Associations of the Serum KL-6 with Severity and Prognosis in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

BACKGROUND: As a biomarker of alveolar-capillary basement membrane injury, Krebs von den Lungen-6 (KL-6) is involved in the occurrence and development of pulmonary diseases. However, the role of the KL-6 in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) has yet to be elucidated. This prospective study was designed to clarify the associations of the serum KL-6 with the severity and prognosis in patients with AECOPD. METHODS: This study enrolled 199 eligible AECOPD patients. Demographic data and clinical characteristics were recorded. Follow-up was tracked to evaluate acute exacerbation and death. The serum KL-6 concentration was measured via an enzyme-linked immunosorbent assay. RESULTS: Serum KL-6 level at admission was higher in AECOPD patients than in control subjects. The serum KL-6 concentration gradually elevated with increasing severity of AECOPD. Pearson and Spearman analyses revealed that the serum KL-6 concentration was positively correlated with the severity score, monocyte count and concentrations of C-reactive protein, interleukin-6, uric acid, and lactate dehydrogenase in AECOPD patients during hospitalization. A statistical analysis of long-term follow-up data showed that elevated KL-6 level at admission was associated with longer hospital stays, an increased risk of future frequent acute exacerbations, and increased severity of exacerbation in COPD patients. CONCLUSION: Serum KL-6 level at admission is positively correlated with increased disease severity, prolonged hospital stay and increased risk of future acute exacerbations in COPD patients. There are positive dose-response associations of elevated serum KL-6 with severity and poor prognosis in COPD patients. The serum KL-6 concentration could be a novel diagnostic and prognostic biomarker in AECOPD patients.

One-pot synthesis and hydrogen peroxide electrochemical sensing of 3D TiO2/MnO2 nanorods assembled microspheres.

Nanorods assembled 3D microspheres of TiO2/MnO2 were prepared via a simple one-pot hydrothermal approach. The resultant composite material exhibited remarkable electrocatalytic activity for hydrogen peroxide (H2O2) in comparison to each single component. The electrochemical sensor constructed with TiO2/MnO2 exhibited a linear relationship within the range 0.0001-5.6 mmol·L-1 for H2O2. The limit of detection (LOD) and sensitivity for H2O2 were 0.03 µmol·L-1 (S/N = 3) and 316.6 µA (mmol·L-1)-1 cm-2. Moreover, this sensor can be employed to detect trace amount of H2O2 in serum and urine samples successfully, supporting an insight and strategy for a more sensitive electrochemical sensor.

Investigation on the interaction of NH3&CH4 co-activated char under reburning conditions.

In the current global context, there is a pressing need to curtail greenhouse gas emissions, making the utilization of a coal and zero-carbon energy blend an imperative strategy for reducing carbon emissions from coal-fired power generation. The planar flame burner serves as a tool to simulate the temperature and atmospheric conditions within the reburning zone, facilitating extensive examination of the physical and chemical structural alterations, as well as the nitrogen oxide reduction potential, during NH3/CH4 activation for reburning pulverized coal. Experimental results underscore that blending high-activity fuels optimizes the combustion performance of coal char. Through the addition of NH3 and CH4, the NO reduction capability of coal char is bolstered by approximately 0.67 times compared to sole reliance on recirculating flue gas transport. Furthermore, NH3 introduction facilitates the conversion of C]O double bonds into C-O single bonds, rendering them more amenable to reduction by NO. While the joint influence of NH3 and CH4 does not significantly impact char particle size, it does foster the evolution of N-Q to N-5 and N-6 on the char surface. Furthermore, there was a significant increase in the BET-specific surface area, which rose by 50%. Additionally, the total pore volume increased by approximately 21.43%. The comprehensive understanding of NH3 and CH4 modified pulverized coal reburning technology holds significant promise for optimizing power plant operations and mitigating carbon dioxide and nitrogen oxide emissions.

Using model systems to unravel host-Pseudomonas aeruginosa interactions.

Using model systems in infection biology has led to the discoveries of many pathogen-encoded virulence factors and critical host immune factors to fight pathogenic infections. Studies of the remarkable Pseudomonas aeruginosa bacterium that infects and causes disease in hosts as divergent as humans and plants afford unique opportunities to shed new light on virulence strategies and host defence mechanisms. One of the rationales for using model systems as a discovery tool to characterise bacterial factors driving human infection outcomes is that many P. aeruginosa virulence factors are required for pathogenesis in diverse different hosts. On the other side, many host signalling components, such as the evolutionarily conserved mitogen-activated protein kinases, are involved in immune signalling in a diverse range of hosts. Some model organisms that have less complex immune systems also allow dissection of the direct impacts of innate immunity on host defence without the interference of adaptive immunity. In this review, we start with discussing the occurrence of P. aeruginosa in the environment and the ability of this bacterium to cause disease in various hosts as a natural opportunistic pathogen. We then summarise the use of some model systems to study host defence and P. aeruginosa virulence.

