The correlation between serum angiopoietin-2 levels and acute kidney injury (AKI): a meta-analysis.

INTRODUCTION: The correlation between serum angiopoietin-2 levels and acute kidney injury (AKI) is a topic of significant clinical interest. This meta-analysis aims to provide a comprehensive evaluation of this relationship. CONTENT: A systematic search was conducted in PubMed, Embase, Web of Science, and Cochrane databases up to October 11, 2023. The included studies were evaluated using the Newcastle-Ottawa Scale (NOS) and Methodological Index for Non-Randomized Studies (MINORS). Weighted mean differences (WMD) and odds ratios (OR) were calculated using random-effects models. Sensitivity analysis, funnel plots, and Egger's test were used to assess the robustness and publication bias of the findings. Subgroup analyses were performed to explore potential variations between adults and children. SUMMARY: Eighteen studies encompassing a total of 7,453 participants were included. The analysis revealed a significant elevation in serum angiopoietin-2 levels in patients with AKI compared to those without (WMD: 4.85; 95 % CI: 0.75 to 0.27; I²=93.2 %, p<0.001). Subgroup analysis indicated significantly higher angiopoietin-2 levels in adults with AKI (WMD: 5.17; 95 % CI: 3.51 to 6.83; I²=82.6 %, p<0.001), but not in children. Additionally, high serum angiopoietin-2 levels were associated with an increased risk of AKI (OR: 1.58; 95 % CI: 1.39 to 1.8; I²=89.1 %, p<0.001). Sensitivity analysis validated the robustness of these results, showing no substantial change in the overall effect size upon the exclusion of individual studies. OUTLOOK: This meta-analysis supports a significant association between elevated serum angiopoietin-2 levels and increased risk of AKI. The observed differential association between adults and children highlights the need for further targeted research to understand these age-specific variations.

WWC1 upregulation accelerates hyperuricemia by reduction in renal uric acid excretion through Hippo signaling pathway.

Hyperuricemia (HUA) is a metabolic disorder characterized by elevated serum uric acid (UA), primarily attributed to the hepatic overproduction and renal underexcretion of UA. Despite the elucidation of molecular pathways associated with this underexcretion, the etiology of HUA remains largely unknown. In our study, using by Uox knockout rats, HUA mouse, and cell line models, we discovered that the increased WWC1 levels were associated with decreased renal UA excretion. Additionally, using knockdown and overexpression approaches, we found that WWC1 inhibited UA excretion in renal tubular epithelial cells. Mechanistically, WWC1 activated the Hippo pathway, leading to phosphorylation and subsequent degradation of the downstream transcription factor YAP1, thereby impairing the ABCG2 and OAT3 expression through transcriptional regulation. Consequently, this reduction led to a decrease in UA excretion in renal tubular epithelial cells. In conclusion, our study has elucidated the role of upregulated WWC1 in renal tubular epithelial cells inhibiting the excretion of UA in the kidneys and causing HUA.

Deciphering the molecular regulatory of RAB32/GPRC5A axis in chronic obstructive pulmonary disease.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a significant public health problem characterized by persistent airflow limitation. Despite previous research into the pathogenesis of COPD, a comprehensive understanding of the cell-type-specific mechanisms in COPD remains lacking. Recent studies have implicated Rab GTPases in regulating chronic immune response and inflammation via multiple pathways. In this study, the molecular regulating mechanism of RAB32 in COPD was investigated by multiple bioinformatics mining and experimental verification. METHODS: We collected lung tissue surgical specimens from Zhongshan Hospital, Fudan University, and RT-qPCR and western blotting were used to detect the expression of Rabs in COPD lung tissues. Four COPD microarray datasets from the Gene Expression Omnibus (GEO) were analyzed. COPD-related epithelial cell scRNA-seq data was obtained from the GSE173896 dataset. Weighted gene co-expression network analysis (WGCNA), mfuzz cluster, and Spearman correlation analysis were combined to obtain the regulatory network of RAB32 in COPD. The slingshot algorithm was used to identify the regulatory molecule, and the co-localization of RAB32 and GPRC5A was observed with immunofluorescence. RESULTS: WGCNA identified 771 key module genes significantly associated with the occurrence of COPD, including five Rab genes. RAB32 was up-regulated in lung tissues from subjects with COPD as contrast to those without COPD on both mRNA and protein levels. Integrating the results of WGCNA, Mfuzz clusters, and Spearman analysis, nine potential interacting genes with RAB32 were identified. Among these genes, GPRC5A exhibited a similar molecular expression pattern to RAB32. Co-expression density analysis at the cell level demonstrated that the co-expression density of RAB32 and GPRC5A was higher in type I alveolar epithelial cells (AT1s) than in type II alveolar epithelial cells (AT2s). The immunofluorescence also confirmed the co-localization of RAB32 and GPRC5A, and the Pearson correlation analysis found the relationship between RAB32 and GPRC5A was significantly stronger in the COPD lungs (r = 0.65) compared to the non-COPD lungs (r = 0.33). CONCLUSIONS: Our study marked endeavor to delineate the molecular regulatory axis of RAB32 in COPD by employing diverse methods and identifying GPRC5A as a potential interacting molecule with RAB32. These findings offered novel perspectives on the mechanism of COPD.

