Analysis of the Class 1 Integrons, Carbapenemase Genes and Biofilm Formation Genes Occurrence in Acinetobacter baumannii Clinical Isolates.

Acinetobacter baumannii is a non-fermentative Gram-negative bacterium that can cause nosocomial infections in critically ill patients. Carbapenem-resistant A. baumannii (CRAB) has spread rapidly in clinical settings and has become a key concern. The main objective of this study was to identify the distribution of integrons and biofilm-formation-related virulence genes in CRAB isolates. A total of 269 A. baumannii isolates (219 isolates of CRAB and 50 isolates of carbapenem-sensitive A. baumannii (CSAB)) were collected. Carbapenemase genes (bla KPC, bla VIM, bla IMP, bla NDM, and bla OXA-23-like) and biofilm-formation-related virulence genes (abal, bfms, bap, and cusE) were screened with PCR. Class 1 integron was screened with PCR, and common promoters and gene cassette arrays were determined with restriction pattern analysis combined with primer walking sequencing. Whole-genome sequencing was conducted, and data were analyzed for a bla OXA-23-like-negative isolate. All 219 CRAB isolates were negative for bla KPC, bla VIM, bla IMP, and bla NDM, while bla OXA-23-like was detected in 218 isolates. The detection rates for abal, bfms, bap, and cusE in 219 CRAB were 93.15%, 63.93%, 88.13%, and 77.63%, respectively. Class 1 integron was detected in 75 CRAB (34.25%) and in 3 CSAB. The single gene cassette array aacA4-catB8-aadA1 with relatively strong PcH2 promoter was detected in class 1 integrons. The bla OXA-23-like-negative CRAB isolate was revealed to be a new sequence type (Oxford 3272, Pasteur 2520) carrying bla OXA-72, bla OXA-259, and bla ADC-26. In conclusion, bla OXA-23-like was the main reason for CRAB's resistance to carbapenems. A new (Oxford 3272, Pasteur 2520) CRAB sequence type carrying the bla OXA-72, bla OXA-259, and bla ADC-26 was reported.

PRMT5-mediated arginine methylation of FXR1 is essential for RNA binding in cancer cells.

Emerging evidence indicates that arginine methylation promotes the stability of arginine-glycine-rich (RGG) motif-containing RNA-binding proteins (RBPs) and regulates gene expression. Here, we report that post-translational modification of FXR1 enhances the binding with mRNAs and is involved in cancer cell growth and proliferation. Independent point mutations in arginine residues of FXR1's nuclear export signal (R386 and R388) and RGG (R453, R455 and R459) domains prevent it from binding to RNAs that form G-quadruplex (G4) RNA structures. Disruption of G4-RNA structures by lithium chloride failed to bind with FXR1, indicating its preference for G4-RNA structure containing mRNAs. Furthermore, loss-of-function of PRMT5 inhibited FXR1 methylation both in vivo and in vitro, affecting FXR1 protein stability, inhibiting RNA-binding activity and cancer cell growth and proliferation. Finally, the enhanced crosslinking and immunoprecipitation (eCLIP) analyses reveal that FXR1 binds with the G4-enriched mRNA targets such as AHNAK, MAP1B, AHNAK2, HUWE1, DYNC1H1 and UBR4 and controls its mRNA expression in cancer cells. Our findings suggest that PRMT5-mediated FXR1 methylation is required for RNA/G4-RNA binding, which promotes gene expression in cancer cells. Thus, FXR1's structural characteristics and affinity for RNAs preferentially G4 regions provide new insights into the molecular mechanism of FXR1 in oral cancer cells.

The P286R mutation of DNA polymerase ε activates cancer-cell-intrinsic immunity and suppresses endometrial tumorigenesis via the cGAS-STING pathway.

