Toward High Contrast and Noninvasive Fluorescence Switches via an O-Fused Ring 5,7-Dihydroxy-4-methyl-2,2,3-triphenylbenzofuran-6(2H)-one Strategy.

An unprecedented O-fused ring 5,7-dihydroxy-4-methyl-2,2,3-triphenylbenzofuran-6(2H)-one (3) was first time synthesized. Further, a series of novel dialkyl/fluoroalkyl derivatives of compound 3, 5,7-dialkoxy/fluoroalkoxy-4-methyl-2,2,3-triphenylbenzofuran-6(2H)-one, were obtained with noninvasive fluorescence switching characteristics and aggregation-induced emission properties. Compared with fluoroalkyl derivatives, the alkyl analogs exhibited a significant bathochromic shift in solid-state fluorescence emission. Notably, these noninvasive fluorescent molecular switches could be facilely tuned through light and heat stimulation, which successfully achieved high contrast and reversible fluorescent emission between orange and yellow endowing them with potential applications in data encryption materials. In addition, the single crystal data of compounds 3 and 7-CF3 displayed weak intermolecular interactions in different directions, resulting in twisted conformation and antiparallel slip stacking. Interestingly, the polymer dimethyl silicone film doped with 7-C3F7 also showed an evident light-responsive behavior, meeting the criterion for fluorescent materials in the optical field.

Progress on H2B as a multifunctional protein related to pathogens.

Histone H2B is a member of the core histones, which together with other histones form the nucleosome, the basic structural unit of chromosomes. As scientists delve deeper into histones, researchers gradually realize that histone H2B is not only an important part of nucleosomes, but also plays a momentous role in regulating gene transcription, acting as a receptor and antimicrobial action outside the nucleus. There are a variety of epigenetically modified sites in the H2B tail rich in arginine and lysine, which can occur in ubiquitination, phosphorylation, methylation, acetylation, etc. When stimulated by foreign factors such as bacteria, viruses or parasites, histone H2B can act as a receptor for the recognition of these pathogens, and induce an intrinsic immune response to enhance host defense. In addition, the extrachromosomal histone H2B is also an important anti-microorganism agent, which may be the key to the development of antibiotics in the future. This review aims to summarize the interaction between histone H2B and etiological agents and explore the role of H2B in epigenetic modifications, receptors and antimicrobial activity.

TO-UGDA: target-oriented unsupervised graph domain adaptation.

Graph domain adaptation (GDA) aims to address the challenge of limited label data in the target graph domain. Existing methods such as UDAGCN, GRADE, DEAL, and COCO for different-level (node-level, graph-level) adaptation tasks exhibit variations in domain feature extraction, and most of them solely rely on representation alignment to transfer label information from a labeled source domain to an unlabeled target domain. However, this approach can be influenced by irrelevant information and usually ignores the conditional shift of the downstream predictor. To effectively address this issue, we introduce a target-oriented unsupervised graph domain adaptive framework for graph adaptation called TO-UGDA. Particularly, domain-invariant feature representations are extracted using graph information bottleneck. The discrepancy between two domains is minimized using an adversarial alignment strategy to obtain a unified feature distribution. Additionally, the meta pseudo-label is introduced to enhance downstream adaptation and improve the model's generalizability. Through extensive experimentation on real-world graph datasets, it is proved that the proposed framework achieves excellent performance across various node-level and graph-level adaptation tasks.

Mechanism and anti-corrosion measures of carbon dioxide corrosion in CCUS: A review.

