Ultra-robust informational metasurfaces based on spatial coherence structures engineering.

Optical information transmission is vital in modern optics and photonics due to its concurrent and multi-dimensional nature, leading to tremendous applications such as optical microscopy, holography, and optical sensing. Conventional optical information transmission technologies suffer from bulky optical setup and information loss/crosstalk when meeting scatterers or obstacles in the light path. Here, we theoretically propose and experimentally realize the simultaneous manipulation of the coherence lengths and coherence structures of the light beams with the disordered metasurfaces. The ultra-robust optical information transmission and self-reconstruction can be realized by the generated partially coherent beam with modulated coherence structure even 93% of light is recklessly obstructed during light transmission, which brings new light to robust optical information transmission with a single metasurface. Our method provides a generic principle for the generalized coherence manipulation on the photonic platform and displays a variety of functionalities advancing capabilities in optical information transmission such as meta-holography and imaging in disordered and perturbative media.

Mechanical insights into desulfurization by peroxymonosulfate oxidation via a non-reactive oxygen species pathway.

Air pollution by sulfur dioxide (SO2) remains a pressing concern for both the environment and human health. Desulfurization enhanced by persulfate based advanced oxidation processes (PS-AOPs) has been proven to be a feasible method. However, the inherent contradiction between the rapid diffusion mass transfer of SO2 in the "gas-liquid-gas" phase and the limited lifespan of reactive oxygen species (ROS) can not be ignored. Excessive investment in PS is required to sustainably generate ROS to achieve continuous desulfurization performance, which may lead to excessive PS consumption. To address this issue, whether PS can achieve the oxidation absorption of SO2 via a non-reactive oxygen species pathway was investigated. Experimental and computational results demonstrated that peroxymonosulfate (PMS) instead of peroxydisulfate (PDS) had a great SO2 removal performance, the utilization of PS could be effectively achieved by maintaining a 1:1 molar ratio of PMS and removed SO2. The presence of HOO bonds in the PMS introduced a partial positive charge to the oxygen atom, making the PMS polar and more susceptible to be attacked by the nucleophile HSO3-. So SO2 underwent a series of processes including dissolution, dissociation, one-oxygen atom transfer, and ionization before ultimately being converted into SO42- ions, effectively achieving its removal from flue gas. This study may presents a novel approach for achieving high-efficiency flue gas desulfurization.

ITGB5 facilitates gastric cancer metastasis by promoting TGFBR2 endosomal recycling.

TGFBR2, a key regulator of the TGFß signaling pathway, plays a crucial role in gastric cancer (GC) metastasis through its endosomal recycling process. Despite its importance, the mechanisms governing this process remain unclear. Here, we identify integrin ß5 (ITGB5) as a critical mediator that promotes TGFBR2 endosomal recycling. Our study reveals elevated expression of ITGB5 in GC, particularly in metastatic cases, correlating with poor patient outcomes. Knockdown of ITGB5 impairs GC cell metastasis both in vitro and in vivo. Mechanistically, ITGB5 facilitates epithelial-mesenchymal transition mediated by TGFß signaling, thereby enhancing GC metastasis. Acting as a scaffold, ITGB5 interacts with TGFBR2 and SNX17, facilitating SNX17-mediated endosomal recycling of TGFBR2 and preventing lysosomal degradation, thereby maintaining its surface distribution on tumor cells. Notably, TGFß signaling directly upregulates ITGB5 expression, establishing a positive feedback loop that exacerbates GC metastasis. Our findings shed light on the role of ITGB5 in promoting GC metastasis through SNX17-mediated endosomal recycling of TGFBR2, providing insights for the development of targeted cancer therapies.

Enhancing the acidic oxygen evolution reaction performance of RuO2-TiO2by a reduction-oxidation process.

