Identification and characterization of the WOX Gene Family revealed two WUS Clade Members associated with embryo development in Cunninghamia lanceolata.

The WUSCHEL-related homeobox (WOX) gene family is vital for plant development and stress response. In this study, we conducted a comprehensive analysis of WOX genes in Cunninghamia lanceolata (C. lanceolata) and subsequently explored the potential roles of two ClWOX genes within the WUS clade. In total, six ClWOX genes were identified through a full-length transcriptome analysis. These genes, exhibiting conserved structural and functional motifs, were assigned to the ancient clade and Modern/WUS clade, respectively, through a phylogenetic analysis. Our expression analysis indicated that these ClWOX genes were highly expressed in the middle and late developmental stages of zygotic embryos in C. lanceolata. Moreover, only ClWOX5 and ClWOX6 within the Modern/WUS clade exhibited transcriptional activity, and their expressions were also induced in response to auxin and wounding. Overexpression of ClWOX5 and ClWOX6 in Arabidopsis caused a partially sterile phenotype, resulting in a very low seed setting rate. Transcriptomic analysis revealed that expressions of many embryo-defective (EMB) genes, phytohormone-related genes, and transcription factors (TFs) were dramatically altered in ClWOX5 and ClWOX6 transgenic plants, which suggested that ClWOX5 and ClWOX6 may play specific important roles in embryo development via complex gene networks. In addition, overexpression of ClWOX5 and ClWOX6 in leaf segments promoted shoot regeneration in tobacco, indicating that ClWOX5 and ClWOX6 can promote plant regeneration and could be used to improve genetic transformation. In conclusion, these results help to elucidate the function of the WOX gene and provide a valuable basis for future studies of the developmental regulation and applications of WOX genes in C. lanceolata.

The persistent inflammation in COPD: is autoimmunity the core mechanism?

COPD poses a significant global public health challenge, primarily characterised by irreversible airflow restriction and persistent respiratory symptoms. The hallmark pathology of COPD includes sustained airway inflammation and the eventual destruction of lung tissue structure. While multiple risk factors are implicated in the disease's progression, the underlying mechanisms remain largely elusive. The perpetuation of inflammation is pivotal to the advancement of COPD, emphasising the importance of investigating these self-sustaining mechanisms for a deeper understanding of the pathogenesis. Autoimmune responses constitute a critical mechanism in maintaining inflammation, with burgeoning evidence pointing to their central role in COPD progression; yet, the intricacies of these mechanisms remain inadequately defined. This review elaborates on the evidence supporting the presence of autoimmune processes in COPD and examines the potential mechanisms through which autoimmune responses may drive the chronic inflammation characteristic of the disease. Moreover, we attempt to interpret the clinical manifestations of COPD through autoimmunity.

Greenhouse gases emissions from aquaculture ponds: Different emission patterns and key microbial processes affected by increased nitrogen loading.

Global aquaculture production is expected to rise to meet the growing demand for food worldwide, potentially leading to increased anthropogenic greenhouse gases (GHG) emissions. As the demand for fish protein increases, so will stocking density, feeding amounts, and nitrogen loading in aquaculture ponds. However, the impact of GHG emissions and the underlying microbial processes remain poorly understood. This study investigated the GHG emission characteristics, key microbial processes, and environmental drivers underlying GHG emissions in low and high nitrogen loading aquaculture ponds (LNP and HNP). The N2O flux in HNP (43.1 ± 11.3 µmol m-2 d-1) was significantly higher than in LNP (-11.3 ± 25.1 µmol m-2 d-1), while the dissolved N2O concentration in HNP (52.8 ± 7.1 nmol L-1) was 150 % higher than in LNP (p < 0.01). However, the methane (CH4) and carbon dioxide (CO2) fluxes and concentrations showed no significant differences (p > 0.05). N2O replaced CH4 as the main source of Global Warming Potential in HNP. Pond sediments acted as a sink for N2O but a source for CH4 and CO2. The △N2O/(△N2O + â–³N2) in HNP (0.015 ± 0.007 %) was 7.7-fold higher than in LNP (0.002 ± 0.001 %) (p < 0.05). The chemical oxygen demand to NO2-N ratio was the most important environmental factor explaining the variability of N2O fluxes. Ammonia-oxidizing bacteria driven nitrification in water was the predominant N2O source, while comammox-driven nitrification and nosZII-driven N2O reduction in water were key processes for reducing N2O emission in LNP but decreased in HNP. The strong CH4 oxidization by Methylocystis and CO2 assimilation by algae resulted in low CH4 emissions and CO2 sink in the aquaculture pond. The Mantel test indicated that HNP increased N2O fluxes mainly through altering functional genes composition in water and sediment. Our findings suggest that there is a significant underestimation of N2O emissions without considering the significantly increased △N2O/(△N2O + â–³N2) caused by increased nitrogen loading.