Pyroptotic T cell-derived active IL-16 has a driving function in ovarian endometriosis development.

Endometriosis, affecting 6%-10% of women, often leads to pain and infertility and its underlying inflammatory mechanisms are poorly understood. We established endometriosis models in wild-type and IL16KO mice, revealing the driver function of IL-16 in initiating endometriosis-related inflammation. Using an in vitro system, we confirmed iron overload-induced GSDME-mediated pyroptosis as a key trigger for IL-16 activation and release. In addition, our research led to the development of Z30702029, a compound inhibiting GSDME-NTD-mediated pyroptosis, which shows promise as a therapeutic intervention for endometriosis. Importantly, our findings extend beyond endometriosis, highlighting GSDME-mediated pyroptosis as a broader pathway for IL-16 release and offering insights into potential treatments for various inflammatory conditions.

Near-edge x-ray absorption fine structure spectra and specific dissociation of small peptoid molecules.

In this study, the total ion yield near-edge x-ray absorption fine structure spectra of four similar peptoid molecules, which differ in the numbers and positions of methyl groups, were investigated experimentally and theoretically. At each excitation energy, the intensity and branching ratio of each ionic product were measured. At a few resonant excitation energies, a specific dissociation of the C-CO bond at the nitrogen and oxygen K-edges and of the N-CO bond at the carbon K-edge was dominant, which correlated well with the predicted destination antibonding orbitals of the core electron excitation. These specific dissociation mechanisms of small peptoid molecules could provide insights into similar phenomena that occur in peptide molecules.

Role of 5-hydroxytryptamine type 3 receptors in the regulation of anxiety reactions. / 5-羟色胺3受体对焦虑反应的调节作用.

5-Hydroxytryptamine (5-HT) type 3 receptor (5-HT3R) is the only type of ligand-gated ion channel in the 5-HT receptor family. Through the high permeability of Na+, K+, and Ca2+ and activation of subsequent voltage-gated calcium channels (VGCCs), 5-HT3R induces a rapid increase of neuronal excitability or the release of neurotransmitters from axon terminals in the central nervous system (CNS). 5-HT3Rs are widely expressed in the medial prefrontal cortex (mPFC), amygdala (AMYG), hippocampus (HIP), periaqueductal gray (PAG), and other brain regions closely associated with anxiety reactions. They have a bidirectional regulatory effect on anxiety reactions by acting on different types of cells in different brain regions. 5-HT3Rs mediate the activation of the cholecystokinin (CCK) system in the AMYG, and the γ|-aminobutyric acid (GABA) "disinhibition" mechanism in the prelimbic area of the mPFC promotes anxiety by the activation of GABAergic intermediate inhibitory neurons (IINs). In contrast, a 5-HT3R-induced GABA "disinhibition" mechanism in the infralimbic area of the mPFC and the ventral HIP produces anxiolytic effects. 5-HT2R-mediated regulation of anxiety reactions are also activated by 5-HT3R-activated 5-HT release in the HIP and PAG. This provides a theoretical basis for the treatment of anxiety disorders or the production of anxiolytic drugs by targeting 5-HT3Rs. However, given the circuit specific modulation of 5-HT3Rs on emotion, systemic use of 5-HT3R agonism or antagonism alone seems unlikely to remedy anxiety, which deeply hinders the current clinical application of 5-HT3R drugs. Therefore, the exploitation of circuit targeting methods or a combined drug strategy might be a useful developmental approach in the future.