Carbon capture, utilization, and storage (CCUS) technology is widely recognized as a key solution for mitigating global climate change. Consequently, it has received significant attention from countries worldwide. However, carbon dioxide corrosion poses a significant challenge to CCUS and represents a bottleneck to the large-scale development and application of this technology. To mitigate this issue, this review starts with a discussion of corrosion problems in CCUS. Later, the fundamentals of the carbon dioxide corrosion mechanism are introduced. Then, the influences of various factors that affect the corrosion are highlighted, such as water content, pH, flow rate, etc. Afterward, we summarize the commonly used methods for corrosion protection, with a particular focus on inhibitor, given their eco-friendly and effective nature. Lastly, challenges and prospects are discussed to motivate future studies on developing novel, high-performance green inhibitor and studying the corresponding protection mechanisms, hoping to make some contributions to carbon emission reduction.

YTHDC1 delays cellular senescence and pulmonary fibrosis by activating ATR in an m6A-independent manner.

Accumulation of DNA damage in the lung induces cellular senescence and promotes age-related diseases such as idiopathic pulmonary fibrosis (IPF). Hence, understanding the mechanistic regulation of DNA damage repair is important for anti-aging therapies and disease control. Here, we identified an m6A-independent role of the RNA-binding protein YTHDC1 in counteracting stress-induced pulmonary senescence and fibrosis. YTHDC1 is primarily expressed in pulmonary alveolar epithelial type 2 (AECII) cells and its AECII expression is significantly decreased in AECIIs during fibrosis. Exogenous overexpression of YTHDC1 alleviates pulmonary senescence and fibrosis independent of its m6A-binding ability, while YTHDC1 deletion enhances disease progression in mice. Mechanistically, YTHDC1 promotes the interaction between TopBP1 and MRE11, thereby activating ATR and facilitating DNA damage repair. These findings reveal a noncanonical function of YTHDC1 in delaying cellular senescence, and suggest that enhancing YTHDC1 expression in the lung could be an effective treatment strategy for pulmonary fibrosis.

The effects of CypA on apoptosis: potential target for the treatment of diseases.

Cyclophilin A (CypA), the first member of cyclophilins, is distributed extensively in eukaryotic and prokaryotic cells, primarily localized in the cytoplasm. In addition to acting as an intracellular receptor for cyclosporin A (CSA), CypA plays a crucial role in diseases such as aging and tumorigenesis. Apoptosis, a form of programmed cell death, is able to balance the rate of cell viability and death. In this review, we focus on the effects of CypA on apoptosis and the relationship between specific mechanisms of CypA promoting or inhibiting apoptosis and diseases, including tumorigenesis, cardiovascular diseases, organ injury, and microbial infections. Notably, the process of CypA promoting or inhibiting apoptosis is closely related to disease development. Finally, future prospects for the association of CypA and apoptosis are discussed, and a comprehensive understanding of the effects of CypA on apoptosis in relation to diseases is expected to provide new insights into the design of CypA as a therapeutic target for diseases. KEY POINTS: • Understand the effect of CypA on apoptosis. • CypA affects apoptosis through specific pathways. • The effect of CypA on apoptosis is associated with a variety of disease processes.

The m6A reader YTHDF2 alleviates the inflammatory response by inhibiting IL-6R/JAK2/STAT1 pathway-mediated high-mobility group box-1 release.

