Enhanced Stable and Efficient of Dual-Ligand Zirconium-Based Metal-Organic Frameworks for Synergistic Photodynamic Inactivation.

Porphyrins, known for generating toxic singlet oxygen (1O2) to combat bacteria, face challenges such as hydrophilicity and limited lifespan and 1O2 yield. Conversely, triterpenoid compounds like ammonium glycyrrhizinate (AG) offer antioxidative and antibacterial properties but lack efficacy and stability. Combining them in Metal-Organic Frameworks (MOFs) yields dual-ligand zirconium (Zr)-basedMOFs (M-TG), capitalizing on porphyrins' membrane-disrupting ability and AG's inhibition of bacterial membrane synthesis for a synergistic antibacterial effect. M-TG resolves activity loss, enhances reactive oxygen species (ROS) yield, and extends stability, achieving a remarkable 99.999% sterilization rate. This innovative approach maximizes ligand properties through synergistic effects, promising significant advancements in antibacterial material design.

Associations of ambient air pollution with incidence and dynamic progression of atrial fibrillation.

The influence of air pollution on dynamic changes in clinical state from healthy to atrial fibrillation (AF), further AF-related complications and ultimately, death are unclear. We aimed to investigate the relationships between air pollution and the occurrence and progression trajectories of AF. We retrieved 442,150 participants free of heart failure (HF), myocardial infarction (MI), stroke and dementia at baseline from UK Biobank. Exposures to air pollution for each transition stage were estimated at the geocoded residential address of each participant using the bilinear interpolation approach. The outcomes were incident AF, complications, and death. Multi-stage models were used to evaluate the associations between air pollution and dynamic progression of AF. Over a 12.6-year median follow-up, a total of 21,670 incident AF patients were identified, of whom, 4103 developed complications and 1331 died. PM2.5, PM10, NOx and NO2 were differentially positively associated, while O3 was negatively associated with risks of progression trajectories of AF. PM2.5 exposure was significantly associated with an increased risk of progression. The associations of PM2.5, PM10, NOx, and NO2 on incident AF were generally more pronounced compared to other transitions. The cumulative transition probabilities were generally higher in individuals with higher exposure levels of PM2.5, PM10, NOx, and NO2 and lower exposure to O3. Air pollution could potentially have a role in increasing the risk of both the occurrence and progression of AF, emphasizing the significance of air pollution interventions in both the primary prevention of AF and the management of AF-related outcomes.

Xiaoqinglong decoction mitigates nasal inflammation and modulates gut microbiota in allergic rhinitis mice.

Introduction: Allergic rhinitis (AR) is a respiratory immune system disorder characterized by dysregulation of immune responses. Within the context of AR, gut microbiota and its metabolites have been identified as contributors to immune modulation. These microorganisms intricately connect the respiratory and gut immune systems, forming what is commonly referred to as the gut-lung axis. Xiaoqinglong Decoction (XQLD), a traditional Chinese herbal remedy, is widely utilized in traditional Chinese medicine for the clinical treatment of AR. In this study, it is hypothesized that the restoration of symbiotic microbiota balance within the gut-lung axis plays a pivotal role in supporting the superior long-term efficacy of XQLD in AR therapy. Therefore, the primary objective of this research is to investigate the impact of XQLD on the composition and functionality of the gut microbiota in a murine model of AR. Methods: An ovalbumin-sensitized mouse model to simulate AR was utilized, the improvement of AR symptoms after medication was investigated, and high-throughput sequencing was employed to analyze the gut microbiota composition. Results: XQLD exhibited substantial therapeutic effects in AR mice, notably characterized by a significant reduction in allergic inflammatory responses, considerable alleviation of nasal symptoms, and the restoration of normal nasal function. Additionally, following XQLD treatment, the disrupted gut microbiota in AR mice displayed a tendency toward restoration, showing significant differences compared to the Western medicine (loratadine) group. Discussion: This results revealed that XQLD may enhance AR allergic inflammatory responses through the regulation of intestinal microbiota dysbiosis in mice, thus influencing the dynamics of the gut-lung axis. The proposal of this mechanism provides a foundation for future research in this area.