As a promising alternative to Ir based acidic oxygen evolution reaction (OER) catalysts, Ru suffers from severe fading issues. Supporting it on robust oxides such as TiO2is a simple and effective way to enhance its lifetime. Here, we find that a simple reduction-oxidation process can further improve both activity and stability of RuO2-TiO2composites at high potentials. In this process, the degree of oxidation was carefully controlled to form Ru/RuO2heterostructure to improve OER activity. Moreover, due to the oxophilicity difference of Ru and Ti, the structure of catalysts was changed from supported to embedded, which enhanced the protective effect of TiO2and mitigated the dissolution of Ru element in acidic electrolyte, making as-prepared Ru/RuO2-TiO2with better durability at all tested potentials.

Spatial Information Lasing Enabled by Full-k-Space Bound States in the Continuum.

Optical amplification and massive information transfer in modern physics depend on stimulated radiation. However, regardless of traditional macroscopic lasers or emerging micro- and nanolasers, the information modulations are generally outside the lasing cavities. On the other hand, bound states in the continuum (BICs) with inherently enormous Q factors are limited to zero-dimensional singularities in momentum space. Here, we propose the concept of spatial information lasing, whose lasing information entropy can be correspondingly controlled by near-field Bragg coupling of guided modes. This concept is verified in gain-loss metamaterials supporting full-k-space BICs with both flexible manipulations and strong confinement of light fields. The counterintuitive high-dimensional BICs exist in a continuous energy band, which provide a versatile platform to precisely control each lasing Fourier component and, thus, can directly convey rich spatial information on the compact size. Single-mode operation achieved in our scheme ensures consistent and stable lasing information. Our findings can be expanded to different wave systems and open new scenarios in informational coherent amplification and high-Q physical frameworks for both classical and quantum applications.

Polarization-insensitive high-numerical-aperture metalens for wide-field super-resolution imaging.

The development of super-oscillatory lens (SOL) offers opportunities to realize far-field label-free super-resolution microscopy. Most microscopes based on a high numerical aperture (NA) SOL operate in the point-by-point scanning mode, resulting in a slow imaging speed. Here, we propose a high-NA metalens operating in the single-shot wide-field mode to achieve real-time super-resolution imaging. An optimization model based on the exhaustion algorithm and angular spectrum (AS) theory is developed for metalens design. We numerically demonstrate that the optimized metalens with an NA of 0.8 realizes the imaging resolution (imaging pixel size) about 0.85 times the Rayleigh criterion. The metalens can achieve super-resolution imaging of an object with over 200 pixels, which is one order of magnitude higher than the unoptimized metalens. Our method provides an avenue toward single-shot far-field label-free super-resolution imaging for applications such as real-time imaging of living cells and temporally moving particles.

Hyperbolic metamaterial empowered controllable photonic Weyl nodal line semimetals.

Motivated by unique topological semimetals in condensed matter physics, we propose an effective Hamiltonian with four degrees of freedom to describe evolutions of photonic double Weyl nodal line semimetals in one-dimensional hyper-crystals, which supports the energy bands translating or rotating independently in the form of Weyl quasiparticles. Especially, owing to the unit cells without inversion symmetry, a pair of reflection-phase singularities carrying opposite topological charges emerge near each nodal line, and result in a unique bilateral drumhead surface state. After reducing radiation leakages and absorption losses, these two singularities gather together gradually, and form a quasi-bound state in the continuum (quasi-BIC) ring at the nodal line ultimately. Our work not only reports the first realization of controllable photonics Weyl nodal line semimetals, establishes a bridge between two independent topological concepts-BICs and Weyl semimetals, but also heralds new possibilities for unconventional device applications, such as dual-mode schemes for highly sensitive sensing and switching.

CircGLIS3 promotes gastric cancer progression by regulating the miR-1343-3p/PGK1 pathway and inhibiting vimentin phosphorylation.