Background: Sepsis is a common severe complication in major burn victims and is characterized by a dysregulated systemic response to inflammation. YTH domain family 2 (YTHDF2), a well-studied N6-methyladenosine (m6A) reader that specifically recognizes and binds to m6A-modified transcripts to mediate their degradation, is connected to pathogenic and physiological processes in eukaryotes, but its effect on sepsis is still unknown. We aimed to discover the effects and mechanisms of YTHDF2 in sepsis. Methods: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blot analyses were used to measure the expression of YTHDF2, the interleukin 6 receptor (IL-6R), high-mobility group box-1 (HMGB1), Janus kinase 2 (JAK2) and signal transducer and activator of transcription 1 (STAT1) under different in vitro conditions. Enzyme-linked immunosorbent assays were utilized to evaluate the expression of HMGB1, IL-6, IL-1ß and tumor necrosis factor-α. To confirm that YTHDF2 specifically targets IL-6R mRNA, RNA immunoprecipitation and dual-luciferase reporter assays were performed. Finally, we utilized a mouse model of lipopolysaccharide (LPS)-induced sepsis to verify the effects of YTHDF2 in vivo. Results: According to our findings, YTHDF2 was expressed at a low level in peripheral blood mononuclear cells from septic mice and patients as well as in LPS-induced RAW264.7 cells. Overexpression of YTHDF2 alleviated the inflammatory response by inhibiting HMGB1 release and JAK2/STAT1 signalling in LPS-stimulated cells. Mechanistically, YTHDF2 suppressed JAK2/STAT1 signalling by directly recognizing the m6A-modified site in IL-6R and decreasing the stability of IL-6R mRNA, thereby inhibiting HMGB1 release. In vivo experiments showed that YTHDF2 played a protective role in septic mice by suppressing the IL-6R/JAK2/STAT1/HMGB1 axis. Conclusions: In summary, these findings demonstrate that YTHDF2 plays an essential role as an inhibitor of inflammation to reduce the release of HMGB1 by inhibiting the IL-6R/JAK2/STAT1 pathway, indicating that YTHDF2 is a novel target for therapeutic interventions in sepsis.

Comparative genomics and DNA methylation analysis of Pseudomonas aeruginosa clinical isolate PA3 by single-molecule real-time sequencing reveals new targets for antimicrobials.

Introduction: Pseudomonas aeruginosa (P.aeruginosa) is an important opportunistic pathogen with broad environmental adaptability and complex drug resistance. Single-molecule real-time (SMRT) sequencing technique has longer read-length sequences, more accuracy, and the ability to identify epigenetic DNA alterations. Methods: This study applied SMRT technology to sequence a clinical strain P. aeruginosa PA3 to obtain its genome sequence and methylation modification information. Genomic, comparative, pan-genomic, and epigenetic analyses of PA3 were conducted. Results: General genome annotations of PA3 were discovered, as well as information about virulence factors, regulatory proteins (RPs), secreted proteins, type II toxin-antitoxin (TA) pairs, and genomic islands. A genome-wide comparison revealed that PA3 was comparable to other P. aeruginosa strains in terms of identity, but varied in areas of horizontal gene transfer (HGT). Phylogenetic analysis showed that PA3 was closely related to P. aeruginosa 60503 and P. aeruginosa 8380. P. aeruginosa's pan-genome consists of a core genome of roughly 4,300 genes and an accessory genome of at least 5,500 genes. The results of the epigenetic analysis identified one main methylation sites, N6-methyladenosine (m6A) and 1 motif (CATNNNNNNNTCCT/AGGANNNNNNNATG). 16 meaningful methylated sites were picked. Among these, purH, phaZ, and lexA are of great significance playing an important role in the drug resistance and biological environment adaptability of PA3, and the targeting of these genes may benefit further antibacterial studies. Disucssion: This study provided a detailed visualization and DNA methylation information of the PA3 genome and set a foundation for subsequent research into the molecular mechanism of DNA methyltransferase-controlled P. aeruginosa pathogenicity.

Transient Magnetoelectric Coupling Induced by the Dynamic Intertwinement between Exchange Striction and Compensation in GdFeO3.

In this study, we investigate the dynamic magnetoelectric (ME) coupling behaviors of GdFeO3 under pulsed magnetic fields. When a magnetic field is applied along the c-axis, and the temperature is near the compensation temperature (Tcomp = 3.5 K), we observe a subtle transition involving the reversal of Fe3+ moments at approximately 0.8 T in magnetization (M) measurements. This transition induces a corresponding jump in electrical polarization (P), which is not present in the static field measurements. The dynamic intertwining between M and P signifies a competition between antiferromagnetic (AFM) coupling between Gd3+ and Fe3+ moments and their Zeeman energies. The robust AFM coupling leads to the reversal of Fe3+ moments near Tcomp, triggering the abrupt change in P. Based on the exchange striction mechanism in the ferrimagnetic GdFeO3, we propose the possibility of achieving highly magnetic field sensitive ME coupling near the compensation temperature in ferrimagnetic multiferroic orthoferrites.

