Natriuretic peptide receptor-C perturbs mitochondrial respiration in white adipose tissue.

Natriuretic peptide receptor-C (NPR-C) is highly expressed in adipose tissues, and regulates obesity related diseases, however the detailed mechanism remains unknown. In this research, we aimed to explore the potential role of NPR-C in cold exposure and high-fat/high-sugar (HF/HS) diet induced metabolic changes, especially in regulating white adipose tissue (WAT) mitochondrial function. Our findings showed that NPR-C expression, especially in epididymal WAT (eWAT), was reduced after cold exposure. Global Npr3 (gene encoding NPR-C protein) deficiency led to reduced body weight, increased WAT browning, thermogenesis, and enhanced expression of genes related to mitochondrial biogenesis. RNA-sequencing of eWAT showed that Npr3 deficiency enhanced expression of mitochondrial respiratory chain complex genes and promoted mitochondrial oxidative phosphorylation in response to cold exposure. In addition, Npr3 KO mice were able to resist obesity induced by HF/HS diet. Npr3 knockdown in stromal vascular fraction (SVF)-induced white adipocytes promoted the expression of proliferator-activated receptor gamma coactivator 1α (PGC1α), uncoupling protein 1 (UCP1) and mitochondrial respiratory chain complexes. Mechanistically, NPR-C inhibited cGMP and calcium signaling in an NPR-B-dependent manner but suppressed cAMP signaling in an NPR-B-independent manner. Moreover, Npr3 knockdown induced browning via AKT and p38 pathway activation, which were attenuated by Npr2 knockdown. Importantly, treatment with the NPR-C specific antagonist, AP-811, decreased WAT mass and increased PGC-1α, UCP1 and mitochondrial complex expression. These findings demonstrate that NPR-C deficiency enhances metabolic health by boosting energy expenditure in WAT, emphasizing the potential of NPR-C inhibition for treating obesity and related metabolic disorders.

Regulation of phosphoglycerate kinase 1 and its critical role in cancer.

Cells that undergo normal differentiation mainly rely on mitochondrial oxidative phosphorylation to provide energy, but most tumour cells rely on aerobic glycolysis. This phenomenon is called the "Warburg effect". Phosphoglycerate kinase 1 (PGK1) is a key enzyme in aerobic glycolysis. PGK1 is involved in glucose metabolism as well as a variety of biological activities, including angiogenesis, EMT, mediated autophagy initiation, mitochondrial metabolism, DNA replication and repair, and other processes related to tumorigenesis and development. Recently, an increasing number of studies have proven that PGK1 plays an important role in cancer. In this manuscript, we discussed the effects of the structure, function, molecular mechanisms underlying PGK1 regulation on the initiation and progression of cancer. Additionally, PGK1 is associated with chemotherapy resistance and prognosis in tumour patients. This review presents an overview of the different roles played by PGK1 during tumorigenesis, which will help in the design of experimental studies involving PGK1 and enhance the potential for the use of PGK1 as a therapeutic target in cancer. Video Abstract.

Determining the Contribution of Micro/Nanoplastics to Antimicrobial Resistance: Challenges and Perspectives.

Microorganisms colonizing the surfaces of microplastics form a plastisphere in the environment, which captures miscellaneous substances. The plastisphere, owning to its inherently complex nature, may serve as a "Petri dish" for the development and dissemination of antibiotic resistance genes (ARGs), adding a layer of complexity in tackling the global challenge of both microplastics and ARGs. Increasing studies have drawn insights into the extent to which the proliferation of ARGs occurred in the presence of micro/nanoplastics, thereby increasing antimicrobial resistance (AMR). However, a comprehensive review is still lacking in consideration of the current increasingly scattered research focus and results. This review focuses on the spread of ARGs mediated by microplastics, especially on the challenges and perspectives on determining the contribution of microplastics to AMR. The plastisphere accumulates biotic and abiotic materials on the persistent surfaces, which, in turn, offers a preferred environment for gene exchange within and across the boundary of the plastisphere. Microplastics breaking down to smaller sizes, such as nanoscale, can possibly promote the horizontal gene transfer of ARGs as environmental stressors by inducing the overgeneration of reactive oxygen species. Additionally, we also discussed methods, especially quantitatively comparing ARG profiles among different environmental samples in this emerging field and the challenges that multidimensional parameters are in great necessity to systematically determine the antimicrobial dissemination risk in the plastisphere. Finally, based on the biological sequencing data, we offered a framework to assess the AMR risks of micro/nanoplastics and biocolonizable microparticles that leverage multidimensional AMR-associated messages, including the ARGs' abundance, mobility, and potential acquisition by pathogens.