Adipocyte dysfunction promotes lung inflammation and aberrant repair: a potential target of COPD.

Background: Obesity and chronic obstructive pulmonary disease (COPD) are prevailing worldwide, bringing a heavy medical burden. Clinical and pathophysiological relationship between obesity and COPD is paradoxical and elusive. We aim to explore their inherent associations from clinical, genetic, and animal levels. Methods: We performed literature review and cohort analysis of patients with COPD to compare lung function, symptom, and prognosis among different weight groups. After retrieving datasets of obesity and COPD in Gene Expression Omnibus (GEO) database, we carried out differentially expressed gene analysis, functional enrichment, protein-protein interactions network, and weighted gene co-expression network analysis. Then, we acquired paraffin-embedded lung tissues of fatty acid-binding protein 4-Cre-BMPR2fl/fl conditional knockout (CKO) mice that were characterized by adipocyte-specific knockout of bone morphogenetic protein receptor 2 (BMPR2) for staining and analysis. Results: Our cohort study reports the effect of obesity on COPD is inconsistent with previous clinical studies. Lung function of overweight group was statistically superior to that of other groups. We also found that the inflammatory factors were significantly increased hub genes, and cytokine-associated pathways were enriched in white adipose tissue of patients with obesity. Similarly, injury repair-associated genes and pathways were further enhanced in the small airways of patients with COPD. CKO mice spontaneously developed lung injury, emphysema, and pulmonary vascular remodeling, along with increased infiltration of macrophages. BMPR2-defiecient adipocytes had dysregulated expression of adipocytokines. Conclusion: Inflammation and abnormal repair might be potential mechanisms of the pathological association between obesity and COPD. BMPR2-associated adipocyte dysfunction promoted lung inflammation and aberrant repair, in which adipocytokines might play a role and thus could be a promising therapeutic target.

Glucose-Triggered Release of trans-N-p-Coumaroyltyramine from Zeolitic Imidazolate Framework-8 (ZIF8) Modified with Dioscorea opposita Thunb Polysaccharide.

A Dioscorea opposita Thunb polysaccharide (DOP)-modified ZIF8 material was developed in this study, which can be used as a "smart" glucose-responsive carrier to control the slow release of drugs. The 3-aminophenylboronic acid (APBA) functionalized carboxylated long-chain polymer poly(ethylene glycol) (PEG) segments, which were first modified on the surface of ZIF8 nanoparticles with a hydrogen bond and then chemically cross-linked with DOP through a borate ester bond, leading to the drugs loaded on ZIF8 being "closed" in PBS but being "open" via taking off the DOP coating in high concentrations of glucose; thus, leakage can be prevented in the drug loaded and a glucose-triggered release can effectively result. Moreover, the materials showed good biocompatibility and the released trans-N-p-coumaroyltyramine (NCT) could work synergistically with the DOP to improve insulin resistance and promote glucose consumption in insulin-resistant HepG2 cells.

Knockdown of versican 1 in lung fibroblasts aggravates Lipopolysaccharide-induced acute inflammation through up-regulation of the SP1-Toll-like Receptor 2-NF-κB Axis: a potential barrier to promising Versican-targeted therapy.

