Protective effect and pharmacokinetics of dihydromyricetin nanoparticles on oxidative damage of myocardium.

PURPOSE: This study aims to investigate the protective mechanism of dihydromyricetin PLGA nanoparticles (DMY-PLGA NPs) against myocardial ischemia-reperfusion injury (MIRI) in vitro and the improvement of oral bioavailability in vivo. METHODS: DMY-PLGA NPs was prepared and characterized by emulsifying solvent volatilization, and the oxidative stress model of rat H9c2 cardiomyocyte induced by H2O2 was established. After administration, cell survival rate, lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) were detected, and the expressions of PGC1α and PPARα were detected by western blot (WB). At the same time, the pharmacokinetics in rats were studied to explore the improvement of bioavailability. RESULTS: DMY-PLGA NPs can significantly increase cell survival rate, decrease LDH and MDA content, increase SOD content and PGC1α、PPARα protein expression. Compared with DMY, the peak time of DMY-PLGA NPs was extended (P<0.1), and the bioavailability was increased by 2.04 times. CONCLUSION: DMY-PLGA NPs has a significant protective effect on H9c2 cardiomyocytes, which promotes the absorption of DMY and effectively improves bioavailability.

Immune cell infiltration and drug response in glioblastoma multiforme: insights from oxidative stress-related genes.

BACKGROUND: GBM, also known as glioblastoma multiforme, is the most prevalent and lethal type of brain cancer. The cell proliferation, invasion, angiogenesis, and treatment of gliomas are significantly influenced by oxidative stress. Nevertheless, the connection between ORGs and GBM remains poorly comprehended. The objective of this research is to investigate the predictive significance of ORGs in GBM and their potential as targets for therapy. METHODS: We identified differentially expressed genes in glioma and ORGs from public databases. A risk model was established using LASSO regression and Cox analysis, and its performance was evaluated with ROC curves. We then performed consistent cluster analysis on the model, examining its correlation with immunity and drug response. Additionally, PCR, WB and IHC were employed to validate key genes within the prognostic model. RESULTS: 9 ORGs (H6PD, BMP2, SPP1, HADHA, SLC25A20, TXNIP, ACTA1, CCND1, EEF1A1) were selected via differential expression analysis, LASSO and Cox analysis, and incorporated into the risk model with high predictive accuracy. Enrichment analyses using GSVA and GSEA focused predominantly on malignancy-associated pathways. Subtype C of GBM had the best prognosis with the lowest risk score. Furthermore, the model exhibited a strong correlation with the infiltration of immune cells and had the capability to pinpoint potential targeted therapeutic medications for GBM. Ultimately, we selected HADHA for in vitro validation. The findings indicated that GBM exhibits a significant upregulation of HADHA. Knockdown of HADHA inhibited glioma cell proliferation and diminished their migration and invasion capacities and influenced the tumor growth in vivo. CONCLUSION: The risk model, built upon 9 ORGs and the identification of GBM subtypes, suggests that ORGs have a broad application prospect in the clinical immunotherapy and targeted drug treatment of GBM. HADHA significantly influences the development of gliomas, both in vivo and in vitro.

Prediction and analysis of quality markers for Chuantieling gel patches based on HPLC fingerprinting and network pharmacology.

The Chuantieling gel patch (CGP), a traditional Chinese medicine compound, is an external treatment for asthma. It has shown remarkable effectiveness in alleviating asthma-related airway hyperresponsiveness and inflammation. Nevertheless, there is currently no information available regarding the analysis of quality markers for CGP, and there is a need for further improvement in quality control research. In this study, we developed an HPLC fingerprinting method for CGP and conducted a comprehensive methodological investigation. We assessed the similarity among 10 batches of CGP, identified common peaks, and quantified the content of seven major quality markers. Furthermore, we built a network pharmacology-based 'active ingredients-targets-pathways-diseases' network to forecast the potential mechanisms of action for the primary active components in asthma treatment. Our findings demonstrated that the developed CGP fingerprinting and content determination methods were consistent and trustworthy. We verified the existence of 25 shared peaks and successfully identified 7 chromatographic peaks, including sinigrin thiocyanate, ephedrine hydrochloride, methyleugenol, imperatorin, cinnamaldehyde, emodin, and 6-gingerol, using reference standards. The network pharmacology analysis suggested that these seven active components may target proteins such as STAT3 (signal transducer and activator of transcription 3), MAPK3 (mitogen-activated protein kinase 3), and TP53 (tumor protein P53) and influence various diseases through pathways including cancer pathways, hepatitis B, and PI3K-Akt (phosphoinositide 3-kinase-protein kinase B) signaling. This study provides insight into the complex multicomponent composition of CGP, and the predictive analysis through network pharmacology sets the stage for uncovering the mechanisms responsible for the therapeutic effects of CGP.

