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Abstract Exposure to certain heavy metals has been demonstrated to be associated with a higher risk of preterm birth (PTB). However, studies focused on the effects of other metal mixtures were limited. A nested case‒control study enrolling 94 PTB cases and 282 controls was conducted. Metallic elements were detected in maternal plasma collected in the first trimester using inductively coupled plasma‒mass spectrometry. The effect of maternal exposure on the risk of PTB was investigated using logistic regression, least absolute shrinkage and selection operator, restricted cubic spline (RCS), quantile g computation (QGC) and Bayesian kernel machine regression (BKMR). Vanadium (V) and arsenic (As) were positively associated with PTB risk in the logistic model, and V remains positively associated in the multi‐exposure logistic model. QGC analysis determined V (69.42%) and nickel (Ni) (70.30%) as the maximum positive and negative contributors to the PTB risk, respectively. BKMR models further demonstrated a positive relationship between the exposure levels of the mixtures and PTB risk, and V was identified as the most important independent variable among the elements. RCS analysis showed an inverted U‐shape effect of V and gestational age, and plasma V more than 2.18 μg/L was considered a risk factor for shortened gestation length. Exposure to metallic elements mixtures consisting of V, As, cobalt, Ni, chromium and manganese in the first trimester was associated with an increased risk of PTB, and V was considered the most important factor in the mixtures in promoting the incidence of PTB.

Abstract Aims The study aims to provide comprehensive evidence for the selection of agents in type 2 diabetes mellitus (T2DM) patients with cardiovascular risk and summarize the lasted evidence for the cardiovascular effects of sodium glucose cotransporter‐2 inhibitor (SGLT2i) in patients with heart failure (HF). Methods and results Several online databases were searched. All studies that explored the cardiovascular effects of SGLT2i or glucagon‐like peptide 1 receptor agonist (GLP1‐RA) were screened and reviewed. A total of 38 studies were included. Compared with GLP1‐RA, the use of SGLT2i significantly reduced the risk of cardiovascular death [risk ratio (RR) = 0.59; 95% confidence interval (CI), 0.44–0.58], hospitalization of heart failure (HHF) (RR = 0.77; 95% CI, 0.74–0.80), death from any cause (RR = 0.64; 95% CI, 0.60–0.68), and myocardial infarction (MI) (RR = 0.81; 95% CI, 0.76–0.87). However, SGLT2i significantly increased the risk of stroke (RR = 1.10; 95% CI, 1.04–1.17). Compared with the control group, SGLT2i treatment reduced the risk of cardiovascular death by 14% (RR = 0.86; 95% CI, 0.79–0.94), HHF by 25%, and death from any cause by 9% in patients with HF, regardless of diabetes status. Conclusions SGLT2i is associated with a lower risk of cardiovascular death, HHF, death from any cause, and MI in patients with T2DM compared with GLP1‐RA. In addition, SGLT2i brought more benefits with respect to the effects of cardiovascular death, HHF, and death from any cause in patients with HF, regardless of diabetes status.

Abstract Due to its inherent ductility, Ag2S shows promise as a flexible thermoelectric material for harnessing waste heat from diverse sources. However, its thermoelectric performance remains subpar, and existing enhancement strategies often compromise its ductility. In this study, a novel Sn‐doping‐induced biphasic structuring approach is introduced to synergistically control electron and phonon transport. Specifically, Sn‐doping is incorporated into Ag2S0.7Se0.3 to form a biphasic composition comprising (Ag, Sn)2S0.7Se0.3 as the primary phase and Ag2S0.7Se0.3 as the secondary phase. This biphasic configuration achieves a competitive figure‐of‐merit ZT of 0.42 at 343 K while retaining exceptional ductility, exceeding 90%. The dominant (Ag, Sn)2S0.7Se0.3 phase bolsters the initially low carrier concentration, with interfacial boundaries between the phases effectively mitigating carrier scattering and promoting carrier mobility. Consequently, the optimized power factor reaches 5 µW cm−1 K−2 at 343 K. Additionally, the formation of the biphasic structure induces diverse micro/nano defects, suppressing lattice thermal conductivity to a commendable 0.18 W m−1 K−1, thereby achieving optimized thermoelectric performance. As a result, a four‐leg in‐plane flexible thermoelectric device is fabricated, exhibiting a maximum power density of ≈49 µW cm−2 under the temperature difference of 30 K, much higher than that of organic‐based flexible thermoelectric devices.