Controlled Synthesis of MOF-Derived Nano-Microstructure toward Lightweight and Wideband Microwave Absorption.

Correlating metal-organic framework (MOF) synthesis processes and microwave absorption (MA) enhancement mechanisms is a pioneer project. Nevertheless, the correlation process still relies mainly on empirical doctrine, which hardly corresponds to the specific mechanism of the effect on the dielectric properties. Hereby, after the strategy of modulation of protonation engineering and solvothermal temperature in the synthesis route, the obtained sheet-like self-assembled nanoflowers were constructed. Porous structures with multiple heterointerfaces, abundant defects, and vacancies are obtained by controlled design of the synthesis procedure. The rearrangement of charges and enhanced polarization can be promoted. The designed electromagnetic properties and special nano-microstructures of functional materials have significant impact on their electromagnetic wave energy conversion effects. As a consequence, the MA performance of the samples has been enhanced toward broadband absorption (6.07 GHz), low thickness (2.0 mm), low filling (20%), and efficient loss (-25 dB), as well as being suitable for practical environmental applications. This work establishes the connection between the MOF-derived materials synthesis process and the MA enhancement mechanism, which provides insight into various microscopic microwave loss mechanisms.

Recent Advances on F-Doped Layered Transition Metal Oxides for Sodium Ion Batteries.

With the development of social economy, using lithium-ion batteries in energy storage in industries such as large-scale electrochemical energy storage systems will cause lithium resources to no longer meet demand. As such, sodium ion batteries have become one of the effective alternatives to LIBs. Many attempts have been carried out by researchers to achieve this, among which F-doping is widely used to enhance the electrochemical performance of SIBs. In this paper, we reviewed several types of transition metal oxide cathode materials, and found their electrochemical properties were significantly improved by F-doping. Moreover, the modification mechanism of F-doping has also been summed up. Therefore, the application and commercialization of SIBs in the future is summarized in the ending of the review.

The identification of Pseudomonas aeruginosa persisters using flow cytometry.

Pseudomonas aeruginosa persisters are a rare and poorly characterized subpopulation of cells that are responsible for many recurrent infections. The lack of knowledge on the mechanisms that lead to persister cell development is mainly a result of the difficulty in isolating and characterizing this rare population. Flow cytometry is an ideal method for identifying such subpopulations because it allows for high-content single-cell analysis. However, there are fewer established protocols for bacterial flow cytometry compared to mammalian cell work. Herein, we describe and propose a flow cytometry protocol to identify and isolate P. aeruginosa persister cells. Additionally, we show that the percentage of potential persister cells increases with increasing antibiotic concentrations above the MIC.

Production of quorum sensing-related metabolites and phytoalexins during Pseudomonas aeruginosa-Brassica napus interaction.

Pseudomonas aeruginosa is an opportunistic bacterial pathogen that has been shown to interact with many organisms throughout the domains of life, including plants. How this broad-host-range bacterium interacts with each of its diverse hosts, especially the metabolites that mediate these interactions, is not completely known. In this work, we used a liquid culture root infection system to collect plant and bacterial metabolites on days 1, 3 and 5 post-P. aeruginosa (strain PA14) infection of the oilseed plant, canola (Brassica napus). Using MS-based metabolomics approaches, we identified the overproduction of quorum sensing (QS)-related (both signalling molecules and regulated products) metabolites by P. aeruginosa while interacting with canola plants. However, the P. aeruginosa infection induced the production of several phytoalexins, which is a part of the hallmark plant defence response to microbes. The QS system of PA14 appears to only mediate part of the canola-P. aeruginosa metabolomic interactions, as the use of isogenic mutant strains of each of the three QS signalling branches did not significantly affect the induction of the phytoalexin brassilexin, while induction of spirobrassinin was significantly decreased. Interestingly, a treatment of purified QS molecules in the absence of bacteria was not able to induce any phytoalexin production, suggesting that active bacterial colonization is required for eliciting phytoalexin production. Furthermore, we identified that brassilexin, the only commercially available phytoalexin that was detected in this study, demonstrated a MIC of 400 µg ml-1 against P. aeruginosa PA14. The production of phytoalexins can be an effective component of canola innate immunity to keep potential infections by the opportunistic pathogen P. aeruginosa at bay.

