to effectively trade-offs and synergies to ecological and socioeconomic is essential to achieving the sustainable development of the grassland ecosystem. However, few studies have addressed the trade-offs and synergies of grassland ecosystem services in terms of coupling the natural ecosystem and the socioeconomic system. Therefore, we constructed an index of the analyzed trade-offs and synergies of grassland ecosystem services from the perspective of "ecological-production-living" functions (EPLFs) and analyzed the spatial-temporal characteristics of grassland EPLF trade-off and synergy relationships based on the data from the implementation of three conservation policies in the Qilian Mountains from 2003 to 2020. The results showed evident spatial and temporal differentiation of the grassland EPLFs. The ecological function was consistent with the production function, trending upward initially and then decreasing. The living function showed a trend of continuous increase. The spatial pattern of grassland EPLFs showed that the northwest and southeast were more active than the middle of the Qilian Mountains, and the regional gradient difference was apparent. The trade-off and synergy relationships of grassland EPLFs have obvious spatial correlations as well; spatial differences were evident under different conservation policies. With national park construction, the synergistic relationship gradually weakened and the trade-off relationship gradually strengthened. These results suggest that the policy of ecological priority increased trade-offs and reduced synergies among EPLFs was not conducive to coupling and coordinating grassland EPLFs for development in the Qilian Mountains. Our study also demonstrates that maintaining moderate grassland grazing pressure and the appropriate number of herdsmen is crucial to sustainably develop the grassland ecosystem in the Qilian Mountains, and further research into coupling mechanisms for grassland EPLFs is needed to reduce trade-offs and increase synergies with grassland ecosystem services.

Resveratrol rescues cutaneous radiation-induced DNA damage via a novel AMPK/SIRT7/HMGB1 regulatory axis.

Cutaneous radiation injury (CRI) interrupts the scheduled process of radiotherapy and even compromises the life quality of patients. However, the current clinical options for alleviating CRI are relatively limited. Resveratrol (RSV) has been shown to be a promising protective agent against CRI; yet the mechanisms of RSV enhancing radioresistance were not fully elucidated and limited its clinical application. In this study, we demonstrate RSV promotes cutaneous radioresistance mainly through SIRT7. During ionizing radiation (IR) treatment, RSV indirectly phosphorylates and activates SIRT7 through AMPK, which is critical for maintaining the genome stability of keratinocytes. Immunoprecipitation and mass spectrometry identified HMGB1 to be the key interacting partner of SIRT7 to mediate the radioprotective function of RSV. Mechanistic study elucidated that SIRT7 interacts with and deacetylates HMGB1 to redistribute it into nucleus and "switch on" its function for DNA damage repair. Our findings establish a novel AMPK/SIRT7/HMGB1 regulatory axis that mediates the radioprotective function of RSV to alleviate IR-induced cutaneous DNA injury, providing an efficiently-curative option for patients with CRI during radiotherapy.

Morphology and Luminescence Regulation for CsPbBr3 Perovskite Light-Emitting Diodes by Controlling Growth of Low-Dimensional Phases.

At present, the high defect density and strong nonradiative recombination rate of all-inorganic cesium lead bromide (CsPbBr3) perovskite light-emitting diodes (PeLEDs) seriously inhibit the improvement of their quantum efficiency. In this paper, the addition of a short-chain additive, diethylammonium bromide (DEABr), aims to control the generation of a quasi-2D large n-phase to optimize the surface morphology and construct two-dimensional/three-dimensional (2D/3D) heterojunction perovskite structures to enhance the EL efficiency of PeLEDs. Through Kelvin probe force microscopy (KPFM) characterization, we confirmed that the 2D phase grains with a low potential are locally formed on the surface of the perovskite film under the action of DEABr. The existence of the 2D phase effectively improved the surface morphology and suppressed surface defects. In addition, the in situ constructed 2D/3D heterojunction perovskite structure further increases the exciton radiative recombination rate and significantly improves the electroluminescent performance. By optimizing its doping concentration, the optimal all-inorganic PeLED displays a current efficiency (CE) of 30.3 cd A-1, an external quantum efficiency (EQE) of 9.6%, and a maximum brightness of 32,500 cd m-2. According to our results, the formation of 2D structures on the surface of the CsPbBr3 film can improve surface morphology issues and optoelectronic properties of the film.

Association of NO2 with daily hospital admissions for mental disorders: Investigation of the modification effects of green spaces and long-term NO2 exposure.

Air pollution is a risk factor for increased hospital admissions due to mental disorders, while green spaces have been linked with better mental health. We linked daily hospital admission records from Wuhan's 74 municipal hospitals from 2017 to 2019 with modeled annual average NO2 concentrations and added data on the residential surrounding green spaces with 250 m and 500 m buffers based on the normalized difference vegetation index (NDVI) using a land use regression model (LUR). The conditional logistic regression model was used to estimate the acute effect of short-term NO2 exposure, and stratification analyses were applied to explore the modification effect of long-term NO2 exposure and green spaces by estimating the odds ratios in the single- and dual-environmental factor groups. A total of 42,705 hospital admissions for mental disorders were identified. Short-term exposure to NO2 was associated with an increased risk of hospital admission for mental disorders. A 10 µg/m3 increase in NO2 (lag01 day) was associated with an increase in hospital admissions of 2.86% (95% CI, 2.05-3.68) for the total mental disorders. Compared with patients in the "low-NDVI/low-NO2" group (ER = 2.27%, 95% CI, 0.27-4.31), patients in the "high-NDVI/low-NO2" group (ER = 1.93%, -0.10-3.99) showed a lower and insignificant increase in hospitalizations for the total mental disorders, while greenness had a slight moderating effect in the high-level long-term NO2 exposure areas. This study suggested that green spaces may moderate the acute effect of NO2 exposure for mental disorder hospitalizations, especially in low-level long-term NO2 exposure areas.