Recognition and detection of histamine in foods using aptamer modified fluorescence polymer dots sensors.

Histamine has been known as a momentous cause of biogenic amine poisoning. Therefore, the content of histamine in foods is strictly required to be controlled within a certain range. Here, an aptamer fluorescent sensor was developed for detection of histamine. Poly [(9, 9-di-n-octylfluorenyl-2, 7-diyl)-alt-(benzo [2,1,3] thiadia-zol-4, 8-diyl)] (PF8BT) and the styrene maleic anhydride copolymer (PSMA) were used for the preparation of PF8BT-Polymer dots (PF8BT-Pdots). PF8BT-Pdots and the cyanine3-phosphoramidite (Cy3) were linked through aptamer to achieve the ratiometric detection for histamine. PF8BT-Pdots were partly quenched by Cy3 due to the fluorescence resonance energy transfer (FRET), when the histamine molecule was recognized by aptamer on the surface of PF8BT-Pdots. A linear range (3-21 µmol/L) was obtained for histamine detection with a low limit of detection (LOD = 0.38 µmol/L). PF8BT aptamer Pdots (PF8BT-A) were used to detect histamine in simply treated aquaculture water and tuna. The cell imaging of HeLa cells presented a good biosecurity and outstanding fluorescent imaging capability of PF8BT-A. The aptamer fluorescent sensors provided a new platform for rapid and accurate detection of histamine in aquatic products and had great potential for the application in food safety and quality control.

Air pollution, APOE genotype and risk of dementia among individuals with cardiovascular diseases: A population-based longitudinal study.

Individuals with cardiovascular disease (CVD) are particularly vulnerable to dementia, but it remains unclear whether air pollution exposure links with higher risk of dementia among those with CVD. The data were derived from the UK Biobank study (UKB). Dementia-free participants with CVD at baseline were included. Air pollution exposure was assessed through land use regression models, including particulate matter (PM2.5, PM2.5-10, and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX). A Cox proportional hazards model was used to investigate the associations between air pollution exposure and incident dementia among individuals with CVD. Air pollution was associated with dementia among individuals with CVD, and the hazard ratios of dementia associated with each interquartile range (IQR) µg/m3 increase in air pollution were 1.07 (95% CI: 1.02, 1.12) for PM2.5, 1.10 (95% CI: 1.04, 1.15) for PM10, 1.08 (95% CI: 1.03, 1.14) for NO2 and 1.05 (95% CI: 1.00, 1.09) for NOx. Associations between air pollution and all-cause dementia were found to be significant among individuals with hypertension. Adverse effects of air pollution were also observed for Alzheimer's dementia (AD) and vascular dementia (VaD), with a higher effect for AD. Observed associations remained similar in subgroups of APOE ε4 carriers and noncarriers, although there was a higher risk difference across different air pollution concentration among these individuals carrying APOE ε4. Air pollution emerges as a critical risk factor for dementia among individuals with CVD, regardless of genetic susceptibility indicated by the APOE genotype. Notably, individuals with hypertension might be susceptible to the adverse effects of air pollution, leading to a higher incidence of dementia. Understanding these impacts on dementia among individuals with CVD may promote better targeted prevention and clinical management strategies.

Ambient fine particulate matter chemical composition associated with in-hospital case fatality, hospital expenses, and length of hospital stay among patients with heart failure in China.