Calunduloside E inhibits HepG2 cell proliferation and migration via p38/JNK-HMGB1 signalling axis.

High-mobility group box 1 (HMGB1), a highly conserved chromosome protein, is considered as a potential therapeutic target and novel biomarker because of its regulation in the proliferation and metastasis of Hepatocellular carcinoma (HCC). Calenduloside E (CE), a natural active product, has been reported to anti-cancer effect. However, the role and underlying molecular mechanism of CE in HCC is still unclear. The purpose of this study is to investigate the effects of CE on the proliferation and migration of HCC, and then explore the possible underlying molecular mechanism. HepG2 cells were treated with CE or transfected with HMGB1 shRNA plasmids, EdU and colony formation assays were used to detect cell proliferation ability. Wound healing and transwell assays were used to determine the role of CE in cell migration. The expression of Cyclins, PCNA, MMPs, HMGB1, N-cadherin, E-cadherin and phosphorylation of p38, ERK and JNK were all detected using Western blotting. Our results showed that CE inhibited HepG2 cells proliferation and migration in a dose dependent manner; reduced the expression levels of Cycins, PCNA, HMGB1, MMPs and N-cadherin; up-regulated E-cadherin expression; enhanced the phosphorylation of p38 and JNK signalling pathways. Blocking the activation of p38 and JNK obviously reversed CE-mediated inhibitory effects on HepG2 cell proliferation and migration; reversed CE-induced down-regulation of Cyclins, PCNA, MMPs, N-cadherin and HMGB1, as well as E-cadherin up-regulation. In conclusion, our study suggested that CE reduces the expression levels of Cyclins, MMPs and epithelial-mesenchymal transformation (EMT) through p38/JNK-HMGB1 signaling axis and then inhibits HepG2 cells proliferation and migration in HepG2 cells. This study provides a new perspective for the anti-tumour molecular mechanism of CE in HCC.

Pathogen-secreted proteases activate a novel plant immune pathway.

Mitogen-activated protein kinase (MAPK) cascades play central roles in innate immune signalling networks in plants and animals. In plants, however, the molecular mechanisms of how signal perception is transduced to MAPK activation remain elusive. Here we report that pathogen-secreted proteases activate a previously unknown signalling pathway in Arabidopsis thaliana involving the Gα, Gß, and Gγ subunits of heterotrimeric G-protein complexes, which function upstream of an MAPK cascade. In this pathway, receptor for activated C kinase 1 (RACK1) functions as a novel scaffold that binds to the Gß subunit as well as to all three tiers of the MAPK cascade, thereby linking upstream G-protein signalling to downstream activation of an MAPK cascade. The protease-G-protein-RACK1-MAPK cascade modules identified in these studies are distinct from previously described plant immune signalling pathways such as that elicited by bacterial flagellin, in which G proteins function downstream of or in parallel to an MAPK cascade without the involvement of the RACK1 scaffolding protein. The discovery of the new protease-mediated immune signalling pathway described here was facilitated by the use of the broad host range, opportunistic bacterial pathogen Pseudomonas aeruginosa. The ability of P. aeruginosa to infect both plants and animals makes it an excellent model to identify novel immunoregulatory strategies that account for its niche adaptation to diverse host tissues and immune systems.

Mice Lacking γδ T Cells Exhibit Impaired Clearance of Pseudomonas aeruginosa Lung Infection and Excessive Production of Inflammatory Cytokines.

Pseudomonas aeruginosa is an opportunistic pathogen that causes chronic and life-threatening infections in immunocompromised patients. A better understanding of the role that innate immunity plays in the control of P. aeruginosa infection is crucial for therapeutic development. Specifically, the role of unconventional immune cells like γδ T cells in the clearance of P. aeruginosa lung infection is not yet well characterized. In this study, the role of γδ T cells was examined in an acute mouse model of P. aeruginosa lung infection. In the absence of γδ T cells, mice displayed impaired bacterial clearance and decreased survival, outcomes which were associated with delayed neutrophil recruitment and impaired recruitment of other immune cells (macrophages, T cells, natural killer cells, and natural killer T [NKT] cells) into the airways. Despite reduced NKT cell recruitment in the airways of mice lacking γδ T cells, NKT cell-deficient mice exhibited wild-type level control of P. aeruginosa infection. Proinflammatory cytokines were also altered in γδ T cell-deficient mice, with increased production of interleukin-1ß, interleukin-6, and tumor necrosis factor. γδ T cells did not appear to contribute significantly to the production of interleukin-17A or the chemokines CXCL1 and CXCL2. Importantly, host survival could be improved by inhibiting tumor necrosis factor signaling with the soluble receptor construct etanercept in γδ cell-deficient mice. These findings demonstrate that γδ T cells play a protective role in coordinating the host response to P. aeruginosa lung infection, both in contributing to early immune cell recruitment and by limiting inflammation.