Atmosphere-inspired multilayered nanoarmor with modulable protection and delivery of Interleukin-4 for inflammatory microenvironment modulation.

Inflammatory bowel disease (IBD) has been closely associated with immune disorders and excessive M1 macrophage activation, which can be reversed by the M2-polarizing effect of interleukin-4 (IL-4). However, maintaining native IL-4 activity with its specific release in the inflammatory microenvironment and efficient biological performance remain a challenge. Inspired by the multilayered defense mechanism of the earth's atmosphere, we constructed a multilayered protective nanoarmor (NA) for IL-4 delivery (termed as IL-4@PEGRA NAs) into an intricate inflammatory microenvironment. The poly(ethylene glycol) (PEG)-ylated phenolic rosmarinic acid (RA)-grafted copolymer contains two protective layers-the intermediate polyphenol (RA molecules) and outermost shield (PEG) layers-to protect the biological activity of IL-4 and prolong its circulation in blood. Moreover, IL-4@PEGRA NAs scavenge reactive oxygen species with the specific release of IL-4 and maximize its biofunction at the site of inflammation, leading to M2 macrophage polarization and downregulation of inflammatory mediators. Simultaneously, gut microbiota dysbiosis can improve to amplify the M2-polarizing effect and inhibit the phosphatidylinositol 3 kinase/Akt signaling pathway, thereby attenuating inflammation and promoting colitis tissue repair. It provides a nature-inspired strategy for constructing an advanced multilayered NA delivery system with protective characteristics and potential for IBD management.

Effect of microbial communities on nitrogen and phosphorus metabolism in rivers with different heavy metal pollution.

Small urban and rural rivers usually face heavy metal pollution as a result of urbanization and industrial and agricultural activities. To elucidate the metabolic capacity of microbial communities on nitrogen and phosphorus cycle in river sediments under different heavy metal pollution backgrounds, this study collected samples in situ from two typical rivers, Tiquan River and Mianyuan River, with different heavy metal pollution levels. The microbial community structure and metabolic capacity of nitrogen and phosphorus cycles of sediment microorganisms were analyzed by high-throughput sequencing. The results showed that the major heavy metals in the sediments of the Tiquan River were Zn, Cu, Pb, and Cd with the contents of 103.80, 30.65, 25.95, and 0.44 mg/kg, respectively, while the major heavy metals in the sediments of the Mianyuan River were Cd and Cu with the contents of 0.60 and 27.81 mg/kg, respectively. The dominant bacteria Steroidobacter, Marmoricola, and Bacillus in the sediments of the Tiquan River had positive correlations with Cu, Zn, and Pb while are negatively correlated with Cd. Cd had a positive correlation with Rubrivivax, and Cu had a positive correlation with Gaiella in the sediments of the Mianyuan River. The dominant bacteria in the sediments of the Tiquan River showed strong phosphorus metabolic ability, and the dominant bacteria in the sediments of the Mianyuan River showed strong nitrogen metabolic ability, corresponding to the lower total phosphorus content in the Tiquan River and the higher total nitrogen content in the Mianyuan River. The results of this study showed that resistant bacteria became dominant bacteria due to the stress of heavy metals, and these bacteria showed strong nitrogen and phosphorus metabolic ability. It can provide theoretical support for the pollution prevention and control of small urban and rural rivers and have positive significance for maintaining the healthy development of rivers.

Effect of La2 O3 and CeO2 on anaerobic methanogenesis process: Kinetics analysis and process mechanism study.