*Joint senior authorship. BACKGROUND: Previous studies have observed the adverse effects of ambient fine particulate matter pollution (PM2.5) on heart failure (HF). However, evidence regarding the impacts of specific PM2.5 components remains scarce. METHODS: We included 58 129 patients hospitalised for HF between 2013 and 2017 in 11 cities of Shanxi, China from inpatient discharge database. We evaluated exposure to PM2.5 and its components ((sulphate (SO42-), nitrate (NO3-), ammonium (NH4+), organic matter (OM) and black carbon (BC)), along with meteorological factors using bilinear interpolation at each patients' residential address. We used multivariable logistic and linear regression models to assess the associations of these components with in-hospital case fatality, hospital expenses, and length of hospital stay. RESULTS: Increase equivalents to the interquartile range (IQR) in OM (odds ratio (OR) = 1.13; 95% confidence interval (CI) = 1.02, 1.26) and BC (OR = 1.14; 95% CI = 1.02, 1.26) were linked to in-hospital case fatality. Per IQR increments in PM2.5, SO42-, NO3-, OM, and BC were associated with cost increases of 420.62 (95% CI = 285.75, 555.49), 221.83 (95% CI = 96.95, 346.71), 214.93 (95% CI = 68.66, 361.21), 300.06 (95% CI = 176.96, 423.16), and 303.09 (95% CI = 180.76, 425.42) CNY. Increases of 1 IQR in PM2.5, SO42-, OM, and BC were associated with increases in length of hospital stay of 0.10 (95% CI = 0.02, 0.19), 0.09 (95% CI = 0.02, 0.17), 0.10 (95% CI = 0.03, 0.17), and 0.16 (95% CI = 0.08, 0.23) days. CONCLUSIONS: Our findings suggest that ambient SO42-, OM, and BC might be significant risk factors for HF, emphasising the importance of formulating customised guidelines for the chemical constituents of PM and controlling the emissions of the most dangerous components.

Alizarin complexone modified UiO-66-NH2 as dual-mode colorimetric and fluorescence pH sensor for monitoring perishable food freshness.

Food prone to spoilage has a huge food safety hazard, threatening people's health, so early detection of food spoilage is a continuous and urgent need. Herein, we developed a dual-mode response sensor, alizarin complexone@UiO-66-NH2, which can accurately detect pH. The sensor demonstrated significant changes in color from pale yellow to deep pink, while the fluorescence shifted from light blue to blue violet. Moreover, both UV absorption and fluorescence intensity showed a linear correlation with pH raging from 4.5 to 7.5. These results indicate that the sensor effectively responds to pH, making it suitable for detecting the freshness of perishable food. To put this into practice, we integrated the sensor with cellulose-based filter paper to determine the freshness of shrimp and beef, which was proved to be effective in assessing freshness. In the future, it can be combined with intelligent colorimetric and fluorescence instruments to achieve visual detection.

Initial Upper Palaeolithic material culture by 45,000 years ago at Shiyu in northern China.

The geographic expansion of Homo sapiens populations into southeastern Europe occurred by ∼47,000 years ago (∼47 ka), marked by Initial Upper Palaeolithic (IUP) technology. H. sapiens was present in western Siberia by ∼45 ka, and IUP industries indicate early entries by ∼50 ka in the Russian Altai and 46-45 ka in northern Mongolia. H. sapiens was in northeastern Asia by ∼40 ka, with a single IUP site in China dating to 43-41 ka. Here we describe an IUP assemblage from Shiyu in northern China, dating to ∼45 ka. Shiyu contains a stone tool assemblage produced by Levallois and Volumetric Blade Reduction methods, the long-distance transfer of obsidian from sources in China and the Russian Far East (800-1,000 km away), increased hunting skills denoted by the selective culling of adult equids and the recovery of tanged and hafted projectile points with evidence of impact fractures, and the presence of a worked bone tool and a shaped graphite disc. Shiyu exhibits a set of advanced cultural behaviours, and together with the recovery of a now-lost human cranial bone, the record supports an expansion of H. sapiens into eastern Asia by about 45 ka.

EPO promotes the progression of rheumatoid arthritis by inducing desialylation via increasing the expression of neuraminidase 3.