Point Chirality Controlled Diastereoselective Self-Assembly and Circularly Polarized Luminescence in Quadruple-Stranded Europium(III) Helicates.

Aromatic ß-diketones have been extensively employed as highly effective sensitizers in luminescent lanthanide complexes. However, the difficulties to make the chiral modified groups effectively participate in the frontier molecular orbital (FMO) distributions limit their applications on lanthanide circularly polarized luminescence (CPL) fields. Considering the inherent chirality of the helical structure, a pair of enantiopure dinuclear europium quadruple-stranded helicates, ΔΔ/ΛΛ-(HNEt3)2(Eu2L4) (ΔΔ/ΛΛ)-1; L = R/S-1,2-bis(4,4'-bis(4,4,4-trifluoro-1,3-dioxobutyl)phenoxyl)propane are assembled via a point chirality induced strategy. The comprehensive spectral characteristics combined with density functional theory (DFT) calculations demonstrate that the one point chirality at the spacer of the ligand successfully controls the Δ or Λ configuration around the Eu(III) ion center and the P or M helical patterns of the helicates. The mirror-image CPL and CD spectra further confirm the formation of the enantiomer pairs. As expected, the helicate presents a higher luminescence quantum yield (QY) of 68% and a large |glum| value (0.146). This study effectively combines the excellent sensitization capability of ß-diketone and the helical chirality of helicates. This strategy provides an effective path for the synthesis of lanthanide material with excellent CPL performance.

Early Growth Response 1 Deficiency Protects the Host against Pseudomonas aeruginosa Lung Infection.

Pseudomonas aeruginosa is an opportunistic pathogen that is a common cause of nosocomial infections. The molecular mechanisms governing immune responses to P. aeruginosa infection remain incompletely defined. Early growth response 1 (Egr-1) is a zinc-finger transcription factor that controls inflammatory responses. Here, we characterized the role of Egr-1 in host defense against P. aeruginosa infection in a mouse model of acute bacterial pneumonia. Egr-1 expression was rapidly and transiently induced in response to P. aeruginosa infection. Egr-1-deficient mice displayed decreased mortality, reduced levels of proinflammatory cytokines (tumor necrosis factor [TNF], interleukin-1ß [IL-1ß], IL-6, IL-12, and IL-17), and enhanced bacterial clearance from the lung. Egr-1 deficiency caused diminished NF-κB activation in P. aeruginosa-infected macrophages independently of IκBα phosphorylation. A physical interaction between Egr-1 and NF-κB p65 was found in P. aeruginosa-infected macrophages, suggesting that Egr-1 could be required for assembly of heterodimeric transcription factors that direct synthesis of inflammatory mediators. Interestingly, Egr-1 deficiency had no impact on neutrophil recruitment in vivo due to its differential effects on chemokine production, which included diminished accumulation of KC (CXCL1), MIP2 (CXCL2), and IP-10 (CXCL10) and increased accumulation of LIX (CXCL5). Importantly, Egr-1-deficient macrophages and neutrophils displayed significant increases in nitric oxide production and bacterial killing ability that correlated with enhanced bacterial clearance in Egr-1-deficient mice. Together, these findings suggest that Egr-1 plays a detrimental role in host defense against P. aeruginosa acute lung infection by promoting systemic inflammation and negatively regulating the nitric oxide production that normally assists with bacterial clearance.

IL-17R deletion predicts high-grade colorectal cancer and poor clinical outcomes.