La2 O3 and CeO2 , as main rare earth oxides, with unique physical and chemical properties have been widely used in catalyst and grinding industry. In this study, the effects of La2 O3 and CeO2 on the anaerobic process were investigated. The biological methane production tests showed that 0-0.05 g/L La2 O3 and 0-0.05 g/L CeO2 enhanced anaerobic methanogenesis process. The result showed maximum specific methanogenic rates of La2 O3 and CeO2 were 56.26 mL/(h·gVSS) and 49.43 mL/(h·gVSS) and, compared with the control, increased 4% and 3%, respectively. La2 O3 significantly reduced the accumulation of volatile fatty acids (VFAs), whereas CeO2 had no similar effect. Dissolution experiments demonstrated that the content of extracellular La in the anaerobic granular sludge reached 404 µg-La/g volatile suspended solid (VSS), which was 134 times higher than that of extracellular Ce (3 µg-Ce/gVSS). The content of intracellular La reached 206 µg-La/gVSS, which was 19 times higher than that of intracellular Ce (11 µg-Ce/gVSS). The different stimulation between La3+ and Ce3+ could be attributed to the different dissolution of La2 O3 and CeO2 . The result of this work is helpful to optimize anaerobic processes and to develop novel additives. PRACTITIONER POINTS: Novel anaerobic additives were developed. La2O3 and CeO2 in 0-0.05 g/L enhanced organics degradation and methane production. The addition of La2O3 significantly reduced the accumulation of volatile fatty acids. The solubilization of La2O3 was stronger than CeO2. The promoting effects of low concentrations of La2O3 and CeO2 were derived from dissolved La and Ce.

Mycoplasma genitalium Protein of Adhesion Suppresses T Cell Activation via CypA-CaN-NFAT Pathway.

Mycoplasma genitalium is a prokaryotic microorganism that causes urogenital tract infections. M. genitalium protein of adhesion (MgPa) was essential for M. genitalium attachment and subsequent invasion into host cells. Our prior research confirmed that Cyclophilin A (CypA) was the binding receptor for MgPa and MgPa-CypA interaction can lead to the production of inflammatory cytokines. In this study, we revealed that the recombinant MgPa (rMgPa) could inhibit the CaN-NFAT signaling pathway to reduce the level of IFN-γ, IL-2, CD25, and CD69 in Jurkat cells by binding to the CypA receptor. Moreover, rMgPa inhibited the expressions of IFN-γ, IL-2, CD25, and CD69 in primary mouse T cells. Likewise, the expressions of these T cells activation-related molecules in CypA-siRNA-transfected cells and CypA-/- mouse primary T cell was strengthened by rMgPa. These findings showed that rMgPa suppressed T cell activation by downregulating the CypA-CaN-NFAT pathway, and as a result, acted as an immunosuppressive agent. IMPORTANCE Mycoplasma genitalium is a sexually transmitted bacterium that can co-infect with other infections and causes nongonococcal urethritis in males, cervicitis, pelvic inflammatory disease, premature birth, and ectopic pregnancy in women. The adhesion protein of M. genitalium (MgPa) is the primary virulence factor in the complicated pathogenicity of M. genitalium. This research proved that MgPa could interact with host cell Cyclophilin A (CypA) and prevent T cell activation by inhibiting Calcineurin (CaN) phosphorylation and NFAT nuclear translocation, which clarified the immunosuppression mechanism of M. genitalium to host T cells. Therefore, this study can provide a new idea that CypA can be used for a therapeutic or prophylactic target for M. genitalium infection.

Vimentin Is an Attachment Receptor for Mycoplasma pneumoniae P1 Protein.

