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1.
Eur J Med Res ; 29(1): 253, 2024 Apr 24.
Article in English | MEDLINE | ID: mdl-38659000

ABSTRACT

The progression of heart failure (HF) is complex and involves multiple regulatory pathways. Iron ions play a crucial supportive role as a cofactor for important proteins such as hemoglobin, myoglobin, oxidative respiratory chain, and DNA synthetase, in the myocardial energy metabolism process. In recent years, numerous studies have shown that HF is associated with iron dysmetabolism, and deficiencies in iron and overload of iron can both lead to the development of various myocarditis diseases, which ultimately progress to HF. Iron toxicity and iron metabolism may be key targets for the diagnosis, treatment, and prevention of HF. Some iron chelators (such as desferrioxamine), antioxidants (such as ascorbate), Fer-1, and molecules that regulate iron levels (such as lactoferrin) have been shown to be effective in treating HF and protecting the myocardium in multiple studies. Additionally, certain natural compounds can play a significant role by mediating the imbalance of iron-related signaling pathways and expression levels. Therefore, this review not only summarizes the basic processes of iron metabolism in the body and the mechanisms by which they play a role in HF, with the aim of providing new clues and considerations for the treatment of HF, but also summarizes recent studies on natural chemical components that involve ferroptosis and its role in HF pathology, as well as the mechanisms by which naturally occurring products regulate ferroptosis in HF, with the aim of providing reference information for the development of new ferroptosis inhibitors and lead compounds for the treatment of HF in the future.


Subject(s)
Biological Products , Heart Failure , Iron , Humans , Heart Failure/metabolism , Heart Failure/drug therapy , Iron/metabolism , Biological Products/therapeutic use , Biological Products/pharmacology , Animals , Ferroptosis/drug effects , Iron Chelating Agents/therapeutic use , Iron Chelating Agents/pharmacology , Antioxidants/therapeutic use
2.
PLoS One ; 19(4): e0301927, 2024.
Article in English | MEDLINE | ID: mdl-38635748

ABSTRACT

Generally, UHS-ECC should consume massive cement, which is negative to its sustainability as cement production leads to 8% of global CO2 emissions. To decrease the cost of production and carbon emissions of UHS-ECC, rice husk ash was employed to replace the cement as a supplementary cementitious material in this study. Experiment results illustrate that blending rice husk ash (RHA) would decrease the fluidity of mortar. Furthermore, the green UHS-ECC shows a maximum compressive strength of 130.3 MPa at 28 days when RHA content was 20% of cement. The ultimate tensile strength of UHS-ECCs first increased and then decreased, while both tensile strain and strain energy presented an opposite tendency. At the micro-scale, if RHA content was lower than 20% of cement, incorporating RHA can significantly decreasing fiber bridging complementary energy of UHS-ECC, thus reducing pseudo strain hardening energy (PSHenergy) index, which finely agrees with the degradation of ductility of UHS-ECCs. To guarantee the features of ultra-high strength, acceptable workability, and high tensile ductility, the RHA dosage should not be in excess 20% of cement. These researched results are prospected to the contribution of pozzolanic RHA on the efficient usage of sustainable UHS-ECC.


Subject(s)
Oryza , Bone Cements , Carbon , Compressive Strength , Glass Ionomer Cements
3.
Ying Yong Sheng Tai Xue Bao ; 35(3): 659-668, 2024 Mar 18.
Article in English | MEDLINE | ID: mdl-38646753