Endometrial carcinoma (EC) is a prevalent gynecological tumor in women, and its treatment and prevention are significant global health concerns. The mutations in DNA polymerase ε (POLE) are recognized as key features of EC and may confer survival benefits in endometrial cancer patients undergoing anti-PD-1/PD-L1 therapy. However, the anti-tumor mechanism of POLE mutations remains largely elusive. This study demonstrates that the hot POLE P286R mutation impedes endometrial tumorigenesis by inducing DNA breakage and activating the cGAS-STING signaling pathway. The POLE mutations were found to inhibit the proliferation and stemness of primary human EC cells. Mechanistically, the POLE mutants enhance DNA damage and suppress its repair through the interaction with DNA repair proteins, leading to genomic instability and the upregulation of cytoplasmic DNA. Additionally, the POLE P286R mutant also increases cGAS level, promotes TBK1 phosphorylation, and stimulates inflammatory gene expression and anti-tumor immune response. Furthermore, the POLE P286R mutation inhibits tumor growth and facilitates the infiltration of cytotoxic T cells in human endometrial cancers. These findings uncover a novel mechanism of POLE mutations in antagonizing tumorigenesis and provide a promising direction for effective cancer therapy.

PRMT1 and PRMT5: on the road of homologous recombination and non-homologous end joining.

DNA double-strand breaks (DSBs) are widely accepted to be the most deleterious form of DNA lesions that pose a severe threat to genome integrity. Two predominant pathways are responsible for repair of DSBs, homologous recombination (HR) and non-homologous end-joining (NHEJ). HR relies on a template to faithfully repair breaks, while NHEJ is a template-independent and error-prone repair mechanism. Multiple layers of regulation have been documented to dictate the balance between HR and NHEJ, such as cell cycle and post-translational modifications (PTMs). Arginine methylation is one of the most common PTMs, which is catalyzed by protein arginine methyltransferases (PRMTs). PRMT1 and PRMT5 are the predominate PRMTs that promote asymmetric dimethylarginine and symmetric dimethylarginine, respectively. They have emerged to be crucial regulators of DNA damage repair. In this review, we summarize current understanding and unaddressed questions of PRMT1 and PRMT5 in regulation of HR and NHEJ, providing insights into their roles in DSB repair pathway choice and the potential of targeting them for cancer therapy.

Autophagy dictates sensitivity to PRMT5 inhibitor in breast cancer.

Protein arginine methyltransferase 5 (PRMT5) catalyzes mono-methylation and symmetric di-methylation on arginine residues and has emerged as a potential antitumor target with inhibitors being tested in clinical trials. However, it remains unknown how the efficacy of PRMT5 inhibitors is regulated. Here we report that autophagy blockage enhances cellular sensitivity to PRMT5 inhibitor in triple negative breast cancer cells. Genetic ablation or pharmacological inhibition of PRMT5 triggers cytoprotective autophagy. Mechanistically, PRMT5 catalyzes monomethylation of ULK1 at R532 to suppress ULK1 activation, leading to attenuation of autophagy. As a result, ULK1 inhibition blocks PRMT5 deficiency-induced autophagy and sensitizes cells to PRMT5 inhibitor. Our study not only identifies autophagy as an inducible factor that dictates cellular sensitivity to PRMT5 inhibitor, but also unearths a critical molecular mechanism by which PRMT5 regulates autophagy through methylating ULK1, providing a rationale for the combination of PRMT5 and autophagy inhibitors in cancer therapy.

TRAF6 Promotes PRMT5 Activity in a Ubiquitination-Dependent Manner.

Protein arginine methyltransferase 5 (PRMT5) is the primary enzyme generating symmetric dimethylarginine (sDMA) on numerous substrates, through which it regulates many cellular processes, such as transcription and DNA repair. Aberrant expression and activation of PRMT5 is frequently observed in various human cancers and associated with poor prognosis and survival. However, the regulatory mechanisms of PRMT5 remain poorly understood. Here, we report that TRAF6 serves as an upstream E3 ubiquitin ligase to promote PRMT5 ubiquitination and activation. We find that TRAF6 catalyzes K63-linked ubiquitination of PRMT5 and interacts with PRMT5 in a TRAF6-binding-motif-dependent manner. Moreover, we identify six lysine residues located at the N-terminus as the primarily ubiquitinated sites. Disruption of TRAF6-mediated ubiquitination decreases PRMT5 methyltransferase activity towards H4R3 in part by impairing PRMT5 interaction with its co-factor MEP50. As a result, mutating the TRAF6-binding motifs or the six lysine residues significantly suppresses cell proliferation and tumor growth. Lastly, we show that TRAF6 inhibitor enhances cellular sensitivity to PRMT5 inhibitor. Therefore, our study reveals a critical regulatory mechanism of PRMT5 in cancers.

