Systemic immune-inflammation index and all-cause and cause-specific mortality in sarcopenia: a study from National Health and Nutrition Examination Survey 1999-2018.

Background: Sarcopenia, common in the elderly, often linked to chronic diseases, correlates with inflammation.The association between SII and mortality in sarcopenia patients is underexplored, this study investigates this relationship in a U.S. adult cohort. Methods: We analyzed 1999-2018 NHANES data, focusing on 2,974 adults with sarcopenia. Mortality outcomes were determined by linking to National Death Index (NDI) records up to December 31, 2019. Using a weighted sampling design, participants were grouped into three groups by the Systemic Immune-Inflammation Index (SII). We used Cox regression models, adjusting for demographic and clinical variables, to explore SII's association with all-cause and cause-specific mortality in sarcopenia, performing sensitivity analyses for robustness. Results: Over a median follow-up of 9.2 years, 829 deaths occurred. Kaplan-Meier analysis showed significant survival differences across SII groups. The highest SII group showed higher hazard ratios (HRs) for all-cause and cause-specific mortality in both crude and adjusted models. The highest SII group had a higher HR for all-cause(1.57, 1.25-1.98), cardiovascular(1.61, 1.00-2.58), cancer(2.13, 1.32-3.44), and respiratory disease mortality(3.21, 1.66-6.19) in fully adjusted models. Subgroup analyses revealed SII's association with all-cause mortality across various demographics, including age, gender, and presence of diabetes or cardiovascular disease. Sensitivity analyses, excluding participants with cardiovascular diseases, those who died within two years of follow-up, or those under 45 years of age, largely reflected these results, with the highest SII group consistently demonstrating higher HRs for all types of mortality in both unadjusted and adjusted models. Conclusion: Our study is the first to demonstrate a significant relationship between SII and increased mortality risks in a sarcopenia population.

PM2.5 exposure upregulates pro-inflammatory protein expression in human microglial cells via oxidant stress and TLR4/NF-κB pathway.

Exposure to ambient PM2.5 is associated with neurodegenerative disorders, in which microglia activation plays a critical role. Thus far, the underlying mechanisms for PM2.5-induced microglia activation have not been well elucidated. In this study, a human microglial cell line (HMC3) was used as the in vitro model to examine the inflammatory effect (hall marker of microglia activation) of PM2.5 and regulatory pathways. The expression of inflammatory mediators including interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2) as well as the brain derived neurotrophic factor (BDNF) were determined by ELISA and/or real-time PCR, respectively. Flow cytometry was used to measure the production of intracellular reactive oxygen species (ROS). Western blot was used to measure protein levels of Toll-like receptor 4 (TLR4), NF-κB inhibitor α (IκBα) and COX-2. It was shown that PM2.5 stimulation increased IL-6 and COX-2 expression but decreased BDNF expression in a dose-dependent manner. Further studies showed that PM2.5 triggered the formation of ROS and pre-treatment with the ROS scavenger acetylcysteine (NAC) significantly suppressed PM2.5-induced IL-6 and COX-2 expression. Moreover, the nuclear factor kappa B (NF-κB) inhibitor BAY11-7085 or the TLR4 neutralizing antibody markedly blocked PM2.5-induced IL-6 and COX-2 expression. However, NAC or BAY11-7085 exhibited minimal effect on PM2.5-induced BDNF down-regulation. In addition, pre-treatment with BAY11-7085 or TLR4 neutralizing antibody reduced ROS production induced by PM2.5, and NAC pre-treatment inhibited TLR4 expression and NF-κB activation induced by PM2.5. Collectively, PM2.5 treatment induced IL-6 and COX-2 but suppressed BDNF expression. PM2.5-induced IL-6 and COX-2 expression was mediated by interactive oxidative stress and TLR4/NF-κB pathway.

The effect of training to target cognitive biases towards social rejection in eating disorders.