ABSTRACT

To accurately monitor the phenology of net ecosystem carbon exchange (NEE) in grasslands with remote sensing, we analyzed the variations in NEE and its phenology in the Stipa krylovii steppe and discussed the remote sensing vegetation index thresholds for NEE phenology, with the observational data from the Inner Mongolia Xilinhot National Climate Observatory's eddy covariance system and meteorological gradient observation system during 2018-2021, as well as Sentinel-2 satellite data from January 1, 2018 to December 31, 2021. Results showed that, from 2018 to 2021, NEE exhibited seasonal variations, with carbon sequestration occurring from April to October and carbon emission in other months, resulting in an overall carbon sink. The average Julian days for the start date (SCUP) and the end date (ECUP) of carbon uptake period were the 95th and 259th days, respectively, with an average carbon uptake period lasting 165 days. Photosynthetically active radiation showed a negative correlation with daily NEE, contributing to carbon absorption of grasslands. The optimal threshold for capturing SCUP was a 10% threshold of the red-edge chlorophyll index, while the normalized difference vegetation index effectively reflected ECUP with a threshold of 75%. These findings would provide a basis for remote sensing monitoring of grassland carbon source-sink dynamics.


Subject(s)
Carbon , Ecosystem , Environmental Monitoring , Grassland , Poaceae , Remote Sensing Technology , China , Carbon/metabolism , Poaceae/metabolism , Poaceae/growth & development , Environmental Monitoring/methods , Carbon Sequestration , Seasons , Carbon Cycle
4.
Int Immunopharmacol ; 133: 112130, 2024 Apr 21.
Article in English | MEDLINE | ID: mdl-38648712

ABSTRACT

Neutrophils and T lymphocytes are closely related to occurrence of immunosuppression in sepsis. Studies have shown that neutrophil apoptosis decreases and T lymphocyte apoptosis increases in sepsis immunosuppression, but the specific mechanism involved remains unclear. In the present study, we found Toll-like Receptor 2 (TLR2) and programmed death-ligand 1 (PD-L1) were significantly activated in bone marrow neutrophils of wild-type mice after LPS treatment and that they were attenuated by treatment with C29, an inhibitor of TLR2. PD-L1 activation inhibits neutrophil apoptosis, whereas programmed death protein 1 (PD-1)activation promotes apoptosis of T lymphocytes, which leads to immunosuppression. Mechanistically, when sepsis occurs, pro-inflammatory factors and High mobility group box-1 protein (HMGB1) passively released from dead cells cause the up-regulation of PD-L1 through TLR2 on neutrophils. The binding of PD-L1 and PD-1 on T lymphocytes leads to increased apoptosis of T lymphocytes and immune dysfunction, eventually resulting in the occurrence of sepsis immunosuppression. In vivo experiments showed that the HMGB1 inhibitor glycyrrhizic acid (GA) and the TLR2 inhibitor C29 could inhibit the HMGB1/TLR2/PD-L1 pathway, and improving sepsis-induced lung injury. In summary, this study shows that HMGB1 regulates PD-L1 and PD-1 signaling pathways through TLR2, which leads to immunosuppression.

5.
Front Pharmacol ; 15: 1250918, 2024.
Article in English | MEDLINE | ID: mdl-38601463

ABSTRACT

Ischemic stroke (IS) is a major cause of mortality and disability among adults. Recanalization of blood vessels to facilitate timely reperfusion is the primary clinical approach; however, reperfusion itself may trigger cerebral ischemia-reperfusion injury. Emerging evidence strongly implicates the NLRP3 inflammasome as a potential therapeutic target, playing a key role in cerebral ischemia and reperfusion injury. The aberrant expression and function of NLRP3 inflammasome-mediated inflammation in cerebral ischemia have garnered considerable attention as a recent research focus. Accordingly, this review provides a comprehensive summary of the signaling pathways, pathological mechanisms, and intricate interactions involving NLRP3 inflammasomes in cerebral ischemia-reperfusion injury. Moreover, notable progress has been made in investigating the impact of natural plant products (e.g., Proanthocyanidins, methylliensinine, salidroside, α-asarone, acacia, curcumin, morin, ginsenoside Rd, paeoniflorin, breviscapine, sulforaphane, etc.) on regulating cerebral ischemia and reperfusion by modulating the NLRP3 inflammasome and mitigating the release of inflammatory cytokines. These findings aim to present novel insights that could contribute to the prevention and treatment of cerebral ischemia and reperfusion injury.

