Prediction of superhard C1+xN1-x compounds with metal-free magnetism and narrow band gaps.

The scarcity of superhard materials with magnetism or a narrow band gap, despite their potential applications in various fields, makes it desirable to design such materials. Here, a series of C1+xN1-x compounds are theoretically designed by replacing different numbers of nitrogen atoms with carbon atoms in the synthesized C1N1 compound. The results indicate that the compounds C5N3 and C7N1 possess both superhardness and antiferromagnetic ordering due to the introduction of low-coordinated carbon atoms. The hardness of the two compounds is about 40.3 and 54.5 GPa, respectively. The magnetism in both compounds is attributed to the unpaired electrons in low-coordinated carbon atoms, and the magnetic moments are 0.42 and 0.39 µB, respectively. Interestingly, the magnetism in C5N3 remains unaffected by the external pressure used in this study, whereas C7N1 becomes nonmagnetic when the pressure exceeds ∼80 GPa. Electronic calculations reveal that both compounds behave as indirect band gap semiconductors, with narrow energy gaps of about 0.30 and 0.20 eV, respectively. Additionally, the other two compounds, C6N2-I and C6N2-III, exhibit nonmagnetic ordering and possess hardness values of 52.6 and 35.0 GPa, respectively. C6N2-I behaves as a semiconductor with an energy gap of 0.79 eV, and C6N2-III shows metallic behavior. Notably, the energy gaps of C5N3 and C6N2-I remain nearly constant under arbitrary pressure due to their porous and superhard structure. These compounds fill the gap in magnetic or narrow band gap superhard materials, and they can be used in the spintronic or optoelectronic fields where conventional superhard materials are not suitable.

Light on Alzheimer's disease: from basic insights to preclinical studies.

Alzheimer's disease (AD), referring to a gradual deterioration in cognitive function, including memory loss and impaired thinking skills, has emerged as a substantial worldwide challenge with profound social and economic implications. As the prevalence of AD continues to rise and the population ages, there is an imperative demand for innovative imaging techniques to help improve our understanding of these complex conditions. Photoacoustic (PA) imaging forms a hybrid imaging modality by integrating the high-contrast of optical imaging and deep-penetration of ultrasound imaging. PA imaging enables the visualization and characterization of tissue structures and multifunctional information at high resolution and, has demonstrated promising preliminary results in the study and diagnosis of AD. This review endeavors to offer a thorough overview of the current applications and potential of PA imaging on AD diagnosis and treatment. Firstly, the structural, functional, molecular parameter changes associated with AD-related brain imaging captured by PA imaging will be summarized, shaping the diagnostic standpoint of this review. Then, the therapeutic methods aimed at AD is discussed further. Lastly, the potential solutions and clinical applications to expand the extent of PA imaging into deeper AD scenarios is proposed. While certain aspects might not be fully covered, this mini-review provides valuable insights into AD diagnosis and treatment through the utilization of innovative tissue photothermal effects. We hope that it will spark further exploration in this field, fostering improved and earlier theranostics for AD.

Role of Qufeng Tongqiao Prescription in the protection of cerebral ischemia and associated molecular network mechanism.