OBJECTIVE: Versican participates in various pathological processes like inflammation and fibrosis and is a potential therapeutic target for inflammatory diseases. Versican 1 (V1) has increased expression in inflammatory diseases, but its role is unclear. We explored the effects of V1 on acute lung inflammation to determine whether targeting V1 had therapeutic potential. METHODS: Human fetal lung fibroblast (HFL1) was transfected with or without V1-inhibiting lentivirus and treated with LPS. The expression levels of inflammatory cytokines, V1, cellular signaling pathway and Toll-like receptors (TLRs) were detected by qPCR, ELISA and western blot. The migration and adhesion of neutrophils and monocytes to HFL1s were performed. The activity of transcriptional factors was determined by dual-luciferase reporter assay. RESULTS: Inflammatory factors increased dramatically and continuously with V1 knockdown and LPS stimulation (P < 0.01), orchestrating migration of inflammatory cells and an enhanced inflammatory reaction. V1-knockdown increased TLR2 (P < 0.01) and activated the NF-κB pathway, which was partially reversed with a TLR2 neutralizing antibody and an NF-κB inhibitor. Explosion of LPS-induced inflammation was induced by knockdown of V1 via the SP1-TLR2-NF-κB axis. CONCLUSION: Increased expression of V1 might be protective in acute inflammation, and an infection-induced cytokine storm might be a severe complication of V1-targeted interventions.

Water Plays Multifunctional Roles in the Intervening Formation of Secondary Organic Aerosols in Ozonolysis of Limonene: A Valence Photoelectron Spectroscopy and Density Functional Theory Study.

Although water may affect aqueous aerosol chemistry, how it intervenes in the formation of secondary organic aerosols (SOAs) at the molecular level remains elusive. Ozonolysis of limonene is one of the most important sources of indoor SOAs. Here, we report the valence electronic properties of limonene aerosols and SOAs derived from limonene ozonolysis (Lim-SOAs) via aerosol vacuum ultraviolet photoelectron spectroscopy, with a focus on the effects of water on Lim-SOAs. The first vertical ionization energy of limonene aerosols is measured to be 8.79 ± 0.07 eV. While water significantly increases the total photoelectron yield of Lim-SOAs, three photoelectron features attributable to Lim-SOAs each exhibit distinct dependence on the fraction of water in aerosols, implying that different formation pathways and molecular origins are involved in the formation of Lim-SOAs. Combined with density functional theory calculation and mass spectrometry measurements, this study reveals that water, particularly the water dimer, enhances the formation of Lim-SOAs by altering the ozonolysis energetics and pathways by intervening in its Criegee chemistry, acting as both a catalyst and a reactant. The atmospheric implication is discussed.

Determination of the optimal concentration and duration of C5aR antagonist application in an inflammatory model of human dental pulp cells.

Deep tooth decay approaching the pulp may develop into pulpitis; to prevent this, pulp cells need to balance the rapid immune response to avoid rapid swelling of the pulp. Current treatment of deep decay that approaches the pulp involves the application of drugs that induce low-level inflammation in the dental pulp to promote its repair, but this treatment is sometimes insufficient. However, the unsuccessful treatment often resulted in pulpitis. The C5a-C5aR is the initial stage of the immune cascade response. Blocking the binding of C5a-C5aR can slow the immune response in the narrow pulp cavity, so that dental pulp cells have enough time to proliferate, migrate, and differentiate. In this study, we compared lipoteichoic acid (LTA) and lipopolysaccharides (LPS) at different concentrations and time points and used the C5aR antagonist W54011 to block the C5a-C5aR axis. The blocking effect was detected by analyzing the expression of C5a, C5aR, interleukin (IL)-6, and Toll-like receptors 2 and 4 (TLR-2, 4). Next, we determined the optimal concentration and duration of LTA and LPS treatment in combination with W54011. Based on our results, we selected 1.0 µg·mL-1 LPS treatment for 48 h to generate an inflammatory model of human dental pulp cells. We then regrouped the cells and conducted expression analyses to monitor the expression of C5a, C5aR, IL-6, and TLR-4 at the protein and mRNA levels. LPS stimulation for 48 h and treatment with W54011 for 48 h effectively inhibited inflammation and did not affect C5a expression. This study provides a basis for follow-up studies of W54011 in dental pulp cells.

The Clinical Impact of Metagenomic Next-Generation Sequencing (mNGS) Test in Hospitalized Patients with Suspected Sepsis: A Multicenter Prospective Study.