The Influence of Thermal Parameters on the Self-Nucleation Behavior of Polyphenylene Sulfide (PPS) during Secondary Thermoforming.

During the secondary thermoforming of carbon fiber-reinforced polyphenylene sulfide (CF/PPS) composites, a vital material for the aerospace field, varied thermal parameters profoundly influence the crystallization behavior of the PPS matrix. Notably, PPS exhibits a distinctive self-nucleation (SN) behavior during repeated thermal cycles. This behavior not only affects its crystallization but also impacts the processing and mechanical properties of PPS and CF/PPS composites. In this article, the effects of various parameters on the SN and non-isothermal crystallization behavior of PPS during two thermal cycles were systematically investigated by differential scanning calorimetry. It was found that the SN behavior was not affected by the cooling rate in the second thermal cycle. Furthermore, the lamellar annealing resulting from the heating process in both thermal cycles affected the temperature range for forming the special SN domain, because of the refined lamellar structure, and expelled various defects. Finally, this study indicated that to control the strong melt memory effect in the first thermal cycle, both the heating rate and processing melt temperature need to be controlled simultaneously. This work reveals that through collaborative control of these parameters, the crystalline morphology, crystallization temperature and crystallization rate in two thermal cycles are controlled. Furthermore, it presents a new perspective for controlling the crystallization behavior of the thermoplastic composite matrix during the secondary thermoforming process.

A Zn-modified PCN-224 fluorescent nanoprobe for selective and sensitive turn-on detection of glutathione.

Monitoring endogenous glutathione (GSH) levels in living cells is essential for cancer diagnose and treatment. In this work, GSH responsive fluorescent nanoprobe with turn-on property was constructed using Zn-modified porphyrinic metal-organic frameworks (PCN-224-Zn). The introduced Zn2+ could quench the fluorescence of PCN-224 by the metallization of organic ligand (TCPP) and serves as sensing site for GSH. When exposed to GSH, the strong binding affinity of GSH generates the formation of Zn-GSH complex, eliminating the fluorescence quenching effect of Zn2+. Based on the constructed PCN-224-Zn nanoprobe, selective determination of GSH was achieved in the range of 0.01-6 µM with a detection limit of 1.5 nM. Furthermore, the constructed nanoprobe can realize the fluorescence imaging of endogenous GSH in MCF-7 and HeLa cells. Meanwhile, PCN-224-Zn could also monitor GSH in cell lysate with recovery rates from 93.8 % to 102.3 %. The performance of PCN-224-Zn demonstrates its capacities in the application of fluorescence sensing and bio-imaging fields.

MTOR Suppresses Cigarette Smoke-Induced Airway Inflammation and MMP12 Expression in Macrophage in Chronic Obstructive Pulmonary Disease.