OBJECTIVE: This study examined the effect of cognitive bias modification for interpretation (CBM-I) training in Korean women with eating disorders (EDs). METHOD: Sixty-three women with EDs participated in the study. Participants were randomly assigned to the intervention group where they received six sessions of CBM-I training (n = 31) in addition to treatment-as-usual or were put on a waiting list (n = 32). Participants' interpretation and attention biases, emotion regulation, affect, and ED psychopathology were assessed at baseline, end-of-intervention (4 weeks), and follow-up (8 weeks). RESULTS: Participants who completed the CBM-I training displayed greater reductions in negative interpretation bias (Δη2 = 0.107) and emotion dysregulation (Δη2  = 0.085) with medium to large effect sizes compared to the control group, which were maintained from baseline to follow-up. Disengagement from negative faces and a focus on positive faces was found in the intervention group with a moderate effect size at the end-of-intervention (Δη2  = 0.090). Both intervention and control groups showed improvements in ED psychopathology. Baseline neuroticism was positively correlated with CBM-I effect. DISCUSSION: The results suggest that modifying interpretation bias towards ambiguous social stimuli might be an effective adjuvant treatment to reduce negative expectations of social situations and improve emotion regulation in women with bulimia nervosa and anorexia nervosa.

One-Step Electrochemical Ethylene-to-Ethylene Glycol Conversion over a Multitasking Molecular Catalyst.

Ethylene glycol is an essential commodity chemical with high demand, which is conventionally produced via thermocatalytic oxidation of ethylene with huge fossil fuel consumption and CO2 emission. The one-step electrochemical approach offers a sustainable route but suffers from reliance on noble metal catalysts, low activity, and mediocre selectivity. Herein, we report a one-step electrochemical oxidation of ethylene to ethylene glycol over an earth-abundant metal-based molecular catalyst, a cobalt phthalocyanine supported on a carbon nanotube (CoPc/CNT). The catalyst delivers ethylene glycol with 100% selectivity and 1.78 min-1 turnover frequency at room temperature and ambient pressure, more competitive than those obtained over palladium catalysts. Experimental data demonstrate that the catalyst orchestrates multiple tasks in sequence, involving electrochemical water activation to generate high-valence Co-oxo species, ethylene epoxidation to afford an ethylene oxide intermediate via oxygen transfer, and eventually ring-opening of ethylene oxide to ethylene glycol facilitated by in situ formed Lewis acid site. This work offers a great opportunity for commodity chemicals synthesis based on a one-step, earth-abundant metal-catalyzed, and renewable electricity-driven route.

Assessment of Human Exposure to Traditional and Novel Organophosphate Esters via Multiple Personal Matrices.

Herein, 16 traditional and 13 novel organophosphate esters (OPEs) in skin wipes, personal PM2.5, sputum, and nails (fingernails and toenails) and 7 OPE metabolites in urine synchronously obtained from 64 college students were analyzed. Similar compositional profiles of the OPEs were found in skin wipes and nails and in personal PM2.5 and induced sputum. Significant correlations were observed between the concentrations of high-lipophilicity low-volatility OPEs in skin wipes and nails and between the concentrations of high-volatility low-lipophilicity OPEs in personal PM2.5 and sputum. These results imply that OPEs in fingernails and toenails may mainly come from external sources rather than internal exposure, and human nails and sputum can be used as indicators of human exposure to OPEs. A comparison between the daily exposure doses of the OPEs in personal PM2.5 and sputum shows that more volatile compounds may have higher inhalation bioavailability, which should be considered to improve the accuracy of inhalation exposure assessments. According to comprehensive external and internal exposure assessment, dermal absorption may be a more dominant pathway than inhalation, and skin wipes may be the best representative environmental matrix of human exposure to OPEs.

Association of short-term PM2.5 exposure with airway innate immune response, microbiota and metabolism alterations in human airways.