Therapeutic Potential of Ginsenoside Rb1-PLGA Nanoparticles for Heart Failure Treatment via the ROS/PPARα/PGC1α Pathway.

(1) Background: Ginsenoside Rb1-PLGA nanoparticles (GRb1@PLGA@NPs) represent a novel nanotherapeutic system, yet their therapeutic efficacy and underlying mechanisms for treating heart failure (HF) remain unexplored. This study aims to investigate the potential mechanisms underlying the therapeutic effects of GRb1@PLGA@NPs in HF treatment; (2) Methods: The left anterior descending coronary artery ligation was employed to establish a HF model in Sprague-Dawley rats, along with an in vitro oxidative stress model using H9c2 myocardial cells. Following treatment with GRb1@PLGA@NPs, cardiac tissue pathological changes and cell proliferation were observed. Additionally, the serum levels of biomarkers such as NT-proBNP, TNF-α, and IL-1ß were measured, along with the expression of the ROS/PPARα/PGC1α pathway; (3) Results: GRb1@PLGA@NPs effectively ameliorated the pathological status of cardiac tissues in HF rats, mitigated oxidative stress-induced myocardial cell damage, elevated SOD and MMP levels, and reduced LDH, MDA, ROS, NT-proBNP, TNF-α, and IL-1ß levels. Furthermore, the expression of PPARα and PGC1α proteins was upregulated; (4) Conclusions: GRb1@PLGA@NPs may attenuate myocardial cell injury and treat HF through the ROS/PPARα/PGC1α pathway.

Preparation, characterization and in vivo pharmacokinetic study of ginsenoside Rb1-PLGA nanoparticles.

This study aimed to construct a Ginsenoside Rb1-PLGA nano drug delivery system, optimize its preparation process, characterize and evaluate the resulting Ginsenoside Rb1-PLGA Nanoparticles (GRb1@PLGA@NPs). GRb1@PLGA@NPs were prepared using the emulsion solvent evaporation method. The optimal preparation process was determined using Plackett-Burman design combined with Box-Behnken experiments. Physical characterization and in vitro release studies were conducted. LC-MS/MS technique was employed to investigate the pharmacokinetic characteristics of GRb1 and GRb1@PLGA@NPs in rat plasma. The optimal preparation process yielded GRb1@PLGA@NPs with a particle size of 120.63 nm, polydispersity index (PDI) of 0.172, zeta potential of - 22.67 mV, encapsulation efficiency of 75%, and drug loading of 11%. In vitro release demonstrated sustained drug release. Compared to GRb1, GRb1@PLGA@NPs exhibited a shortened time to peak concentration by approximately 0.72-fold. The area under the plasma concentration-time curve significantly increased to 4.58-fold of GRb1. GRb1@PLGA@NPs formulated using the optimal process exhibited uniform distribution and stable quality, its relative oral bioavailability was significantly improved compared to free GRb1.

Electrically programmable magnetic coupling in an Ising network exploiting solid-state ionic gating.

Two-dimensional arrays of magnetically coupled nanomagnets provide a mesoscopic platform for exploring collective phenomena as well as realizing a broad range of spintronic devices. In particular, the magnetic coupling plays a critical role in determining the nature of the cooperative behavior and providing new functionalities in nanomagnet-based devices. Here, we create coupled Ising-like nanomagnets in which the coupling between adjacent nanomagnetic regions can be reversibly converted between parallel and antiparallel through solid-state ionic gating. This is achieved with the voltage-control of the magnetic anisotropy in a nanosized region where the symmetric exchange interaction favors parallel alignment and the antisymmetric exchange interaction, namely the Dzyaloshinskii-Moriya interaction, favors antiparallel alignment of the nanomagnet magnetizations. Applying this concept to a two-dimensional lattice, we demonstrate a voltage-controlled phase transition in artificial spin ices. Furthermore, we achieve an addressable control of the individual couplings and realize an electrically programmable Ising network, which opens up new avenues to design nanomagnet-based logic devices and neuromorphic computers.