BACKGROUND: Circular RNAs (circRNAs) have been proved to play crucial roles in the development of various cancers. However, the molecular mechanism of circGLIS3 involved in gastric cancer (GC) tumorigenesis has not been elucidated. METHODS: The higher expression level of circGLIS3 was identified in GC through RNA sequencing and subsequent tissue verification using Quantitative real-time PCR (qRT-PCR). A series of functional experiments in vitro and in vivo were performed to evaluated the effects of circGLIS3 on tumor growth and metastasis in GC. The interaction and regulation of circGLIS3/miR-1343-3p/PGK1 axis was confirmed by RNA pulldown, western blot, and rescue experiments. RIP and western blot were performed to demonstrate the role of circGLIS3 in regulating phosphorylation of VIMENTIN. We then used qRT-PCR and co culture system to trace circGLIS3 transmission via exosomal communication and identify the effect of exosomal circGLIS3 on gastric cancer and macrophages. Finally, RIP experiments were used to determine that EIF4A3 regulates circGLIS3 expression. RESULTS: CircGLIS3(hsa_circ_0002874) was significantly upregulated in GC tissues and high circGLIS3 expression was associated with advanced TNM stage and lymph node metastasis in GC patients. We discovered that overexpression of circGLIS3 promoted GC cell proliferation, migration, invasion in vitro and in vivo, while suppression of circGLIS3 exhibited the opposite effect. Mechanistically, circGLIS3 could sponge miR-1343-3p and up-regulate the expression of PGK1 to promote GC tumorigenesis. We also found that circGLIS3 reduced the phosphorylation of VIMENTIN at ser 83 site by binding with VIMENTIN. Moreover, it was proven that exosomal circGLIS3 could promote gastric cancer metastasis and the M2 type polarization of macrophages. In the final step, the mechanism of EIF4A3 regulating the generation of circGLIS3 was determined. CONCLUSION: Our findings demonstrate that circGLIS3 promotes GC progression through sponging miR-1343-3p and regulating VIMENTIN phosphorylation. CircGLIS3 is a potential therapeutic target for GC patients.

Novel copy number variations and phenotypes of infantile epileptic spasms syndrome.

We summarize the copy number variations (CNVs) and phenotype spectrum of infantile epileptic spasms syndrome (IESS) in a Chinese cohort. The CNVs were identified by genomic copy number variation sequencing. The CNVs and clinical data were analyzed. 74 IESS children with CNVs were enrolled. 35 kinds of CNVs were identified. There were 11 deletions and 5 duplications not reported previously in IESS, including 2 CNVs not reported in epilepsy. 87.8% were de novo, 9.5% were inherited from mother and 2.7% from father. Mosaicism occurred in one patient with Xq21.31q25 duplication. 16.2% (12/74) were 1p36 deletion, and 20.3% (15/74) were 15q11-q13 duplication. The age of seizure onset ranged from 17 days to 24 months. Seizure types included epileptic spasms, focal seizures, tonic seizures, and myoclonic seizures. All patients displayed developmental delay. Additional features included craniofacial anomaly, microcephaly, congenital heart defects, and hemangioma. 29.7% of patients were seizure-free for more than 12 months, and 70.3% still had seizures after trying 2 or more anti-seizure medications. In conclusion, CNVs is a prominent etiology of IESS. 1p36 deletion and 15q duplication occurred most frequently. CNV detection should be performed in patients with IESS of unknown causes, especially in children with craniofacial anomalies and microcephaly.

Bisphenol F exposure induces depression-like changes: Roles of the kynurenine metabolic pathway along the "liver-brain" axis.

