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Directionally duplexed metalenses manipulated by the geometric phase of a silicon nano-bar are theoretically designed to generate multifunctional structured light. It is numerically demonstrated that incident light with different linear and circular polarization states, along forward and backward propagation directions, can be differentially converted into multiple focusing structured beams of arbitrary topological charges, either of vector light with azimuthally variant polarizations or of vortex light with helical phases. Due to the all-silicon and nonresonant metastructural design, the resultant high working efficiencies of our proposed metalens are promising for applications such as optical communication, nanoparticle manipulation, and other direction-duplexed multifunctional optical meta-devices.
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AIMS: Cognitive frailty can increase the risk of adverse health outcomes in older adults. Estimates of the prevalence of cognitive frailty among older adults with diabetes varied widely in literature. This study aimed to conduct a systematic review and meta-analysis to assess the pooled prevalence of cognitive frailty and risk factors in community-dwelling older adults with diabetes, providing evidence for healthcare professionals to better understand the status of cognitive frailty and help develop effective interventions. METHODS: Databases of PubMed, Web of Science, Cochrane Library, Embase, Cumulative Index of Nursing and Allied Health, Proquest, China National Knowledge Infrastructure and China Biology Medicine were searched from inception to February 10th, 2022. The reviewers independently selected studies, extracted data and assessed the quality of studies. Pooled prevalence of cognitive frailty and risk factors were estimated. Subgroup analysis, meta-regression analysis, sensitivity analysis and publication bias were also conducted. RESULTS: A total of 15 studies with 6391 participants were included in this review. The pooled prevalence of cognitive frailty was 11% (95%CI = 7.9-14%) in community-dwelling older adults with diabetes. Pooled estimates showed that increasing age, higher level of HbA1c, shorter night sleep duration and depression were risk factors, and regular exercise was the protective factor of cognitive frailty in community-dwelling older adults with diabetes. CONCLUSION: Cognitive frailty was common in community-dwelling older adults with diabetes. Routine screening of cognitive frailty and effective interventions should be implemented for this population in community settings. REGISTRATION: PROSPERO ID CRD42021276973.
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Diabetes Mellitus , Fragilidad , Humanos , Anciano , Fragilidad/epidemiología , Vida Independiente , Anciano Frágil , Prevalencia , Factores de Riesgo , Diabetes Mellitus/epidemiología , CogniciónRESUMEN
In this study, we report a facile synthesis of a novel N, S, B, and O-codoped carbon nanosphere-armored Co9S8 nanoparticle composite (Co9S8@NSBOC) and its superior activation performance toward peroxymonosulfate (PMS) for methylene blue (MB) and ofloxacin degradation. The effects of various experimental parameters and the general applicability of the catalyst were investigated. Particularly, Co9S8@NSBOC exhibited high catalytic activity in a wide pH range of 3-12 and HPO42- exhibited a synergic catalytic effect with Co9S8@NSBOC in the degradation system. Radical quenching tests, EPR measurements and electrochemical analysis demonstrated that the degradation mechanism of pollutants in the Co9S8@NSBOC/PMS system included both radical and non-radical pathways, in which ËO2-, 1O2 and electron transfer played dominant roles. Co2+, S2-, carbon defects, C[double bond, length as m-dash]O/C-O-C, pyridinic-N, graphitic-N, BC2O and C-S-C species on Co9S8@NSBOC, all contributed to PMS activation. The degradation pathways of MB and ofloxacin were proposed based on HPLC-MS/MS analysis of their degradation intermediates. This work not only presents a facile and practical synthetic method of cobalt sulfide-coupled multi-heteroatom-doped carbocatalysts, but also provides useful insights into their active sites and activation mechanisms toward PMS activation.