Abstract The DC‐side stability of the grid‐tied converter under different control modes is fully investigated using electrical torque analysis. The small‐signal model of a single converter connected to an ideal DC bus under various control modes is formulated. Accordingly, the damping and synchronising coefficient contributed by the DC network and controllers of grid‐tied converter are separately accessed using the electrical torque analysis method and the stabilising conditions of the grid‐tied converter operating under different control modes are further derived. The system stability mainly corresponds with DC network dynamics under constant active power control mode. On the contrary, the grid‐tied converter under constant DC‐link voltage control mode has no stability problem. Generally, elevating the DC‐link capacitance or decreasing the droop gain can greatly improve the stability margin reserve of the VSC‐HVDC links. In addition, the control gains of the classical PQ controller are proven to have limited impacts on DC‐side system stability. Finally, the results of numerical simulation prove the validity of the proposed stability analysis method and the stable boundary for the grid‐tied converter with different control modes.

Abstract Objective As of 2022, 36 anti‐seizure medications (ASMs) have been licensed for the treatment of epilepsy, however, adverse effects (AEs) are commonly reported. Therefore, ASMs with a wide margin between therapeutic effects and AEs are preferred over ASMs that are associated with a narrow margin between efficacy and risk of AEs. E2730 was discovered using in vivo phenotypic screening and characterized as an uncompetitive, yet selective, inhibitor of γ‐aminobutyric acid (GABA) transporter 1 (GAT1). Here, we describe the preclinical characteristics of E2730. Methods Anti‐seizure effects of E2730 were evaluated in several animal models of epilepsy: corneal kindling, 6 Hz–44 mA psychomotor seizure, amygdala kindling, Fragile X syndrome, and Dravet syndrome models. Effects of E2730 on motor coordination were assessed in accelerating rotarod tests. The mechanism of action of E2730 was explored by [3H]E2730 binding assay. The GAT1‐selectivity over other GABA transporters was examined by GABA uptake assay of GAT1, GAT2, GAT3, or betaine/GABA transporter 1 (BGT‐1) stably expressing HEK293 cells. To further investigate the mechanism for E2730‐mediated inhibition of GAT1, in vivo microdialysis and in vitro GABA uptake assays were conducted under conditions of different GABA concentrations. Results E2730 showed anti‐seizure effects in the assessed animal models with an approximately >20‐‍fold margin between efficacy and motor incoordination. [3H]E2730 binding on brain synaptosomal membrane was abolished in GAT1‐deficient mice, and E2730 selectively inhibited GAT1‐mediated GABA uptake over other GABA transporters. In addition, results of GABA uptake assays showed that E2730‐mediated inhibition of GAT1 positively correlated to the level of ambient GABA in vitro. E2730 also increased extracellular GABA concentration in hyperactivated conditions but not under basal levels in vivo. Significance E2730 is a novel, selective, uncompetitive GAT1 inhibitor, which acts selectively under the condition of increasing synaptic activity, contributing to a wide margin between therapeutic effect and motor incoordination.

Abstract Singe‐phase single‐stage AC–DC converters exhibit the advantages of lower cost, higher efficiency, and lower power semiconductor device count compared with traditional two‐stage topologies. However, most existing single‐stage AC–DC topologies encounter some or all the following drawbacks: hard‐switching operation, bulky bus or output capacitor, uncontrolled bus voltage, not actively shaped input current, a large amount of power semiconductor devices, etc. The bridgeless single‐stage full‐bridge AC–DC converter can be considered a promising solution for high power capacity and efficiency. However, this topology still suffers from most of the drawbacks. In this paper, a new asymmetric modulation method of bridgeless single‐stage full‐bridge AC–DC converter is proposed to achieve active power factor (PF) correction and zero‐voltage switching. Topology description, the proposed modulation and control methods, theoretical analysis progress, and reference design procedure are presented in detail. Finally, a 2‐kW laboratory prototype is implemented with experimental results presented to validate the principle and design.