Bisphenol F (BPF), one of the major alternatives of Bisphenol A (BPA), is becoming extensively used in industrial production with great harm to human beings and environment. Recent studies have revealed that environmental exposure is crucial to the initiation and development of depression. Thereby, the aim the present study is to ascertain the correlationship between the BPF exposure and depression occurrence. In the current study, BPF strikingly triggered depression-like changes in mice through the sucrose preference test (SPT), tail suspension test (TST) and forced swim test (FST), accompanied by the perturbation of the kynurenine (KYN) metabolic pathway along the "liver-brain" axis. Mechanistically, the neurotransmitters from the tryptophan metabolic pathway were converted to the toxic KYN pathway after BPF treatment. With the ELISA assay, it revealed that the toxic KYN metabolites, including KYN and 3-hydroxykynurenine (3-HK), were strikingly increased in the mouse brains which was ascribed to the enhanced expression of the rate-limiting enzymes Indoleamine 2,3-dioxygenase (IDO1) and Kynurenine 3-monooxygenase (KMO) respectively. Interestingly, the increased brain KYN induced by BPF was also validated partially from the periphery, since the ELISA and western blotting results indicated the significantly increased KYN in the serum and L-type amino acid transporter 1 (LAT1) in the brain, the key transporter responsible for KYN and 3-HK crossing the blood-brain barrier. Intriguingly, the liver-derived KYN metabolic pathway was the important source of the peripheral KYN and 3-HK, as BPF substantially enhanced hepatic IDO1, Tryptophan, 2, 3-dioxygenase (TDO2), and KMO levels indicated by western blotting. This study is the first to delineate previously unrecognized BPF-induced depression by regulating the KYN metabolic pathway along the "liver-brain" axis; therefore, targeting LAT1 or hepatic KYN signaling may provide a potentially unique therapeutic intervention in BPF-induced depression.

RP11-789C1.1 inhibits gastric cancer cell proliferation and accelerates apoptosis via the ATR/CHK1 signaling pathway.

BACKGROUND: Long non-coding RNAs (lncRNAs) plays an important role in the progression of gastric cancer (GC). Their involvement ranges from genetic regulation to cancer progression. However, the mechanistic roles of RP11-789C1.1 in GC are not fully understood. METHODS: We identified the expression of lncRNA RP11-789C1.1 in GC tissues and cell lines by real-time fluorescent quantitative polymerase chain reaction. A series of functional experiments revealed the effect of RP11-789C1.1 on the proliferation of GC cells. In vivo experiments verified the effect of RP11-789C1.1 on the biological behavior of a GC cell line. RNA pull-down unveiled RP11-789C1.1 interacting proteins. Western blot analysis indicated the downstream pathway changes of RP11-789C1.1, and an oxaliplatin dosing experiment disclosed the influence of RP11-789C1.1 on the drug sensitivity of oxaliplatin. RESULTS: Our results demonstrated that RP11-789C1.1 inhibited the proliferation of GC cells and promoted the apoptosis of GC cells. Mechanistically, RP11-789C1.1 inhibited checkpoint kinase 1 (CHK1) phosphorylation by binding ataxia-telangiectasia mutated and Rad3 related (ATR), a serine/threonine-specific protein kinase, promoted GC apoptosis, and mediated oxaliplatin sensitivity. CONCLUSION: In general, we discovered a tumor suppressor molecule RP11-789C1.1 and confirmed its mechanism of action, providing a theoretical basis for targeted GC therapy.

A lipidomic approach to bisphenol F-induced non-alcoholic fatty liver disease-like changes: altered lipid components in a murine model.

Bisphenol A (BPA), a typical environmental endocrine disruptor, is an "obesogen" that can induce lipid accumulation in the liver. Highly similar in structure to BPA, bisphenol F (BPF) is becoming the dominant BPA substitute on the market, which attracts more and more attention due to its potential adverse effects. Recently, BPF exposure is found to cause non-alcoholic fatty liver disease (NAFLD)-like changes; however, the underlying toxic effects remain poorly understood. Therefore, in the current study, we focused on BPF-mediated lipid homeostasis, especially the alterations of lipid components and metabolism. In human serum, the BPF levels in healthy controls and NAFLD patients were assessed by ELISA, and BPF-induced disturbance of lipid metabolism was evaluated in mouse model via non-targeted lipomic methods with ultra-high performance liquid chromatography-quadrupole time-of-flight mass spectrometry. It suggested that BPF exposure was positively correlated with NAFLD severity and triglyceride level in patients. Based on the relationships, lipid metabolites were assessed in mouse livers between control and BPF-treated group, and it revealed that twenty-six lipid metabolites (including phospholipids, sphingolipids, and glycerides) were significantly changed in mouse livers. Phosphatidylcholine, phosphatidylethanolamine, and diglyceryl ester levels were lower than those in the control mice; hexose ceramide content in sphingolipids markedly increased in BPF-treated mouse livers. Noteworthily, the glycerophospholipid metabolic pathway was found to be the most pronounced in BPF-induced disturbance of lipid metabolism. Therefore, the current study, for the first time, is deciphering the BPF-induced lipid metabolic disturbance, which may provide novel intervention strategies for BPF-induced NAFLD-like changes.