Exposure to fine particulate matter (PM2.5) has been associated with impaired airway innate immunity, leading to diverse lung disorders. However, the mechanisms of the adverse effects of PM2.5 on the airway innate immune system has not been adequately elucidated. This study aimed to investigate the association between short-term exposure to ambient PM2.5 and airway innate immune responses. A panel study of 53 undergraduate students was conducted in November 2020 and April 2021. Levels of airway innate immune biomarkers including interleukin-1ß (IL-1ß), IL-4, IL-6, IL-8, IL-17, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), myeloperoxidase (MPO), and matrix metalloproteinase-9 (MMP-9) in induced sputum were measured, and airway microbiota and metabolites examined. Linear mixed-effect model was used to evaluate the effects of short-term exposure to PM2.5 on the above-listed airway immune biomarkers. The results indicated that for every 10 µg/m3 increase in PM2.5 concentration (at lag3), was associated with an increase of 21.3 % (5.4 %-37.1 %), 26.2 % (0.30 %-52.1 %), 22.4 % (0.70 %-44.2 %), 27.4 % (6.6 %-48.3 %), 18.3 % (4.6 %-31.9 %), 3.9 % (0.20 %-7.6 %) or 2.4 % (0.10 %-4.7 %) in IL-6, TNF-α, IL-17, IL-4, IFN-γ, MPO, or MMP-9 levels, respectively. Meanwhile, exposure to higher levels of ambient PM2.5 was found to significantly modulate airway microbiota and metabolite profile. Specifically, Prevotella and Fusobacterium, as well as 96 different metabolites were associated with PM2.5 levels. The metabolic pathways associated with these metabolites mainly included amino acid biosynthesis and metabolism. Notably, PM2.5 exposure-induced alterations of some airway microbiota were significantly correlated with specific airway metabolic change. Taken together, these results demonstrated that short-term exposure to PM2.5 was associated with alterations of airway immune response, microbial dysbiosis and changes of metabolites. This study provided insights into the mechanisms underlying PM2.5-induced airway innate immune responses.

Recovery-focused self-help intervention using vodcasts for patients with personality disorder: feasibility randomised controlled trial.

BACKGROUND: Availability of long-term psychological interventions for personality disorders is limited because of their high intensity and cost. Research in evidence-based, low-intensity interventions is needed. AIMS: This study aimed to examine the feasibility, acceptability and potential impact of a low-intensity, digital guided self-help (GSH) intervention that is focused on emotion regulation, recovery-oriented and provides in-the-moment delivery for patients with personality disorders. METHOD: We conducted a single-blind feasibility trial. A total of 43 patients with a personality disorder were recruited and randomly assigned to either a GSH arm (n = 22) or a treatment-as-usual arm (n = 21). The GSH intervention included a series of short videos offering psychoeducation and support, personalised feedback using text messages, and supportive telephone calls, for 4 weeks in addition to treatment as usual. Outcomes of emotional disturbance, emotion dysregulation, self-harm behaviours and decentring ability were measured at baseline, 4 weeks (end of intervention) and 8 weeks (follow-up). RESULTS: All patients who attended the first session continued until the last session. There was an interaction effect between time and group on anxiety (P = 0.027, Δη2 = 0.10), where the GSH group showed a significant reduction in anxiety at follow-up (P = 0.003, d = 0.25). The GSH group increased in decentring ability at the end of intervention (P = 0.007, d = -0.65), and the decrease in self-harm behaviours continued until follow-up (P = 0.02, d = 0.57). CONCLUSIONS: The results suggest that a personalised digital GSH with a focus on recovery could reduce anxiety and self-harm behaviours at short-term follow-up.

The relationship between air pollution and depression and anxiety disorders - A systematic evaluation and meta-analysis of a cohort-based study.