Jujuboside A ameliorates cognitive deficiency in delirium through promoting hippocampal E4BP4 in mice.

OBJECTIVE: Delirium (acute brain syndrome) is a common and serious neuropsychiatric disorder characterized by an acute decline in cognitive function. However, there is no effective treatment clinically. Here we investigated the potential effect of jujuboside A (JuA, a natural triterpenoid saponin) on cognitive impairment in delirium. METHODS: Delirium models of mice were established by injecting lipopolysaccharide (LPS) plus midazolam and implementing a jet lag protocol. Novel object recognition test and Y maze test were used to evaluate the effects of JuA on delirium-associated cognitive impairment. The mRNA and protein levels of relevant clock factors and inflammatory factors were measured by qPCR and Western blotting. Hippocampal Iba1+ intensity was determined by immunofluorescence staining. KEY FINDINGS: JuA ameliorated delirium (particularly delirium-associated cognitive impairment) in mice, which was proved by the behavioural tests, including a preference for new objects, an increase of spontaneous alternation and improvement of locomotor activity. Furthermore, JuA inhibited the expression of ERK1/2, p-p65, TNFα and IL-1ß in hippocampus, and repressed microglial activation in delirious mice. This was attributed to the increased expression of E4BP4 (a negative regulator of ERK1/2 cascade and microglial activation). Moreover, loss of E4bp4 in mice abrogated the effects of JuA on delirium as well as on ERK1/2 cascade and microglial activation in the hippocampus of delirious mice. Additionally, JuA treatment increased the expression of E4BP4 and decreased the expression of p-p65, TNFα and IL-1ß in LPS-stimulated BV2 cells, supporting a protective effect of JuA on delirium. CONCLUSIONS: JuA protects against delirium-associated cognitive impairment through promoting hippocampal E4BP4 in mice. Our findings are of great significance to the drug development of JuA against delirium and related disorders.

Reprogramming of rhythmic liver metabolism by intestinal clock.

BACKGROUND & AIMS: Temporal oscillations in intestinal nutrient processing and absorption are coordinated by the local clock, which leads to the hypothesis that the intestinal clock has major impacts on shaping peripheral rhythms via diurnal nutritional signals. Here, we investigate the role of the intestinal clock in controlling liver rhythmicity and metabolism. METHODS: Transcriptomic analysis, metabolomics, metabolic assays, histology, quantitative (q)PCR, and immunoblotting were performed with Bmal1-intestine-specific knockout (iKO), Rev-erba-iKO, and control mice. RESULTS: Bmal1 iKO caused large-scale reprogramming of the rhythmic transcriptome of mouse liver with a limited effect on its clock. In the absence of intestinal Bmal1, the liver clock was resistant to entrainment by inverted feeding and a high-fat diet. Importantly, Bmal1 iKO remodelled diurnal hepatic metabolism by shifting to gluconeogenesis from lipogenesis during the dark phase, leading to elevated glucose production (hyperglycaemia) and insulin insensitivity. Conversely, Rev-erba iKO caused a diversion to lipogenesis from gluconeogenesis during the light phase, resulting in enhanced lipogenesis and an increased susceptibility to alcohol-related liver injury. These temporal diversions were attributed to disruption of hepatic SREBP-1c rhythmicity, which was maintained via gut-derived polyunsaturated fatty acids produced by intestinal FADS1/2 under the control of a local clock. CONCLUSIONS: Our findings establish a pivotal role for the intestinal clock in dictating liver rhythmicity and diurnal metabolism, and suggest targeting intestinal rhythms as a new avenue for improving metabolic health. IMPACT AND IMPLICATIONS: Our findings establish the centrality of the intestinal clock among peripheral tissue clocks, and associate liver-related pathologies with its malfunction. Clock modifiers in the intestine are shown to modulate liver metabolism with improved metabolic parameters. Such knowledge will help clinicians improve the diagnosis and treatment of metabolic diseases by incorporating intestinal circadian factors.