Contributions of local emissions and regional background to summertime ozone in central China.

Source contributions and regional transport of maximum daily average 8-h (MDA8) O3 during a high O3 month (June 2019) in Henan province in central China are explored using a source-oriented Community Multiscale Air Quality (CMAQ) model. The monthly average MDA8 O3 exceeds ∼70 ppb in more than half of the areas and shows a clear spatial gradient, with lower O3 concentrations in the southwest and higher in the northeast. Significant contributions of anthropogenic emissions to monthly average MDA8 O3 concentrations of more than 20 ppb are predicted in the provincial capital Zhengzhou, mostly due to emissions from the transportation sector (∼50%) and in the areas in the north and northeast regions where industrial and power generation-related emissions are high. Biogenic emissions in the region only contribute to approximately 1-3 ppb of monthly average MDA8 O3. In industrial areas north of the province, their contributions reach 5-7 ppb. Two CMAQ-based O3-NOx-VOCs sensitivity assessments (the local O3 sensitivity ratios based on the direct decoupled method and the production ratio of H2O2 to HNO3) and the satellite HCHO to NO2 column density ratio consistently show that most of the areas in Henan are in NOx-limited regime. In contrast, the high O3 concentration areas in the north and at the city centers are in the VOC-limited or transition regimes. The results from this study suggest that although reducing NOx emissions to reduce O3 pollution in the region is desired in most areas, VOC reductions must be applied to urban and industrial regions. Source apportionment simulations with and without Henan anthropogenic emissions show that the benefit of local anthropogenic NOx reduction might be lower than expected from the source apportionment results because the contributions of Henan background O3 increase in response to the reduced local anthropogenic emissions due to less NO titration. Thus, collaborative O3 controls in neighboring provinces are needed to reduce O3 pollution problems in Henan effectively.

CDK5-PRMT1-WDR24 signaling cascade promotes mTORC1 signaling and tumor growth.

The mammalian target of rapamycin complex1 (mTORC1) is a central regulator of metabolism and cell growth by sensing diverse environmental signals, including amino acids. The GATOR2 complex is a key component linking amino acid signals to mTORC1. Here, we identify protein arginine methyltransferase 1 (PRMT1) as a critical regulator of GATOR2. In response to amino acids, cyclin-dependent kinase 5 (CDK5) phosphorylates PRMT1 at S307 to promote PRMT1 translocation from nucleus to cytoplasm and lysosome, which in turn methylates WDR24, an essential component of GATOR2, to activate the mTORC1 pathway. Disruption of the CDK5-PRMT1-WDR24 axis suppresses hepatocellular carcinoma (HCC) cell proliferation and xenograft tumor growth. High PRMT1 protein expression is associated with elevated mTORC1 signaling in patients with HCC. Thus, our study dissects a phosphorylation- and arginine methylation-dependent regulatory mechanism of mTORC1 activation and tumor growth and provides a molecular basis to target this pathway for cancer therapy.

[Variation Characteristics and Source Apportionment of Atmospheric VOCs at Multi-sites in Zhengzhou].

From July 2020 to June 2021, monthly offline sampling of atmospheric VOCs was carried out and analyzed at three urban sites and one suburban site in Zhengzhou. Then, the volume fraction levels, composition characteristics, reactivity, and source apportionment of atmospheric VOCs were discussed. The results showed that the volume fraction of atmospheric VOCs in Zhengzhou was (37.50±14.30)×10-9 during the sampling period, and the proportion of components was represented by alkanes (33%)>OVOCs (24%)>halogenated hydrocarbons (23%)>aromatic hydrocarbons (8%)>alkenes (7%)>alkynes (4%)>sulfides (1%). The seasonal variation characteristics were winter>autumn>summer>spring, and the monthly average value of VOCs had the highest value in January and the lowest value in May; the spatial variation characteristics were Zhengzhou University (ZD)>Jiancezhan (JCZ)>Jingkaiqu (JKQ)>Gangli Reservoir (GLR). The average·OH loss rate (L·OH) was 4.24 s-1, and the average ozone formation potential (OFP) was 172.27 µg·m-3; the top ten species of L·OH and OFP at each site and in each season were dominated by alkenes, OVOCs, and aromatic hydrocarbons. The results of positive matrix factorization (PMF) showed that the main sources of VOCs were vehicle emissions (28%), solvent utilization (24%), industrial emissions (24%), and oil and gas volatilization (19%) and plant emissions (5%).