Abstract Objective To explore whether narrow‐band imaging (NBI) endoscopy is accurate in the diagnosis of malignant transformation of vocal cord leukoplakia. Methods The PubMed, Embase, Cochrane Library and Web of Science databases were searched to collect data on studies reporting the use of NBI endoscopy as a diagnostic test for diagnosing vocal cord leukoplakia from January 2015 to December 2021. Study design, analysis method, and extraction results were performed according to the PRISMA guidelines. The sensitivity, specificity, pooled positive likelihood ratio (PLR), negative likelihood ratio (NLR) and area under the curve (AUC) were used to summarize the performance metrics of the meta‐analysis. Risk of bias data and the quality of the included studies was evaluated according to the Quality Assessment of Diagnostic Accuracy Studies‐2 tool (QUADAS‐2). Results Nine studies were finally included in the analysis. The results of the meta‐analysis showed that the pooled sensitivity and specificity of NBI endoscopy for diagnosing leukoplakia lesions were 0.76 (95% CI: 0.72–0.8) and 0.93 (95% CI: 0.91–0.95), respectively. The PLR and NLR were 10.09 (95% CI: 6.53–15.59) and 0.22 (95% CI: 0.13–0.38), respectively. The comprehensive diagnostic odds ratio (DOR) was 54.96 (95% CI: 24.32–124.17), and the area under the curve was 0.9584. The eight articles had a low risk of bias risk and one article was unclear. Conclusion NBI likely has good accuracy for diagnosing malignant transformation of vocal cord leukoplakia. However, multicenter studies and large samples are still needed.

Abstract This case study aimed to identify rare viral myocarditis combined with encephalitis as a COVID‐19 vaccine complication. A 59‐year‐old male patient with a 2 day history of headache and rapidly progressive cognitive decline, who had received the third dose of COVID‐19 vaccine 12 days before, was admitted to our hospital. The patient had no underlying systemic conditions, no prior medical history, and no prior history of COVID‐19 infection. The patient was diagnosed with viral myocarditis and encephalitis by two neurologists and two cardiologists after laboratory examination, head computed tomography, and magnetic resonance imaging evaluation. The patient experienced cardiogenic shock and developed severe arrhythmia, resulting in his death 10 h after admission. Clinically suspected lethal viral myocarditis combined with encephalitis in the patient could be related to COVID‐19 vaccination. Adverse effects of the Chinese COVID‐19 vaccine, especially serious complications, have been uncommon. This case study highlights a rare complication after COVID‐19 vaccination that needs high attention.

Abstract In turbulent mixed convection conditions, flow and heat transfer can deteriorate under specific conditions, thus affecting the performance of the safety of the system, which could imperil the safety of the nuclear reactor. In this paper, by analyzing the velocity, temperature distributions, and other thermal‐hydraulic parameters, the steady‐state computational fluid dynamics approach with the SST k–ω turbulence model used in this study was verified. Then, flow and heat transfer characteristics in turbulent mixed convection inside 2 × 2 subchannels with and without spacer grids were investigated. The results showed that the velocity profiles were distorted and the heat transfer capacity was impaired due to the influence of buoyancy. The Nusselt number ratio (Nu/Nuf) between turbulent mixed convection and forced convection increased with the increase of Reynolds number (Re) until unity but decreased with the increases of Grashof number (Gr) and Buoyancy parameter (Bo*).

Abstract The lethality and chemotherapy resistance of pancreatic cancer necessitates the urgent development of innovative strategies to improve patient outcomes. To address this issue, we designed a novel drug delivery system named GDMCN2,which uses iron‐based metal organic framework (Fe‐MOF) nanocages encased in a covalent organic framework (COF) and modified with the pancreatic cancer‐specific antibody, NRP2. After being targeted into tumor cells, GDMCN2 gradually release the sonosensitizer sinoporphyrin sodium (DVDMS) and chemotherapeutic gemcitabine (GEM) and simultaneously generated reactive oxygen species (ROS) under ultrasound (US) irradiation. This system can overcome gemcitabine resistance in pancreatic cancer and reduce its toxicity to non‐targeted cells and tissues. In a mechanistic cascade, the release of ROS activates the mitochondrial transition pore (MPTP), leading to the release of Ca2+ and induction of endoplasmic reticulum (ER) stress. Therefore, microtubule‐associated protein 1A/1B‐light chain 3 (LC3) is activated, promoting lysosomal autophagy. This process also induces autophagy‐dependent ferroptosis, aided by the upregulation of Nuclear Receptor Coactivator 4 (NCOA4). This mechanism increases the sensitivity of pancreatic cancer cells to chemotherapeutic drugs and increases mitochondrial and DNA damage. The findings demonstrate the potential of GDMCN2 nanocages as a new avenue for the development of cancer therapeutics.