6.
Pestic Biochem Physiol ; 200: 105845, 2024 Mar.
Article in English | MEDLINE | ID: mdl-38582577

ABSTRACT

7-dehydrocholesterol (7-DHC) is a key intermediate product used for biosynthesis of molting hormone. This is achieved through a series of hydroxylation reactions catalyzed by the Halloween family of cytochrome P450s. Neverland is an enzyme catalyzes the first reaction of the ecdysteroidogenic pathway, which converts dietary cholesterol into 7-DHC. However, research on the physiological function of neverland in orthopteran insects is lacking. In this study, neverland from Locusta migratoria (LmNvd) was cloned and analyzed. LmNvd was mainly expressed in the prothoracic gland and highly expressed on days 6 and 7 of fifth instar nymphs. RNAi-mediated silencing of LmNvd resulted in serious molting delays and abnormal phenotypes, which could be rescued by 7-DHC and 20-hydroxyecdysone supplementation. Hematoxylin and eosin staining results showed that RNAi-mediated silencing of LmNvd disturbed the molting process by both promoting the synthesis of new cuticle and suppressing the degradation of the old cuticle. Quantitative real-time PCR results suggested that the mRNA expression of E75 early gene and chitinase 5 gene decreased and that of chitin synthase 1 gene was markedly upregulated after knockdown of LmNvd. Our results suggest that LmNvd participates in the biosynthesis process of molting hormone, which is involved in regulating chitin synthesis and degradation in molting cycles.


Subject(s)
Locusta migratoria , Molting , Animals , Molting/genetics , Ecdysone/metabolism , Locusta migratoria/genetics , Locusta migratoria/metabolism , RNA Interference , Gene Expression Regulation, Developmental , Insect Proteins/genetics , Insect Proteins/metabolism
7.
Curr Med Imaging ; 2024 Mar 07.
Article in English | MEDLINE | ID: mdl-38462828

ABSTRACT

BACKGROUND: The Glypican 3 (GPC3)-positive expression in Hepatocellular Carcinoma (HCC) is associated with a worse prognosis. Moreover, GPC3 has emerged as an immunotherapeutic target in advanced unresectable HCC systemic therapy. It is significant to diagnose GPC3-positive HCCs before therapy. Regarding imaging diagnosis of HCC, dynamic contrast-enhanced CT is more common than MRI in many regions. OBJECTIVE: The aim of this study was to construct and validate a radiomics model based on contrast-enhanced CT to predict the GPC3 expression in hepatocellular carcinoma. METHODS: This retrospective study included 141 (training cohort: n = 100; validation cohort: n = 41) pathologically confirmed HCC patients. Radiomics features were extracted from the Artery Phase (AP) images of contrast-enhanced CT. Logistic regression with the Least Absolute Shrinkage and Selection Operator (LASSO) regularization was used to select features to construct radiomics score (Rad-score). A final combined model, including the Rad-score of the selected features and clinical risk factors, was established. Receiver Operating Characteristic (ROC) curve analysis, Delong test, and Decision Curve Analysis (DCA) were used to assess the predictive performance of the clinical and radiomics models. RESULTS: 5 features were selected to construct the AP radiomics model of contrast-enhanced CT. The radiomics model of AP from contrast-enhanced CT was superior to the clinical model of AFP in training cohorts (P < 0.001), but not superior to the clinical model in validation cohorts (P = 0.151). The combined model (AUC = 0.867 vs. 0.895), including AP Rad-score and serum Alpha-Fetoprotein (AFP) levels, improved the predictive performance more than the AFP model (AUC = 0.651 vs. 0.718) in the training and validation cohorts. The combined model, with a higher decision curve indicating more net benefit, exhibited a better predictive performance than the AP radiomics model. DCA revealed that at a range threshold probability approximately above 60%, the combined model added more net benefit compared to the AP radiomics model of contrastenhanced CT. CONCLUSION: A combined model including AP Rad-score and serum AFP levels based on contrast-enhanced CT could preoperatively predict GPC3-positive expression in HCC.