Mifepristone increases AQP1 mRNA expression, angiogenesis, and cell permeability through the ERK MAPK pathway.

AIMS: The purpose of this study was to investigate the mechanism of mifepristone serves as an anti-implantation contraceptive drug on aquaporins 1 (AQP1) expression. METHODS: Human umbilical vein endothelial cells (HUVECs) were used to detect the effects of different concentrations of mifepristone (0, 0.065, 0.2, and 1 µmol/L) on the activity of angiogenesis and AQP1 expression. The expression of AQP1 was tested by the real-time PCR. The angiogenesis and penetration function of HUVECs was investigated by Matrigel lumen formation and trans-well assay, respectively. RESULTS: The expression of AQP1, angiogenesis and cell permeability were significantly higher than control groups in HUVECs treatment with mifepristone at 1 µmol/L for 12 h. Estrogen and progesterone decreased the up-regulation of AQP1 and cell permeability, not angiogenesis, induced by mifepristone. Mifepristone increased protein levels of p-ERK, not p-p38 or p-JNK, and pre-treatment with ERK MAPK-specific inhibitor significantly inhibited the up-regulation of AQP1 mRNA expression, angiogenesis and cell permeability induced by mifepristone. si-AQP1 significantly reduced the up-regulation of angiogenesis, cell permeability and p-ERK/ERK ratio expression induced by mifepristone treatment. Overexpression of AQP1 enhanced the increase of expression ratio of p-ERK/ERK induced by mifepristone. CONCLUSIONS: Low-dose mifepristone increased cell permeability, angiogenesis and AQP1 expression, which was involved in MAPK pathways. This provides new insights into the molecular mechanism of mifepristone serves as an anti-implantation contraceptive drug.

Hyperthermia promotes degradation of the acute promyelocytic leukemia driver oncoprotein ZBTB16/RARα.

The acute promyelocytic leukemia (APL) driver ZBTB16/RARα is generated by the t(11;17) (q23;q21) chromosomal translocation, which is resistant to combined treatment of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) or conventional chemotherapy, resulting in extremely low survival rates. In the current study, we investigated the effects of hyperthermia on the oncogenic fusion ZBTB16/RARα protein to explore a potential therapeutic approach for this variant APL. We showed that Z/R fusion protein expressed in HeLa cells was resistant to ATO, ATRA, and conventional chemotherapeutic agents. However, mild hyperthermia (42 °C) rapidly destabilized the ZBTB16/RARα fusion protein expressed in HeLa, 293T, and OCI-AML3 cells, followed by robust ubiquitination and proteasomal degradation. In contrast, hyperthermia did not affect the normal (i.e., unfused) ZBTB16 and RARα proteins, suggesting a specific thermal sensitivity of the ZBTB16/RARα fusion protein. Importantly, we found that the destabilization of ZBTB16/RARα was the initial step for oncogenic fusion protein degradation by hyperthermia, which could be blocked by deletion of nuclear receptor corepressor (NCoR) binding sites or knockdown of NCoRs. Furthermore, SIAH2 was identified as the E3 ligase participating in hyperthermia-induced ubiquitination of ZBTB16/RARα. In short, these results demonstrate that hyperthermia could effectively destabilize and subsequently degrade the ZBTB16/RARα fusion protein in an NCoR-dependent manner, suggesting a thermal-based therapeutic strategy that may improve the outcome in refractory ZBTB16/RARα-driven APL patients in the clinic.

Engineered Biomaterials Trigger Remineralization and Antimicrobial Effects for Dental Caries Restoration.