Regulation of BCRP expression and sulfasalazine pharmacokinetics by the nuclear receptor REV-ERBα.

BCRP (breast cancer resistance protein) is a crucial efflux transporter involved in the regulation of the pharmacokinetics and pharmacodynamics of a wide range of drugs. Herein, we aimed to investigate a potential role for the nuclear receptor REV-ERBα in the regulation of BCRP expression and sulfasalazine (a BCRP probe substrate) pharmacokinetics.Regulation of BCRP expression by REV-ERBα was assessed using Rev-erbα-/- mice and AML12 and CT26 cells. Pharmacokinetic analysis was performed with Rev-erbα-/- and wild-type mice after sulfasalazine administration.We found that the expression levels of BCRP mRNA and protein were downregulated in the liver and small intestine of Rev-erbα-dificient mice. In line with this, Rev-erbα ablation increased the systemic exposures of oral sulfasalazine.Positive regulation of BCRP expression and function by REV-ERBα was furtherly confirmed in AML12 and CT26 cells. Moreover, indirect regulation of Bcrp expression by REV-ERBα was potentially mediated by a negative transcription factor DEC2, which is a downstream target of REV-ERBα.In conclusion, REV-ERBα positively regulates BCRP expression in mice, thereby affecting sulfasalazine pharmacokinetics.

Integration of GWAS, linkage analysis and transcriptome analysis to reveal the genetic basis of flowering time-related traits in maize.

Maize (Zea mays) inbred lines vary greatly in flowering time, but the genetic basis of this variation is unknown. In this study, three maize flowering-related traits (DTT, days to tasselling; DTP, days to pollen shed; DTS, days to silking) were evaluated with an association panel consisting of 226 maize inbred lines and an F2:3 population with 120 offspring from a cross between the T32 and Qi319 lines in different environments. A total of 82 significant single nucleotide polymorphisms (SNPs) and 117 candidate genes were identified by genome-wide association analysis. Twenty-one quantitative trait loci (QTLs) and 65 candidate genes were found for maize flowering time by linkage analysis with the constructed high-density genetic map. Transcriptome analysis was performed for Qi319, which is an early-maturing inbred line, and T32, which is a late-maturing inbred line, in two different environments. Compared with T32, Qi319 showed upregulation of 3815 genes and downregulation of 3906 genes. By integrating a genome-wide association study (GWAS), linkage analysis and transcriptome analysis, 25 important candidate genes for maize flowering time were identified. Together, our results provide an important resource and a foundation for an enhanced understanding of flowering time in maize.

Understanding and revealing the intrinsic impacts of the COVID-19 lockdown on air quality and public health in North China using machine learning.

To avoid the spread of COVID-19, China implemented strict prevention and control measures, resulting in dramatic variations in urban and regional air quality. With the complex effect from long-term emission mitigation and meteorology variation, an accurate evaluation of the net effect from lockdown on air quality changes has not been fully quantified. Here, we combined machine learning algorithm and Theil-Sen regression technique to eliminate meteorological and long-term trends effects on air pollutant concentrations and precisely detect concentrations changes those ascribed to lockdown measures in North China. Our results showed that, compared to the same period in 2015-2019, the adverse meteorology during the lockdown period (January 25th to March 15th) in early 2020 increased PM2.5 concentration in North China by 9.8 %, while the reduction of anthropogenic emissions led to a 32.2 % drop. Stagnant meteorological conditions have a more significant impact on the ground-level air quality in the Beijing-Tianjin-Hebei Region than that in Shanxi and Shandong provinces. After further striping out the effect of long-term emission reduction trend, the lockdown-derived NO2, PM2.5, and O3 shown variety change trend, and at -30.8 %, -27.6 %, and +10.0 %, respectively. Air pollutant changes during the lockdown could be overestimated up to 2-fold without accounting for the influences of meteorology and long-term trends. Further, with pollution reduction during the lockdown period, it would avoid 15,807 premature deaths in 40 cities. If with no deteriorate meteorological condition, the total avoided premature should increase by 1146.

Exploring the driving factors of haze events in Beijing during Chinese New Year holidays in 2020 and 2021 under the influence of COVID-19 pandemic.