Insight into the mechanisms of neuroendocrine toxicity induced by 6:2FTCA via thyroid hormone disruption.

6:2 fluorotonic carboxylic acid (6:2 FTCA), a novel substitute for perfluorooctanoic acid (PFOA), is being used gradually in industrial production such as coatings or processing aids, and its detection rate in the aqueous environment is increasing year by year, posing a potential safety risk to aquatic systems and public health. However, limited information is available on the effects and mechanism of 6:2 FTCA. Therefore, this study was conducted to understand better the neuroendocrine effects of early exposure to 6:2 FTCA and the underlying mechanisms on zebrafish. In this study, zebrafish embryos were treated to varied doses of 6:2 FTCA (0, 0.08 µg/mL, 0.8 µg/mL and 8 µg/mL) at 4 h post-fertilization (hpf) for a duration of six days, which exhibited a pronounced inhibition of early growth and induced a disorganized swim pattern characterized by reduced total swim distance and average swim speed. Simultaneously, the thyroid development of zebrafish larvae was partially hindered, accompanied by decreased T3 levels, altered genes associated with the expression of thyroid hormone synthesis, transformation and transportation and neurotransmitters associated with tryptophan and tyrosine metabolic pathways. Molecular docking results showed that 6:2 FTCA has a robust binding energy with the thyroid hormone receptor (TRß). Moreover, exogenous T3 supplementation can partially restore the adverse outcomes. Our findings indicated that 6:2 FTCA acts as a thyroid endocrine disruptor and can induce neuroendocrine toxic effects. Furthermore, our results show that targeting TRß may be a potentially therapeutic strategy for 6:2 FTCA-induced neuroendocrine disrupting effects.

Mystery of bisphenol F-induced nonalcoholic fatty liver disease-like changes: Roles of Drp1-mediated abnormal mitochondrial fission in lipid droplet deposition.

As one of the major substitutes for bisphenol A (BPA), bisphenol F (BPF) has been widely used. Our previous study demonstrated that BPF exposure facilitates lipid droplet deposition in hepatic cells, contributing to nonalcoholic fatty liver disease (NAFLD)-like changes. However, the underlying mechanisms remain poorly understood. Here, with a metabolic cage system, we observed the perturbation of energy metabolism in mice treated with BPF. BPF obviously suppressed metabolic capacity, which manifested as decreased energy expenditure, low O2 consumption and CO2 levels in mice. Consistent with the in vivo results, a Seahorse XF Cell Mito Stress Test showed significant reductions in mitochondrial ATP production capacity, maximum respiratory capacity, and residual respiratory capacity after BPF treatment in an in vitro study. Electron microscopy revealed a striking increase in mitochondrial fission that was synchronous with excessive expression and activation of dynamin-related protein 1 (Drp1). Intriguingly, chemical inhibition of Drp1 by Mdivi-1 and/or silencing of Drp1 dramatically hampered mitochondrial fission and ameliorated BPF-induced lipid droplet deposition both in mouse liver and human hepatic cells. Mechanistically, mitochondrial dynamics imbalance played prominent roles in these processes, since suppression of Drp1 by chemical inhibition or knockdown substantially reversed BPF-induced mitochondrial fission and ameliorated the suppression of mitochondrial metabolism as well as excessive mitochondrial ROS, which was verified to be key to lipid droplet deposition. Collectively, the findings of the current study reveal previously unrecognized effects involving Drp1-mediated mitochondrial injury in BPF-induced lipid droplet deposition. Therefore, targeted intervention against mitochondrial dysfunction may be a promising therapeutic strategy for BPF-induced NAFLD-like changes.