Mycoplasma pneumoniae is the most common pathogen causing respiratory tract infection, and the P1 protein on its adhesion organelle plays a crucial role during the pathogenic process. Currently, there are many studies on P1 and receptors on host cells, but the adhesion mechanism of P1 protein is still unclear. In this study, a modified virus overlay protein binding assay (VOPBA) and liquid chromatography-mass spectrometry (LC-MS) were performed to screen for proteins that specifically bind to the region near the carboxyl terminus of the recombinant P1 protein (rP1-C). The interaction between rP1-C and vimentin or ß-4-tubulin were confirmed by far-Western blotting and coimmunoprecipitation. Results verified that vimentin and ß-4-tubulin were mainly distributed on the cell membrane and cytoplasm of human bronchial epithelial (BEAS-2B) cells, but only vimentin could interact with rP1-C. The results of the adhesion and adhesion inhibition assays indicated that the adhesion of M. pneumoniae and rP1-C to cells could be partly inhibited by vimentin and its antibody. When vimentin was downregulated with the corresponding small interfering RNA (siRNA) or overexpressed in BEAS-2B cells, the adhesion of M. pneumoniae and rP1-C to cells was decreased or increased, respectively, which indicated that vimentin was closely associated with the adhesion of M. pneumoniae and rP1-C to BEAS-2B cells. Our results demonstrate that vimentin could be a receptor on human bronchial epithelial cells for the P1 protein and plays an essential role in the adhesion of M. pneumoniae to cells, which may clarify the pathogenesis of M. pneumoniae. IMPORTANCE Mycoplasma pneumoniae is the most common pathogen causing respiratory tract infection, and the P1 protein on its adhesion organelle plays a crucial role during the pathogenic process. A variety of experiments, including enzyme-linked immunosorbent assay (ELISA), coimmunoprecipitation, adhesion, and adhesion inhibition assay, have demonstrated that the M. pneumoniae P1 protein can interact with vimentin, that the adhesion of M. pneumoniae and recombinant P1 protein to BEAS-2B cells was affected by the expression level of vimentin. This provides a new idea for the prevention and treatment of Mycoplasma pneumoniae infection.

Spin Reorientation Transition and Negative Magnetoresistance in Ferromagnetic NdCrSb3 Single Crystals.

High-quality NdCrSb3 single crystals are grown using a Sn-flux method, for electronic transport and magnetic structure study. Ferromagnetic ordering of the Nd3+ and Cr3+ magnetic sublattices are observed at different temperatures and along different crystallographic axes. Due to the Dzyaloshinskii-Moriya interaction between the two magnetic sublattices, the Cr moments rotate from the b axis to the a axis upon cooling, resulting in a spin reorientation (SR) transition. The SR transition is reflected by the temperature-dependent magnetization curves, e.g., the Cr moments rotate from the b axis to the a axis with cooling from 20 to 9 K, leading to a decrease in the b-axis magnetization f and an increase in the a-axis magnetization. Our elastic neutron scattering along the a axis shows decreasing intensity of magnetic (300) peak upon cooling from 20 K, supporting the SR transition. Although the magnetization of two magnetic sublattices favours different crystallographic axes and shows significant anisotropy in magnetic and transport behaviours, their moments are all aligned to the field direction at sufficiently large fields (30 T). Moreover, the magnetic structure within the SR transition region is relatively fragile, which results in negative magnetoresistance by applying magnetic fields along either a or b axis. The metallic NdCrSb3 single crystal with two ferromagnetic sublattices is an ideal system to study the magnetic interactions, as well as their influences on the electronic transport properties.

LncRNA GAS5 suppresses inflammatory responses by inhibiting HMGB1 release via miR-155-5p/SIRT1 axis in sepsis.

Sepsis comprises a lethal immunologic response due to infection. Increasingly, evidence has demonstrated the important role of long non-coding RNA growth arrest-specific transcript 5 (GAS5) in the regulation of sepsis. Nevertheless, the mechanisms by which GAS5 participates in the progression of sepsis remain unclear. Our study demonstrated the role and underlying mechanism of GAS5 in regulating lipopolysaccharide (LPS)-induced inflammation. In this study, GAS5 expression was found to be markedly decreased in serum samples of sepsis patients and a sepsis mouse model, and was negatively related with HMGB1 expression. GAS5 overexpression inhibited cell inflammatory responses by decreasing HMGB1 release. Furthermore, GAS5 inhibited LPS-mediated hyperacetylation and the release of HMGB1 by increasing the expression of sirtuin1 (SIRT1). Additionally, upregulated GAS5 attenuated inflammatory responses in vitro and vivo, and the knockdown of a miR-155-5p mimic and SIRT1 rescued the effects of GAS5 upregulation. Mechanistically, GAS5 sponged miR-155-5p to upregulate SIRT1, thereby inhibiting HMGB1 acetylation and release. In conclusion, our findings indicate that GAS5 suppresses inflammatory responses by modulating the miR-155-5p/SIRT1/HMGB1 axis in sepsis, providing a novel therapeutic target for inflammation in sepsis.