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Fine particulate matter (PM2.5) has been shown to induce DNA damage. Circular RNAs (circRNAs) have been implicated in various disease processes related to environmental chemical exposure. However, the role of circRNAs in the regulation of DNA damage response (DDR) after PM2.5 exposure remains unclear. In this study, male ICR mice were exposed to PM2.5 at a daily mean concentration of 382.18 µg/m3 for 3 months in an enriched-ambient PM2.5 exposure system in Shijiazhuang, China, and PM2.5 collected form Shijiazhuang was applied to RAW264.7 cells at 100 µg/mL for 48 h. The results indicated that exposure to PM2.5 induced histopathological changes and DNA damage in the lung, kidney and spleen of male ICR mice, and led to decreased cell viability, increased LDH activity and DNA damage in RAW264.7 cells. Furthermore, circ_Cabin1 expression was significantly upregulated in multiple mouse organs as well as in RAW264.7 cells upon exposure to PM2.5. PM2.5 exposure also resulted in impairment of non-homologous end joining (NHEJ) repair via the downregulation of Lig4 or Dclre1c expression in vivo and in vitro. Importantly, circ_Cabin1 promoted PM2.5-induced DNA damage via inhibiting of NHEJ repair. Moreover, the expression of circ_Cabin1 and Lig4 or Dclre1c was strongly correlated in multiple mouse organs, as well as in the blood. In summary, our study provides a new perspective on circRNAs in the regulation of DDR after environmental chemical exposure.
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Proteínas Adaptadoras Transductoras de Señales/genética , Daño del ADN/efectos de los fármacos , Material Particulado/toxicidad , ARN Circular/genética , Animales , Supervivencia Celular/efectos de los fármacos , Reparación del ADN por Unión de Extremidades/genética , ADN Ligasa (ATP)/genética , Endonucleasas/genética , Masculino , Ratones , Ratones Endogámicos ICR , Proteínas Nucleares/genética , Células RAW 264.7RESUMEN
BACKGROUND: Lung cancer has high morbidity and mortality worldwide with non-small cell lung cancer (NSCLC) accounting for 85% of the cases. Therapies for lung cancer have relatively poor outcomes and further improvements are required. Circular RNAs have been reported to participate in the occurrence and progression of cancer. Information on the functions and mechanism of circRNAs in lung cancer is limited and needs more exploration. METHODS: We detected expression of genes and proteins by qPCR and western blot. Function of circSATB2 was investigated using RNA interference and overexpression assays. Location of circSATB2 was assessed by fluorescence in situ hybridization (FISH). Interaction of circSATB2, miR-326 and FSCN1 was confirmed by dual-luciferase reporter assay. RESULTS: Data from the investigation showed that circSATB2 was highly expressed in NSCLC cells and tissues. circSATB2 positively regulated fascin homolog 1, actin-bundling protein 1 (FSCN1) expression via miR-326 in lung cancer cells. Furthermore, circSATB2 can be transferred by exosomes and promote the proliferation, migration and invasion of NSCLC cells, as well as induce abnormal proliferation in normal human bronchial epithelial cells. Also, circSATB2 was highly expressed in serumal exosomes from lung cancer patients with high sensitivity and specificity for clinical detection and was related to lung cancer metastasis. CONCLUSIONS: circSATB2 participated in the progression of NSCLC and was differentially expressed in lung cancer tissue and serumal exosomes. circSATB2 may be potential biomarker for the diagnosis of NSCLC.
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Biomarcadores de Tumor/metabolismo , Carcinoma de Pulmón de Células no Pequeñas/patología , Proteínas Portadoras/metabolismo , Neoplasias Pulmonares/patología , Proteínas de Unión a la Región de Fijación a la Matriz/genética , MicroARNs/genética , Proteínas de Microfilamentos/metabolismo , ARN Circular/genética , Factores de Transcripción/genética , Apoptosis , Biomarcadores de Tumor/genética , Carcinoma de Pulmón de Células no Pequeñas/genética , Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Proteínas Portadoras/genética , Movimiento Celular , Proliferación Celular , Progresión de la Enfermedad , Regulación Neoplásica de la Expresión Génica , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/metabolismo , Proteínas de Microfilamentos/genética , Pronóstico , Células Tumorales CultivadasRESUMEN