8.
BMC Med ; 22(1): 110, 2024 Mar 13.
Article in English | MEDLINE | ID: mdl-38475833

ABSTRACT

BACKGROUND: Previous randomized controlled trials (RCTs) suggested that gut microbiota-based therapies may be effective in treating autoimmune diseases, but a systematic summary is lacking. METHODS: Pubmed, EMbase, Sinomed, and other databases were searched for RCTs related to the treatment of autoimmune diseases with probiotics from inception to June 2022. RevMan 5.4 software was used for meta-analysis after 2 investigators independently screened literature, extracted data, and assessed the risk of bias of included studies. RESULTS: A total of 80 RCTs and 14 types of autoimmune disease [celiac sprue, SLE, and lupus nephritis (LN), RA, juvenile idiopathic arthritis (JIA), spondyloarthritis, psoriasis, fibromyalgia syndrome, MS, systemic sclerosis, type 1 diabetes mellitus (T1DM), oral lichen planus (OLP), Crohn's disease, ulcerative colitis] were included. The results showed that gut microbiota-based therapies may improve the symptoms and/or inflammatory factor of celiac sprue, SLE and LN, JIA, psoriasis, PSS, MS, systemic sclerosis, Crohn's disease, and ulcerative colitis. However, gut microbiota-based therapies may not improve the symptoms and/or inflammatory factor of spondyloarthritis and RA. Gut microbiota-based therapies may relieve the pain of fibromyalgia syndrome, but the effect on fibromyalgia impact questionnaire score is not significant. Gut microbiota-based therapies may improve HbA1c in T1DM, but its effect on total insulin requirement does not seem to be significant. These RCTs showed that probiotics did not increase the incidence of adverse events. CONCLUSIONS: Gut microbiota-based therapies may improve several autoimmune diseases (celiac sprue, SLE and LN, JIA, psoriasis, fibromyalgia syndrome, PSS, MS, T1DM, Crohn's disease, and ulcerative colitis).


Subject(s)
Autoimmune Diseases , Celiac Disease , Colitis, Ulcerative , Crohn Disease , Diabetes Mellitus, Type 1 , Fibromyalgia , Gastrointestinal Microbiome , Lupus Erythematosus, Systemic , Psoriasis , Scleroderma, Systemic , Spondylarthritis , Humans , Randomized Controlled Trials as Topic
9.
Behav Sci (Basel) ; 14(3)2024 Mar 14.
Article in English | MEDLINE | ID: mdl-38540539

ABSTRACT

Due to the increasing competition in the market and the limited availability of high-quality employment opportunities, an increasing number of employees struggle to maintain a balance between their physical conditions and performance demands, resulting in a more widespread occurrence of "working while ill". However, little is known about the controlled motivation behind the phenomenon under pressure. Drawing on self-determination theory, this study utilized 281 questionnaire data to examine the positive effect of performance pressure on employee presenteeism, and to explore the moderating role of authoritarian leadership and its joint moderation function effect with independent self-construal. The results indicated that performance pressure had a significant positive effect on employee presenteeism. Authoritarian leadership imposed an enhanced moderating effect between performance pressure and employee presenteeism, while independent self-construal diminished the augmentative moderating role played by authoritarian leadership in the relationship between performance pressure and employee presenteeism. This study reveals the controlled motivation of employee presenteeism under performance pressure, taking into account the cultural background and organizational context of China. Moreover, it also offers novel perspectives for effectively managing this phenomenon.