OBJECTIVE: Erythropoietin (EPO) known as an erythrocyte-stimulating factor is increased in patients with rheumatoid arthritis (RA). Nevertheless, the function of EPO in the process of RA and relative mechanism needs to be further clarified. METHODS: The level of EPO in serum and synovial fluid from patients with RA and healthy controls was determined by . Collagen-induced arthritis (CIA) mice were constructed to confirm the role of EPO on RA pathogenesis. Differentially expressed genes (DEGs) of EPO-treated fibroblast-like synoviocyte (FLS) were screened by transcriptome sequencing. The transcription factor of neuraminidase 3 (NEU3) of DEGs was verified by double luciferase reporting experiment, DNA pulldown, electrophoretic mobility shift assay and chromatin immunoprecipitation-quantitative PCR (qPCR) assay. RESULTS: The overexpression of EPO was confirmed in patients with RA, which was positively associated with Disease Activity Score 28-joint count. Additionally, EPO intervention could significantly aggravate the joint destruction in CIA models. The upregulation of NEU3 was screened and verified by transcriptome sequencing and qPCR in EPO-treated FLS, and signal transducer and activator of transcription 5 was screened and verified to be the specific transcription factor of NEU3. EPO upregulates NEU3 expression via activating the Janus kinase 2 (JAK2)-STAT5 signalling pathway through its receptor EPOR, thereby to promote the desialylation through enhancing the migration and invasion ability of FLS, which is verified by JAK2 inhibitor and NEU3 inhibitor. CONCLUSION: EPO, as a proinflammatory factor, accelerates the process of RA through transcriptional upregulation of the expression of NEU3 by JAK2/STAT5 pathway.

Interactive effects of physical activity and sarcopenia on incident ischemic heart disease: Results from a nation-wide cohort study.

BACKGROUND AND AIMS: Lack of physical activity (PA) and sarcopenia is a known risk factors for ischemic heart disease (IHD). However, considering their coexistence in the middle-aged and elderly population, the interaction of these two factors remains uncertain. Here, we investigated the interactive effects of PA and sarcopenia on IHD. METHODS: We extracted 344,688 participants free of IHD at baseline from the UK Biobank. PA was classified into low, moderate, and high according to the International Physical Activity Questionnaire. Sarcopenia was identified in accordance with the European Working Group on Sarcopenia in Older People 2. Cox proportional hazard models were applied to estimate the effect of PA and sarcopenia on incident IHD and its subtypes. We also used objective PA data measured by wrist-worn devices to repeat these analyses. RESULTS: Over a median follow-up of 11.7 years, 24,809 (7.2%) participants developed incident IHD. Lack of PA was associated with a higher risk of IHD after adjusting for potential confounders. The hazard ratio (HR) was 1.09 (95% CI: 1.05-1.13) for individuals without sarcopenia and 1.29 (95% CI: 1.17-1.42) for those with sarcopenia. Regarding the joint effect, the combination of low PA and sarcopenia was associated with the highest risk of IHD, with an HR of 1.54 (95% CI: 1.44-1.66), and both additive and multiplicative interactions were significant (RERI 0.27, 95% CI: 0.14-0.39, p-interaction <0.01). For subtypes of IHD, the interaction was pronounced in acute myocardial infarction and chronic ischemic heart disease. CONCLUSIONS: These results suggest a synergistic interaction between lack of PA and sarcopenia on the risk of IHD. Findings from this study may help facilitate more effective primary prevention of IHD.

Sarcopenia and mild kidney dysfunction and risk of all-cause and cause-specific mortality in older adults.