In this study, Co nanoparticle-embedded N,O-codoped porous carbon nanospheres (C@Co) with abundant N and O doping, high graphitization, large specific surface area (319 m2 g-1) and a well-developed mesoporous structure were synthesized and characterized thoroughly, and were applied to activate peroxymonosulfate (PMS) for the degradation of methylene blue (MB). Various influential factors affecting the catalytic performance including C@Co dosage, PMS dosage, MB concentration, initial pH, temperature, and co-existing common anions and humic acid (HA) on the MB degradation were systematically investigated. The increase of the C@Co dosage (15-60 mg), PMS dosage (25-100 mg) and reaction temperature (278-308 K) promoted the MB degradation in the C@Co/PMS system. The best performance of the C@Co/PMS system was observed under weakly acidic or nearly neutral conditions. Both the MB concentration (25-100 mg L-1) and Cl- (5-100 mM), NO3- (10-500 mM), CO32- (10-300 mM), HCO3- (1-30 mM) and HA (2-40 mg L-1) had an inhibitory effect on MB degradation, and the degree of decrease in MB degradation increased as their concentrations were enhanced. Interestingly, HPO42- (1-100 mM) had an overall inhibitory effect on the degradation process of MB; however, in comparison with lower concentrations (1-10 mM), an attenuation of the inhibitory effect at higher concentrations (50-100 mM) could be observed. Moreover, the C@Co/PMS system also exhibited general applicability in eliminating various organic pollutants from water such as methyl orange, malachite green, safranine T, Congo red, Rhodamine B, ofloxacin and tetracycline. Classical radical-quenching tests and EPR measurements showed that both the non-radical pathway (major route, involving 1O2) and radical pathway (minor route, involving ËOH, ËSO4- and ËO2-) contribute to the MB degradation. DFT calculations disclosed that the combination of Co-C interactions with graphitic N doping brought in catalytically active sites in C@Co where the charge states of some C atoms were significantly increased. The degradation intermediates of MB during the catalytic reaction were also identified by HPLC-MS and the possible degradation pathway was proposed. Overall, the resultant C@Co can be developed as a novel and efficient heterogeneous catalyst for activating PMS to degrade organic pollutants, and has potential application in environmental remediation.
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BACKGROUND: ST-segment elevation (STE) and an increased Tpeak-Tend interval (Tp-e) have prognostic value for malignant arrhythmia events (MAEs) in patients with ST-segment elevation myocardial infarction (STEMI) and Brugada syndrome. Whether STE could predict MAEs and has an electrophysiological relationship with Tp-e in electrocardiogram (ECG) of vasospastic angina (VA) patients needs to be elucidated. METHODS: Sixty-five patients with VA and 23 patients with VA complicated by MAEs were enrolled. The relationship of ECG parameters and MAEs (defined as ventricular tachycardia/ventricular fibrillation (VT/VF), syncope, and aborted sudden death) was analyzed by t-test, regression and receiver operating characteristic (ROC) curve analyses. RESULTS: Patients with MAEs showed greater STE (P<0.001) and corrected QT dispersion (cQTd) (P=0.021), a longer corrected Tp-e interval (cTp-e) (P<0.001), and a larger Tp-e/QT ratio (P<0.001) than those in non-MAE groups. Univariate analysis revealed that cQTd (odds ratio (OR)=1.065; P=0.020), cTp-e (OR=1.159; P=0.001), Tp-e/QT (OR=1.344, P=0.002), and STE (OR=5.655, P<0.001) were significantly associated with MAEs. In the multivariate analysis, Tp-e/QT and STE remained predictors of MAEs. ROC curve analysis showed that the areas under curve (AUCs) for Tp-e/QT (AUC=0.944) and STE (AUC=0.974) were not significantly different (P>0.05), but both were significantly different than AUCs for cQTd (AUC=0.724) and cTp-e (AUC=0.841) (all P<0.05). STE was well fitted with the Tp-e/QT ratio in a multivariable linear regression model. CONCLUSIONS: STE and increased Tp-e/QT ratio had related electrophysiological properties and were independent prognostic indicators of MAEs in patients with VA.