To explore the of Qufeng Tongqiao Prescription in the treatment of cerebral ischemia-reperfusion (CIR) and associated molecular network mechanism. Venny diagram, gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) analysis, protein-protein interaction (PPI), hub genes mining, molecular docking, combined with animal experiments and Nissl stain were performed to determine the molecular network mechanism of Qufeng Tongqiao Prescription for CIR treatment. Fifty three intersecting genes between Qufeng Tongqiao Prescription and cerebral ischemia reperfusion were acquired from Venny analysis. GO analysis showed that the main biological process (BP) was response to lipopolysaccharide, and the main cell localization (CC) process was membrane raft, while the most important molecular function (MF) process is Cytokine receptor binding. Moreover, AGE-RAGE signaling pathway in diabetic complications is the most important signaling pathway in KEGG pathway. Through molecular docking, it was found that Astragalus membranaceus was docked with MAPK14, IL4, FOS, IL6, and JUN; pueraria membranaceus was directly docked with JUN and IL4; Acorus acorus was linked to JUN and MAPK14; Ganoderma ganoderma and human were involved in JUN docking, and Ligusticum chuanqi and pueraria could not be docked with MAPK14, respectively. The results of animal experiments showed that Qufeng Tongqiao Prescription significantly improved behavioral performance and reduced the number of neuronal deaths in rats subjected to CIR, and molecular mechanisms are associated with FOS, IL-6, IL4, JUN, and MAPK14, of there, IL-6, as a vital candidator, which has been confirmed by immunostaining detection. Together, Qufeng Tongqiao Prescription has positive therapeutic effect on CIR, and the underlying mechanism is involved MAPK14, FOS, IL4, and JUN network, while IL-6 may be as a vital target.

LINC00158 modulates the function of BEAS-2B cells via targeting BCL11B and ameliorates OVA-LPS-induced severe asthma in mice models.

Persistent type (T) 2 airway inflammation plays an important role in the development of severe asthma. However, the molecular mechanisms leading to T2 severe asthma have yet to be fully clarified. Human normal lung epithelial cells (BEAS-2B cells) were transfected with LINC00158/BCL11B plasmid/small interfering RNA (siRNA). Levels of epithelial-mesenchymal transition (EMT)-related markers were measured using real-time qPCR (RT-qPCR) and western blot. A dual luciferase reporter assay was used to validate the targeting relationship between LINC00158 and BCL11B. The effects of LINC00158-lentivirus vector-mediated overexpression and dexamethasone on ovalbumin (OVA)/lipopolysaccharide (LPS)-induced severe asthma were investigated in mice in vivo. Our study showed that overexpression of LINC00158/BCL11B inhibited the levels of EMT-related proteins, apoptosis, and promoted the proliferation of BEAS-2B cells. BCL11B was a direct target of LINC00158. And LINC00158 targeted BCL11B to regulate EMT, apoptosis, and cell proliferation of BEAS-2B cells. Compared with severe asthma mice, LINC00158 overexpression alleviated OVA/LPS-induced airway hyperresponsiveness and airway inflammation, including reductions in T helper 2 cells factors in lung tissue and BALF, serum total- and OVA-specific IgE, inflammatory cell infiltration, and goblet cells hyperplasia. In addition, LINC00158 overexpression alleviated airway remodeling, including reduced plasma TGF-ß1 and collagen fiber deposition, as well as suppression of EMT. Additionally, overexpression of LINC00158 enhanced the therapeutic effect of dexamethasone in severe asthmatic mice models. LINC00158 regulates BEAS-2B cell biological function by targeting BCL11B. LINC00158 ameliorates T2 severe asthma in vivo and provides new insights into the clinical treatment of severe asthma.

Advances in Dyslipidaemia Treatments: Focusing on ApoC3 and ANGPTL3 Inhibitors.

Apolipoprotein C3 (apoC3) and angiopoietin-like protein 3 (ANGPTL3) inhibit lipolysis by lipoprotein lipase and may influence the secretion and uptake of various lipoproteins. Genetic studies show that depletion of these proteins is associated with improved lipid profiles and reduced cardiovascular events so it was anticipated that drugs which mimic the effects of loss-of-function mutations would be useful lipid treatments. ANGPTL3 inhibitors were initially developed as a treatment for severe hypertriglyceridaemia including familial chylomicronaemia syndrome (FCS), which is usually not adequately controlled with currently available drugs. However, it was found ANGPTL3 inhibitors were also effective in reducing low-density lipoprotein cholesterol (LDL-C) and they were studied in patients with homozygous familial hypercholesterolaemia (FH). Evinacumab targets ANGPTL3 and reduced LDL-C by about 50% in patients with homozygous FH and it has been approved for that indication. The antisense oligonucleotide (ASO) vupanorsen targeting ANGPTL3 was less effective in reducing LDL-C in patients with moderate hypertriglyceridaemia and its development has been discontinued but the small interfering RNA (siRNA) ARO-ANG3 is being investigated in Phase 2 studies. ApoC3 can be inhibited by the ASO volanesorsen, which reduced triglycerides by >70% in patients with FCS and it was approved for FCS in Europe but not in the United States because of concerns about thrombocytopaenia. Olezarsen is an N-acetylgalactosamine-conjugated ASO targeting apoC3 which appears as effective as volanesorsen without the risk of thrombocytopaenia and is undergoing Phase 3 trials. ARO-APOC3 is an siRNA targeting apoC3 that is currently being investigated in Phase 3 studies.