OBJECTIVE: To explore the correlation between air pollution and the onset of depression and anxiety disorders, to draw more comprehensive and integrated conclusions, and to provide recommendations for maintaining mental health and developing policies to reduce mental health risks caused by air pollution. METHODS: Meta-analysis of cohort study articles exploring the relationship between air pollution and depression or anxiety disorders included in Pubmed, Web Of Science, CNKI, and Wan Fang database before October 31, 2022, and subgroup analysis of the association between air pollution and depression and anxiety disorders regarding the air pollutants studied, the study population, and Publication bias analysis and sensitivity analysis. RESULTS: A total of 25 articles meeting the criteria were included in this study, including 23 articles examining the relationship between air pollution and depression and 5 articles examining the relationship between air pollution and anxiety disorders. The results of the meta-analysis were based on the type of pollutant and showed that there was a high degree of heterogeneity among the studies on the relationship between air pollution and depression and a significant heterogeneity among the studies on PM2.5 and the risk of anxiety disorders (I2 = 71%, p < .01), so a random-effects model was selected for the analysis. CO, O3, and SO2 and depression onset had combined RR values of 1.10 (1.00, 1.20), 1.06 (0.87, 1.29), 1.17 (1.06, 1.31), 1.19 (0.90, 1.58), 1.03 (0.99, 1.07), and 1.09 (0.97, 1.24), respectively, and PM2.5 and anxiety The combined RR value for morbidity was 1.10 (0.99, 1.22). The results of sensitivity analysis showed that the combined results were stable and reliable. The results of Egger regression method test showed that none of them had significant publication bias (p > .05). LIMITATION: Combined exposure to air pollutants on depression and anxiety, further studies by other researchers are needed in the future. CONCLUSIONS: PM2.5 and NO2 exposure, especially long-term exposure, may be associated with the onset of depression, and no association was found for the time being between PM10, CO, O3, SO2 exposure and depression and PM2.5 exposure and anxiety disorders.

Visible light-driven C/O-g-C3N4 activating peroxydisulfate to effectively inactivate antibiotic resistant bacteria and inhibit the transformation of antibiotic resistance genes: Insights on the mechanism.

Antibiotic resistant bacteria (ARB) and antibiotic resistance genes (ARGs) dissemination within water pose a serious threat to public health. Herein, C and O dual-doped g-C3N4 (C/O-g-C3N4) photocatalyst, fabricated via calcination treatment, was utilized to activate peroxydisulfate (PDS) to investigate the disinfection effect on tetracycline-resistant Escherichia coli and the transformation frequency of ARGs. As a result, approximately 7.08 log E. coli were inactivated, and 72.36 % and 53.96 % of antibiotics resistance gene (tetB) and 16 S rRNA were degraded respectively within 80 min. Futhermore, the transformation frequency was reduced to 0.8. Characterization and theoretical results indicated that C and O doping in g-C3N4 might lead to the electronic structure modulation and band gap energy reduction, resulting in the production of more free radicals. The mechanism analysis revealed that C/O-g-C3N4 exhibited a lower adsorption energy and reaction energy barrier for PDS compared to g-C3N4. This was beneficial for the homolysis of O-O bonds, forming SO4•- radicals. The attack of the generated active species led to oxidative stress in cells, resulting in damage to the electron transport chain and inhibition of ATP production. Our findings disclose a valuable insight for inactivating ARB, and provide a prospective strategy for ARGs dissemination in water contamination.

MMP-Responsive Nanoparticle-Loaded, Injectable, Adhesive, Self-Healing Hydrogel Wound Dressing Based on Dynamic Covalent Bonds.

Developing a multifunctional hydrogel wound dressing with good injectability, self-healing, tissue adhesion, biocompatibility, and fast skin wound healing efficiency remains challenging. In this work, an injectable adhesive dopamine-functionalized oxidized hyaluronic acid/carboxymethyl chitosan/collagen (AHADA/CCS/Col) hydrogel was constructed. The Schiff dynamic bond between AHADA and CCS, the N-Ag-N bond between CCS and Ag ions, and the S-Ag-S dynamic bond between sulfhydryl-modified collagen (ColSH) and Ag ions allowed the hydrogel to be both injectable and self-healing. Moreover, the aldehyde groups and catechol groups presented in the hydrogel could generate force with several groups on the tissue interface; therefore, the hydrogel also had good tissue adhesion. In vitro experiments proved that this hydrogel exhibited good biocompatibility and could promote cell proliferation. Additionally, curcumin (Cur)-loaded gelatin nanoparticles (Cur@Gel NPs) were prepared, which could respond to matrix metalloproteinases (MMPs) and controllably release Cur to hasten wound healing efficiency. Animal experiment results showed that this AHADA/CCS/Col hydrogel loaded with Cur@Gel NPs promoted wound repairing better, indicating its potential as a wound dressing.