BACKGROUND: Sarcopenia has been identified as a risk factor for increased mortality in individuals with CKD. However, when considering individuals with mild kidney dysfunction prior to CKD, the impact of sarcopenia on adverse outcomes, particularly mortality, remains uncertain. METHODS: This study included 323 801 participants from the UK Biobank. Mild kidney dysfunction was defined as eGFR between 60 and 89.9 mL/min/1.73 m2, and sarcopenia was defined according to the criteria of the 2019 European Working Group of Sarcopenia in Older People. Cox proportional hazard models with inverse probability weighting and competing risk models were used for analysis. RESULTS: During a median follow-up of 11.8 years, 20 146 participants died from all causes. Compared with participants with normal kidney function and without sarcopenia, those with mild kidney dysfunction or sarcopenia had significantly increased risks of all-cause mortality [hazard ratio (HR): 1.16, 95% confidence interval (CI): 1.12 to 1.19; HR: 1.29, 95% CI: 1.20 to 1.37]; those with both mild kidney dysfunction and sarcopenia had an even higher risk of all-cause mortality (HR: 1.61, 95% CI: 1.52 to 1.71), with a significant overall additive interaction (relative risk due to interaction 0.17, 95% CI: 0.05 to 0.29). Further subgroup analyses revealed that the associations of probable sarcopenia with all-cause and cause-specific mortality (non-accidental cause, non-communicable diseases, and cancer) were stronger among participants with mild kidney dysfunction than those with normal kidney function. CONCLUSIONS: The study indicates that sarcopenia and mild kidney dysfunction synergistically increase the risk of all-cause and cause-specific mortality. Early recognition and improvement of mild kidney function or sarcopenia in older people may reduce mortality risk but would require more prospective confirmation.

Recent Study of Separation and Identification of Micro- and Nanoplastics for Aquatic Products.

Micro- and nanoplastics (MNPs) are polymeric compounds widely used in industry and daily life. Although contamination of aquatic products with MNPs exists, most current research on MNPs focuses on environmental, ecological, and toxicological studies, with less on food safety. Currently, the extent to which aquatic products are affected depends primarily on the physical and chemical properties of the consumed MNPs and the content of MNPs. This review presents new findings on the occurrence of MNPs in aquatic products in light of their properties, carrier effects, chemical effects, seasonality, spatiality, and differences in their location within organisms. The latest studies have been summarized for separation and identification of MNPs for aquatic products as well as their physical and chemical properties in aquatic products using fish, bivalves, and crustaceans as models from a food safety perspective. Also, the shortcomings of safety studies are reviewed, and guidance is provided for future research directions. Finally, gaps in current knowledge on MNPs are also emphasized.

Perfect Talbot self-imaging effect of aperiodic gratings.

We propose and investigate a class of aperiodic grating structure which can achieve perfect Talbot effect under certain conditions. The aperiodic grating structure is obtained by the superposition of two or more sine terms. In the case of two sine terms, the Talbot effect can be realized when the period ratio of two terms is arbitrary. While in the case of more than two sine terms, the period ratios of each term must meet certain extra conditions. The theory has been further verified by numerical simulations. It expands the field of Talbot effect and is of potential significance for subsequent research applications such as optical imaging and measurement.

Ambient air pollution associated with incident asthma, subsequent cardiovascular disease and death: A trajectory analysis of a national cohort.

No previous study has examined the impact of air pollution on the cardiovascular disease (CVD) trajectory, especially among asthmatic subjects. Based on the UK Biobank cohort, we retrieved 292,227 adults free of asthma and CVD aged 37-73 years at recruitment (2006-2010). Annual mean concentrations of particulate matter (PM10 and PM2.5) and nitrogen oxides (NO2 and NOx) were assessed at each individual's addresses. We used multi-state models to estimate the associations of air pollution with the trajectory from healthy to incident asthma, subsequent CVD, and death. During a median follow-up of 11.7 years, a total of 6338 (2.2%) participants developed asthma, among which, 638 (10.1%) subsequently proceeded to CVD. We observed significant impacts of various air pollutants on the CVD dynamic transitions, with a more substantial effect of particulate matter pollutants than gaseous air pollutants. For example, the hazard ratios (95% confidence intervals) for per interquartile range increase in PM2.5 and PM10 were 1.28 (1.13, 1.44) and 1.27 (1.13, 1.43) for transitions from incident asthma to subsequent CVD. In conclusion, long-term air pollution exposure could affect the CVD trajectory. Distinguishing the effect of air pollutants on CVD transition stages has great significance for CVD health management and clinical prevention, especially among asthma patients.