Background: Macrophage-derived matrix metalloproteinase 12 (MMP12) can cause destruction of lung tissue structure and plays a significant role in the development and progression of chronic obstructive pulmonary disease (COPD). MTOR is a serine/threonine kinase that plays a crucial role in cell growth and metabolism. The activity of MTOR in the lung tissues of COPD patients also shows significant changes. However, it is unclear whether MTOR can regulate the development and progression of COPD by controlling MMP12. This study primarily investigates whether MTOR in macrophages can affect the expression of MMP12 and participate in the progression of COPD. Methods: We tested the changes in MTOR activity in macrophages exposed to cigarette smoke (CS) both in vivo and in vitro. Additionally, we observed the effect of MTOR on the expression of MMP12 in macrophages and on lung tissue inflammation and structural damage in mice, both in vivo and in vitro, using MTOR inhibitors or gene knockout mice. Finally, we combined inhibitor treatment with gene knockout to demonstrate that MTOR primarily mediates the expression of MMP12 through the NF-κB signaling pathway. Results: Exposure to CS can enhance MTOR activity in mouse alveolar macrophages. Inhibiting the activity of MTOR or suppressing its expression leads to increased expression of MMP12. Myeloid-specific knockout of MTOR expression can promote the occurrence of CS-induced pulmonary inflammation and emphysema in mice. Inhibiting the activity of NF-κB can eliminate the effect of MTOR on MMP12. Conclusion: Macrophage MTOR can reduce the expression of MMP12 by inhibiting NF-κB, thereby inhibiting the occurrence of COPD inflammation and destruction of lung tissue structure. Activating the activity of macrophage MTOR may be beneficial for the treatment of COPD.

Pregnancy-associated gynecological cancer in New South Wales, Australia 1994-2013: A population-based historical cohort study.

INTRODUCTION: Pregnancy-associated gynecological cancer (PAGC) refers to cancers of the ovary, uterus, fallopian tube, cervix, vagina, and vulva diagnosed during pregnancy or within 12 months postpartum. We aimed to describe the incidence of, and perinatal outcomes associated with, invasive pregnancy-associated gynecological cancer. MATERIAL AND METHODS: We conducted a population-based historical cohort study using linked data from New South Wales, Australia. We included all women who gave birth between 1994 and 2013, with a follow-up period extending to September 30, 2018. Three groups were analyzed: a gestational PAGC group (women diagnosed during pregnancy), a postpartum PAGC group (women diagnosed within 1 year of giving birth), and a control group (women with control diagnosis during pregnancy or within 1 year of giving birth). We used generalized estimation equations to compare perinatal outcomes between study groups. RESULTS: There were 1 786 137 deliveries during the study period; 70 women were diagnosed with gestational PAGC and 191 with postpartum PAGC. The incidence of PAGC was 14.6/100 000 deliveries and did not change during the study period. Women with gestational PAGC (adjusted odds ratio [aAOR] 6.81, 95% confidence interval [CI] 2.97-15.62) and with postpartum PAGC (aOR 2.65, 95% CI 1.25-5.61) had significantly increased odds of a severe maternal morbidity outcome compared with the control group. Babies born to women with gestational PAGC were more likely to be born preterm (aOR 3.11, 95% CI 1.47-6.59) and were at increased odds of severe neonatal complications (aOR 3.47, 95% CI 1.45-8.31) compared with babies born to women without PAC. CONCLUSIONS: The incidence of PAGC has not increased over time perhaps reflecting, in part, the effectiveness of cervical screening and early impacts of human papillomavirus vaccination programs in Australia. The higher rate of preterm birth among the gestational PAGC group is associated with adverse outcomes in babies born to these women.

Pan-Cancer Single-Nucleus Total RNA Sequencing Using snHH-Seq.

Tumor heterogeneity and its drivers impair tumor progression and cancer therapy. Single-cell RNA sequencing is used to investigate the heterogeneity of tumor ecosystems. However, most methods of scRNA-seq amplify the termini of polyadenylated transcripts, making it challenging to perform total RNA analysis and somatic mutation analysis.Therefore, a high-throughput and high-sensitivity method called snHH-seq is developed, which combines random primers and a preindex strategy in the droplet microfluidic platform. This innovative method allows for the detection of total RNA in single nuclei from clinically frozen samples. A robust pipeline to facilitate the analysis of full-length RNA-seq data is also established. snHH-seq is applied to more than 730 000 single nuclei from 32 patients with various tumor types. The pan-cancer study enables it to comprehensively profile data on the tumor transcriptome, including expression levels, mutations, splicing patterns, clone dynamics, etc. New malignant cell subclusters and exploring their specific function across cancers are identified. Furthermore, the malignant status of epithelial cells is investigated among different cancer types with respect to mutation and splicing patterns. The ability to detect full-length RNA at the single-nucleus level provides a powerful tool for studying complex biological systems and has broad implications for understanding tumor pathology.