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Angina Pectoris Variable/fisiopatología , Arritmias Cardíacas/fisiopatología , Síndrome de Brugada/fisiopatología , Vasoespasmo Coronario/fisiopatología , Electrocardiografía , Infarto del Miocardio con Elevación del ST/fisiopatología , Adulto , Anciano , Angina Pectoris Variable/complicaciones , Arritmias Cardíacas/etiología , Síndrome de Brugada/complicaciones , Angiografía Coronaria , Vasoespasmo Coronario/complicaciones , Muerte Súbita Cardíaca/etiología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Pronóstico , Factores de Riesgo , Infarto del Miocardio con Elevación del ST/complicacionesRESUMEN
PURPOSE: Previous studies have evaluated intra-study heterogeneities of heart failure with preserved ejection fraction (HFpEF), but inter-study heterogeneities remain poorly understood. We investigate the heterogeneities of outcomes among control groups of HFpEF trials. METHODS: We included randomized controlled trials recruiting HFpEF patients with ejection fraction ≥ 40% and reporting Kaplan-Meier curves for at least 36 months. The Kaplan-Meier curves of control groups were extracted and calculated for hazard ratios and 95% confidence intervals. Two virtual trials were developed to validate the reliability and accuracy of our method. RESULTS: Of 4161 studies, we included six trials containing 7682 HFpEF patients in control groups. The DIG trial had the highest all-cause mortality, cardiovascular mortality, heart failure mortality, and composite endpoints of cardiovascular mortality and heart failure hospitalization (all p < 0.001). The TOPCAT trial had the lowest all-cause mortality, cardiovascular mortality, heart failure hospitalization, and composite of cardiovascular mortality and heart failure hospitalization (all p < 0.001). Adoption of different ejection fraction cut-off values for HFpEF diagnosis did not significantly change the outcomes of control groups in the DIG trial (45% vs. 50%: hazard ratio, 1.05, 95% confidence interval, 0.97-1.13, p = 0.271), or in the CHARM-Preserved trial (40% vs. 50%: hazard ratio, 1.01, 95% confidence interval, 0.93-1.09, p = 0.864) during 36-month follow-up. CONCLUSIONS: The control groups of HFpEF trials have heterogeneous outcomes. Future trials should consider these heterogeneities when designing protocols.
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Insuficiencia Cardíaca/terapia , Ensayos Clínicos Controlados Aleatorios como Asunto/métodos , Proyectos de Investigación , Volumen Sistólico , Función Ventricular Izquierda , Anciano , Causas de Muerte , Interpretación Estadística de Datos , Determinación de Punto Final , Femenino , Insuficiencia Cardíaca/diagnóstico , Insuficiencia Cardíaca/mortalidad , Insuficiencia Cardíaca/fisiopatología , Hospitalización , Humanos , Estimación de Kaplan-Meier , Masculino , Ensayos Clínicos Controlados Aleatorios como Asunto/estadística & datos numéricos , Reproducibilidad de los Resultados , Proyectos de Investigación/estadística & datos numéricos , Factores de Riesgo , Factores de Tiempo , Resultado del TratamientoRESUMEN
PURPOSE: Sepsis is characterized by an acute inflammatory response to infection, often with multiple organ failures, especially severe lung injury. This study was implemented to probe circular RNA (circRNA) protein tyrosine kinase 2 (circPTK2)-associated regulatory mechanisms in septic acute lung injury (ALI). METHODS: A cecal ligation and puncture-based mouse model and an lipopolysaccharides (LPS)-based alveolar type II cell (RLE-6TN) model were generated to mimic sepsis. In the two models, inflammation- and pyroptosis-related genes were measured. RESULTS: The degree of lung injury in mice was analyzed by hematoxylin and eosin (H&E) staining and the apoptosis was by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining. In addition, pyroptosis and toxicity were detected in cells. Finally, the binding relationship between circPTK2, miR-766, and eukaryotic initiation factor 5A (eIF5A) was detected. Data indicated that circPTK2 and eIF5A were up-regulated and miR-766 was down-regulated in LPS-treated RLE-6TN cells and lung tissue of septic mice. Lung injury in septic mice was ameliorated after inhibition of circPTK2. CONCLUSIONS: It was confirmed in the cell model that knockdown of circPTK2 effectively ameliorated LPS-induced ATP efflux, pyroptosis, and inflammation. Mechanistically, circPTK2 mediated eIF5A expression by competitively adsorbing miR-766. Taken together, circPTK2/miR-766/eIF5A axis ameliorates septic ALI, developing a novel therapeutic target for the disease.