Ambient air pollution and incidence, progression to multimorbidity and death of hypertension, diabetes, and chronic kidney disease: A national prospective cohort.

BACKGROUND: The link between ambient air pollution and the incidence of hypertension, diabetes, and chronic kidney disease (CKD) has been widely studied. However, the associations of air pollution with the dynamic progression to multimorbidity and mortality of these diseases are unknown. METHODS: This study included 162,334 participants from the UK Biobank. Multimorbidity was defined as the coexistence of at least two of hypertension, diabetes, and CKD. Land use regression was used to estimate annual concentrations of particulate matter (PM2.5), PM10, nitrogen dioxide (NO2), and nitrogen oxides (NOx). Multi-state models were used to assess the association between ambient air pollutants and the dynamic progression of hypertension, diabetes, and CKD. RESULTS: During a median follow-up of 11.7 years, 18,496 participants experienced at least one of hypertension, diabetes, and CKD, 2216 experienced multimorbidity, and 302 died afterwards. We observed differential associations of four air pollutants on different transitions from healthy status to incident disease (hypertension, diabetes, or CKD), to multimorbidity, and to death. The hazard ratios (HRs) of each IQR increment in PM2.5, PM10, NO2, and NOx for the transition to incident disease were 1.07 [95 % confidence intervals (CI): 1.04, 1.09], 1.02 (1.00, 1.03), 1.07 (1.04, 1.09), and 1.05 (1.03, 1.07), but the associations with the transition to death were significant for NOx only [HR: 1.04 (95 % CI: 1.01, 1.08)]. CONCLUSIONS: Air pollution exposure might be one important determinant for the incidence and dynamic progression of hypertension, diabetes, and CKD, suggesting that more attention should be paid to ambient air pollution control in the prevention of hypertension, diabetes, and CKD, as well as their progression.

Nanoscale semiconducting polymer dots with rhodamine spirolactam as fluorescent sensor for mercury ions in living systems.

Mercury ion (Hg2+), as one of the most poisonous heavy metal ions, could seriously damage mental and neurological functions thus causing severe diseases. A fluorescent ratiometric sensor based on semiconducting polymer dots (Pdots) and rhodamine spirolactam derivate was developed for the detection of Hg2+. The Pdots were prepared by Poly [(9,9-dioctylfluorenyl-2,7-diyl)-co-(1,4-diphenylene-vinylene-2-methoxy-5-{2-ethylhexyloxy}-benzene)] (PDDB) with emitting strong green fluorescence. The organic fluorescence dye N-(rhodamine-B) lactam-hydrazine (RhBH), as Hg2+-recognizing monomer, was conjugated to the surface of Pdots. Hg2+ could specifically trigger ring-opening process of RhBH and thus induce strong Förster resonance energy transfer (FRET) effect, resulting in the green fluorescence decrease of Pdots (energy donor) and red emission derived from the ring-opened RhBH (energy acceptor) increasing. PDDB@RhBH showed a sensitive and reversible response toward Hg2+ and had a great performance on resisting interferences from various biological analytes. Additionally, both fluorescent imaging in living cells and zebrafish, and systemic toxicity analysis in rats demonstrated that PDDB@RhBH was a great potential fluorescent sensor for quantitative Hg2+ imaging in living systems.

A fully human connective tissue growth factor blocking monoclonal antibody ameliorates experimental rheumatoid arthritis through inhibiting angiogenesis.