Transcriptomics profile of human bronchial epithelial cells exposed to ambient fine particles and influenza virus (H3N2).

Fine particulate matter (PM2.5) pollution remains a major threat to public health. As the physical barrier against inhaled air pollutants, airway epithelium is a primary target for PM2.5 and influenza viruses, two major environmental insults. Recent studies have shown that PM2.5 and influenza viruses may interact to aggravate airway inflammation, an essential event in the pathogenesis of diverse pulmonary diseases. Airway epithelium plays a critical role in lung health and disorders. Thus far, the mechanisms for the interactive effect of PM2.5 and the influenza virus on gene transcription of airway epithelial cells have not been fully uncovered. In this present pilot study, the transcriptome sequencing approach was introduced to identify responsive genes following individual and co-exposure to PM2.5 and influenza A (H3N2) viruses in a human bronchial epithelial cell line (BEAS-2B). Enrichment analysis revealed the function of differentially expressed genes (DEGs). Specifically, the DEGs enriched in the xenobiotic metabolism by the cytochrome P450 pathway were linked to PM2.5 exposure. In contrast, the DEGs enriched in environmental information processing and human diseases, such as viral protein interaction with cytokines and cytokine receptors and epithelial cell signaling in bacterial infection, were significantly related to H3N2 exposure. Meanwhile, co-exposure to PM2.5 and H3N2 affected G protein-coupled receptors on the cell surface. Thus, the results from this study provides insights into PM2.5- and influenza virus-induced airway inflammation and potential mechanisms.

Overexpression of Lias Gene Alleviates Cadmium-Induced Kidney Injury in Mice Involving Multiple Effects: Metabolism, Oxidative Stress, and Inflammation.

Oxidative stress is an important mechanism underlying toxicity induced by cadmium (Cd) exposure. However, there are significant differences of the antioxidant baseline in different populations. This means that different human has different intensity of oxidative stress in vivo after exposure to toxicants. LiasH/H mouse is a specific model which is created by genetically modifying the Lias 3'-untranslated region (3'-UTR). LiasH/H mice express high levels of LA and have high endogenous antioxidant capacity which is approximately 150% higher than wild-type C57BL/6 J mice (WT, Lias+/+). But more importantly, they have dual roles of metal chelator and antioxidant. Here, we applied this mouse model to evaluate the effect of endogenous antioxidant levels in the body on alleviating Cd-induced renal injury including Cd metabolism, oxidative stress, and inflammation. In the experiment, mice drank water containing Cd (50 mg/L), for 12 weeks. Many biomarkers of Cd metabolism, oxidative stress, inflammation, and major pathological changes in the kidney were examined. The results showed overexpression of the Lias gene decreased Cd burden in the body of mice, mitigated oxidative stress, attenuated the inflammatory response, and subsequent alleviated cadmium-induced kidney injury in mice.

Electrochemical carbon-carbon coupling with enhanced activity and racemate stereoselectivity by microenvironment regulation.

Enzymes are characteristic of catalytic efficiency and specificity by maneuvering multiple components in concert at a confined nanoscale space. However, achieving such a configuration in artificial catalysts remains challenging. Herein, we report a microenvironment regulation strategy by modifying carbon paper with hexadecyltrimethylammonium cations, delivering electrochemical carbon-carbon coupling of benzaldehyde with enhanced activity and racemate stereoselectivity. The modified electrode-electrolyte interface creates an optimal microenvironment for electrocatalysis-it engenders dipolar interaction with the reaction intermediate, giving a 2.2-fold higher reaction rate (from 0.13 to 0.28 mmol h-1 cm-2); Moreover, it repels interfacial water and modulates the conformational specificity of reaction intermediate by facilitating intermolecular hydrogen bonding, affording 2.5-fold higher diastereomeric ratio of racemate to mesomer (from 0.73 to 1.82). We expect that the microenvironment regulation strategy will lead to the advanced design of electrode-electrolyte interface for enhanced activity and (stereo)selectivity that mimics enzymes.

Unraveling the potential-dependent structure evolution in CuO for electrocatalytic biomass valorization.