Unexpected outbreak of the 2019 novel coronavirus (COVID-19) has profoundly altered the way of human life and production activity, which posed visible impacts on PM2.5 and its chemical species. The abruptly emergency reduction in human activities provided an opportunity to explore the synergetic impacts of multi-factors on shaping PM2.5 pollution. Here, we conducted two comprehensive observation measurements of PM2.5 and its chemical species from 1 January to 16 February in Beijing 2020 and the same lunar date in 2021, to investigate temporal variations and reveal the driving factors of haze before and after Chinese New Year (CNY). Results show that mean PM2.5 concentrations during the whole observation were 63.83 and 66.86 µg/m3 in 2020 and 2021, respectively. Higher secondary inorganic species were observed after CNY, and K+, Cl- showed three prominent peaks which associated closely with fireworks burnings from suburb Beijing and surroundings, verifying that they could be used as two representative tracers of fireworks. Further, we explored the impacts of meteorological conditions, regional transportation as well as chemical reactions on PM2.5. We found that unfavorable meteorological conditions accounted for 11.0 % and 16.9 % of PM2.5 during CNY holidays in 2020 and 2021, respectively. Regional transport from southwest and southeast (south) played an important role on PM2.5 during the two observation periods. Higher ratio of NO3-/SO42- were observed under high OX and low RH conditions, suggesting the major pathway of NO3- and SO42- formation could be photochemical process and aqueous-phase reaction. Additionally, nocturnal chemistry facilitated the formation of secondary components of both inorganic and organic. This study promotes understandings of PM2.5 pollution in winter under the influence of COVID-19 pandemic and provides a well reference for haze and PM2.5 control in future.

Tangeretin prevents cognitive deficit in delirium through activating RORα/γ-E4BP4 axis in mice.

Delirium is a common and serious neuropsychiatric syndrome characterized with acute cognitive and attentional deficits, however, the effective therapies are lacking. Here, using mouse models of delirium, we investigated the effects of tangeretin (TAN, a natural flavonoid) on cognitive impairment by assessing object preference with novel object recognition (NOR) test and spontaneous alternation with Y maze test. We found that TAN, as a RORα/γ agonist, prevented cognitive decline in delirious mice as evidenced by a normal novel object preference and increased spontaneous alternation. This was accompanied by decreased expression of ERK1/2, TNFα and IL-1ß as well as diminished microglial activation in delirious mice. The protective effect of TAN on delirium was mainly attributed to increased hippocampal E4BP4 expression (a known target of RORs and a regulator of cognition in delirium through modulating the ERK1/2 cascade and microglial activation) via activation of RORα/γ. In addition, TAN treatment modulated the expression of RORα/γ target genes (such as E4bp4 and Bmal1) and inhibited the expression of TNFα and IL-1ß in lipopolysaccharide (LPS)-stimulated cells, supporting a beneficial effect of TAN on delirium. In conclusion, TAN is identified as a RORα/γ agonist which promotes E4BP4 expression to prevent cognitive decline in delirious mice. Our findings may have implications for drug development of TAN for prevention and treatment of various diseases associated with cognitive deficiency.

The nuclear receptor REV-ERBα regulates CYP2E1 expression and acetaminophen hepatotoxicity.

CYP2E1 plays an important role in drug metabolism and drug-induced hepatotoxicity. Here, we aimed to investigate a potential role for the nuclear receptor REV-ERBα in regulation of CYP2E1 expression and acetaminophen (APAP)-induced hepatotoxicity, and to determine the underlying mechanisms.Regulatory effects of REV-ERBα on CYP2E1 expression were assessed in vivo (using Rev-erbα-/- mice) and in vitro (using AML12 and HepG2 cells). In vitro microsomal CYP2E1 activity was probed using its specific substrate p-nitrophenol. Pharmacokinetic and acute toxicity studies were performed with Rev-erbα-/- and wild-type mice after APAP administration.We found that Rev-erbα ablation led to decreases in hepatic CYP2E1 expression and activity in mice. In line with this, APAP-induced hepatotoxicity was attenuated in Rev-erbα-deficient mice. The attenuated toxicity was due to down-regulation of APAP metabolism mediated by CYP2E1, which was evidenced by a decrease in formation of the toxic intermediate metabolite NAPQI (i.e. reduced APAP-cysteine and APAP-N-acetylcysteine levels). Furthermore, positive regulation of CYP2E1 expression by REV-ERBα was confirmed in both AML12 and HepG2 cells. Based on luciferase reporter assays, it was found that REV-ERBα regulated Cyp2e1 transcription and expression through repression of DEC2.In conclusion, REV-ERBα positively regulates CYP2E1 expression in mice, thereby affecting APAP metabolism and hepatotoxicity.