Abstract Background Advanced glycation end products (AGEs) that abnormally accumulate in diabetic patients have been reported to damage bone health. We aimed to investigate the association between skin autofluorescence (SAF)‐AGEage (SAF − AGEs × age/100) and low bone density (LBD)/osteoporosis or major osteoporotic fractures (MOFs) in patients with type 2 diabetes mellitus (T2DM). Methods This study was nested in the prospective REACTION (Risk Evaluation of Cancers in Chinese Diabetic Individuals) study and included 1214 eligible participants. SAF was used to measure skin AGEs (SAF‐AGEs). Fracture events were determined by an in‐person clinical follow‐up. Binary logistic regression analysis, linear regression analysis, and a restricted cubic spline nested in logistic models were used to test outcomes. Results The overall prevalence of LBD/osteoporosis in middle‐aged or elderly T2DM patients was 35.7% (n = 434), and the overall incidence of MOFs was 10.5% (n = 116). Logistic analysis showed a significantly positive relationship between quartiles of SAF‐AGEage and the risk of LBD/osteoporosis (odds ratio [OR] 2.02, 95% CI 1.34–3.03; OR 3.63, CI 2.44–5.39; and OR 6.51, CI 4.34–9.78) for the multivariate‐adjusted models, respectively. SAF‐AGEage was associated with MOFs with a multivariate‐adjusted OR of 1.02 (CI 0.52–2.02), 2.42 (CI 1.32–4.46), and 2.70 (CI 1.48–4.91), respectively. Stratified analyses showed that SAF‐AGEage was significantly associated with MOFs only in females, nonsmokers, nondrinkers, individuals with lower body mass index, and those without LBD/osteoporosis. Linear regression analyses showed that higher SAF‐AGEs were associated with a higher level of serum N‐terminal propeptide of type I procollagen (s‐PINP) and serum carboxy‐terminal cross‐linking peptide of type I collagen (s‐CTX), with a multivariate‐adjusted OR of 1.02 (CI 0.24–1.80) and 6.30 (CI 1.77–10.83), respectively. Conclusions In conclusion, SAF‐AGEage was positively associated with the prevalence of LBD/osteoporosis or MOFs in patients with T2DM. A positive association between SAF‐AGEs and the level of s‐PINP and s‐CTX was found.

Abstract The impact of renin on kidney remain unclear among hypertensives with glucose metabolic disorders (GMD). We aimed to evaluate the association between plasma renin activity (PRA) and kidney damage in hypertensive patients with GMD. Overall, 2033 inpatients with hypertension and GMD free of chronic kidney disease (CKD) at baseline were included. CKD was defined using estimated glomerular filtration rate (eGFR) and urine protein. PRA was treated as continuous variable, and also dichotomized as high (≥0.65) or low (