Arginine methylation of BRD4 by PRMT2/4 governs transcription and DNA repair.

BRD4 functions as an epigenetic reader and plays a crucial role in regulating transcription and genome stability. Dysregulation of BRD4 is frequently observed in various human cancers. However, the molecular details of BRD4 regulation remain largely unknown. Here, we report that PRMT2- and PRMT4-mediated arginine methylation is pivotal for BRD4 functions on transcription, DNA repair, and tumor growth. Specifically, PRMT2/4 interacts with and methylates BRD4 at R179, R181, and R183. This arginine methylation selectively controls a transcriptional program by promoting BRD4 recruitment to acetylated histones/chromatin. Moreover, BRD4 arginine methylation is induced by DNA damage and thereby promotes its binding to chromatin for DNA repair. Deficiency in BRD4 arginine methylation significantly suppresses tumor growth and sensitizes cells to BET inhibitors and DNA damaging agents. Therefore, our findings reveal an arginine methylation-dependent regulatory mechanism of BRD4 and highlight targeting PRMT2/4 for better antitumor effect of BET inhibitors and DNA damaging agents.

Histone Deacetylase 3 Governs ß-Estradiol-ERα-Involved Endometrial Tumorigenesis via Inhibition of STING Transcription.

PURPOSE: The stimulator of interferon genes (STING) pathway plays a crucial role in antitumor immunity, and it is strictly regulated by many types of post-translational modifications. However, the contribution of acetylation involved in the regulation of STING to endometrial tumorigenesis remains unclear. METHODS: We attempted to identify the key role of STING in endometrial carcinoma (EC) tissue and cell lines and explore its epigenetic regulation mechanism by HDACs that are critically involved in EC. We used IHC and qRT-PCR to detect the protein level and mRNA level of STING expression in endometrial carcinoma tissues, then explored the potential role of STING in tumor proliferation and apoptosis by CCK8 and flow cytometry, and identified the STING effect in the tumorigenicity by a mouse xenograft assay. We explored the possible relationship of acetylation alteration in STING regulation by ChIP analysis and Co-IP, and we knocked out STING in ECC1 and Ishikawa cells using CRISPR-Cas9 to further confirm the critical role of STING restoration induced by HDAC3 inhibitor RGFP-966 in the proliferation and apoptosis. RESULTS: We found that STING expression was largely decreased and worked as an important regulator of cell proliferation and apoptosis; either activated or overexpressed STING, with both pharmacological and genetic approaches, largely blocked cell proliferation and induced apoptosis in EC. Moreover, STING expression was deregulated by both ß-estradiol and HDAC3. Mechanically, we determined that HDAC3 can interact with ß-estradiol-ERα and induce deacetylation of histone 3 lysine 4 at the STING promoter, thereby decreasing STING expression. Inhibition of HDAC3 increased STING expression, thereby inhibiting tumorigenesis. CONCLUSION: This study reveals a novel molecular mechanism by which HDAC3 inhibits STING transcription via ß-estradiol-ERα and provides a promising therapy (a combination of HDAC and STING) for combating endometrial cancer.

The Role of Protein Arginine Methyltransferases in DNA Damage Response.

In response to DNA damage, cells have developed a sophisticated signaling pathway, consisting of DNA damage sensors, transducers, and effectors, to ensure efficient and proper repair of damaged DNA. During this process, posttranslational modifications (PTMs) are central events that modulate the recruitment, dissociation, and activation of DNA repair proteins at damage sites. Emerging evidence reveals that protein arginine methylation is one of the common PTMs and plays critical roles in DNA damage response. Protein arginine methyltransferases (PRMTs) either directly methylate DNA repair proteins or deposit methylation marks on histones to regulate their transcription, RNA splicing, protein stability, interaction with partners, enzymatic activities, and localization. In this review, we summarize the substrates and roles of each PRMTs in DNA damage response and discuss the synergistic anticancer effects of PRMTs and DNA damage pathway inhibitors, providing insight into the significance of arginine methylation in the maintenance of genome integrity and cancer therapies.