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Lesión Pulmonar Aguda , MicroARNs , Sepsis , Animales , Ratones , Piroptosis , ARN Circular/genética , ARN Circular/farmacología , Quinasa 1 de Adhesión Focal/farmacología , Lipopolisacáridos/efectos adversos , Pulmón/metabolismo , Apoptosis , Lesión Pulmonar Aguda/metabolismo , Sepsis/genética , Factores de Iniciación de Péptidos/farmacología , MicroARNs/genética , MicroARNs/metabolismo , Adenosina Trifosfato/farmacologíaRESUMEN
OBJECTIVES: To systematically estimate the global prevalence of burnout among nursing students, and examine the associated factors of burnout in this population. DESIGN: A systematic review and meta-analysis. REVIEW METHODS AND DATA SOURCES: PubMed, Embase, Web of Science, and CINAHL were searched from inception to June 30th, 2022. Two researchers independently screened studies, extracted data and assessed the quality of included studies. The random-effects model was used to estimate the global prevalence of burnout among nursing students. Subgroup analysis, meta-regression analysis, publication bias, and sensitivity analysis were also conducted. RESULTS: A total of 21 studies were included, involving 10,861 nursing students. In the random-effects model, the pooled prevalence of burnout was 23.0 % (95 % CI = 15.6-30.5 %) in nursing students. The pooled prevalence of emotional exhaustion, depersonalization, and reduced personal accomplishment was 47.1 %, 32.2 %, and 43.5 %, respectively. Main associated factors of burnout included demographic (e.g., age and grade), educational (e.g., workload, academic satisfaction, and incivility experience), physical (e.g., sleep quality and physical activity), and psychological (e.g., self-efficacy and personality traits) factors. CONCLUSIONS: Burnout is common in nursing students, with demographic, educational, physical, and psychological factors affecting their burnout. Early screening of burnout and interventions to prevent and reduce burnout should be considered for nursing students.
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Agotamiento Profesional , Estudiantes de Enfermería , Humanos , Prevalencia , Estudiantes de Enfermería/psicología , Agotamiento Profesional/epidemiología , Agotamiento Profesional/psicología , Agotamiento Psicológico , EmocionesRESUMEN
Benzo [a]pyrene (B [a]P) is a widespread environmental chemical pollutant that has been linked to the development of various diseases. However, the specific mechanism of action remains unclear. In this study, human bronchial epithelial 16HBE and BEAS-2B cells were exposed to B [a]P at 0-32 µM to assess the DNA-damaging effects. B [a]P exposure resulted in elevated expression of γ-H2AX, a marker of DNA damage. The m6A RNA methylation assay showed that B [a]P exposure increased the extent of m6A modification and the demethylase ALKBH5 played an integral role in this process. Moreover, the results of the comet assay and Western blot analysis showed an increase in m6A modification mediated by ALKBH5 that promoted DNA damage. Furthermore, the participation of a novel circular RNA, circ_0003552, was assessed by high-throughput sequencing under the condition of high m6A modification induced by B [a]P exposure. In subsequent functional studies, an interference/overexpression system was created to confirm that circ_0003552 participated in regulation of DNA damage. Mechanistically, circ_0003552 had an m6A binding site that could regulate its generation. This study is the first to report that B [a]P upregulated circ_0003552 through m6A modification, thereby promoting DNA damage. These findings revealed that epigenetics played a key role in environmental carcinogen-induced DNA damage, and the quantitative changes it brought might provide an early biomarker for future medical studies of genetic-related diseases and a new platform for investigations of the interaction between epigenetics and genetics.
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The health hazards of nanoparticles of neodymium oxide (NPs-Nd2O3) have aroused public concern in recent years. Exposure to NPs-Nd2O3 can change the level of reactive oxygen species (ROS) that cause DNA damage and alter whole transcriptome expression profiles for micro (mi)RNA, circular (circ)RNA, long noncoding (lnc)RNA, and mRNA. However, there have been no reports to our knowledge about the role of circRNAs in DNA damage caused by NPs-Nd2O3. In our study, we analyzed the circRNA expression profile of human bronchial epithelial cells(16HBE)exposed to 40 µg/ml NPs-Nd2O3. Our results indicated that exposure produced 1025 up-regulated and 890 down-regulated circRNAs. Real-time quantitative polymerase chain reaction (qRT-PCR) was applied to verify some of the significantly changed circRNAs and demonstrated that circ_009773 was apparently down-regulated. Through exploration of its host gene function, we found that circ_009773 may be related to DNA damage. Functional experiments found that circ_009773 regulated NPs-Nd2O3-induced DNA damage in 16HBE cells. A circ_009773-associated competing endogenous (ce)RNA network was constructed based on one differentially expressed (DE) circRNA, 74 DE miRNAs and 208 DE mRNAs. Module analysis identified hub genes related to DNA damage and repair and a protein-protein interaction (PPI) network was created.