Dental caries is the most prevalent chronic disease globally, significantly impacting individuals' quality of life. A key reason behind the failure of implanted restorations is their biological inactivity, meaning they are unable to form crosslinks with the surrounding tooth structures, thus making patients susceptible to implant loss and recurrent tooth decay. For the treatment of caries, antibacterial medicine and remineralization are effective means of treating the recurrence of caries. Owing to the rapid progression in the biomaterials field, several biomaterials have been reported to display antimicrobial properties and aid in dentin remineralization. Bioactive materials hold considerable potential in diminishing biofilm accumulation, inhibiting the process of demineralization, enabling dentin remineralization, and combating bacteria related to caries. Bioactive materials, such as fluoride, amorphous calcium phosphate, bioactive glass, collagen, and resin-based materials, have demonstrated their effectiveness in promoting dentin remineralization and exerting antibacterial effects on dental caries. However, the concentration of fluoride needs to be strictly controlled. Although amorphous calcium phosphate can provide the necessary calcium and phosphorus ions for remineralization, it falls short in delivering the mechanical strength required for oral mastication. Resin-based materials also offer different advantages due to the complexity of their design. In this review, we delve into the application of advanced bioactive materials for enhancing dentin remineralization and antibacterial properties. We eagerly anticipate future developments in bioactive materials for the treatment of dental caries.

Reliability and validity of the 15-item Chronic Oral Mucosal Disease Questionnaire in China: A short-form instrument to measure quality of life.

BACKGROUND: Chronic oral mucosal diseases have been a common problem, which affected individuals' health and social functions seriously. Although there has been a rigorous Chinese version of the Chronic Mucosal Diseases Questionnaire (COMDQ-26) to measure the quality of life of patients with chronic oral mucosal diseases, 26 items were so redundant to be a burden for patients. It was necessary to make a brief, practical, and easy-to-use tool in China. This study aimed to test the validity and reliability of the Chinese version of the short-form Chronic Mucosal Diseases Questionnaire (COMDQ-15). METHODS: A total of 165 respondents from a tertiary stomatological hospital were recruited in this study from July to December, 2020. Internal consistency, test-retest reliability, criterion validity, confirmatory factor analysis, and exploratory factor analysis were used to evaluate the reliability and validity of the Chinese version of Chronic Mucosal Diseases Questionnaire-15. RESULTS: The total Cronbach's α of 0.841 and subscale ranging from 0.736 to 0.965 revealed good internal consistency of the reliability. The intraclass correlation coefficients exceeded 0.80 indicated excellent test-retest reliability. Compared with the Oral Health Impact Profile-14, the criterion validity was 0.549. The confirmatory factor analysis results supported acceptable validity of the Chinese version of Chronic Mucosal Diseases Questionnaire-15, and the exploratory factor analysis demonstrated that the 15 items were classified into four domains, with a cumulative proportion of 71.52%. CONCLUSION: The Chinese version of Chronic Mucosal Diseases Questionnaire-15 is a brief and low-burden tool, and has been proved reliable and valid to assess the quality of life of patients with chronic oral mucosal diseases in China (the Chinese Clinical Trial Registry (no. ChiCTR2000031607).

Alteration of CTCF-associated chromatin neighborhood inhibits TAL1-driven oncogenic transcription program and leukemogenesis.

Aberrant activation of the TAL1 is associated with up to 60% of T-ALL cases and is involved in CTCF-mediated genome organization within the TAL1 locus, suggesting that CTCF boundary plays a pathogenic role in T-ALL. Here, we show that -31-Kb CTCF binding site (-31CBS) serves as chromatin boundary that defines topologically associating domain (TAD) and enhancer/promoter interaction required for TAL1 activation. Deleted or inverted -31CBS impairs TAL1 expression in a context-dependent manner. Deletion of -31CBS reduces chromatin accessibility and blocks long-range interaction between the +51 erythroid enhancer and TAL1 promoter-1 leading to inhibition of TAL1 expression in erythroid cells, but not T-ALL cells. However, in TAL1-expressing T-ALL cells, the leukemia-prone TAL1 promoter-IV specifically interacts with the +19 stem cell enhancer located 19 Kb downstream of TAL1 and this interaction is disrupted by the -31CBS inversion in T-ALL cells. Inversion of -31CBS in Jurkat cells alters chromatin accessibility, histone modifications and CTCF-mediated TAD leading to inhibition of TAL1 expression and TAL1-driven leukemogenesis. Thus, our data reveal that -31CBS acts as critical regulator to define +19-enhancer and the leukemic prone promoter IV interaction for TAL1 activation in T-ALL. Manipulation of CTCF boundary can alter TAL1 TAD and oncogenic transcription networks in leukemogenesis.