Adipose triglyceride lipase suppresses noncanonical inflammasome by hydrolyzing LPS.

Intracellular recognition of lipopolysaccharide (LPS) by mouse caspase-11 or human caspase-4 is a vital event for the activation of the noncanonical inflammasome. Whether negative regulators are involved in intracellular LPS sensing is still elusive. Here we show that adipose triglyceride lipase (ATGL) is a negative regulator of the noncanonical inflammasome. Through screening for genes participating in the noncanonical inflammasome, ATGL is identified as a negative player for intracellular LPS signaling. ATGL binds LPS and catalyzes the removal of the acylated side chains that contain ester bonds. LPS with under-acylated side chains no longer activates the inflammatory caspases. Cells with ATGL deficiency exhibit enhanced immune responses when encountering intracellular LPS, including an elevated secretion of interleukin-1ß, decreased cell viability and increased cell cytotoxicity. Moreover, ATGL-deficient mice show exacerbated responses to endotoxin challenges. Our results uncover that ATGL degrades cytosolic LPS to suppress noncanonical inflammasome activation.

Commonly used software tools produce conflicting and overly-optimistic AUPRC values.

The precision-recall curve (PRC) and the area under it (AUPRC) are useful for quantifying classification performance. They are commonly used in situations with imbalanced classes, such as cancer diagnosis and cell type annotation. We evaluated 10 popular tools for plotting PRC and computing AUPRC, which were collectively used in >3,000 published studies. We found the AUPRC values computed by the tools rank classifiers differently and some tools produce overly-optimistic results.

Astrocyte-Derived Exosomal miR-148a-3p Suppresses Neuroinflammation and Restores Neurological Function in Traumatic Brain Injury by Regulating the Microglial Phenotype.

Interactions between astrocytes and microglia play an important role in the regeneration and repair of traumatic brain injury (TBI), and exosomes are involved in cell-cell interactions. A TBI model was constructed in rats. Brain extract (Ext) was isolated 1 d after TBI. Astrocyte-derived exosomes were obtained by coculturing Ext with primary astrocytes, and the morphology of exosomes was observed by electron microscopy. The isolated exosomes were cocultured with microglia to observe phenotypic changes in M1 and M2 markers. Aberrant RNA expression was detected in necrotic brain tissue and edematous brain tissue. The role of miR-148a-3p in regulating microglial phenotype was explored by knocking down or overexpressing miR-148a-3p. Finally, the effect of miR-148a-3p on TBI was studied in a rat TBI model. Astrocyte-derived exosomes stimulated by Ext promoted the transition of microglia from the M1 phenotype to the M2 phenotype. MiR-148a-3p was highly expressed in TBI. Transfecting miR-148a-3p promoted the transition of microglia from the M1 phenotype to the M2 phenotype and inhibited the lipopolysaccharide-induced inflammatory response in pre-microglia. In a rat TBI model, miR-148a-3p significantly improved the modified neurological severity score and attenuated brain injury, which promoted the transition of microglia from the M1 phenotype to the M2 phenotype. MiR-148a-3p alleviated TBI by inhibiting the nuclear factor κB pathway. Astrocyte-derived exosomal miR-148a-3p regulates the microglial phenotype, inhibits neuroinflammation, and restores neurological function in TBI. These results provide new potential targets for the treatment of TBI.