Heterogeneous Variations on Historical and Future Trends of CO2 and Multiple Air Pollutants from the Cement Production Process in China: Emission Inventory, Spatial-Temporal Characteristics, and Scenario Projections.

Cement production is a major contributor to carbon dioxide (CO2) and multiple hazardous air pollutant (HAP) emissions, threatening climate mitigation and urban/regional air quality improvement. In this study, we established a comprehensive emission inventory by coupling the unit-based bottom-up and mass balance methods, revealing that emissions of most HAPs have been remarkably controlled. However, an increasing 6.0% of atmospheric mercury emissions, as well as 14.1 and 23.7% of fuel-related and process-related CO2 emission growth were witnessed unexpectedly. Industrial adjustment policies have imposed a great impact on the spatiotemporal changes in emission characteristics. Monthly emissions of CO2 and multiple HAPs decreased from December to February due to the "staggered peak production," especially in northern China after implementing the intensified action plan for air pollution control in winter. Upgrading environmental technologies and adjusting capacity structures are identified as dominant driving forces for reducing HAP emissions. Besides, energy intensity improvement can help offset some of the impact caused by the increase in clinker/cement production. Furthermore, scenario analysis results show that ultra-low emission and low-carbon technology transformation constitute the keys to achieve the synergic reduction of CO2 and multiple HAP emissions in the future.

E4BP4 Coordinates Circadian Control of Cognition in Delirium.

Improved understanding of the etiologies of delirium, a common and severe neuropsychiatric syndrome, would facilitate the disease prevention and treatment. Here, the authors invesitgate the role of circadian rhythms in the pathogenesis of delirium. They observe perturbance of circadian rhythms in mouse models of delirium and disrupted clock gene expression in patients with delirium. In turn, physiological and genetic circadian disruptions sensitize mice to delirium with aggravated cognitive impairment. Likewise, global deletion of E4bp4 (E4 promoter-binding protein), a clock gene markedly altered in delirium conditions, results in exacerbated delirium-associated cognitive decline. Cognitive decline in delirium models is attributed to microglial activation and impaired long-term potentiation in the hippocampus. Single-cell RNA-sequencing reveals microglia as the regulatory target of E4bp4. E4bp4 restrains microglial activation via inhibiting the ERK1/2 signaling pathway. Supporting this, mice lacking in microglial E4bp4 are delirious prone, whereas mice with E4bp4 specifically deleted in hippocampal CA1 neurons have a normal phenotype. Mechanistically, E4bp4 inhibits ERK1/2 signaling by trans-repressing Mapk1/3 (genes encoding ERK1/2) via direct binding to a D-box element in the promoter region. These findings define a causal role of clock dysfunction in delirium development and indicate E4bp4 as a regulator of cognition at the crosstalk between circadian clock and delirium.

Meteorology-normalized variations of air quality during the COVID-19 lockdown in three Chinese megacities.

To avoid the spread of COVID-19, China implemented strict prevention and control measures, resulting in dramatic variations in air quality. Here, we applied a machine learning algorithm (random forest model) to eliminate meteorological effects and characterize the high-resolution variation characteristics of air quality induced by COVID-19 in Beijing, Wuhan, and Urumqi. Our RF model estimates showed that the highest decrease in deweathered PM2.5 in Wuhan (-43.6%) and Beijing (-14.0%) was at traffic stations during lockdown period (February 1- March 15, 2020), while it was at industry stations in Urumqi (-54.2%). Deweathered NO2 decreased significantly in each city (∼30%-50%), whereas accompanied by a notable increase in O3. The diurnal patterns show that the morning peaks of traffic-related NO2 and CO almost disappeared. Additionally, our results suggested that meteorological effects offset some of the reduction in pollutant concentrations. Adverse meteorological conditions played a leading role in the variation in PM2.5 concentration in Beijing, which contributed to +33.5%. The true effect of lockdown reduced the PM2.5 concentrations in Wuhan, Beijing, and Urumqi by approximately 14.6%, 17.0%, and 34.0%, respectively. In summary, lockdown is the most important driver of the decline in pollutant concentrations, but the reduction of SO2 and CO is limited and they are mainly influenced by changing trends. This study provides insights into quantifying variations in air quality due to the lockdown by considering meteorological variability, which varies greatly from city to city, and provides a reference for changes in city scale pollutant concentrations during the lockdown.