Background Pulmonary arterial hypertension (PAH) is a complex, fatal disease where disease severity has been associated with the single nucleotide polymorphism (SNP) rs2856830, located near the human leukocyte antigen DPA1 (HLA‐DPA1) gene. We aimed to define the genetic architecture of functional variants associated with PAH disease severity by identifying allele‐specific binding transcription factors and downstream targets that control endothelial pathophenotypes and PAH. Methods and Results Electrophoretic mobility shift assays of oligonucleotides containing SNP rs2856830 and 8 SNPs in linkage disequilibrium revealed functional SNPs via allele‐imbalanced binding to human pulmonary arterial endothelial cell nuclear proteins. DNA pulldown proteomics identified SNP‐binding proteins. SNP genotyping and clinical correlation analysis were performed in 84 patients with PAH at University of Pittsburgh Medical Center and in 679 patients with PAH in the All of Us database. SNP rs9277336 was identified as a functional SNP in linkage disequilibrium (r2>0.8) defined by rs2856830, and the minor allele was associated with decreased hospitalizations and improved cardiac output in patients with PAH, an index of disease severity. SNP pulldown proteomics showed allele‐specific binding of nuclear ACTN4 (alpha actinin 4) protein to rs9277336 minor allele. Both ACTN4 and HLA‐DPA1 were downregulated in pulmonary endothelium in human patients and rodent models of PAH. Via transcriptomic and phenotypic analyses, knockdown of HLA‐DPA1 phenocopied knockdown of ACTN4, both similarly controlling cell structure pathways, immune pathways, and endothelial dysfunction. Conclusions We defined the pathogenic activity of functional SNP rs9277336, entailing the allele‐specific binding of ACTN4 and controlling expression of the neighboring HLA‐DPA1 gene. Through inflammatory or genetic means, downregulation of this ACTN4‐HLA‐DPA1 regulatory axis promotes endothelial pathophenotypes, providing a mechanistic explanation for the association between this SNP and PAH outcomes.

Abstract Purpose The ability of the T‐cell–inflamed gene expression profile (GEP) to predict clinical outcome in esophageal cancer (EC) is unknown. This retrospective observational study assessed the prognostic value of GEP and programmed death ligand 1 (PD‐L1) expression in patients with EC treated in routine clinical practice. Methods Tumor samples of 294 patients from three centers in Denmark, South Korea, and the United States, collected between 2005 and 2017, were included. T‐cell–inflamed GEP score was defined as non‐low or low using a cutoff of −1.54. A combined positive score (CPS) ≥10 was defined as PD‐L1 expression positivity. Associations between overall survival (OS) and GEP status and PD‐L1 expression were explored by Cox proportional hazards models adjusting for age, sex, histology, stage, and performance status. Results Median age was 65 years; 63% of patients had adenocarcinoma (AC) and 37% had squamous cell carcinoma (SCC). Thirty‐six percent of tumors were GEP non‐low, with higher prevalence in AC (46%) than SCC (18%). Twenty‐one percent were PD‐L1–positive: 32% in South Korean samples versus 16% in non‐Asian samples and 26% in SCC versus 18% in AC. GEP scores and PD‐L1 CPS were weakly correlated (Spearman’s R = 0.363). OS was not significantly associated with GEP status (non‐low vs low; adjusted hazard ratio, 0.91 [95% CI, 0.69–1.19]) or PD‐L1 expression status. Conclusion Neither GEP nor PD‐L1 expression was a prognostic marker in Asian and non‐Asian patients with EC.

Abstract Background PRKAG2 cardiac syndrome is a rare autosomal dominant genetic disorder caused by a PRKAG2 gene variant. There are several major adverse cardiac presentations, including hypertrophic cardiomyopathy (HCM) and life‐threatening arrhythmia. Two cases with pathogenic variants in the PRKAG2 gene are reported here who presents different cardiac phenotypes. Methods Exome sequencing and variant analysis of PRKAG2 were performed to obtain genetic data, and clinical characteristics were determined. Results The first proband was a 9‐month‐old female infant (Case 1), and was identified with severe DCM and resistant heart failure. The second proband was a 10‐year‐old female infant (Case 2), and presented with HCM and ventricular preexcitation. Exome sequencing identified a de novo c.425C > T (p.T142I) heterozygous variant in the PRKAG2 gene for Case 1, and a c.869A > T (p.K290I) for Case 2. The mutated sites in the protein were labeled and identified as p.K290 in the CBS domain and p.T142 in the non‐CBS domain. Differences in the molecular functions of CBS and non‐CBS domains have not been resolved, and variants might lead to the different cardiomyopathy phenotypes. Single‐cell RNA analysis demonstrated similar expression levels of PRKAG2 in cardiomyocytes and conductive tissues. These results suggest that the arrhythmia induced by the PRKAG2 variant was the primary change, and not secondary to cardiomyopathy. Conclusion In summary, this is the first case report to describe a DCM phenotype with early onset in patients possessing a PRKAG2 c.425C > T (p.T142I) pathogenic variant. Our results aid in understanding the molecular function of non‐CBS variants in terms of the disordered sequence of transcripts. Moreover, we used scRNA‐seq to show that electrically conductive cells express a higher level of PRKAG2 than do cardiomyocytes. Therefore, variants in PRKAG2 are expected to also alter the biological function of the conduction system.