Deubiquitylase USP31 Induces Autophagy and Promotes the Progression in Lung Squamous Cell Carcinoma Cells by Stabilizing E2F1 Expression.

BACKGROUND: Autophagy exerts a vital role in the progression of lung squamous cell carcinoma (LUSC). Ubiquitin-specific peptidase 31 (USP31) has recently been found to be involved in the development of a variety of cancers. However, whether USP31 modulates autophagy in LUSC remains unclear. METHODS: This study revealed that high levels of USP31 were discovered in LUSC tissue samples employing the Gene Expression Profiling Interactive Analysis (GEPIA) database, quantitative real- time PCR (qRT-PCR), and Western blot analysis. Cell proliferation was tested via cell counting kit 8 (CCK-8) as well as colony formation, demonstrating that USP31-stable knockdown reduced cell viability. RESULTS: Immunofluorescence analysis illustrated that USP31 knockdown blocked the occurrence of LUSC autophagy. Meanwhile, USP31 has been shown to stabilize the expression of E2F transcription factor 1 (E2F1) through the proteasome pathway. Furthermore, overexpressed E2F1 effectively eliminated the effect of USP31 knockdown on LUSC cell proliferation and autophagy. CONCLUSION: In summary, this investigation proved that USP31 promoted LUSC cell growth and autophagy, at least in part by stabilizing E2F1 expression, which provided a potential therapeutic gene for the treatment of LUSC.

Effects of Voltage and Treatment Time of Pulsed Electric Field on Electroporation in Rhizoctonia solani.

The pulsed electric field (PEF) of µs duration can induce electroporation by causing permanent damage to the membrane, leading to cell death. The microbe was treated by a homemade PEF generator instrument. The sterilization effect of PEF on the Rhizoctonia solani was observed by scanning electron microscope (SEM) and transmission electron microscope (TEM), and the leakage of the intracellular contents was measured with a conductometer and an ultraviolet spectrophotometer. The increases in the electrical conductivity and the optical density (OD) value indicated that the cell membrane was damaged, and the intracellular contents overflowed. As a result, according to our experimental conditions, the optimum condition was the high-pulsed electric voltage of 26 kV, and the treatment time was 4 min. It could be concluded that the PEF could damage the cell membrane, and the ratio of electroporation reached 100%, which provides a new method of killing R. solani efficiently.

Reproducible and High-Performance WOLEDs Based on Independent High-Efficiency Triplet Harvesting of Yellow Hot-Exciton ESIPT and Blue TADF Emitters.

Hot exciton organic light-emitting diode (OLED) emitters can balance the high performance of a device and reduce efficiency roll-off by fast reverse intersystem crossing from high-lying triplets (hRISC). In this study, an excited-state intramolecular proton transfer (ESIPT) fluorophore of 2-(benzo[d]thiazol-2-yl)-4-(pyren-1-yl)phenol (PyHBT) with the typical characteristic properties of a hot exciton is developed. With high efficiency of utilization of the exciton (91%), its yellow OLED exhibited high external quantum efficiency (EQE) of 5.6%, current efficiency (CE) of 16.8 cd A-1 , and power efficiency (PE) of 17.3 lm W-1 . The performance of the yellow emissive "hot exciton" ESIPT fluorophores is among the highest recorded. Due to the large Stokes shift of the ESIPT emitter, non-energy-transferred high-performance white OLEDs (WOLEDs) are developed, which are reproducible and highly efficient. This is possible because of the independent harvesting of most of the triplets in both complementary-color emitters without the interference of energy transfer. The PyHBT-based WOLEDs exhibit a maximum EQE of 14.3% and CE of 41.1 cd A-1 , which facilitates the high-yield mass production of inexpensive WOLEDs.