Field measurements on emission characteristics, chemical profiles, and emission factors of size-segregated PM from cement plants in China.

Cement manufacturing is a major contributor to ambient particulate matter (PM) pollution in China, threatening urban and regional air quality improvement. Here, we tested the typical outlets (kiln tail, kiln head, and coal mill) in one shaft kiln and three rotary kilns to investigate the mass concentrations, size distributions, and chemical compositions of size-segregated PM. Results show that the concentrations of PM in most samples are lower than the strict local emission standards (10 mg/Nm3). We show that the characteristic chemical compositions in PM for most tested outlets are Ca and Ca2+, while for shaft kiln are K, S, K+, and SO42-, and organic carbon. Elemental carbon accounts for a relatively high proportion of PM emitted from coal mills. Meanwhile, unstable and abnormal operating conditions and variations on feed coal compositions will cause high levels of NH4+ and Cl- in PM from the kiln tail/head. Besides, the emission factors (EFs) of PM2.5, PM10, and PM after air pollution control devices for typical outlets of cement plants are calculated, which fall in ranges of 0.16-2.48, 1.49-18.46, and 3.32-35.35 g/(t of clinker), respectively. It suggests that mass emission characteristics, source profiles, and EFs of PM have changed notably as emission standards become more stringent. We believe the newly detailed size-segregated PM EFs and chemical profiles will help update and compile the refined emission inventory for current cement production in China.

ZIF-L membrane with a membrane-interlocked-support composite architecture for H2/CO2 separation.

Metal-organic framework (MOF) membranes hold great promise in energy-efficient chemical separations. The outstanding challenges of the microstructural design stem from (1) thinning of membranes to immensely reduce the mass-transfer resistance (for high permeances); (2) tuning of orientation to optimize the selective transport of gas molecules, and (3) reinforcement of intercrystalline structure to subside leakage through defective gaps (for high selectivity). Here, we propose the ZIF-L membrane that is completely confined into the voids of the alumina support through an interfacial assembly process, producing an appealing membrane-interlocked-support (MIS) composite architecture that meets the requirements of the microstructural design of MOF membranes. Consequently, the membranes show average H2 permeances of above 4000 GPU and H2/CO2 separation factor (SF) of above 200, representing record-high separation performances of ZIF-L membranes and falling into the industrial target zone (H2 permeance > 1000 GPU and H2/CO2 SF > 60). Furthermore, the ZIF-L membrane possessing the MIS composite architecture that is established with alumina particles as scaffolds shows mechanical stability, scraped repeatedly by a piece of silicon rubber causing no selectivity loss.

Cloning and Characterization of a Cold-adapted Chitosanase from Marine Bacterium Bacillus sp. BY01.

Chitosanase plays an important role in the production of chitooligosaccharides (CHOS), which possess various biological activities. Herein, a glycoside hydrolase (GH) family 46 chitosanase-encoding gene, csnB, was cloned from marine bacterium Bacillus sp. BY01 and heterologously expressed in Escherichia coli. The recombinant chitosanase, CsnB, was optimally active at 35 °C and pH 5.0. It was also revealed to be a cold-adapted enzyme, maintaining 39.5% and 40.4% of its maximum activity at 0 and 10 °C, respectively. Meanwhile, CsnB showed wide pH-stability within the range of pH 3.0 to 7.0. Then, an improved reaction condition was built to enhance its thermostability with a final glycerol volume concentration of 20%. Moreover, CsnB was determined to be an endo-type chitosanase, yielding chitosan disaccharides and trisaccharides as the main products. Overall, CsnB provides a new choice for enzymatic CHOS production.