Background: Metagenomic Next Generation Sequencing (mNGS) has the potential to detect pathogens rapidly. We aimed to assess the diagnostic performance of mNGS in hospitalized patients with suspected sepsis and evaluate its role in guiding antimicrobial therapy. Methods: A multicenter, prospective cohort study was performed. We enrolled patients with suspected sepsis, collected clinical characteristics and blood samples, and recorded the 30-day survival. Diagnostic efficacy of mNGS test and blood culture was compared, and the clinical impact of mNGS on antibiotic regimen modification was analyzed. Results: A total of 277 patients were enrolled, and 162 were diagnosed with sepsis. The mortality was 44.8% (121/270). The mNGS test exhibited shorter turn-out time (27.0 (26.0, 29.0) vs. 96.0 (72.0, 140.3) hours, p < 0.001) and higher sensitivity (90.5% vs. 36.0%, p < 0.001) compared with blood culture, especially for fungal infections. The mNGS test showed better performance for patients with mild symptoms, prior antibiotic use, and early stage of infection than blood culture, and was capable of guiding antibiotic regimen modification and improving prognosis. Higher reads of pathogens detected by mNGS were related to 30-day mortality (p = 0.002). Conclusions: Blood mNGS testing might be helpful for early etiological diagnosis of patients with suspected sepsis, guiding the antibiotic regimen modification and improving prognosis.

ROS induced the Rab26 promoter hypermethylation to promote cigarette smoking-induced airway epithelial inflammation of COPD through activation of MAPK signaling.

Cigarette smoking (CS) exposure-induced airway inflammatory responses drive the occurrence and development of emphysema and chronic obstructive pulmonary disease (COPD). However, its precise mechanisms have not been fully elucidated. In this study, we explore the role of Rab26 in CS exposure modulating the inflammatory response of airway epithelium and the novel mechanism of CS exposure regulation Rab26. These data showed that CS exposure and H2O2 (a type of ROS) suppressed the expression of Rab26 and increased the expression of DNMT3b in vivo and in vitro. GEO data analysis found the level of Rab26 was decreased in the lung tissue of COPD patients. CSE-induced ROS promoted DNA methylation of the Rab26 promoter and inhibited its promoter activity by elevating the DNMT3b level. Antioxidants N-Acetyl-l-cysteine (NAC), 5-Aza-2'-deoxycytidine (5-AZA) (DNA methylation inhibitor) and DNMT3B siRNA alleviated CSE's inhibitory effect on Rab26 expression in vitro. Importantly, NAC alleviated the improved expression of Rab26 and reduced DNMT3B expression, in the airway of smoking exposure as well as attenuated the inflammatory response in vivo. Overexpression of Rab26 attenuated CSE-induced production of inflammatory mediators through part inactivation of p38 and JNK MAPK. On the contrary, silencing Rab26 enhanced p38 and JNK activation and aggravated inflammatory response. These findings suggest that ROS-mediated Rab26 promoter hypermethylation is a critical step in cigarette smoking-induced airway epithelial inflammatory response. Restoring Rab26 in the airway epithelium might be a potential strategy for treating airway inflammation and COPD.

The effects of social comparison and self-construal on creative idea generation: An EEG study.

Social comparisons usually occur in teams when members are tasked with generating creative ideas. However, it is unclear how these comparisons influence creative idea generation, which may be due to a lack of research on the interpretations of social comparison feedback. Self-construal is a psychological characteristic wherein individuals attempt to explain their cooperation and personal behaviours. Therefore, this study explored the influence of social comparison and self-construal on creative idea generation and the underlying neural mechanisms by recording electroencephalogram (EEG) activity. Individuals with independent and interdependent self-construal were randomly assigned to upward or downward comparison conditions and completed an alternative uses task. Results indicated that interdependent self-construal individuals had better originality and flexibility performance in the upward comparison condition compared to those in the downward comparison condition. The EEG results further revealed that, among interdependent self-construal individuals, the upward comparison condition elicited greater alpha synchronization in the bilateral frontal, right parietal, and right temporal regions compared to the downward comparison condition. Moreover, in the upward comparison condition, left frontal alpha synchronization mediated the effect of interdependent self-construal on creative idea generation. These findings support the notion of the joint effect of self-construal and social comparison on creative idea generation and suggest that interdependent self-construal individuals are better able to control irrelevant interfering information and form novel associations during an upward comparison situation compared to a downward comparison situation.