RNA Sequencing and Bioinformatics Analysis to Reveal Potential Biomarkers in Patients with Combined Allergic Rhinitis and Asthma Syndrome.

Introduction: Combined allergic rhinitis and asthma syndrome (CARAS) is a concurrent clinical or subclinical allergic symptom of diseases of the upper and lower respiratory tract. This study is the first to explore the expression profiles of mRNA, lncRNA, and circRNA in CARAS using RNA sequencing, which may provide insight into the mechanisms underlying CARAS. Material and Methods: Whole blood samples from nine participants (three CARAS patients, three AR patients, and three normal control participants) were subjected to perform RNA sequencing, followed by identification of differentially expressed lncRNAs (DElncRNAs), circRNAs (DEcircRNAs) and mRNAs (DEmRNAs). Then, lncRNA/circRNA-mRNA regulatory pairs were constructed, followed by functional analysis, immune infiltration analysis, drug prediction, and expression validation with RT-qPCR and ELISA. Results: The results showed that 61 DEmRNAs, 23 DElncRNAs and 3 DEcircRNAs may be related to the occurrence and development of CARAS. KRT8 may be implicated in the development of AR into CARAS. Three immunity-related mRNAs (IDO1, CYSLTR2, and TEC) and two hypoxia-related mRNAs (TKTL1 and VLDLR) were associated with the occurrence and development of CARAS. TEC may be considered a drug target for Dasatinib in treating CARAS. Several lncRNA/circRNA-mRNA regulatory pairs were identified in CARAS, including LINC00452/MIR4280HG/hsa_circ_0007272/hsa_circ_0070934-CLC, HEATR6-DT/LINC00639/LINC01783/hsa_circ_0008903-TEC, RP11-71L14.3-IDO1/SMPD3, RP11-178F10.2-IDO1/HRH4, and hsa_circ_0008903-CYSLTR2, which may indicate potential regulatory effects of lncRNAs/circRNAs in CARAS. Dysregulated levels of immune cell infiltration may be closely related to CARAS. Conclusion: The regulating effect of lncRNA/circRNA-immunity/hypoxia-related mRNA regulatory pairs may be involved in the occurrence and development of CARAS.

ALKBH5-mediated CHAC1 depletion promotes malignant progression and decreases cisplatin-induced oxidative stress in gastric cancer.

The m6a demethyltransferase ALKBH5 dynamically modulates gene expression and intracellular metabolic molecules by modifying RNA m6a in cancer cells. However, ALKBH5's function in gastric cancer (GC) has remained controversial. This study demonstrates that ALKBH5 is highly expressed in GC. Silencing ALKBH5 hampers proliferation, and metastatic potential, and induces cell death in GC cells. Through a comprehensive analysis of the transcriptome and m6A sequencing, alterations in certain ALKBH5 target genes, including CHAC1, were identified. ALKBH5's demethylation effect regulates CHAC1 RNA stability, leading to reduced CHAC1 expression. Moreover, CHAC1 modulates intracellular ROS levels, influencing the chemotherapy sensitivity of gastric cancer. In summary, our study unveils the pivotal role of the ALKBH5-CHAC1-ROS axis and highlights the significance of m6A methylation in gastric cancer.

The role of oestrogen therapy in reducing risk of Alzheimer's disease: systematic review.