A ratiometric fluorescent nanoprobe based on CdSe quantum dots for the detection of Ag+ in environmental samples and living cells.

With the widespread application of Ag+ in modern life and industry, the potential hazardous effects of Ag+ to environment and humans have attracted great concerns. Thus, effective and rapid strategies for Ag+ detection are highly desirable. In this paper, a novel ratiometric fluorescence sensor using CdSe quantum dots (QDs) has been constructed for sensitive and selective detection of Ag+, which is based on the formation of Ag2Se QDs. CdSe QDs were initially prepared and showed single wavelength emission at 510 nm. When Ag+ exists, a rising peak appeared at 650 nm and the emission at 510 nm declined, exhibiting distinct ratiometric fluorescence emission (I650/I510) characteristic with a linear response over the Ag+ concentration range of 0.01-4 µM. Significantly, the fluorescence changed from green to red. The detection limit of the constructed sensor is 1.4 nM. Furthermore, the sensing assay can be successfully applied to detect Ag+ in real water samples and living cells.

Methane production from peroxymonosulfate pretreated algae biomass: Insights into microbial mechanisms, microcystin detoxification and heavy metal partitioning behavior.

This study investigated the methane production potential of algal biomass by anerobic digestion with the addition of peroxymonosulfate (PMS), the removal of microcystin were analyzed and discussed. The microcystin concentration in the collected algal sludge was 1.20 µg/L in the liquid phase and 1393 µg/g in the algal sludge before anaerobic fermentation. The microcystin concentration decreased to 0.20-0.35 µg/L in the liquid phase and 4.16-11.51 µg/g in the sludge phase after 60 days of digestion. The initial PMS dose and residue microcystin concentration could be simulated with a logarithmic decay model (R2 > 0.87). Anaerobic digestion could recover energy from algal source in the form of methane gas, which was not affected in the presence of microcystin, and the microcystin removal rate was >99%. Digestion decreased the total contents of Cd and Zn in the liquid phase and increased the total contents of Cr and Pb in the liquid phase. The microbial community and function prediction results indicated that the PMS0.1 system had the highest methane production, which was attributed to the high abundance of Mechanosaeta (40.52%). This study provides insights into microbial mechanisms, microcystin detoxification and the heavy metal partitioning behavior of the algal biomass during methane production.

Corrigendum: Autophagy Promotes Cigarette Smoke-Initiated and Elastin-Driven Bronchitis-Like Airway Inflammation in Mice.

[This corrects the article DOI: 10.3389/fimmu.2021.594330.].

Improving methane production from algal sludge anaerobic fermentation by peroxydisulfate (PDS) pretreatment.

This study investigated the potential of improving methane production from algal sludge anaerobic digestion by peroxydisulfate (PDS) pretreatment. The results show that with PDS dosage at 0.02 g PDS/g algal sludge TSS, PDS added system has highest accumulative methane production after 60 days fermentation. The accumulative methane production was 1.08, 1.15, 1.14, 1.13, 1.08, 0.76, and 0.15 times as compared with control, at 0.01, 0.02, 0.05, 0.1, 0.2, 0.5, and 1 g PDS/g algal sludge TSS added, respectively. The SCOD in the system was keep increasing with the increment of PDS dosage after 120 min pretreatment. The algal sludge dewatering rate was increased with adding of PDS as pretreatment. The addition of PDS has inhibited the activities of microbes involved in digestion, while the short chain fatty acids production was improved after 3 days digestion. One-substrate model can be used to simulate the methane yield. The hydrolysis rate was decreased after dosing with PDS, while highest actual and predicted accumulative methane yield was occurred at 0.02 g PDS/g algal sludge TSS. Proteobacteria has higher percentage when the PDS was not higher than 0.1 g PDS/g algal sludge TSS, Acetothermia has higher percentage at 0.01 g PDS/g algal sludge TSS. The microcystin-LR (MC-LR) in algal sludge was largely removed after digestion, including the intracellular MC-LR. The higher PDS dosage could cause heavy metal release from algae cell to the digestate during fermentation. The addition of PDS to algal sludge can improve the accumulative methane production and mitigate microcystin concentration.