Effects of Tearing Conditions on the Crack Propagation in a Monolayer Graphene Sheet.

The path of crack propagation in a graphene sheet is significant for graphene patterning via the tearing approach. In this study, we evaluate the fracture properties of pre-cracked graphene during the tearing process, with consideration of the effects of the aspect ratio, loading speed, loading direction, and ambient temperatures on the crack propagation in the monolayer sheet. Some remarkable conclusions are drawn based on the molecular dynamic simulation results, i.e., a higher loading speed may result in a complicated path of crack propagation, and the propagation of an armchair crack may be accompanied by sp carbon links at high temperatures. The reason for this is that the stronger thermal vibration reduces the load stress difference near the crack tip and, therefore, the crack tip can pass through the sp link. A crack propagates more easily along the zigzag direction than along the armchair direction. The out-of-plane tearing is more suitable than the in-plane tearing for graphene patterning. The path of crack propagation can be adjusted by changing the loading direction, e.g., a rectangular graphene ribbon can be produced by oblique tearing. This new understanding will benefit the application of graphene patterning via the tearing approach.

Continuous positive airway pressure adherence and blood pressure lowering in patients with obstructive sleep apnoea syndrome and nocturnal hypertension.

PURPOSE: We investigated continuous positive airway pressure (CPAP) adherence and its association with the blood pressure (BP) and pulse rate changes in patients with obstructive sleep apnoea syndrome (OSAS) and hypertension. MATERIALS AND METHODS: In a single-blind trial, patients were randomly assigned to CPAP or sham CPAP treatment for 3 months. We performed clinic, ambulatory and home BP measurements at baseline and during follow-up. CPAP adherence was assessed as the CPAP frequency per week and time per night. Non-adherence was defined as a CPAP use for <5 days/week or <4 h/night. RESULTS: In the CPAP (n = 26) and sham CPAP groups (n = 21), the CPAP frequency was 5.5 and 4.8 days/week (p = 0.17), respectively, and the CPAP time was 5.0 and 4.1 h/night (p = 0.03), respectively. The corresponding prevalence of non-adherence was 46.2% and 66.7% (p = 0.16), respectively. The CPAP frequency but not time tended to be associated with the changes in BP and pulse rate at 3 months of follow-up, especially home systolic/diastolic BP in the CPAP group (3.2/1.3 mmHg greater reductions per 1 day increment, p ≤ 0.01). Adherent, compared with non-adherent patients, had greater reductions in BP or pulse rate at 3 months of follow-up. In the CPAP and sham CPAP groups combined, statistical significance was achieved for the adjusted between adherence and non-adherence differences in home systolic/diastolic BP (-5.0/-3.8 mmHg) and 24-h, daytime and night-time ambulatory pulse rate (-6.2, -7.8 and -4.4 beats/min, respectively, p ≤ 0.04). CONCLUSION: CPAP adherence was associated with the BP lowering and pulse rate slowing effects, especially the CPAP frequency.

Comparative genome analysis of programmed DNA elimination in nematodes.

Programmed DNA elimination is a developmentally regulated process leading to the reproducible loss of specific genomic sequences. DNA elimination occurs in unicellular ciliates and a variety of metazoans, including invertebrates and vertebrates. In metazoa, DNA elimination typically occurs in somatic cells during early development, leaving the germline genome intact. Reference genomes for metazoa that undergo DNA elimination are not available. Here, we generated germline and somatic reference genome sequences of the DNA eliminating pig parasitic nematode Ascaris suum and the horse parasite Parascaris univalens. In addition, we carried out in-depth analyses of DNA elimination in the parasitic nematode of humans, Ascaris lumbricoides, and the parasitic nematode of dogs, Toxocara canis. Our analysis of nematode DNA elimination reveals that in all species, repetitive sequences (that differ among the genera) and germline-expressed genes (approximately 1000-2000 or 5%-10% of the genes) are eliminated. Thirty-five percent of these eliminated genes are conserved among these nematodes, defining a core set of eliminated genes that are preferentially expressed during spermatogenesis. Our analysis supports the view that DNA elimination in nematodes silences germline-expressed genes. Over half of the chromosome break sites are conserved between Ascaris and Parascaris, whereas only 10% are conserved in the more divergent T. canis. Analysis of the chromosomal breakage regions suggests a sequence-independent mechanism for DNA breakage followed by telomere healing, with the formation of more accessible chromatin in the break regions prior to DNA elimination. Our genome assemblies and annotations also provide comprehensive resources for analysis of DNA elimination, parasitology research, and comparative nematode genome and epigenome studies.