BACKGROUND: Studies have shown a relationship between oestrogen and Alzheimer's disease. However, there is neither clear nor strong evidence on the use of oestrogen-only therapy in reducing the risk of Alzheimer's disease. AIMS: To assess the effects of oestrogen-only therapy on reducing the risk of Alzheimer's disease. METHOD: Inclusion criteria was determined with the PICO framework. Outcome was cognitive function measured by neuropsychological tests and strict protocols. Exclusion criteria included non-Alzheimer's dementia, progesterone-only therapy and pre-menopausal women. Searches were conducted in nine electronic healthcare databases, last searched in July 2022. Quality assessments conducted on randomised controlled trials (RCTs) were performed with the GRADE assessment, and cohort studies and case-control studies were assessed with the Newcastle-Ottawa Scale. Extracted data were used to analyse participants, interventions and outcomes. RESULTS: Twenty-four studies satisfied the search criteria (four RCTs, nine cohort studies, 11 case-control studies). Fifteen studies showed positive associations for oestrogen-only therapy reducing the risk of Alzheimer's disease, and the remaining nine found no evidence of association. CONCLUSIONS: Fifteen studies showed that oestrogen-only therapy effectively reduced the risk of Alzheimer's disease, whereas nine showed no correlation. Studies also investigated oestrogen-related variables such as length of oestrogen exposure, being an apolipoprotein E ε4 carrier and concomitant use of non-steroidal anti-inflammatory drugs, and their role in neuroprotection. This review was limited by the limited ranges of duration of oestrogen treatment and type of oestrogen-only therapy used. In conclusion, oestrogen-only therapy has potential for use in preventing Alzheimer's disease, although current evidence is inconclusive and requires further study.

Ambient black carbon variations and emission characteristics of typical Chinese vessels in the Yangtze River Delta, China.

Black carbon (BC) has a significant impact on air quality, climate change, and human health. Studies on BC from vessel exhaust have been focused on in recent years. To realize the contribution of BC from vessels to ambient air quality, 28 months of BC variation were observed from February 2019 to May 2022, including 3 fishing moratoriums and 2 normal periods. The results showed that the average daily concentration of BC in the fishing moratorium was significantly lower than that in the normal period. The difference proportion of the BC concentration between 370 and 880 nm was calculated over the whole period. As a result, the mean difference value in the fishing moratorium from February to May was 0.06 ± 0.07, and the normal period was -0.02 ± 0.05. The aethalometer model indicated that BC was greatly affected by fossil fuel combustion in the normal period. The effect of vessel emissions on regional BC concentrations was considerable. In addition, 16 PAHs and 21 elements in PM emitted from 24 vessels of different types were sampled and analyzed in Dianshan Lake and the Taipu River. EC accounted for the highest proportion (23.64%) in the sample of small trawlers compared to the emissions from cargo ships with large tonnages. The component profiles of vessel exhaust showed that Zn, As, phenanthrene (Phe), anthracene (Ant), fluoranthene (Fla), and pyrene (Pyr) were the dominant species, although some of these species were mainly recognized as characteristic factors of coal combustion. To improve the accuracy of identifying the vessel source, the diagnostic ratios of Ant/(Ant + Phe), BaA/(BaA + Chr), Phe/Ant, and BaA/Chr were provided, and they exhibited the obvious characteristics of fuel combustion.

Anti-reflux effects of a novel esophagogastric asymmetric anastomosis technique after laparoscopic proximal gastrectomy.

BACKGROUND: Reflux esophagitis is a common postoperative complication of proximal gastrectomy. There is an urgent need for a safer method of performing esophageal-gastric anastomosis that reduces the risk of reflux after proximal gastrectomy. We hypothesize that a novel technique termed esophagogastric asymmetric anastomosis (EGAA) can prevent postoperative reflux in a safe and feasible manner. AIM: To observe a novel method of EGAA to prevent postoperative reflux. METHODS: Initially, we employed a thermal stress computer to simulate and analyze gastric peristalsis at the site of an esophagogastric asymmetric anastomosis. This was done in order to better understand the anti-reflux function and mechanism. Next, we performed digestive tract reconstruction using the EGAA technique in 13 patients who had undergone laparoscopic proximal gastrectomy. Post-surgery, we monitored the structure and function of the reconstruction through imaging exams and gastroscopy. Finally, the patients were followed up to assess the efficacy of the anti-reflux effects. RESULTS: Our simulation experiments have demonstrated that the clockwise contraction caused by gastric peristalsis and the expansion of the gastric fundus caused by the increase of intragastric pressure could significantly tighten the anastomotic stoma, providing a means to prevent the reverse flow of gastric fluids. Thirteen patients with esophagogastric junction tumors underwent laparoscopic proximal gastrectomy, with a mean operation time of 304.2 ± 44.3 min. After the operation, the upper gastroenterography in supine/low head positions showed that eight patients exhibited no gastroesophageal reflux, three had mild reflux, and two had obvious reflux. The abdominal computed tomography examination showed a valve-like structure at the anastomosis. During follow-up, gastroscopy revealed a closed valve-like form at the anastomosis site without stenosis or signs of reflux esophagitis in 11 patients. Only two patients showed gastroesophageal reflux symptoms and mild reflux esophagitis and were treated with proton pump inhibitor therapy. CONCLUSION: EGAA is a feasible and safe surgical method, with an excellent anti-reflux effect after proximal gastrectomy.