Microbiome and tryptophan metabolomics analysis in adolescent depression: roles of the gut microbiota in the regulation of tryptophan-derived neurotransmitters and behaviors in human and mice.

BACKGROUND: Adolescent depression is becoming one of the major public health concerns, because of its increased prevalence and risk of significant functional impairment and suicidality. Clinical depression commonly emerges in adolescence; therefore, the prevention and intervention of depression at this stage is crucial. Recent evidence supports the importance of the gut microbiota (GM) in the modulation of multiple functions associated with depression through the gut-brain axis (GBA). However, the underlying mechanisms remain poorly understood. Therefore, in the current study, we aimed to screen the microbiota out from healthy and depressive adolescents, delineate the association of the targeted microbiota and the adolescent depression, address the salutary effects of the targeted microbiota on anti-depressive behaviors in mice involving the metabolism of the tryptophan (Trp)-derived neurotransmitters along the GBA. RESULTS: Here, we found the gut microbiota from healthy adolescent volunteers, first diagnosis patients of adolescent depression, and sertraline interveners after first diagnosis displayed significant difference, the relative abundance of Faecalibacterium, Roseburia, Collinsella, Blautia, Phascolarctobacterium, Lachnospiraceae-unclassified decreased in adolescent depressive patients, while restored after sertraline treatment. Of note, the Roseburia abundance exhibited a high efficiency in predicting adolescent depression. Intriguingly, transplantation of the fecal microbiota from healthy adolescent volunteers to the chronic restraint stress (CRS)-induced adolescent depressed mice significantly ameliorated mouse depressive behaviors, in which the Roseburia exerted critical roles, since its effective colonization in the mouse colon resulted in remarkably increased 5-HT level and reciprocally decreased kynurenine (Kyn) toxic metabolites quinolinic acid (Quin) and 3-hydroxykynurenine (3-HK) levels in both the mouse brain and colon. The specific roles of the Roseburia were further validated by the target bacteria transplantation mouse model, Roseburia intestinalis (Ri.) was gavaged to mice and importantly, it dramatically ameliorated CRS-induced mouse depressive behaviors, increased 5-HT levels in the brain and colon via promoting tryptophan hydroxylase-2 (TPH2) or -1 (TPH1) expression. Reciprocally, Ri. markedly restrained the limit-step enzyme responsible for kynurenine (indoleamine2,3-dioxygenase 1, IDO1) and quinolinic acid (3-hydroxyanthranilic acid 3,4-dioxygenase, 3HAO) generation, thereby decreased Kyn and Quin levels. Additionally, Ri. administration exerted a pivotal role in the protection of CRS-induced synaptic loss, microglial activation, and astrocyte maintenance. CONCLUSIONS: This study is the first to delineate the beneficial effects of Ri. on adolescent depression by balancing Trp-derived neurotransmitter metabolism and improving synaptogenesis and glial maintenance, which may yield novel insights into the microbial markers and therapeutic strategies of GBA in adolescent depression. Video Abstract.

Seizure features and outcomes in 50 children with GATOR1 variants: A retrospective study, more favorable for epilepsy surgery.