10.
Int J Surg ; 2024 Mar 28.
Article in English | MEDLINE | ID: mdl-38537085

ABSTRACT

BACKGROUND: Robotic gastrectomy is a safe and feasible approach for gastric cancer (GC); however, its long-term oncological efficacy remains unclear. We evaluated the long-term survival outcomes and recurrence patterns of patients with locally advanced proximal GC who underwent robotic total gastrectomy (RTG). METHODS: This prospective study (FUGES-014 study) enrolled 48 patients with locally advanced proximal GC who underwent RTG between March 2018 and February 2020 at a tertiary referral teaching hospital. Patients who underwent laparoscopic total gastrectomy (LTG) in the FUGES-002 study were enrolled in a 2:1 ratio to compare the survival outcomes between RTG and LTG. The primary endpoint of the FUGES-014 study was postoperative 30-day morbidity and has been previously reported. Here we reported the results of 3-year disease-free survival (DFS), 3-year overall survival (OS), and recurrence patterns. RESULTS: After propensity score matching, 48 patients in the RTG and 96 patients in the LTG groups were included. The 3-year DFS rates were 77.1% (95% confidence interval [CI] 66.1-89.9%) for the RTG and 68.8% (95% CI 60.1-78.7%) for the LTG groups ( P =0.261). The 3-year OS rates were not significantly different between the groups (85.4% vs. 74.0%, P =0.122). Recurrence occurred in nine patients (18.8%) in the RTG and 27 (28.1%) patients in the LTG groups ( P =0.234). Recurrence patterns and causes of death were similar between the groups ( P >0.05). CONCLUSIONS: The oncological outcome of RTG was non-inferior to that of LTG. Thus, RTG might be an alternative surgical treatment for locally advanced proximal GC.

11.
Gels ; 10(3)2024 Mar 02.
Article in English | MEDLINE | ID: mdl-38534595

ABSTRACT

Ethylhexyl methoxycinnamate (EHMC) is frequently employed as a photoprotective agent in sunscreen formulations. EHMC has been found to potentially contribute to health complications as a result of its propensity to produce irritation and permeate the skin. A microgel carrier, consisting of poly(ethylene glycol dimethacrylate) (pEDGMA), was synthesized using interfacial polymerization with the aim of reducing the irritation and penetration of EHMC. The thermogravimetric analysis (TGA) indicated that the EHMC content accounted for 75.72% of the total composition. Additionally, the scanning electron microscopy (SEM) images depicted the microgel as exhibiting a spherical morphology. In this study, the loading of EHMC was demonstrated through FTIR and contact angle tests. The UV resistance, penetration, and skin irritation of the EHMC-pEDGMA microgel were additionally assessed. The investigation revealed that the novel sunscreen compound, characterized by limited dermal absorption, had no irritant effects and offered sufficient protection against ultraviolet radiation.

12.
Eur J Surg Oncol ; 50(6): 108280, 2024 Mar 21.
Article in English | MEDLINE | ID: mdl-38537365

ABSTRACT

BACKGROUND: The impact of achieving textbook oncological outcome (TOO) as a multimodal therapy quality indicator on the prognosis of advanced gastric cancer (AGC) remains inadequately assessed. METHODS: Patients with AGC who underwent curative gastrectomy between January 2010 and December 2017 at two East Asian medical centers were included. TOO was defined as achieving the textbook outcome (TO) and receiving neoadjuvant and/or adjuvant chemotherapy (NCT or ACT). Cox and logistic regression models were used to identify prognostic and non-TOO-associated risk factors. RESULTS: Among 3626 patients, 57.6% achieved TOO (TOO group), exhibiting significantly better 5-year overall survival (OS) and disease-free survival (DFS) than the non-TOO group (both p < 0.05). Multivariate Cox regression identified TOO as an independent prognostic factor for 5-year OS (HR, 0.67; 95% CI, 0.61-0.74; p < 0.001) and DFS (HR, 0.73; 95% CI, 0.66-0.81; p < 0.001). Multivariate logistic regression showed that open gastrectomy, lack of health insurance, age ≥65 years, ASA score ≥ Ⅲ, and tumor size ≥50 mm are independent risk factors for non-achievement of TOO (all p < 0.05). On a sensitivity analysis of TOO's prognostic value using varying definitions of chemotherapy parameters, a stricter definition of chemotherapy resulted in a decrease in the TOO achievement rate from 57.6 to 22.3%. However, the associated reductions in the risk of death and recurrence fluctuated within the ranges of 33-39% and 28-37%, respectively. CONCLUSIONS: TOO is a reliable and stable metric for favorable prognosis in AGC. Optimizing the surgical approach and improving health insurance status may enhance TOO achievement.