Abstract Aims Adenoid cystic carcinoma (ACC) is a distinctive tumour. Limited studies involving a large population have reported multicentre systematic analyses of the clinical, pathological and immunohistochemical (IHC) features of ACC as well as the potential role of IHC markers in the prognosis of ACC. Methods and Results The clinical, histopathological and IHC data of 296 cases obtained from two tertiary hospitals were analysed. The age at onset ranged from 12 to 87 years with a median age of 52 years. The male‐to‐female ratio was 1:1.3. Patients with ACC arising from the lacrimal gland were younger than those with tumours arising from other sites. Patients with tumours in the extra auditory canal and nasopharynx were older than those with tumours in other locations. Histopathologically, solid type ACC was the most frequent in the nasal cavity and paranasal sinus (6/51) group. Tumours arising from the oral cavity most commonly showed perineural invasion (10/60) and margin positivity (11/60). IHC analyses showed that CK8/18, CK7, CK14, epithelial membrane antigen and CD117 were expressed in 35/35 (100%), 87/88 (98.8%), 26/27 (96.2%), 42/43 (97.6%) and 113/120 (94.1%) patients, respectively. CK5/6, P63, smooth muscle actin, calponin and S100 were positively expressed in 73/73 (100%), 111/124 (89.5%), 38/43 (88.3%), 41/50 (82.0%) and 61/92 (66.3%) cases, respectively. S100 proteins were expressed in 54 (54/77) primary cases and two (2/9) metastatic cases (p = 0.013). Conclusions ACC is a distinctive tumour that mainly affects middle‐aged and elderly individuals, with a mild female predominance. Loss of expression of S100 proteins may be a poor prognostic factor associated with metastasis.

Abstract Pancreatic cancer is one of the most lethal malignancies. With the promising prospects conveyed by immunotherapy in cancers, we aimed to construct an immune‐related gene pairs (IRGPs) signature to predict the prognosis of pancreatic cancer patients. We downloaded clinical and transcriptional data of pancreatic cancer patients from The Cancer Genome Atlas data set as the training group and GSE57495 data set as the verification group. We filtered immune‐related transcriptional data by IMMPORT. With the assistance of lasso penalized Cox regression, we constructed our prognostic IRGPs signature and divided all samples into high‐/low‐risk groups by receiver operating characteristic curve for further comparisons. The comparisons between high‐ and low‐risk groups including survival rate, multivariate, and univariate Cox proportional‐hazards analysis, infiltration of immune cells, and Gene Set Enrichment Analysis (GSEA). Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) are facilitated to analyze the proceedings in which our IRGPs signature may involve in. The results revealed that 18 IRGPs were defined as our prognostic signature. The prognostic value of this IRGPs signature was verified from the GSE57495 data set. We further demonstrated the independent prognostic value of this IRGPs signature. The contents of six immune cells between high‐/low‐risk groups were different, which was associated with the progression of diverse cancers. Results from GO, KEGG, and GSEA revealed that this IRGPs signature was involved in extracellular space, immune response, cancer pathways, cation channel, and gated channel activities. Evidently, this IRGPs signature will provide remarkable value for the therapy of pancreatic cancer patients.

Abstract Urea‐based fertilizers are commonly used in the agricultural rice production. Urea produces gaseous ammonia upon contact with plants and soil. Although rice is considered to be a relatively ammonium‐tolerant crop, urea fertilization can have a negative impact on seedling establishment because of tissue ammonia accumulation. We investigated the molecular/genetic regulation of ammonia tolerance in rice using a multidisciplinary approach consisting of high‐resolution LC‐MS/MS analysis and bioinformatics, together with plant molecular physiology and biochemistry. Growth with 10 or 80 mM NH4Cl led to an inhibition of photosynthesis and ROS accumulation. Proteomic analysis revealed changes in the levels of 266 proteins, which function in translation and protein metabolism, amino acid and carbon metabolism/transport, antioxidant and redox metabolism. The abundance of the transcripts encoding these proteins was increased under high ammonium. Data are presented showing that ammonia‐induced changes in metabolism are linked to a strong antioxidant response but little change in secondary metabolism.