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Daño del ADN/genética , Nanopartículas/toxicidad , Neodimio/toxicidad , Óxidos/toxicidad , ARN Circular/metabolismo , Bronquios/efectos de los fármacos , Línea Celular , Células Epiteliales/efectos de los fármacos , Perfilación de la Expresión Génica , Redes Reguladoras de Genes , Humanos , ARN Circular/genética , Análisis de Secuencia de ARNRESUMEN
Exposure to high concentrations of copper is associated with pulmonary inflammation and chronic respiratory disease (CRD). Epigenetic modulation of noncoding RNAs contributes to the development of several CRDs. It is unknown whether epigenetic modulation is involved in copper mediated pulmonary inflammation and CRD. We conducted a case-control study of 101 CRD cases and 161 control subjects in Shijiazhuang, China, and evaluated circRNAs and cytokine levels (IL-6 and IL-8) by qPCR and ELISA. Urinary copper concentration was determined by inductively coupled plasma mass spectrometry. Linear mixed models and generalized linear mixed models were used to assess the associations of circRNAs with CRD, urinary copper, and cytokines. We exposed the human bronchial epithelial cell line, 16HBE, to copper and assessed the functional role of a circRNA, circ_0008882, by RNA overexpression. Cellular location of circ_0008882 was assessed by separation of nuclear and cytoplasmic RNAs. Nine circRNAs were associated with an increased risk for CRDs, while the relative expression of circ_0008882 was decreased after copper exposure in vitro and in vivo. Copper exposure stimulated 16HBE cells to release proinflammatory IL-6 and IL-8. The release of the cytokines was inhibited by overexpression of circ_0008882. These results suggest a role for circ_0008882 in the regulation of CRD associated inflammation following copper exposure.
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MicroARNs , Neumonía , Trastornos Respiratorios , Estudios de Casos y Controles , Enfermedad Crónica , Cobre/toxicidad , Citocinas , Humanos , Interleucina-6/metabolismo , Interleucina-8 , MicroARNs/genética , ARN/genética , ARN Circular/genética , Trastornos Respiratorios/inducido químicamenteRESUMEN
Coronary heart disease (CHD) is one of the most vital reasons for death and disability all over the world. miRNA, as a plasma index, is quite valuable for disease screening and prognosis prediction in CHD. Mining the molecular mechanism behind miRNA is also helpful for us to find molecular therapeutic strategies. In this research, we found that the expression of plasma miR-30c-5p in CHD patients was obviously lower than that in the control group (CG), which had a high differential value for CHD. We also discovered that miR-30c-5p was obviously correlated with clinical characteristics of CHD patients such as age, NYHA grade, smoking history, hypertension, hyperlipidemia, etc. In prognosis analysis, the miR-30c-5p expression in patients with poor prognosis was dramatically lower than that in those with good one, and the AUC for predicting poor prognosis of CHD was not lower than 0.850. In addition, we also induced myocardial ischemia/reperfusion (I/R) injury model of H9C2 cells through hypoxia/reoxygenation, and found that H9C2 cells also had abnormally down-regulated miR-30c-5p and up-regulated BCL2-like 11 (BCL2L11). Up-regulating miR-30c-5p or down-regulating BCL2L11 were helpful to improve proliferation and apoptosis of I/R injury model. Mechanically, BCL2L11 was also negatively regulated by miR-30c-5p, and up-regulating the former could cancel the in vitro protective effect of up-regulating the latter on H9C2 cell I/R injury model. In vivo research, up-regulating miR-30c-5p or down-regulating BCL2L11 can improve myocardial injury, histopathological changes and apoptosis in rat I/R model.