Epithelium-derived IL17A Promotes Cigarette Smoke-induced Inflammation and Mucus Hyperproduction.

The airway epithelium is a central modulator of innate and adaptive immunity in the lung. IL17A expression was found to be increased in the airway epithelium; however, the role of epithelium-derived IL17A in chronic obstructive pulmonary disease (COPD) remains unclear. In this study, we aimed to determine whether epithelium-derived IL17A regulates inflammation and mucus hyperproduction in COPD by using a cultured human bronchial epithelial (HBE) cell line in vitro and an airway epithelium IL17A-specific knockout mouse in vivo. Increased IL17A expression was observed in the mouse airway epithelium upon cigarette smoke (CS) exposure or in a mouse model of COPD that was induced by using CS and Eln (elastin). CS extract (CSE) also triggered IL17A expression in HBE cells. Blocking IL17A or IL17RA (IL17 receptor A) effectively attenuated CSE-induced MUC5AC and the inflammatory cytokines IL6, TNF-α, and IL1ß in HBE cells, suggesting that IL17A mediates CSE-induced inflammation and mucin production in an autocrine manner. CSE activated p-JUN (phospho-JUN) and p-JNK (phospho-c-Jun N-terminal kinase), which were also reduced by IL17RA siRNA, and JUN siRNA attenuated CSE-induced IL6 and MUC5AC. In vivo, selective knockout of IL17A in the airway epithelium markedly reduced the neutrophilic infiltration in BAL fluid, peribronchial inflammation, proinflammatory mediators (CXCL1 [CXC ligand 1] and CXCL2), and mucus production in a COPD mouse model. We showed a novel function of airway epithelium-derived IL17A, which can act locally in an autocrine manner to amplify inflammation and increase mucus production in COPD pathogenesis.

Prenatal and postnatal exposure to Bisphenol A and Asthma: a systemic review and meta-analysis.

BACKGROUND: Bisphenol A (BPA) is a plasticizer with high production and ubiquitous usage in polycarbonate plastics and epoxy resins. The association between prenatal or postnatal exposure to BPA and childhood wheeze/asthma has not been well established. Our study aimed to provide further justification for the current studies. METHODS: Studies were searched from PubMed, Web of Science, Scopus and Embase from inception until Sep 15, 2020. Meta-analysis was performed to calculate pooled adjusted odds ratios (aOR). The methodological quality of included studies was assessed by using the Newcastle Ottawa Scale (NOS). RESULTS: Of 2,814 screened articles, 9 studies with 3,885 participants were included in the final analysis. When all studies were pooled, postnatal exposure to BPA was associated with a higher risk of childhood asthma (aOR =1.43; 95% CI: 1.28-1.59) or childhood wheeze (aOR =1.38; 95% CI: 1.18-1.62). Prenatal exposure to BPA had a small but significant increased risk of childhood asthma (aOR =1.17; 95% CI: 1.01-1.34). An increased risk of childhood wheeze was related to prenatal exposure to BPA at 16 weeks' gestation (aOR =1.29; 95% CI: 1.07-1.55), but not at 26 weeks' gestation (aOR =1.07; 95% CI: 0.88-1.29) nor at random-time gestation (aOR =1.02; 95% CI: 0.89-1.16). CONCLUSIONS: Prenatal and postnatal exposure to BPA was related to an increased risk of childhood asthma. However, only postnatal and early gestational exposure (at 16 weeks) to BPA could induce the risk of childhood wheeze, but not late gestational exposure (at 26 weeks).

Autophagy Promotes Cigarette Smoke-Initiated and Elastin-Driven Bronchitis-Like Airway Inflammation in Mice.