Carbon monoxide attenuates lipopolysaccharide-induced lung injury by mitofusin proteins via p38 MAPK pathway.

BACKGROUND: The protective effects of carbon monoxide against the lipopolysaccharide (LPS)-induced lung injury were attributed to maintenance of mitochondrial dynamics, but the mechanisms remain unexplored. MATERIALS AND METHODS: Using a rat model of acute lung injury induced by LPS and the LPS attacking cell model, we investigated the effects of pretreatment of carbon monoxide molecule-2 (CORM-2) on the acute lung injury and expressions of mitofusin proteins that play a critical role in mitochondrial dynamics. RESULTS: We found that preadministration of CORM-2, not the inactive form of CORM-2, significantly reduced the lung injury, levels of inflammatory cytokines, and the degree of oxidative stress caused by LPS. What was more, it increased the expressions of mitofusin proteins. Similar findings were also found in LPS-stimulating cell model. However, when the cells were treated in combination with LPS, CORM-2, and SB203580, it completely abolished the protection of CORM-2, reflected by increased levels of inflammatory cytokines and malonaldehyde, decreased activities of superoxide dismutase, along with the lower expressions of mitofusin proteins and the ratio of p-p38 mitogen activated protein kinase to p38 mitogen activated protein kinase. CONCLUSIONS: Our observations suggest that pretreatment with CORM-2 could attenuate LPS-induced lung injury by inducing the expressions of mitofusin proteins via p38 mitogen activated protein kinase pathway.

The prevalence, incidence, management and risks of atrial fibrillation in an elderly Chinese population: a prospective study.

BACKGROUND: There is limited information on prevalent and incident atrial fibrillation in Chinese. We aimed to investigate the prevalence, incidence, management and risks of atrial fibrillation in an elderly Chinese population. METHODS: In a population--based prospective study in elderly (≥ 60 years) Chinese, we performed cardiovascular health examinations including a 12-lead electrocardiogram at baseline in 3,922 participants and biennially during follow-up in 2,017 participants. We collected information on vital status during the whole follow-up period. RESULTS: The baseline prevalence of atrial fibrillation was 2.0 % (n = 34) in 1718 men and 1.6 % (n = 36) in 2204 women. During a median 3.8 years of follow-up, the incidence rate of atrial fibrillation (n = 34) was 4.9 per 1000 person-years (95 % confidence interval [CI], 3.4-6.9). In univariate analysis, both the prevalence and incidence of atrial fibrillation were higher with age advancing (P < 0.0001) and in the presence of coronary heart disease (P ≤ 0.02). Of the 104 prevalent and incident cases of atrial fibrillation, only 1 (1.0 %) received anticoagulant therapy (warfarin). These patients with atrial fibrillation, compared with those with sinus rhythm, had significantly higher risks of all-cause (n = 261, hazard ratio [HR] 1.87, 95 % CI, 1.09-3.20, P = 0.02), cardiovascular (n = 136, HR 3.78, 95 % CI 2.17-6.58, P < 0.0001) and stroke mortality (n = 44, HR 6.31, 95 % CI 2.81-14.19, P = 0.0003). CONCLUSIONS: Atrial fibrillation was relatively frequent in elderly Chinese, poorly managed and associated with higher risks of mortality.

Advancements in Spinal Cord Injury Repair: Insights from Dental-Derived Stem Cells.