Regulation of Embryonic Stem Cell Self-Renewal.

Embryonic stem cells (ESCs) are a type of cells capable of self-renewal and multi-directional differentiation. The self-renewal of ESCs is regulated by factors including signaling pathway proteins, transcription factors, epigenetic regulators, cytokines, and small molecular compounds. Similarly, non-coding RNAs, small RNAs, and microRNAs (miRNAs) also play an important role in the process. Functionally, the core transcription factors interact with helper transcription factors to activate the expression of genes that contribute to maintaining pluripotency, while suppressing the expression of differentiation-related genes. Additionally, cytokines such as leukemia suppressor factor (LIF) stimulate downstream signaling pathways and promote self-renewal of ESCs. Particularly, LIF binds to its receptor (LIFR/gp130) to trigger the downstream Jak-Stat3 signaling pathway. BMP4 activates the downstream pathway and acts in combination with Jak-Stat3 to promote pluripotency of ESCs in the absence of serum. In addition, activation of the Wnt-FDZ signaling pathway has been observed to facilitate the self-renewal of ESCs. Small molecule modulator proteins of the pathway mentioned above are widely used in in vitro culture of stem cells. Multiple epigenetic regulators are involved in the maintenance of ESCs self-renewal, making the epigenetic status of ESCs a crucial factor in this process. Similarly, non-coding RNAs and cellular energetics have been described to promote the maintenance of the ESC's self-renewal. These factors regulate the self-renewal and differentiation of ESCs by forming signaling networks. This review focused on the role of major transcription factors, signaling pathways, small molecular compounds, epigenetic regulators, non-coding RNAs, and cellular energetics in ESC's self-renewal.

[Trend Changes in Ozone Pollution and Sensitivity Analysis of Ozone in Henan Province].

Based on air quality station data and satellite remote sensing data, the interannual variation characteristics and seasonal variation trends of near-surface ozone (O3) in Henan province were studied, and the variation in O3 sensitivity was analyzed. The results showed that the O3 concentration near the surface of Henan province increased first and then decreased from 2015 to 2020. The highest O3 concentration was found in 2018, and the annual mean of the maximum daily 8 h moving mean (MDA8) of O3 was 110.70 µg·m-3. The difference in MDA8 values among different stations gradually decreased. From 2015 to 2020, the average monthly MDA8 in Henan province showed an upward trend, with a growth rate of 2.46 µg·(m3·a)-1. According to the MK trend test, except for in Luohe, Nanyang, and Pingdingshan, the rising trend in other cities was significant (P<0.05). The concentration of MDA8 in the four seasons also showed an increasing trend during the 6 years as follows:autumn (19.31%)>winter (17.09%)>spring (16.82%)>summer (7.24%). From 2015 to 2019, the high value of tropospheric NO2 was concentrated in the northwest of Henan province, and the concentration showed a decreasing trend with a decreasing rate of 0.34×1015 molecules·(cm2·a)-1, whereas the tropospheric HCHO showed a slow rising trend with an annual growth rate of 0.19×1015 molecules·(cm2·a)-1, with a higher concentration in the northern urban area. The O3 sensitivity control area from 2015 to 2019 showed that most of the eastern part of Henan province belonged to the VOCs limited category.

[Characteristics and Source Apportionment of Vehicular VOCs Emissions in a Tunnel Study].