13.
Cell Commun Signal ; 22(1): 182, 2024 03 15.
Article in English | MEDLINE | ID: mdl-38491522

ABSTRACT

BACKGROUND: Diabetic angiogenesis is closely associated with disabilities and death caused by diabetic microvascular complications. Advanced glycation end products (AGEs) are abnormally accumulated in diabetic patients and are a key pathogenic factor for diabetic angiogenesis. The present study focuses on understanding the mechanisms underlying diabetic angiogenesis and identifying therapeutic targets based on these mechanisms. METHODS: In this study, AGE-induced angiogenesis serves as a model to investigate the mechanisms underlying diabetic angiogensis. Mouse aortic rings, matrigel plugs, and HUVECs or 293T cells were employed as research objects to explore this pathological process by using transcriptomics, gene promoter reporter assays, virtual screening and so on. RESULTS: Here, we found that AGEs activated Wnt/ß-catenin signaling pathway and enhanced the ß-catenin protein level by affecting the expression of ß-catenin degradation-related genes, such as FZDs (Frizzled receptors), LRPs (LDL Receptor Related Proteins), and AXIN1. AGEs could also mediate ß-catenin Y142 phosphorylation through VEGFR1 isoform5. These dual effects of AGEs elevated the nuclear translocation of ß-catenin and sequentially induced the expression of KDR (Kinase Insert Domain Receptor) and HDAC9 (Histone Deacetylase 9) by POU5F1 and NANOG, respectively, thus mediating angiogenesis. Finally, through virtual screening, Bioymifi, an inhibitor that blocks VEGFR1 isoform5-ß-catenin complex interaction and alleviates AGE-induced angiogenesis, was identified. CONCLUSION: Collectively, this study offers insight into the pathophysiological functions of ß-catenin in diabetic angiogenesis.


Subject(s)
Diabetes Complications , Diabetes Mellitus , Animals , Humans , Mice , Angiogenesis , beta Catenin/metabolism , Histone Deacetylases/metabolism , Phosphorylation , Repressor Proteins/metabolism , Up-Regulation , Vascular Endothelial Growth Factor Receptor-2/metabolism , Wnt Signaling Pathway
14.
J Hazard Mater ; 469: 134022, 2024 May 05.
Article in English | MEDLINE | ID: mdl-38484662

ABSTRACT

Sulfidized nanoscale zero-valent iron (S-nZVI) showed excellent removal capacity for cadmium (Cd) in aqueous phase. However, the remediation effects of S-nZVI on Cd-contaminated sediment and its interactions with microorganisms in relation to Cd fate remain unclear. The complexity of the external environment posed a challenge for Cd remediation. This study synthesized S-nZVI with different S and Fe precursors to investigate the effect of precursors and applied the optimal material to immobilize Cd in sediments. Characterization analysis revealed that the precursor affected the morphology, Fe0 crystallinity, and the degree of oxidation of the material. Incubation experiments demonstrated that the immobilization efficiency of Cd using S-nZVIFe3++S2- (S/Fe = 0.14) reached the peak value of 99.54%. 1% and 5% dosages of S-nZVI significantly reduced Cd concentration in the overlying water, DTPA-extractable Cd content, and exchangeable (EX) Cd speciation (P < 0.05). Cd leaching in sediment and total iron in the overlying water remained at low levels during 90 d of incubation. Notably, each treatment maintained a high Cd immobilization efficiency under different pH, water/sediment ratio, organic acid, and coexisting ion conditions. Sediment physicochemical properties, functional bacteria, and a range of adsorption, complexation and precipitation of CdS effects dominated Cd immobilization.