Cigarette smoke (CS)-induced macrophage activation and airway epithelial injury are both critical for the development of chronic obstructive pulmonary disease (COPD), while the eventual functions of autophagy in these processes remain controversial. We have recently developed a novel COPD mouse model which is based on the autoimmune response sensitized by CS and facilitated by elastin. In the current study, we therefore utilized this model to investigate the roles of autophagy in different stages of the development of bronchitis-like airway inflammation. Autophagic markers were increased in airway epithelium and lung tissues, and Becn+/- or Lc3b-/- mice exhibited reduced neutrophilic airway inflammation and mucus hyperproduction in this COPD mouse model. Moreover, treatment of an autophagic inhibitor 3-methyladenine (3-MA) either during CS-initiated sensitization or during elastin provocation significantly inhibited the bronchitis-like phenotypes in mice. Short CS exposure rapidly induced expression of matrix metallopeptidase 12 (MMP12) in alveolar macrophages, and treatment of doxycycline, a pan metalloproteinase inhibitor, during CS exposure effectively attenuated the ensuing elastin-induced airway inflammation in mice. CS extract triggered MMP12 expression in cultured macrophages, which was attenuated by autophagy impairment (Becn+/- or Lc3b-/-) or inhibition (3-MA or Spautin-1). These data, taken together, demonstrate that autophagy mediates both the CS-initiated MMP12 activation in macrophages and subsequent airway epithelial injury, eventually contributing to development COPD-like airway inflammation. This study reemphasizes that inhibition of autophagy as a novel therapeutic strategy for CS-induced COPD.

Short-chain fatty acids resource recovery potential from algal sludge via anaerobic fermentation under various pH values.

The harvesting of algal sludge from eutrophic lakes, including the large quantity of organic matters, has the potential to be used as valuable products through the process of resource recovery. This study investigates the fatty acid production potential from algal sludge via anaerobic fermentation under different pH values. The results indicated that the recovery of short-chain fatty acids (SCFAs) was the highest (3269.25 ± 32.89 mg·COD/L) at pH 11 after 7 days of fermentation. The SCFAs concentration at pH value 11 was 6.24, 1.27, 4.90, and 0.53 times higher compared with that at pH value 3, 5, 7, and 9, respectively. The SCFAs production was continually increased from day 1 to day 7 at pH value 7, 9, and 11. Much fewer middle- and long-chain fatty acids were produced compared with SCFAs. Gross. fatty acid production was the highest at pH 11. The concentrations of soluble protein and polysaccharide were the highest at pH 11, implying that the disruption of algal cells could have a high value at pH 11. The polysaccharide concentration was the lowest at pH 7. The fluorescence excitation-emission matrix profile implied that the disruption of algal cells was the greatest at pH 11. Methane production was greatest at pH 7 and 9. Overall, the results of this study revealed that a pH of 11 was optimal for the recovery of SCFAs from algal sludge due to the higher cell disruption, suitable ORP condition for SCFAs production and inhibition of methanogens.

COVID-19: Performance study of microplastic inhalation risk posed by wearing masks.

Wearing face masks has become the new normal worldwide due to the global spread of the coronavirus disease 2019. The inhalation of microplastics due to the wearing of masks has rarely been reported. The present study used different types of commonly used masks to conduct breathing simulation experiments and investigate microplastic inhalation risk. Microplastic inhalation caused by reusing masks that underwent various treatment processes was also tested. Results implied that wearing masks considerably reduces the inhalation risk of particles (e.g., granular microplastics and unknown particles) even when they are worn continuously for 720 h. Surgical, cotton, fashion, and activated carbon masks wearing pose higher fiber-like microplastic inhalation risk, while all masks generally reduced exposure when used under their supposed time (<4 h). N95 poses less fiber-like microplastic inhalation risk. Reusing masks after they underwent different disinfection pretreatment processes can increase the risk of particle (e.g., granular microplastics) and fiber-like microplastic inhalation. Ultraviolet disinfection exerts a relatively weak effect on fiber-like microplastic inhalation, and thus, it can be recommended as a treatment process for reusing masks if proven effective from microbiological standpoint. Wearing an N95 mask reduces the inhalation risk of spherical-type microplastics by 25.5 times compared with not wearing a mask.