To explore the emission characteristics of volatile organic compounds (VOCs) from vehicular exhaust sources and evaporative sources with ethanol gasoline (E10) as the main fuel, VOCs sampling campaigns were carried out in the north third ring tunnel of Zhengzhou city for two consecutive weeks in December 2019. In addition, the characteristics of traffic flow and environmental information were also monitored in the tunnel. Firstly, 106 VOCs were quantified using gas chromatography/mass spectrometry (GC/MS), and then source apportionment of VOCs in the tunnel was carried out using a positive matrix factorization (PMF5.0)-chemical mass balance (CMB8.2) composite model. Finally, the ozone formation potential (OFP) and secondary organic aerosol formation potential (SOAFP) of vehicle exhaust sources and evaporative sources were analyzed using the maximum incremental reactivity (MIR) and fractional aerosol coefficient (FAC). The results showed that ρ(VOCs) in the tunnel was (2794.5±147.4) µg·m-3 during the experiment, among which halogenated hydrocarbons[(32.4±2.0)%] accounted for the highest proportion, followed by aromatic hydrocarbons[(27.5±0.6)%] and alkanes[(23.3±0.8)%]. Source apportionment of vehicular VOCs showed that exhaust emissions (62.5%)>evaporative emissions (37.5%), whereas the contribution of OFP was that exhaust emissions (71.9%)>evaporative emissions (28.1%), and the contribution of SOAFP was that exhaust emissions (75.8%)>evaporative emissions (24.2%). The dominant components of OFP in evaporative sources were m,p-diethylbenzene, isoprene, and trans-2-pentene, whereas m,p-diethylbenzene, m,p-xylene, and 1,2,3-trimethylbenzene were the dominant components of SOAFP. The major components of OFP in exhaust sources were m,p-xylene, 1,2,4-trimethylbenzene, and 1,3,5-trimethylbenzene, whereas m,p-xylene, m,p-diethylbenzene, and 1,3,5-trimethylbenzene were the dominant components of SOAFP. In regions where ethanol gasoline is used, special attention should be paid not only to the exhaust emissions control but also to strengthening the emissions reduction of VOCs from vehicle evaporative sources, especially the high active components such as aromatic hydrocarbons and alkenes.

DNA-PK promotes activation of the survival kinase AKT in response to DNA damage through an mTORC2-ECT2 pathway.

The kinase AKT (also known as protein kinase B) is a key regulator of cell proliferation, survival, and metabolism. In addition to being activated by growth factors, AKT is activated in response to DNA damage. Here, we found that the DNA damage response kinase DNA-PK sustains cell survival through a phosphorylation event that leads to increased AKT activity. In various cancer and noncancer cells in culture, DNA damage caused by ionizing radiation or topoisomerase inhibitors triggered DNA-PK­dependent phosphorylation of the mTOR complex 2 (mTORC2) subunit Sin1, which enabled its interaction with the guanine nucleotide exchange factor ECT2. Depleting Sin1 or ECT2 or disrupting the protein interaction or catalytic function of ECT2 attenuated DNA damage­induced AKT activation, thereby enhancing cellular sensitivity to DNA-damaging agents. Our findings elucidate a mechanism mediating DNA damage­induced AKT activation and cell survival.

Increased expression of PD-L1 in endometrial cancer stem-like cells is regulated by hypoxia.

BACKGROUND: The expression levels of the programmed cell death ligand 1 (PD-L1), known as an immune-inhibitory molecule, are closely associated with cancer stem cell (CSCs) immune escape. Recently, PD-L1 has also been reported to be able to regulate the self-renewal of cancer stem cells. However, The expression and intrinsic role of PD-L1 in endometrial cancer stem-like cell (ECSC) maintenance and its underlying mechanism of action remain unclear. METHODS: Using flow cytometry and western blot assays, we have demonstrated that PD-L1 expression is higher in ECSCs derived from endometrial cancer than in nonstem-like cancer cells. Using mouse xenograft assays for ECSC tumorigenicity. Using gene reporter assay for uncovering the regulation mechanism of PD-L1 in the hypoxia. RESULTS: We revealed the high expression levels of PD-L1 in ECSCs and its correlation with self-renewal. We further found that PD-L1 knockdown reduced expression of several pluripotency-related genes (aldehyde dehydrogenase 1 (ALDH1), CD133, OCT4, SOX2, NANOG), impaired ECSC proliferation and undifferentiated colonies and decreased the number of CD133 positive ECSCs and the number of stem-like spheres. Furthermore, we found that PD-L1 knockdown inhibited ECSC tumorigenicity and the PD-L1 induced self-renewal capability of ECSCs was dependent upon hypoxia HIF-1α and HIF-2α activation. CONCLUSIONS: These data link ECSC maintenance to PD-L1 expression through hypoxia and suggest a promising target for PD1/PD-L1 immunotherapy.

Assessment of summertime O3 formation and the O3-NOX-VOC sensitivity in Zhengzhou, China using an observation-based model.