Electrocatalytic oxidation of renewable biomass (such as glucose) into high-value-added chemicals provides an effective approach to achieving carbon neutrality. CuO-derived materials are among the most promising electrocatalysts for biomass electrooxidation, but the identification of their active sites under electrochemical conditions remains elusive. Herein, we report a potential-dependent structure evolution over CuO in the glucose oxidation reaction (GOR). Through systematic electrochemical and spectroscopic characterizations, we unveil that CuO undergoes Cu2+/Cu+ and Cu3+/Cu2+ redox processes at increased potentials with successive generation of Cu(OH)2 and CuOOH as the active phases. In addition, these two structures have distinct activities in the GOR, with Cu(OH)2 being favorable for aldehyde oxidation, and CuOOH showed faster kinetics in carbon-carbon cleavage and alcohol/aldehyde oxidation. This work deepens our understanding of the dynamic reconstruction of Cu-based catalysts under electrochemical conditions and may guide rational material design for biomass valorization.

High temperature exacerbates ozone-induced airway inflammation: Implication of airway microbiota and metabolites.

Short-term exposure to ozone (O3) has been associated with airway inflammation. Given that high temperature (HT) accelerates O3 production, it is of significance to determine whether co-exposure to HT exacerbates O3-induced airway inflammation. The aim of this study was to examine the possible promotive effect of HT on O3-induced airway inflammation and underlying mechanisms. Forty-eight C57BL/6 N male mice were randomly divided into four groups: filtered air (control), O3, HT, and HT + O3 (co-exposure) groups. Mice in control and O3 groups were exposed to filtered air or 1 ppm O3 at 24 °C, respectively, while mice in HT and co-exposure groups were exposed to filtered air or 1 ppm O3 at 36 °C, respectively. The exposure scenario for four groups was 4 h/d for 5 consecutive days. Bronchoalveolar lavage fluids (BALF) were collected 24 h after the last exposure and subjected to examinations of oxidative stress and inflammation biomarkers, 16S rRNA sequencing, and metabolic profiling. Lung tissues were processed for H&E histological staining. The results showed that O3 inhalation triggered oxidative stress and inflammation in the airways, which was worsen by co-exposure to HT. Further studies revealed that co-exposure to HT strengthened O3-induced decline in Firmicutes and Allobaculum in airways. Moreover, co-exposure to HT promoted O3-induced airway metabolic disorder. Spearman correlation analysis revealed correlations among microbiota dysbiosis, metabolic disorder, oxidative stress and inflammation induced by co-exposure to HT and O3. Taken together, HT exposure aggravates O3-induced airway oxidative stress and inflammation, possibly through modulation of microbiota and metabolism of the airways.

Short-term ozone exposure and serum neural damage biomarkers in healthy elderly adults: Evidence from a panel study.

BACKGROUND: Although converging lines of research have pointed to the adverse neural effects of air pollution, evidence linking ozone (O3) and neural damage remains limited. OBJECTIVES: To investigate the subclinical neural effects of short-term ozone (O3) exposure in elderly adults. METHODS: A panel of healthy elderly individuals was recruited, and five repeated measurements were conducted from December 2018 to April 2019 in Xinxiang, China. Serum neural damage biomarkers, including brain-derived neurotrophic factor (BDNF), neurofilament light chain (NfL), neuron-specific enolase (NSE), protein gene product 9.5 (PGP9.5), and S100 calcium-binding protein B (S100B) were measured at each follow-up session. Personal O3 exposure levels were calculated based on outdoor monitoring and sampling times. A linear mixed-effects model was adopted to quantify the acute effect of O3 on serum neural damage biomarkers. Stratification analysis based on sex, education level, physical activity, and glutathione S-transferases (GST) gene polymorphism analysis was performed to explore their potential modifying effects. RESULTS: A total of 34 healthy volunteers aged 63.7 ± 5.7 y were enlisted and completed the study. The concentration of the daily maximum 8-h average O3 (O3-8h) ranged from 19.5 to 160.5 µg/m3 during the study period. Regression analysis showed that short-term O3 exposure was associated positively with serum concentrations of neural damage biomarkers. A 10 µg/m3 increase in O3-8h exposure was associated with an increment of 74 % (95 % CI:1 %-146 %) and 197 % (95 % CI:39 %-356 %) in BDNF (lag 2 d) and NfL (lag 1 d), respectively. The stratification results suggest that males, people with lower education levels, lower physical activity, and GST theta 1 (GSTT1)-sufficient genotype might be marginally more vulnerable. CONCLUSIONS: This study provides new evidence for the neural damage risk posed by O3 exposure, even at relatively low concentrations, which, therefore, requires that stringent air quality standards be developed and implemented.