A biomarker-responsive nanoprobe for detecting hepatic ischemia-reperfusion injury via optoacoustic/NIR-II fluorescence imaging.

A nanoprobe for detecting hepatic ischemia-reperfusion injury has been developed. Apparent optoacoustic and NIR-II fluorescent signals are given out upon the nanoprobe's response to the in situ biomarker H2O2 in the liver in the case of ischemia-reperfusion injury.

Ecological risk assessment and identification of the distinct microbial groups in heavy metal-polluted river sediments.

To assess the health of river ecosystems, it is essential to quantify the ecological risk of heavy metals in river sediments and the structure of microbial communities. As important tributaries of the Tuo River in the upper reaches of the Yangtze River, the Mianyuan River and the Shiting River, are closely related to the economic development and human daily life in the region. This study assessed the ecological risks of heavy-metal-polluted river sediments, the heavy-metal-driven bacterial communities were revealed, and the relationships between the ecological risks and the identical bacterial communities were discussed. The Cd content was significantly greater than the environmental background value, leading to a serious pollution and very high ecological risk at the confluence of the two rivers and the upper reaches of the Mianyuan River. Microbial community analysis showed that Rhodobacter, Nocardioides, Sphingomonas, and Pseudarthrobacter were the dominant bacterial genera in the sediments of the Shiting River. However, the dominant bacterial genera in the Mianyuan River were Kouleothrix, Dechloromonas, Gaiella, Pedomicrobium, and Hyphomicrobium. Mantel test results showed (r = 0.5977, P = 0.005) that the Cd, As, Zn, Pb, Cr, and Cu were important factors that influenced differences in the distribution of sediment bacterial communities Mianyuan and Shiting rivers. A correlation heatmap showed that heavy metals were negatively correlated for most bacterial communities, but some bacterial communities were tolerant and showed a positive correlation. Overall, the microbial structure of the river sediments showed a diverse spatial distribution due to the influence of heavy metals. The results will improve the understanding of rivers contaminated by heavy metals and provide theoretical support for conservation and in situ ecological restoration of river ecosystems.

Histones: The critical players in innate immunity.

The highly conserved histones in different species seem to represent a very ancient and universal innate host defense system against microorganisms in the biological world. Histones are the essential part of nuclear matter and act as a control switch for DNA transcription. However, histones are also found in the cytoplasm, cell membranes, and extracellular fluid, where they function as host defenses and promote inflammatory responses. In some cases, extracellular histones can act as damage-associated molecular patterns (DAMPs) and bind to pattern recognition receptors (PRRs), thereby triggering innate immune responses and causing initial organ damage. Histones and their fragments serve as antimicrobial peptides (AMPs) to directly eliminate bacteria, viruses, fungi, and parasites in vitro and in vivo. Histones are also involved in phagocytes-related innate immune response as components of neutrophil extracellular traps (NETs), neutrophil activators, and plasminogen receptors. In addition, as a considerable part of epigenetic regulation, histone modifications play a vital role in regulating the innate immune response and expression of corresponding defense genes. Here, we review the regulatory role of histones in innate immune response, which provides a new strategy for the development of antibiotics and the use of histones as therapeutic targets for inflammatory diseases, sepsis, autoimmune diseases, and COVID-19.