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The Mg/Al hydrotalcite (Mg/Al HT) was firstly used as a heterogeneous ozonation catalyst and 2,4-dichlorophenoxyacetic acid (2,4-D) was efficiently degraded by Mg3/Al HT with a COD removal of 68 %. It was higher than that of α-FeOOH with a COD removal of 50 %. The effects of Mg/Al atomic ratio, phosphate and pyrrole on the ozonation performance of Mg/Al HTs were also investigated. The X-ray photoelectron spectroscopy (XPS), nitrogen adsorption-desorption experiment and temperature programmed desorption of adsorbed CO2 or NH3 were used to characterize the surface properties of Mg/Al HT. The surface acidity and basity was proven to be responsible to the excellent ozonation activity of Mg/Al HT. The results of electron spin resonance (ESR) analysis and probe experiments confirmed that OH, O2- and 1O2 were involved in the 2,4-D degradation process and their contributions are as followed: OH > O2- > 1O2. The synergistic effect of surface acid (ozone adsorption center) and base sites (catalytic center) determines Mg/Al HT in the enhanced catalytic ozone decomposition into reactive species. More important, the transition metal free based Mg/Al HTs is steady, non-toxic, naturally abundant and environment friendly, which provided a promising alternative in practical water treatment by catalytic ozonation.
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Long-term exposure to particulate matter 2.5 (PM2.5) is closely related to the occurrence and development of airway inflammation. Exploration of the role of PM2.5 in inflammation is the first step towards clarifying the harmful effects of particulate pollution. However, the molecular mechanisms underlying PM2.5-induced airway inflammation are yet to be fully established. In this study, we focused on the specific roles of non-coding RNAs (ncRNAs) in PM2.5-induced airway inflammation. In a human bronchial epithelial cell line, BEAS-2B, PM2.5 at a concentration of 75 µg/mL induced the inflammatory response. Microarray and quantitative real-time polymerase chain reaction (qRT-PCR) analyses revealed significant upregulation of circRNA104250 and lncRNAuc001.dgp.1 during the PM2.5-induced inflammatory response in this cell line. Data from functional analyses further showed that both molecules promote an inflammatory response. CircRNA104250 and lncRNAuc001.dgp.1 target miR-3607-5p and affect expression of interleukin 1 receptor 1 (IL1R1), which influences the nuclear factor κB (NF-κB) signaling pathway. In summary, we have uncovered an underlying mechanism of airway inflammation by PM2.5 involving regulation of ncRNA for the first time, which provides further insights into the toxicological effects of PM2.5.
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Contaminantes Atmosféricos/efectos adversos , Células Epiteliales/efectos de los fármacos , MicroARNs/genética , ARN Circular/genética , ARN Largo no Codificante/genética , Bronquios/citología , Línea Celular , Humanos , Inflamación , FN-kappa B , Material Particulado/efectos adversos , Receptores Tipo I de Interleucina-1RESUMEN
Fine particulate matter (PM2.5) has been verified to augmented the incidence of pneumonia, asthma, pulmonary fibrosis, and other pulmonary diseases. Airway inflammation is the pathological basis of the respiratory system, and understanding the molecular mechanisms responsible for airway inflammation may thus support the diagnosis and treatment of respiratory diseases. In our study, human bronchial epithelial cells (BEAS-2B) were exposed to various concentrations of PM2.5 for 48 h. PM2.5 entered the cells, resulting in increased production of interleukin 6 (IL-6) and interleukin 8 (IL-8) and decreased the expression of circular RNA 406961 (circ_406961). Further, PM2.5 with a concentration of 75 µg/mL was applied to mechanism study. Functional experiments further confirmed that circ_406961 inhibited PM2.5-induced BEAS-2B cell inflammation. RNA pull-down and mass spectrometry showed that circ_406961 interacted with interleukin enhancer-binding factor 2 (ILF2), which could regulate phosphorylation of signal transducer and activator of transcription 3 (STAT3) and mitogen-activated protein kinase 8 (MAPK8, JNK). Our studies showed that circ_406961 inhibited activation of STAT3/JNK pathways via interacting with ILF2 protein, thereby inhibiting the PM2.5-induced inflammatory reaction.