Adsorption Recycling and High-Value Reutilization of Heavy-Metal Ions from Wastewater: As a High-Performance Anode Lithium Battery.

The dazzling adsorbent products make people overlook the harm of heavy metals adsorbed on them. Hazardous waste adsorbents cause secondary pollution. In this study, waste lignocellulose was dissolved by alkaline urea solvent and high-intensity ultrasound, then cross-linked by epichlorohydrin to make hydrogel, which was utilized to adsorb toxic heavy-metal wastewater. In situ deposition and high-temperature carbonization turn the gel that has absorbed heavy metals into carbon aerogel-loaded metal oxide energy storage materials that may be employed as anodes in lithium-ion batteries with excellent electrochemical performance. The best reversible capacity was 435.86 mAh g-1 after 100 cycles at 0.2C, indicating that the hazardous solid waste generated by the removal of heavy metals using biomass-based adsorbent has potential lithium battery applications. Thus, we provide a fresh perspective on the efficient recycling of heavy metals as well as an environmentally friendly, high-value conservation strategy for lowering the danger of heavy-metal hazardous wastes.

Secondary Metabolite Analysis of Phomopsis sp. LGT-5 Based on the Dual Guidance of Whole-Genome Sequencing and HPLC-Q-ToF-MS/MS.

Microorganisms produce a wealth of structurally diverse specialized metabolites with a remarkable range of biological activities. The Phomopsis sp. LGT-5 was obtained through tissue block and repeatedly crossed methods from Tripterygium wilfordii Hook. F. The antibacterial experiments of LGT-5 showed that it has high inhibitory activity against Staphylococcus aureus and Pseudomonas aeruginosa, and moderate inhibitory activity against Candida albicans. To research the generation of the antibacterial phenomenon of LGT-5 and provide support for further research and application, the whole genome sequencing (WGS) of LGT-5 was obtained by single-molecule real-time DNA sequencing platform Pacific Biosciences (PacBio) sequencing and Illumina paired-end sequencing. The final assembled LGT-5 genome is 54.79 Mb with a contig N50 of 290.07 kb; in addition, its secondary metabolites were detected through HPLC-Q-ToF-MS/MS. By comparing its MS/MS data, the secondary metabolites were analyzed based on visual network maps obtained on the Global Natural Products Social Molecular Networking (GNPS). The analysis results showed that the secondary metabolites of LGT-5 were triterpenes and various cyclic dipeptides.

Progress in quality control, detection techniques, speciation and risk assessment of heavy metals in marine traditional Chinese medicine.

Marine traditional Chinese medicines (MTCMs) hold a significant place in the rich cultural heritage in China. It plays an irreplaceable role in addressing human diseases and serves as a crucial pillar for the development of China's marine economy. However, the rapid pace of industrialization has raised concerns about the safety of MTCM, particularly in relation to heavy metal pollution. Heavy metal pollution poses a significant threat to the development of MTCM and human health, necessitating the need for detection analysis and risk assessment of heavy metals in MTCM. In this paper, the current research status, pollution situation, detection and analysis technology, removal technology and risk assessment of heavy metals in MTCM are discussed, and the establishment of a pollution detection database and a comprehensive quality and safety supervision system for MTCM is proposed. These measures aim to enhance understanding of heavy metals and harmful elements in MTCM. It is expected to provide a valuable reference for the control of heavy metals and harmful elements in MTCM, as well as the sustainable development and application of MTCM.