Spinal cord injury (SCI), a prevalent and disabling neurological condition, prompts a growing interest in stem cell therapy as a promising avenue for treatment. Dental-derived stem cells, including dental pulp stem cells (DPSCs), stem cells from human exfoliated deciduous teeth (SHED), stem cells from the apical papilla (SCAP), dental follicle stem cells (DFSCs), are of interest due to their accessibility, minimally invasive extraction, and robust differentiating capabilities. Research indicates their potential to differentiate into neural cells and promote SCI repair in animal models at both tissue and functional levels. This review explores the potential applications of dental-derived stem cells in SCI neural repair, covering stem cell transplantation, conditioned culture medium injection, bioengineered delivery systems, exosomes, extracellular vesicle treatments, and combined therapies. Assessing the clinical effectiveness of dental-derived stem cells in the treatment of SCI, further research is necessary. This includes investigating potential biological mechanisms and conducting Large-animal studies and clinical trials. It is also important to undertake more comprehensive comparisons, optimize the selection of dental-derived stem cell types, and implement a functionalized delivery system. These efforts will enhance the therapeutic potential of dental-derived stem cells for repairing SCI.

Ambulatory blood pressure monitoring in the prediction and prevention of coronary heart disease.

We reviewed studies of ambulatory blood pressure monitoring (ABPM) in patients with symptomatic coronary heart disease (CHD) or asymptomatic coronary lesions and in patients at high coronary risk, such as in the presence of hypertension. We identified ten cross-sectional and seven prospective studies in patients with CHD or coronary lesions. These studies showed that patients with CHD or coronary lesions often had nocturnal non-dipping or increased blood pressure variability, and might have increased risk of coronary events, due to either uncontrolled hypertension or treatment-induced hypotension identified by ABPM. We identified ten observational studies in hypertensive patients and normotensive subjects and five therapeutic trials in hypertension. These observational studies demonstrated that one or more ambulatory blood pressure components might provide predictive value for coronary events above and beyond clinic blood pressure. The therapeutic trials were less conclusive, but suggestive of additional value for the prevention of coronary events.

Divergent BRAF Inhibitor Resistance Mechanisms Revealed through Epigenetic Mapping.

Although tremendous progress has been made in targeted and immune-based treatments for advanced melanoma, there remains a substantial therapeutic failure rate. For patients with BRAF(V600)-mutant melanomas, resistance to BRAF inhibitors remains a significant survival hurdle. Although multiple compensatory mechanisms to bypass BRAF blockade have been discovered, the epigenetic patterns are still poorly characterized. In this report, we generated eight matched pairs of vemurafenib-sensitive/-resistant melanoma lines and subjected these to concurrent RNA-sequencing and H3K27ac chromatin immunoprecipitation sequencing analysis. Globally, we identified two classes of epigenetic profiles that correlate with resistance. Class 1 resistance involves fewer RNA expression alterations accompanied by fewer enhancer mark changes with H3K27ac. Class 2 resistance shows widespread alterations in transcription and enhancer profiles, which converge on epithelial‒mesenchymal transition and hypoxia-related pathways. We also observed significant and dynamic changes in superenhancers that underpin these transcriptomic patterns. We subsequently verified the two-class structure in pre-BRAF inhibitors and postrelapse human melanoma specimens. Our findings reveal a broad and underappreciated spectrum of epigenetic plasticity during acquired BRAF inhibitor resistance.

Micro-arc oxidation (MAO) and its potential for improving the performance of titanium implants in biomedical applications.

Titanium (Ti) and its alloys have good biocompatibility, mechanical properties and corrosion resistance, making them attractive for biomedical applications. However, their biological inertness and lack of antimicrobial properties may compromise the success of implants. In this review, the potential of micro-arc oxidation (MAO) technology to create bioactive coatings on Ti implants is discussed. The review covers the following aspects: 1) different factors, such as electrolyte, voltage and current, affect the properties of MAO coatings; 2) MAO coatings affect biocompatibility, including cytocompatibility, hemocompatibility, angiogenic activity, corrosion resistance, osteogenic activity and osseointegration; 3) antibacterial properties can be achieved by adding copper (Cu), silver (Ag), zinc (Zn) and other elements to achieve antimicrobial properties; and 4) MAO can be combined with other physical and chemical techniques to enhance the performance of MAO coatings. It is concluded that MAO coatings offer new opportunities for improving the use of Ti and its alloys in biomedical applications, and some suggestions for future research are provided.

Atrazine decontamination by a newly screened psychrotroph Paenarthrobacter sp. KN0901 in an aquatic system: Metabolic pathway, kinetics, and hydroponics experiment.