Reduced brain activity and functional connectivity during creative idea generation in individuals with smartphone addiction.

Since the coronavirus disease 2019 outbreak, the frequency of smartphone use has surged, which has caused an increase in smartphone addiction among individuals. Smartphone addiction can impair various cognitive abilities. However, to date, the impact of smartphone addiction on creative cognition remains unclear. The current functional near-infrared spectroscopy study compared neural differences between smartphone addiction tendency (SAT) and healthy control (HC) individuals during creative idea generation. In particular, by manipulating a key component of creative cognition, that is, overcoming semantic constraints, we explored whether SAT individuals could overcome semantic constraints. Both the SAT and HC groups completed the alternate uses task (AUT) in semantic constraint and unconstraint conditions. The results indicated that the prefrontal cortex (PFC) and temporal regions were less active during AUT in the SAT group than in the HC group. In the SAT group, the PFC was less active under constraint than unconstraint conditions. Moreover, both task-related and resting-state functional connectivity analyses indicated weaker coupling between the PFC and temporal regions in the SAT than in the HC group. Furthermore, the left dorsolateral PFC mediated the effect of smartphone addiction on creative performance. These findings provide unprecedented neuroimaging evidence on the negative impact of smartphone addiction on creative cognition.

The role of nutrients, wind speed, and rainfall in determining the composition of the algal community of shallow lakes in the Taoge water system, upstream from Lake Taihu, China.

Gaining a deeper understanding of factors that influence changes in phytoplankton community has significant implications for shallow lake management. The present study examined changes in the algae community of three shallow eutrophic lakes of the Taoge water system between 2008 and 2018 and the related factors influencing these changes. The composition of the algal community varied significantly during this period with the relative diatom biomass in lakes Changdanghu and Gehu increasing between 2014 and 2016 and again decreasing after 2017. However, relative cyanobacteria biomass initially decreased and later increased; meanwhile, the proportion of biomass of other phyla decreased continuously in the study period. Lake Zhushanhu showed similar trends, although it eventually returned to its initial state with absolute Microcystis dominance. Furthermore, the analysis of driving factors revealed that the concentrations of total nitrogen (TN), nitrate (NO3), and orthophosphate (PO4) were significantly associated with a significant increase in Microcystis biomass. Meteorological conditions also influenced changes in total algal and diatom biomasses, which were inversely related to the daily mean and daily maximum wind speeds. Monthly cumulative precipitation was only significantly associated with diatom biomass. Meanwhile, rainfall primarily affected the algal community structure between 2013 and 2017; an increase in the relative biomass of diatoms coincided with increased precipitation. Coordinating nitrogen and phosphorous use within the Taoge water system should improve lake habitat management; a broader perspective in attempts to control global and regional climate change may be needed.

Addiction-Prone Personality and Creative Cognitive Styles: A Moderated Mediation Model of Novelty Seeking and Depression Tendency.

This study attempted to examine the mechanism of the impact of Addiction-Prone Personality (APP) on creative cognitive styles (idea generation, idea selection), especially to explore the mediating role of novelty seeking and the moderating role of depression tendency on the relationship between APP and creative cognitive styles. College students (N = 576, 79% female) participated in and completed measures of APP, idea generation and selection, novelty seeking, and depression tendency. Results showed that (1) APP was positively related with idea generation while negatively related with idea selection; (2) novelty seeking played a partial mediating role in the relationship between APP and idea generation and a suppressing effect between APP and idea selection; (3) depression tendency moderated the indirect relationship between APP and creative cognitive styles through novelty seeking. Therefore, APP has different indirect effects on idea generation and idea selection via novelty seeking. When there was a higher depression tendency, there was a stronger indirect effect. The study highlights the significant importance of the underlying processes between APP and creative cognitive styles and offers implications for rethinking the relationship between addiction and creativity.

Pathological Voice Detection Based on Phase Reconstitution and Convolutional Neural Network.