OBJECTIVES: To summarize the clinical features of epilepsy related to DEPDC5, NPRL2, and NPRL3 genes encoding the GATOR1 complex in children and to evaluate the factors affecting the prognosis of these epilepsies. METHODS: In this retrospective study, we reviewed the clinical and genetic characteristics of children with epilepsy related to GATOR1 variants who were admitted to the Peking University First Hospital between January 2016 and December 2021. Potential prognostic factors were assessed by comparing children with and without ongoing seizures. RESULTS: Fifty probands, including 31 boys and 19 girls were recruited. The median age at onset of epilepsy was 4 months, and 64% of patients had early-onset epilepsy (≤1 year). The most frequent epileptic seizure type was focal seizure (86%). Among the 50 patients, only six were with de novo variants. According to the novel classification framework for GATOR1 variants, 36 patients were with pathogenic variants and 14 with likely pathogenic variants. DEPDC5 variants were found in 37 patients, NPRL3 in 9, and NPRL2 in 4. The phenotype was similar among the probands, with variants in DEPDC5, NRPL2, or NPRL3. 76% (38/50) of epilepsy related to GATOR1 variants was neuroimaging positive, including brain MRI positive in 31 patients, and MRI combined F-18-fluorodeoxyglucose positron emission tomography positive in the other seven patients. Twenty-seven patients underwent epilepsy surgery. In total, after initial antiseizure medications alone, 92% (46/50) of patients were drug-resistant epilepsies, only 8% (4/50) of the probands became seizure-free but seizure-free (≥6 m) occurred in 92.6% (25/27) of patients with drug-resistant epilepsy after epilepsy surgery at the last follow-up. Patients undergoing epilepsy surgery had better epilepsy prognosis. SIGNIFICANCE: Epilepsy related to GATOR1 variants had high possibility to be drug-resistant epilepsy and to have positive neuroimaging finding. Epilepsy surgery is the only favorable factor for better seizure prognosis in this kind epilepsy.

Long-Term Atmosphere Surveillance (2016-2021) of PM2.5-bound Polycyclic Aromatic Hydrocarbons and Health Risk Assessment in Yangtze River Delta, China.

Long-term atmospheric quality monitoring of fine particulate matter (PM2.5) and PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) was performed in Wuxi from 2016 to 2021. In total, 504 atmospheric PM2.5 samples were collected, and PM2.5-bound 16 PAHs were detected. The PM2.5 and ∑PAHs level decreased annually from 2016 to 2021, from 64.3 to 34.0 µg/m3 and 5.27 to 4.22 ng/m3, respectively. The benzo[a]pyrene (BaP) levels of 42% of the monitoring days in 2017 exceeded the recommended European Union (EU) health-based standard of 1 ng/m3. Five- and six-ring PAHs were found, including benz[a]anthracene, benzo[k]fluoranthene (Bkf), BaP, and benzo[g,h,i]perylene, which were the dominant components (indicating a prominent petroleum, biomass, and coal combustion contribution) using molecular diagnostic ratios and positive matrix factorization analysis. Moreover, PM2.5 and PAHs were significantly negatively associated with local precipitation over a period of six years. Statistically significant temporal and spatial distribution differences of PM2.5, and ∑PAHs were also found. The toxicity equivalent quotient (TEQ) of total PAHs was 0.70, and the TEQ of BaP (0.178) was the highest, followed by that of Bkf (0.090), dibenz[a,h]anthracene (Dah) (0.048), and indeno[1,2,3-cd]pyrene (0.034). The medians of the incremental lifetime cancer risk for long-term exposure to PAHs were 2.74E-8, 1.98E-8, and 1.71E-7 for children, teenagers, and adults, respectively, indicating that the carcinogenic risk of PAHs pollution in air was acceptable to local residents in this area. Sensitivity analysis revealed that BaP, Bkf, and Dah significantly contributed to carcinogenic toxicity. This research provides comprehensive statistics on the local air persistent organic pollutants profile, helps to identify the principal pollution source and compounds, and contributes to the prevention of regional air pollution. Supplementary Information: The online version contains supplementary material available at 10.1007/s12403-023-00572-x.

Design Strategies and Applications of Dimensional Optical Field Manipulation Based on Metasurfaces.