Atrazine residues running off the fields and entering water resources are a major threat to food security and the ecosystem. In this study, a psychrotrophic functional strain named KN0901 to remove atrazine residues was screened. KN0901 could degrade 30 mg·L-1 atrazine in 4 days at 15ºC with 105 CFU·mL-1 incubation. The phylogenetic results showed KN0901 belonged to Paenarthrobacter sp. PCR results showed that the functional genes consist of trzN, atzB, and atzC, suggesting atrazine was transformed to cyanuric acid by KN0901. KN0901 could degrade atrazine without adding exogenous carbon and nitrogen sources. What's more, KN0901 could tolerate extreme low temperature (5ºC) and high atrazine concentration (100 mg·L-1). When growth and degradation curves were compared, the results indicated the length of lag time showed significant correlation to atrazine degradation rate. The hydroponic experiments showed that the toxicity of atrazine was significantly reduced with KN0901 treatment. The study provided an effective, economic, and eco-friendly bioremediation measure to address atrazine contamination.

Microplastics extraction from wastewater treatment plants: Two-step digestion pre-treatment and application.

As the gathering place of urban wastewater, wastewater treatment plants (WWTPs) are indispensable for removing microplastics (MPs), one of the emerging contaminants of great concern, from cities into the natural environment. A reliable and efficient extraction method for MPs, especially in organic-rich matrices, such as sludge samples, is the basis for studying MPs contamination, while it is still lacking. The digestion process, which requires further optimisation, is the most important step during extraction. In this study, we developed and optimised a two-step digestion process to extract MPs and proposed a recommended dosage of digestion reagents based on the mixed liquid volatile suspended solids (MLVSS) level of the sample. Successive addition of 30% H2O2 + 1 M HNO3 (v:v = 1:1, T = 60 °C, t = 5 h + 5 h) could efficiently extract MPs from sludge samples (over 90%), and the recommended dosage of digestion reagent was 100 ml 30% H2O2+100 ml 1 M HNO3 with the sample MLVSS lower than approximately 0.43 g. This new method was also applied to examine the characteristics of MPs in two typical WWTPs (anaerobic-anoxic-oxic and biofilter processes) in Shenzhen. The concentrations of MPs in the influent, effluent and dewatered sludge were approximately 114.00 n/L, 6.00 n/L, and 126.00 n/g (dry weight) in WWTP A, whereas 404.00 n/L, 22.00 n/L, and 204.00 n/g (dry weight) in WWTP B, respectively. Rayon and polyester were the dominant polymers in both the WWTPs. Fibers accounted for the largest proportion of the influent and effluent. Sizes between 0.20-0.50 mm were most detected. This study provides a new and efficient reference method to extract MPs from WWTPs samples, especially sludge sample, with less MPs loss and more beneficial to subsequent identification.

Removing microplastics from aquatic environments: A critical review.

As one of the typical emerging contaminants, microplastics exist widely in the environment because of their small size and recalcitrance, which has caused various ecological problems. This paper summarizes current adsorption and removal technologies of microplastics in typical aquatic environments, including natural freshwater, marine, drinking water treatment plants (DWTPs), and wastewater treatment plants (WWTPs), and includes abiotic and biotic degradation technologies as one of the removal technologies. Recently, numerous studies have shown that enrichment technologies have been widely used to remove microplastics in natural freshwater environments, DWTPs, and WWTPs. Efficient removal of microplastics via WWTPs is critical to reduce the release to the natural environment as a key connection point to prevent the transfer of microplastics from society to natural water systems. Photocatalytic technology has outstanding pre-degradation effects on microplastics, and the isolated microbial strains or enriched communities can degrade up to 50% or more of pre-processed microplastics. Thus, more research focusing on microplastic degradation could be carried out by combining physical and chemical pretreatment with subsequent microbial biodegradation. In addition, the current recovery technologies of microplastics are introduced in this review. This is incredibly challenging because of the small size and dispersibility of microplastics, and the related technologies still need further development. This paper will provide theoretical support and advice for preventing and controlling the ecological risks mediated by microplastics in the aquatic environment and share recommendations for future research on the removal and recovery of microplastics in various aquatic environments, including natural aquatic environments, DWTPs, and WWTPs.