The nonlinear dynamic features can effectively describe the acoustic characteristics of normal and pathological voice. In this paper, the phase space reconstruction and convolution neural network are used to classify the normal and pathological voice. The phase space information of normal and pathological voice is reconstructed using delay time and embedding dimension, the one-dimensional signal is converted to a two-dimensional matrix, and the reconstructed trajectory graph sample of the signal is generated. The trajectory graph samples are used as the input of the VGG-like convolutional neural network, and the graphical features are extracted to achieve a classification of normal and pathological voice. In order to overcome the lack of clinical data, a data enhancement scheme is used. The experiment which classifies the normal and pathological voice is carried out on three pathological databases respectively, i.e. the Massachusetts eye and ear infirmary (MEEI) database, Saarbrücken voice database (SVD) database, and a clinical database collected by the authors. Five-fold cross validation is used and the average recognition rates on the three databases are 99.42%, 97.30% and 95.88% respectively. The average recognition rates are 96.04% and 92.27% for normal, vocal fold paralysis and vocal fold non-paralysis voice in MEEI database and SVD database. The experimental results show that the method has high classification recognition rate and good robustness, and has certain universal applicability for the recognition of the normal and pathological voice.

Fibroblast growth factor 10 attenuates chronic obstructive pulmonary disease by protecting against glycocalyx impairment and endothelial apoptosis.

BACKGROUND: The defects and imbalance in lung repair and structural maintenance contribute to the pathogenesis of chronic obstructive pulmonary diseases (COPD), yet the molecular mechanisms that regulate lung repair process are so far incompletely understood. We hypothesized that cigarette smoking causes glycocalyx impairment and endothelial apoptosis in COPD, which could be repaired by the stimulation of fibroblast growth factor 10 (FGF10)/FGF receptor 1 (FGFR1) signaling. METHODS: We used immunostaining (immunohistochemical [IHC] and immunofluorescence [IF]) and enzyme-linked immunosorbent assay (ELISA) to detect the levels of glycocalyx components and endothelial apoptosis in animal models and in patients with COPD. We used the murine emphysema model and in vitro studies to determine the protective and reparative role of FGF10/FGFR1. RESULTS: Exposure to cigarette smoke caused endothelial glycocalyx impairment and emphysematous changes in murine models and human specimens. Pretreatment of FGF10 attenuated the development of emphysema and the shedding of glycocalyx components induced by CSE in vivo. However, FGF10 did not attenuate the emphysema induced by endothelial-specific killing peptide CGSPGWVRC-GG-D(KLAKLAK)2. Mechanistically, FGF10 alleviated smoke-induced endothelial apoptosis and glycocalyx repair through FGFR1/ERK/SOX9/HS6ST1 signaling in vitro. FGF10 was shown to repair pulmonary glycocalyx injury and endothelial apoptosis, and attenuate smoke-induced COPD through FGFR1 signaling. CONCLUSIONS: Our results suggest that FGF10 may serve as a potential therapeutic strategy against COPD via endothelial repair and glycocalyx reconstitution.

Environmental mechanism of capturing nutrient-rich particles by the lake bottom trap in a large, shallow lake.

Bottom traps capture and preserve nutrient-rich mobile bottom sediments by forming a weak hydrodynamic environment. In this study, Lake Chaohu, a large shallow lake in China, was considered the research object, and the influence of trap at the bottom of the lake on the physical, chemical, and biological characteristics of sediments and water were analysed by combining on-site monitoring and laboratory analysis. The results showed that the hydrodynamic intensity was attenuated by more than 65% at the bottom of the trap compared with that of the upper surface of the water body under different weather conditions, forming an obviously weak hydrodynamic environment. The weak dynamic environment and large sedimentation rate at the bottom of the trap were beneficial to the sedimentation and storage of fine particles that adsorb nutrients, such as nitrogen and phosphorus, in the water. Owing to the increase in local water depth, a low-temperature and low-dissolved oxygen environment was formed inside the trap. The abundance and diversity of microorganisms in the sediments inside the trap were reduced, and the abundance of nitrifying and denitrifying bacteria in the sediment was reduced by approximately 50%, indicating an environment favourable for nitrogen accumulation in the sediment in the trap. Therefore, the environment inside the bottom trap is favourable for capturing the high nutrient-rich particulate matter in the water, which provides theoretical support for use of the lake bottom traps for controlling the endogenous pollution of shallow lakes.