The IL-17 receptor (IL-17R) has a perplexing role in cancer, which may be explained by its yin-yang signaling pathways. Recently, the critical role of IL-17R in maintaining basal levels of A20-a key negative regulator of NF-κB and JNK-c-Jun pathways has been demonstrated in cancer cell lines. Cross-cancer analyses of somatic copy number alterations in IL-17RA, IL-17RC and A20 genes reveal that IL-17RA-deletion is common in colorectal cancer (CRC) patients, representing 24, 26, 37 and 49% of stage I, II, III and IV of patients, respectively, and mutually exclusive with patients displaying microsatellite instability. Importantly, patients with IL-17R-deletion or concurrent deletions of A20 show significantly reduced overall survival. Analysis of multiple published microarray studies confirms that IL-17RA expression is significantly reduced in CRC samples compared to normal counterparts, and its level is closely associated with A20 expression. Analyses of RNAseq data indicate that tumors with IL-17R-deletion express strong molecular markers of tumor invasion, growth and metastasis. Notably, approximately 20 genes responsible for protein synthesis and mitochondrial metabolism are inversely correlated with both IL-17RA and A20. Immunohistochemistry staining in human colorectal tissue arrays further reveals that high-grade tumors have significantly reduced IL-17RA staining compared to low-grade tumors. Thus, collective evidence strongly supports a previously unrecognized CRC-promoting mechanism triggered by IL-17RA-deletion and highlights its utility as a prognostic marker in CRC.

Marine Bacteria, A Source for Alginolytic Enzyme to Disrupt Pseudomonas aeruginosa Biofilms.

Pseudomonas aeruginosa biofilms are typically associated with the chronic lung infection of cystic fibrosis (CF) patients and represent a major challenge for treatment. This opportunistic bacterial pathogen secretes alginate, a polysaccharide that is one of the main components of its biofilm. Targeting this major biofilm component has emerged as a tempting therapeutic strategy for tackling biofilm-associated bacterial infections. The enormous potential in genetic diversity of the marine microbial community make it a valuable resource for mining activities responsible for a broad range of metabolic processes, including the alginolytic activity responsible for degrading alginate. A collection of 36 bacterial isolates were purified from marine water based on their alginolytic activity. These isolates were identified based on their 16S rRNA gene sequences. Pseudoalteromonas sp. 1400 showed the highest alginolytic activity and was further confirmed to produce the enzyme alginate lyase. The purified alginate lyase (AlyP1400) produced by Pseudoalteromonas sp. 1400 showed a band of 23 KDa on a protein electrophoresis gel and exhibited a bifunctional lyase activity for both poly-mannuronic acid and poly-glucuronic acid degradation. A tryptic digestion of this gel band analyzed by liquid chromatography-tandem mass spectrometry confirmed high similarity to the alginate lyases in polysaccharide lyase family 18. The purified alginate lyase showed a maximum relative activity at 30 °C at a slightly acidic condition. It decreased the sodium alginate viscosity by over 90% and reduced the P. aeruginosa (strain PA14) biofilms by 69% after 24 h of incubation. The combined activity of AlyP1400 with carbenicillin or ciprofloxacin reduced the P. aeruginosa biofilm thickness, biovolume and surface area in a flow cell system. The present data revealed that AlyP1400 combined with conventional antibiotics helped to disrupt the biofilms produced by P. aeruginosa and can be used as a promising combinational therapeutic strategy.

A Pseudomonas aeruginosa-secreted protease modulates host intrinsic immune responses, but how?

Recently, we found that the Pseudomonas aeruginosa type II secreted protease IV functions as a unique Arabidopsis innate immunity elicitor. The protease IV-activated pathway involves G protein signaling and raises the question of how protease elicitation leads to the activation of G protein-mediated signaling, because plants do not appear to have metazoan-like G protein-coupled receptors. Importantly, our data suggest that Arabidopsis has evolved a mechanism to detect the proteolytic activity of a pathogen-encoded protease, supporting the host-pathogen arms race model. In the case of opportunistic multi-host pathogens like P. aeruginosa, however, it is not plausible that P. aeruginosa is simultaneously co-evolving in a gene-for-gene manner with all of its potential hosts, which include plants, nematodes, insects, and mammals. This prompts us to ask what is the driving force for co-evolution of defense response in Arabidopsis and pathogenesis of P. aeruginosa, which might not have been subject to iterative cycles of evolutionary selections.

Seaweed Extract (Stella Maris®) Activates Innate Immune Responses in Arabidopsis thaliana and Protects Host against Bacterial Pathogens.