Effect of microplastic particle size to the nutrients removal in activated sludge system.

Microplastics as emerging environmental pollutants, its effect to the bioprocess of water and wastewater treatment has aroused concern. This study investigated the effects of microplastic polystyrene (PS) particle size to the activated sludge nutrient removal process. The ammonia, nitrite, nitrate and phosphorus removal under various PS particle size during nitrification and denitrification process was tested. The results indicated that with PS particle size 150-300 µm, the ammonia oxidation during nitrification process was inhibited to 71%, 92%, and 80% as compared with the blank reactor, for PS concentration at 0.01 g/L, 0.05 g/L and 0.10 g/L, respectively. The nitrite accumulation during nitrification process was also high at PS particle size 150-300 µm and concentration no less than 0.05 g/L. The nitrate reduction during the denitrification process was all inhibited to 69%-94% as compared with the blank, except for reactor No.4. The phosphate removal during nitrification process was not affected by the existence of microplastics PS, the average removal rate was over 80% after 2 h and over 95% after 3 h, respectively. The microplastics particle size plays important role in affecting the activated sludge nutrient removal process.

Evaluation of microplastic polyvinylchloride and antibiotics tetracycline co-effect on the partial nitrification process.

This study investigated the co-effect of microplastic polyvinylchloride and antibiotics tetracycline to partial nitrification process in treating high ammonia wastewater. The average ammonia oxidation rate of all reactors was 53.58, 56.17 and 42.08 mg·N/L·h in round 1, round 7 and round 13, respectively. The ammonia oxidation rate was reduced to 89.40%, 79.08%, 80.60%, 73.37%, 69.50%, 75.72%, 98.93% and 66.04% from 1st round of test to 13th round of test at reactor R1 to R8. The average nitrosation rate was always over 80% in all conditions tested. Tetracycline removal rate was attributed to sludge adsorption in all reactors and was increased continuously with the increment of tetracycline concentration. The nitrous oxide emission was keep decreasing from round 1 to round 13 in all reactors tested. The microbial community results revealed that with the existence of tetracycline and microplastics, the relative abundance of Bacteroidetes were reduced and Proteobacteria were increased.

MTOR suppresses autophagy-mediated production of IL25 in allergic airway inflammation.

INTRODUCTION: Airway epithelial cells are recognised as an essential controller for the initiation and perpetuation of asthmatic inflammation, yet the detailed mechanisms remain largely unknown. This study aims to investigate the roles and mechanisms of the mechanistic target of rapamycin (MTOR)-autophagy axis in airway epithelial injury in asthma. METHODS: We examined the MTOR-autophagy signalling in airway epithelium from asthmatic patients or allergic mice induced by ovalbumin or house dust mites, or in human bronchial epithelial (HBE) cells. Furthermore, mice with specific MTOR knockdown in airway epithelium and autophagy-related lc3b-/- mice were used for allergic models. RESULTS: MTOR activity was decreased, while autophagy was elevated, in airway epithelium from asthmatic patients or allergic mice, or in HBE cells treated with IL33 or IL13. These changes were associated with upstream tuberous sclerosis protein 2 signalling. Specific MTOR knockdown in mouse bronchial epithelium augmented, while LC3B deletion diminished allergen-induced airway inflammation and mucus hyperproduction. The worsened inflammation caused by MTOR deficiency was also ameliorated in lc3b-/- mice. Mechanistically, autophagy was induced later than the emergence of allergen-initiated inflammation, particularly IL33 expression. MTOR deficiency increased, while knocking out of LC3B abolished the production of IL25 and the eventual airway inflammation on allergen challenge. Blocking IL25 markedly attenuated the exacerbated airway inflammation in MTOR-deficiency mice. CONCLUSION: Collectively, these results demonstrate that allergen-initiated inflammation suppresses MTOR and induces autophagy in airway epithelial cells, which results in the production of certain proallergic cytokines such as IL25, further promoting the type 2 response and eventually perpetuating airway inflammation in asthma.