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Sistema de Señalización de MAP Quinasas , ARN Circular , Bronquios , Células Epiteliales , Humanos , Proteína del Factor Nuclear 45 , Material Particulado/toxicidad , Factor de Transcripción STAT3RESUMEN
Fine particulate matter (PM2.5) is one of the most important components of environmental pollutants, and is associated with pulmonary injury. However, the biological mechanisms of pulmonary damage caused by PM2.5 are poorly defined, especially the molecular pathways related to inflammation. Following system exposure to PM2.5 for 3 months in normal mice and in chronic obstructive pulmonary disease (COPD) model mice, it was found that PM2.5 exposure increased the expression of IL-1ß and IL-18 in lung tissues via NLRP3 activation, and these effects were more intense in COPD model mice. Circular RNA (circRNA) sequencing showed that the expression profiles of circRNAs were changed after PM2.5 exposure, and the positive roles of circBbs9 in inflammation induced by PM2.5 were verified. The circBbs9 knockdown alleviated PM2.5-induced inflammation via NLRP3 inflammasome inactivation, as well as IL-1ß and IL-18 inhibition in RAW264.7 cells, while overexpression of circBbs9 had the opposite effect. Bioinformatics and luciferase reporter assays showed that circBbs9 bound to microRNA-30e-5p (miR-30e-5p) and co-regulated the expression of Adar, a downstream target gene of miR-30e-5p. Taken together, these results revealed that PM2.5 induced pulmonary inflammation through NLRP3 inflammasome activation regulated by the circBbs9-miR-30e-5p-Adar pathway. Our findings provide a new target, circBbs9, for the assessment of lung inflammation and COPD exacerbation induced by PM2.5 exposure.
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Inflamasomas , Neumonía , Animales , Inflamación/inducido químicamente , Ratones , Proteína con Dominio Pirina 3 de la Familia NLR/genética , Material Particulado/toxicidad , Neumonía/inducido químicamente , ARN CircularRESUMEN
AimsStem cell-derived extracellular vesicles (EVs) have emerged as a promising therapy for myocardial infarction, but its effects remain incompletely understood. We aim to systematically review the efficacy of EVs on myocardial infarction in both small and large animals.MethodsOn April 5, 2018, we searched the PubMed, Embase and Web of Science databases using variations of "myocardial infarction" and "extracellular vesicle". Controlled studies about the treatment effects of stem cell-derived EVs in myocardial infarction animal model were included. Meta-regression analysis was used to reveal the factors affecting the EVs treatments.ResultsOf 1210 studies retrieved, 24 were eligible for meta-analysis. EVs injection was associated with the improvements of left ventricular ejection fraction (12.65%), fractional shortening (7.54%) and the reduction of infarct size/area at risk (-15.55%). Meta-regression analysis did not reveal the association between treatment efficacy and type of stem cell, ligation-to-injection interval, route of delivery, dosage of delivery or follow-up period (all P values > 0.05). The median quality score of eligible studies was only 1, indicating potential risks of bias.ConclusionStem cell-derived EVs improve cardiac function and reduce infarct size in myocardial infarction animals, but current pool-up study reveals no associations between common factors and treatment effects.
Asunto(s)
Vesículas Extracelulares/fisiología , Infarto del Miocardio/metabolismo , Células Madre/fisiología , AnimalesRESUMEN
Purpose: Sepsis is characterized by an acute inflammatory response to infection, often with multiple organ failures, especially severe lung injury. This study was implemented to probe circular RNA (circRNA) protein tyrosine kinase 2 (circPTK2)-associated regulatory mechanisms in septic acute lung injury (ALI). Methods: A cecal ligation and puncture-based mouse model and an lipopolysaccharides (LPS)-based alveolar type II cell (RLE-6TN) model were generated to mimic sepsis. In the two models, inflammation- and pyroptosisrelated genes were measured. Results: The degree of lung injury in mice was analyzed by hematoxylin and eosin (H&E) staining and the apoptosis was by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining. In addition, pyroptosis and toxicity were detected in cells. Finally, the binding relationship between circPTK2, miR-766, and eukaryotic initiation factor 5A (eIF5A) was detected. Data indicated that circPTK2 and eIF5A were up-regulated and miR-766 was down-regulated in LPS-treated RLE-6TN cells and lung tissue of septic mice. Lung injury in septic mice was ameliorated after inhibition of circPTK2. Conclusion: It was confirmed in the cell model that knockdown of circPTK2 effectively ameliorated LPS-induced ATP efflux, pyroptosis, and inflammation. Mechanistically, circPTK2 mediated eIF5A expression by competitively adsorbing miR-766. Taken together, circPTK2/ miR-766/eIF5A axis ameliorates septic ALI, developing a novel therapeutic target for the disease.