Insects and pathogenic infections (bacteria, viruses and fungi) cause huge losses in agriculturally important crops yearly. Due to the rise in pesticide and antibiotic resistance, our crops and livestock are increasingly at risk. There is a rising demand for environmentally friendly solutions to prevent crop decreases. Components of Ascophyllum nodosum seaweed extracts were recently found to boost plant immunity. The stimulatory activities of the A.nodosum marine alga-derived extract (Stella Maris®) were investigated in a broad range of immune assays. Elevated hydrogen peroxide production measured in a chemiluminescence assay suggested that the extract elicited a strong burst of reactive oxygen species. Arabidopsis seedlings treated with Stella Maris® activated the expression of WRKY30, CYP71A12 and PR-1 genes, the induction of which represent early, mid and late plant immune response, respectively. Finally, this study found that Stella Maris® inhibited the growth of multiple bacterial pathogens, including an opportunistic human pathogen that has demonstrated pathogenicity in plants. In summary, the pre-treatment with the seaweed extract protected Arabidopsis against subsequent infection by these pathogens.

Plant immunity triggered by engineered in vivo release of oligogalacturonides, damage-associated molecular patterns.

Oligogalacturonides (OGs) are fragments of pectin that activate plant innate immunity by functioning as damage-associated molecular patterns (DAMPs). We set out to test the hypothesis that OGs are generated in planta by partial inhibition of pathogen-encoded polygalacturonases (PGs). A gene encoding a fungal PG was fused with a gene encoding a plant polygalacturonase-inhibiting protein (PGIP) and expressed in transgenic Arabidopsis plants. We show that expression of the PGIP-PG chimera results in the in vivo production of OGs that can be detected by mass spectrometric analysis. Transgenic plants expressing the chimera under control of a pathogen-inducible promoter are more resistant to the phytopathogens Botrytis cinerea, Pectobacterium carotovorum, and Pseudomonas syringae. These data provide strong evidence for the hypothesis that OGs released in vivo act as a DAMP signal to trigger plant immunity and suggest that controlled release of these molecules upon infection may be a valuable tool to protect plants against infectious diseases. On the other hand, elevated levels of expression of the chimera cause the accumulation of salicylic acid, reduced growth, and eventually lead to plant death, consistent with the current notion that trade-off occurs between growth and defense.

The apoplastic oxidative burst peroxidase in Arabidopsis is a major component of pattern-triggered immunity.

In plants, reactive oxygen species (ROS) associated with the response to pathogen attack are generated by NADPH oxidases or apoplastic peroxidases. Antisense expression of a heterologous French bean (Phaseolus vulgaris) peroxidase (FBP1) cDNA in Arabidopsis thaliana was previously shown to diminish the expression of two Arabidopsis peroxidases (peroxidase 33 [PRX33] and PRX34), block the oxidative burst in response to a fungal elicitor, and cause enhanced susceptibility to a broad range of fungal and bacterial pathogens. Here we show that mature leaves of T-DNA insertion lines with diminished expression of PRX33 and PRX34 exhibit reduced ROS and callose deposition in response to microbe-associated molecular patterns (MAMPs), including the synthetic peptides Flg22 and Elf26 corresponding to bacterial flagellin and elongation factor Tu, respectively. PRX33 and PRX34 knockdown lines also exhibited diminished activation of Flg22-activated genes after Flg22 treatment. These MAMP-activated genes were also downregulated in unchallenged leaves of the peroxidase knockdown lines, suggesting that a low level of apoplastic ROS production may be required to preprime basal resistance. Finally, the PRX33 knockdown line is more susceptible to Pseudomonas syringae than wild-type plants. In aggregate, these data demonstrate that the peroxidase-dependent oxidative burst plays an important role in Arabidopsis basal resistance mediated by the recognition of MAMPs.

Amygdala and cognitive impairment in cerebral small vessel disease: structural, functional, and metabolic changes.

Cerebral small vessel disease (CSVD) is a prevalent vascular disorder that has been consistently associated with vascular cognitive impairment (VCI). The diagnosis of CSVD continues to rely on magnetic resonance imaging (MRI). Epidemiological data indicate that the characteristic MRI features of CSVD, including white matter hyperintensity (WMH) and lacunar infarction, are very common among individuals over 40 years of age in community studies. This prevalence poses a significant burden on many low- and middle-income families. The amygdala plays a crucial role in integrating sensory and associative information to regulate emotional cognition. Although many previous studies have linked alterations in the amygdala to various diseases, such as depression, there has been little research on CSVD-associated alterations in the amygdala due to the complexity of CSVD. In this paper, we summarize the various imaging features of CSVD and discuss the correlation between amygdala changes and VCI. We also explore how new neuroimaging methods can assess amygdala changes early, laying a foundation for future comprehensive exploration of the pathogenesis of CSVD.