Abstract Understanding the feasibility to couple semiconducting and magnetic properties in metal halide perovskites through interface design opens new opportunities for creating the next generation spin‐related optoelectronics. In this work, a fundamentally new phenomenon of optically induced magnetization achieved by coupling photoexcited orbital magnetic dipoles with magnetic spins at perovskite/ferromagnetic interface is discovered. The depth‐sensitive polarized neutron reflectometry combined with in situ photoexcitation setup, constitutes key evidence of this novel effect. It is demonstrated that a circularly polarized photoexcitation induces a stable magnetization signal within the depth up to 7.5 nm into the surface of high‐quality perovskite (MAPbBr3) film underneath a ferromagnetic cobalt layer at room temperature. In contrast, a linearly polarized light does not induce any detectable magnetization in the MAPbBr3. The observation reveals that photoexcited orbital magnetic dipoles at the surface of perovskite are coupled with the spins of the ferromagnetic atoms at the interface, leading to an optically induced magnetization within the perovskite’s surface. The finding demonstrates that perovskite semiconductor can be bridged with magnetism through optically controllable method at room temperature in this heterojunction design. This provides the new concept of utilizing spin and orbital degrees of freedom in new‐generation spin‐related optoelectronic devices.

Abstract Room‐temperature shelf life is a key factor in fresh market apple (Malus domestica Borkh.) quality and commercial value. To investigate the genetic and molecular mechanism underlying apple shelf life, quantitative trait loci (QTL) were identified using bulked segregant analysis via sequencing (BSA‐seq). Ethylene emission, flesh firmness, or crispness of apple fruit from 1,273 F1 plants of M. asiatica Nakai ‘Zisai Pearl’ × M. domestica ‘Golden Delicious’ were phenotyped prior to and during 6 wk of room‐temperature storage. Segregation of ethylene emission and the flesh firmness or crispness traits was detected in the population. Thirteen QTL, including three major ones, were identified on chromosome 03, 08, and 16. A candidate gene encoding pectin acetylesterase, MdPAE10, from the QTL Z16.1 negatively affected fruit shelf life. A 379‐bp deletion in the coding sequence of MdPAE10 disrupted its function. A single nucleotide polymorphism (SNP) in the MdPAE10 promoter region reduced its transcription activity. These findings provided insight into the genetic control of fruit shelf life and can be potentially used in apple marker‐assisted selection.

Abstract Apple fruit cover color is an important appearance trait determining fruit quality, high degree of fruit cover color or completely red fruit skin is also the ultimate breeding goal. MdMYB1 has repeatedly been reported as a major gene controlling apple fruit cover color. There are also multiple minor‐effect genes affecting degree of fruit cover color (DFC). This study was to identify genome‐wide quantitative trait loci (QTLs) and to develop genomics‐assisted prediction for apple DFC. The DFC phenotype data of 9,422 hybrids from five full‐sib families of Malus asiatica ‘Zisai Pearl’, M. domestica ‘Red Fuji’, ‘Golden Delicious’, and ‘Jonathan’ were collected in 2014–2017. The phenotype varied considerably among hybrids with the same MdMYB1 genotype. Ten QTLs for DFC were identified using MapQTL and bulked segregant analysis via sequencing. From these QTLs, ten candidate genes were predicted, including MdMYB1 from a year‐stable QTL on chromosome 9 of ‘Zisai Pearl’ and ‘Red Fuji’. Then, kompetitive allele‐specific polymerase chain reaction (KASP) markers were designed on these candidate genes and 821 randomly selected hybrids were genotyped. The genotype effects of the markers were estimated. MdMYB1‐1 (represented by marker H162) exhibited a partial dominant allelic effect on MdMYB1‐2 and showed non‐allelic epistasis on markers H1245 and G6. Finally, a non‐additive QTL‐based genomics assisted prediction model was established for DFC. The Pearson's correlation coefficient between the genomic predicted value and the observed phenotype value was 0.5690. These results can be beneficial for apple genomics‐assisted breeding and may provide insights for understanding the mechanism of fruit coloration.