Subject(s)
Iron , Water Pollutants, Chemical , Iron/chemistry , Cadmium/chemistry , Water Pollutants, Chemical/chemistry , Water , Adsorption
15.
Biomed Pharmacother ; 172: 116230, 2024 Mar.
Article in English | MEDLINE | ID: mdl-38350366

ABSTRACT

Ferroptosis, a distinct form of cell death, is characterized by the iron-mediated oxidation of lipids and is finely controlled by multiple cellular metabolic pathways. These pathways encompass redox balance, iron regulation, mitochondrial function, as well as amino acid, lipid, and sugar metabolism. Additionally, various disease-related signaling pathways also play a role in the regulation of ferroptosis. In recent years, with the introduction of the concept of ferroptosis and the deepening of research on its mechanism, ferroptosis is closely related to various biological conditions of eye diseases, including eye organ development, aging, immunity, and cancer. This article reviews the development of the concept of ferroptosis, the mechanism of ferroptosis, and its latest research progress in ophthalmic diseases and reviews the research on ferroptosis in ocular diseases within the framework of metabolism, active oxygen biology, and iron biology. Key regulators and mechanisms of ferroptosis in ocular diseases introduce important concepts and major open questions in the field of ferroptosis and related natural compounds. It is hoped that in future research, further breakthroughs will be made in the regulation mechanism of ferroptosis and the use of ferroptosis to promote the treatment of eye diseases. At the same time, natural compounds may be the direction of new drug development for the potential treatment of ferroptosis in the future. Open up a new way for clinical ophthalmologists to research and prevent diseases.


Subject(s)
Eye Diseases , Ferroptosis , Humans , Eye Diseases/drug therapy , Eye , Iron
17.
Water Res ; 253: 121309, 2024 Apr 01.
Article in English | MEDLINE | ID: mdl-38367381

ABSTRACT

Antibiotics and antibiotic resistance genetic pollution have become a global environmental and health concern recently, with frequent detection in various environmental media. Therefore, finding ways to control antibiotics and antibiotic resistance genes (ARGs) is urgently needed. Nano zero-valent iron (nZVI) has shown a positive effect on antibiotics degradation and restraining ARGs, making it a promising solution for controlling antibiotics and ARGs. However, given the current increasingly fragmented research focus and results, a comprehensive review is still lacking. In this work, we first introduce the origin and transmission of antibiotics and ARGs in various environmental media, and then discuss the affecting factors during the degradation of antibiotics and the control of ARGs by nZVI and modified nZVI, including pH, nZVI dose, and oxidant concentration, etc. Then, the mechanisms of antibiotic and ARGs removal promoted by nZVI are also summarized. In general, the mechanism of antibiotic degradation by nZVI mainly includes adsorption and reduction, while promoting the biodegradation of antibiotics by affecting the microbial community. nZVI can also be combined with persulfates to degrade antibiotics through advanced oxidation processes. For the control of ARGs, nZVI not only changes the microbial community structure, but also affects the proliferation of ARGs through affecting the fate of mobile genetic elements (MGEs). Finally, some new ideas on the application of nZVI in the treatment of antibiotic resistance are proposed. This paper provides a reference for research and application in this field.