Zhengzhou, the provincial capital of Henan province in Central China and a major hub of the country's transportation network, has been suffering from severe summertime ozone (O3) pollution. Simultaneous field measurements of O3 and its precursors, including NOx, CO, HONO, and 106 volatile organic compounds (VOCs), were conducted at an urban site (the municipal environmental monitoring station, MEM) in Zhengzhou in July 2019. The Community Multiscale Air Quality (CMAQ) model, which incorporates the Master Chemical Mechanism (MCMv3.3.1), was modified to work as a 0-D observation-based photochemical box model to assess the sources and sinks of HOx radicals and O3, and the OH reactivity (KOH) and ozone formation potential (OFP) of major VOC groups. In addition, the O3-NOx-VOC sensitivity was evaluated using the relative incremental reactivity (RIR) and O3 formation isopleth techniques. The OH radicals were mainly generated from the propagation reaction of HO2 + NO (91-95%). The daily average mixing ratios of OH and HO2 radicals were significantly higher during high O3 days, reaching as high as 4.8 × 106 and 7.7 × 108 molecules cm-3, respectively. Photochemical O3 formation was mostly due to the conversion of NO to NO2 by HO2 radicals (52-54%), while the NO2 + OH reaction was the main contributor to O3 destruction (70- 76%). Alkenes and aromatics were the main anthropogenic VOC contributors to KOH and OFP. Contributions of biogenic VOCs became much more important on high O3 days, correlating with the increase in temperature and solar radiation. RIR analysis showed that the O3 formation was under the VOC-limited on low O3 days but was in the transition regime during the O3 pollution buildup and persisting days. These results are generally consistent with those based on the O3 formation isopleth. This paper provides important corroborative scientific evidence urgently needed by local governments to formulate O3 pollution control strategies.

Elevated particle acidity enhanced the sulfate formation during the COVID-19 pandemic in Zhengzhou, China.

The significant reduction in PM2.5 mass concentration after the outbreak of COVID-19 provided a unique opportunity further to study the formation mechanism of secondary inorganic aerosols. Hourly data of chemical components in PM2.5, gaseous pollutants, and meteorological data were obtained from January 1 to 23, 2020 (pre-lockdown) and January 24 to February 17, 2020 (COVID-lockdown) in Zhengzhou, China. Sulfate, nitrate, and ammonium were the main components of PM2.5 during both the pre-lockdown and COVID-lockdown periods. Compared with the pre-lockdown period, even though the concentration and proportion of nitrate decreased, nitrate was the dominant component in PM2.5 during the COVID-lockdown period. Moreover, nitrate production was enhanced by the elevated O3 concentration, which was favorable for the homogeneous and hydrolysis nitrate formation despite the drastic decrease of NO2. The proportion of sulfate during the COVID-lockdown period was higher than that before. Aqueous-phase reactions of H2O2 and transition metal (TMI) catalyzed oxidations were the major pathways for sulfate formation. During the COVID-lockdown period, TMI-catalyzed oxidation became the dominant pathway for aqueous-phase sulfate formation because the elevated acidity favored the dissolution of TMI. Therefore, the enhanced TMI-catalyzed oxidation affected by the elevated particle acidity dominated the sulfate formation, resulting in the slight increase of sulfate concentration during the COVID-lockdown period in Zhengzhou.

[Atmospheric NH3 Emission Inventory and Analysis of the Driving Force in Zhengzhou City].

In this study, a 2017-based emission inventory of ammonia(NH3) was established for Zhengzhou by using the emission factor method. The 1 km×1 km gridded emission inventory was mapped using GIS technology. The NH3 emissions between 2007 and 2017 and driving force between 1989 and 2017 were also analyzed. Results showed that the total 2017-based NH3 emission in Zhengzhou was 18143.3 t, and the average emission intensity reached 2.4 t·km-2. The top emission source was from agriculture, accounting for 63.4% of the total emission, followed by fugacity(11.3%). The main contribution sources of livestock were egg poultry, pigs, and cattle. Dengfeng, Xingyang, and Xinmi had the highest emissions, accounting for 19.3%, 16.5%, and 15.6% of the total emission, respectively. The NH3 emission was higher in the southern and central western regions of Zhengzhou and lower in the northeastern region. The NH3 emission in Zhengzhou showed a downward trend from 2007 to 2017. The NH3 emissions from 1987 to 2017 were similar to the environmental Kuznets Curve, i.e., the emissions increased first and then decreased with the increase of per capita gross domestic product(GDP) and urbanization rate.