Ambient Volatile Organic Compound Characterization, Source Apportionment, and Risk Assessment in Three Megacities of China in 2019.

In order to illustrate pollution characterization, source apportionment, and risk assessment of VOCs in Beijing, Baoding, and Shanghai, field observations of CO, NO, NO2, O3, and volatile organic compounds (VOCs) were conducted in 2019. Concentrations of VOCs were the highest in Beijing (105.4 ± 52.1 ppb), followed by Baoding (97.1 ± 47.5 ppb) and Shanghai (91.1 ± 41.3 ppb). Concentrations of VOCs were the highest in winter (120.3 ± 61.5 ppb) among the three seasons tested, followed by summer (98.1 + 50.8 ppb) and autumn (75.5 + 33.4 ppb). Alkenes were the most reactive VOC species in all cities, accounting for 56.0%, 53.7%, and 39.4% of ozone formation potential in Beijing, Baoding, and Shanghai, respectively. Alkenes and aromatics were the reactive species, particularly ethene, propene, 1,3,5-trimethylbenzene, and m/p-xylene. Vehicular exhaust was the principal source in all three cities, accounting for 27.0%, 30.4%, and 23.3% of VOCs in Beijing, Baoding, and Shanghai, respectively. Industrial manufacturing was the second largest source in Baoding (23.6%) and Shanghai (21.3%), and solvent utilization was the second largest source in Beijing (25.1%). The empirical kinetic modeling approach showed that O3 formation was limited by both VOCs and nitric oxides at Fangshan (the suburban site) and by VOCs at Xuhui (the urban site). Acrolein was the only substance with an average hazard quotient greater than 1, indicating significant non-carcinogenic risk. In Beijing, 1,2-dibromoethane had an R-value of 1.1 × 10-4 and posed a definite carcinogenic risk.

Superhard bulk C4N3 compounds with metal-free magnetism assembled from two-dimensional C4N3: a first-principles study.

Enriching the electronic properties of superhard materials is very important to extend their applications, and some superhard materials with metallic or superconducting characteristics have been designed via theoretical or experimental methods. However, their magnetic features have scarcely been studied, since most of them are limited to nonmagnetic ordering. Here, with the help of first-principles calculations, a series of C4N3 compounds are designed by stacking C4N3 sheets with different sequences. As expected, some of them exhibit both magnetic and superhard characteristics. Notably, all these compounds exhibit dynamic and mechanical stabilities, indicating that their dynamic and mechanical stabilities are independent of the stacking sequence. Among them, the ABC-stacked one is energetically favorable, and it exhibits antiferromagnetic ordering and has a hardness of ∼54.0 GPa, and the electronic calculations show that it is a semiconductor with a direct band gap of ∼1.20 eV. Besides, the magnetism of all magnetic C4N3 compounds is caused by the lower coordinated atoms, and the magnetic moments are located on three-fold C or two-fold coordinated N atoms. Additionally, the magnetic property is deeply dependent on the external pressure. This work opens a potential way to design magnetic superhard materials and can arouse their applications in the spintronic field.