Subject(s)
Anti-Bacterial Agents , Water Pollutants, Chemical , Anti-Bacterial Agents/pharmacology , Iron/chemistry , Oxidation-Reduction , Drug Resistance, Microbial/genetics , Adsorption , Water Pollutants, Chemical/chemistry
18.
J Trace Elem Med Biol ; 83: 127415, 2024 May.
Article in English | MEDLINE | ID: mdl-38377659

ABSTRACT

BACKGROUND: Environmental arsenic (As) exposure is strongly related to the progression of chronic obstructive pulmonary disease (COPD). Pulmonary epithelial cells apoptosis is implicated in the pathophysiological mechanisms of COPD. However, the role of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), one biomarker of apoptosis, remains unclear in As-mediated pulmonary function alternations in COPD patients. METHODS: This study included 239 COPD patients. The serum level of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was measured by enzyme-linked immunosorbent assay (ELISA). The blood As level was determined through inductively coupled plasma mass spectrometry (ICP-MS). RESULTS: Blood As levels exhibited a negative and dose-dependent correlation with pulmonary function. Per unit elevation of blood arsenic concentrations was related to reductions of 0.339 L in FEV1, 0.311 L in FVC, 1.171% in FEV1/FVC%, and 7.999% in FEV1% in COPD subjects. Additionally, a positive dose-response correlation of blood As with serum TRAIL was found in COPD subjects. Additionally, the level of serum TRAIL was negatively linked to lung function. Elevated TRAIL significantly mediated As-induced decreases of 11.05%, 13.35%, and 31.78% in FVC, FEV1, and FEV1%, respectively among the COPD patients. CONCLUSION: Blood As level is positively correlated with pulmonary function decline and serum TRAIL increase in individuals with COPD. Our findings suggest that elevated TRAIL levels may serve as a mediating mechanism through which As contributes to declining lung function in COPD patients.


Subject(s)
Arsenic , Pulmonary Disease, Chronic Obstructive , Humans , Ligands , Lung/pathology , Pulmonary Disease, Chronic Obstructive/pathology , Tumor Necrosis Factor-alpha , Apoptosis
19.
Article in English | MEDLINE | ID: mdl-38327141

ABSTRACT

Schizophrenia is a chronic, debilitating mental illness caused by both genetic and environmental factors. Genetic factors play a major role in schizophrenia development. Early growth response 3 (EGR3) is a member of the EGR family, which is associated with schizophrenia. Accumulating studies have investigated the relationship between EGR3 and schizophrenia. However, the role of EGR3 in schizophrenia pathogenesis remains unclear. In the present review, we focus on the progress of research related to the role of EGR3 in schizophrenia, including association studies between EGR3 and schizophrenia, abnormal gene expressional analysis of EGR3 in schizophrenia, biological function studies of EGR3 in schizophrenia, the molecular regulatory mechanism of EGR3 and schizophrenia susceptibility candidate genes, and possible role of EGR3 in the immune system function in schizophrenia. In summary, EGR3 is a schizophrenia risk candidate factor and has comprehensive regulatory roles in schizophrenia pathogenesis. Further studies investigating the molecular mechanisms of EGR3 in schizophrenia are warranted for understanding the pathophysiology of this disorder as well as the development of new therapeutic strategies for the treatment and control of this disorder.

20.
Adv Sci (Weinh) ; 11(15): e2305530, 2024 Apr.
Article in English | MEDLINE | ID: mdl-38353337

ABSTRACT

Considerable efforts have recently been made to augment the power density of moisture-enabled electric generators. However, due to the unsustainable ion/water molecule concentration gradients, the ion-directed transport gradually diminishes, which largely affects the operating lifetime and energy efficiency of generators. This work introduces an electrode chemistry regulation strategy into the ionic diode-type energy conversion structure, which demonstrates 1240 h power generation in ambient humidity. The electrode chemical regulation can be achieved by adding Cl-. The purpose is to destroy the passivation film on the electrode interface and provide a continuous path for ion-electron coupling conduction. Moreover, this device simultaneously satisfies the requirements of fast trapping of moisture molecules, high rectification ratio transport of ions, and sustained ion-to-electron current conversion. A single device can deliver an open-circuit voltage of about 1 V and a peak short-circuit current density of 350 µA cm-2. Finally, the first-principle calculations are carried out to reveal the mechanism by which the electrode surface chemistry affects the power generation performance.

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