Recent rapid progress in metasurfaces is underpinned by the physics of local and nonlocal resonances and the modes coupling among them, leading to tremendous applications such as optical switching, information transmission, and sensing. In this review paper, an overview of the recent advances in a broad range of dimensional optical field manipulation based on metasurfaces categorized into different classes based on design strategies is provided. This review starts from the near-field optical resonances of artificial nanostructures and discusses the far-field optical wave manipulation based on fundamental mechanisms such as mode generation and mode coupling. The recent advances in optical field manipulation based on metasurfaces in different optical dimensions such as phase and polarization are summarized, and newly-developed dimensions such as the orbital angular momentum and the coherence dimensions resulting from phase modulation are discussed. Then, the recent achievements of multiplexing and multifunctional metasurfaces empowered by multidimensional optical field manipulation for optical information transmission and integrated applications are reviewed. Finally, the paper concludes with a few perspectives on emerging trends, possible directions, and existing challenges in this fast-developing field.

Mesoporous Surface-Sulfurized Fe-Co3O4 Nanosheets Integrated with N/S Co-Doped Graphene as a Robust Bifunctional Electrocatalyst for Oxygen Evolution and Reduction Reactions.

Playing a significant role in electrochemical energy conversion and storage systems, heteroatom-doped transition metal oxides are key materials for oxygen-involving reactions. Herein, mesoporous surface-sulfurized Fe-Co3O4 nanosheets integrated with N/S co-doped graphene (Fe-Co3O4-S/NSG) were designed as composite bifunctional electrocatalysts for the oxygen evolution reaction (OER) and the oxygen reduction reaction (ORR). Compared with the Co3O4-S/NSG catalyst, it exhibited superior activity in the alkaline electrolytes by delivering an OER overpotential of 289 mV at 10 mA cm-2 and an ORR half-wave potential of 0.77 V vs. RHE. Additionally, Fe-Co3O4-S/NSG kept stable at 4.2 mA cm-2 for 12 h without significant attenuation to render robust durability. This work not only demonstrates the satisfactory effect of the transition-metal cationic modification represented by iron doping on the electrocatalytic performance of Co3O4, but it also provides a new insight on the design of OER/ORR bifunctional electrocatalysts for efficient energy conversion.

DYNC1H1-related epilepsy: Genotype-phenotype correlation.

AIM: To explore the phenotypic spectrum and refine the genotype-phenotype correlation of DYNC1H1-related epilepsy. METHOD: The clinical data of 15 patients with epilepsy in our cohort and 50 patients with epilepsy from 24 published studies with the DYNC1H1 variants were evaluated. RESULTS: In our cohort, 13 variants were identified from 15 patients (seven males, eight females). Twelve variants were de novo and seven were new. Age at seizure onset ranged from 3 months to 4 years 5 months (median age 1 year). Common seizure types were epileptic spasms, focal seizures, tonic seizures, and myoclonic seizures. Mild-to-severe developmental delay was present in all patients. Six patients were diagnosed with West syndrome and one was diagnosed with epileptic encephalopathy with continuous spikes and waves during slow sleep (CSWS). Collectively, in our cohort and published studies, 17% had ophthalmic diseases, 31% of variants were located in the stalk domain, and 92% patients with epilepsy had a malformation of cortical development (MCD). INTERPRETATION: The phenotypes of DYNC1H1-related epilepsy included multiple seizure types; the most common epileptic syndrome was West syndrome. CSWS is a new phenotype of DYNC1H1-related epilepsy. One-third of the variants in patients with epilepsy were located in the stalk domain. Most patients had a MCD and developmental delay. WHAT THIS PAPER ADDS: Nearly 40% of patients with DYNC1H1 variants had epilepsy. Ninety-two percent of patients with DYNC1H1-related epilepsy had malformation of cortical development. More than 10% of patients with DYNC1H1-related epilepsy were diagnosed with West syndrome. Continuous spikes and waves during slow sleep could be a new phenotype of DYNC1H1 variants. One-third of the variants in patients with epilepsy were located in the stalk domain.