BACKGROUND: Connective tissue growth factor (CTGF) plays a pivotal role in the pathogenesis of rheumatoid arthritis (RA) by facilitating angiogenesis and is a promising therapeutic target for RA treatment. Herein, we generated a fully human CTGF blocking monoclonal antibody (mAb) through phage display technology. RESULTS: A single-chain fragment variable (scFv) with a high affinity to human CTGF was isolated through screening a fully human phage display library. We carried out affinity maturation to elevate its affinity for CTGF and reconstructed it into a full-length IgG1 format for further optimization. Surface plasmon resonance (SPR) data showed that full-length antibody IgG mut-B2 bound to CTGF with a dissociation constant (KD) as low as 0.782 nM. In the collagen-induced arthritis (CIA) mice, IgG mut-B2 alleviated arthritis and decreased the level of pro-inflammatory cytokines in a dose-dependent manner. Furthermore, we confirmed that the TSP-1 domain of CTGF is essential for the interaction. Additionally, the results of Transwell assays, tube formation experiments, and chorioallantoic membrane (CAM) assays showed that IgG mut-B2 could effectively inhibit angiogenesis. CONCLUSION: The fully human mAb that antagonizes CTGF could effectively alleviate arthritis in CIA mice, and its mechanism is tightly associated with the TSP-1 domain of CTGF.

Construction of a nanoscale metal-organic framework aptasensor for fluorescence ratiometric sensing of AFB1 in real samples.

Aflatoxins B1 (AFB1) that could contaminate agricultural products has received sustained attention due to its high toxicity and wide distribution. Therefore, sensitive and facile detection method for AFB1 is significant for food safety and control. In this work, a ratiometric fluorescence NMOFs-Aptasensor was developed based on the combination of Cy3-modified aptamer and zirconium-based nanoscale metal-organic frameworks (NMOFs). NMOFs served as energy donors, and Cy3 labeled on the AFB1 aptamer was used as an acceptor. An energy donor-acceptor pair was fabricated in the NMOFs-Aptasensor. With AFB1 selectively caught by the AFB1 aptamer, the fluorescence of the NMOFs-Aptasensor changed via fluorescence resonance energy transfer (FRET), and the fluorescence spectra changed accordingly. The ratiometric fluorescence signal was utilized to quantitatively measure AFB1. The reported NMOFs-Aptasensor presented great detection performance from 0 to 3.33 ng mL-1, with an LOD of 0.08 ng mL-1. Moreover, the fluorescence sensor was successfully applied to detect AFB1 in real samples.

Enhanced Oxygen Evolution of a Magnetic Catalyst by Regulating Intrinsic Magnetism.

The promotion of magnetic field on catalytic performance has attracted extensive attention. However, little research has been reported on the performance of the oxygen evolution reaction (OER) for the modulating intrinsic magnetism of the catalyst under a magnetic field. Herein, we adjusted the intrinsic magnetism of the CoxNi1-xFe2O4-nanosheet by adjusting the ratio of Co and Ni, and researched the relationship between the OER activity and the intrinsic magnetism. The results indicate that the CoFe2O4-nanosheet has the most OER activity increases in the magnetic field due to the optimal intrinsic magnetism. The required overpotential of CoFe2O4-nanosheet@NF to reach a current density of 10 mA cm-2 was reduced by 21 mV under about 100 mT magnetic field compared with no magnetic field, and the degree of improvement of OER activity of different magnetic catalysts in the same magnetic field is positively correlated with the intrinsic magnetism of the catalyst. Therefore, magnetic field assistance provides a new, effective, and general strategy to improve the activity of electrodes for water splitting.

Connective tissue growth factor-targeting DNA aptamer suppresses pannus formation as diagnostics and therapeutics for rheumatoid arthritis.

Connective tissue growth factor (CTGF) has been recently acknowledged as an ideal biomarker in the early disease course, participating in the pathogenesis of pannus formation in rheumatoid arthritis (RA). However, existing approaches for the detection of or antagonist targeting CTGF are either lacking or unsatisfactory in the diagnosis and treatment of RA. To address this, we synthesized and screened high-affinity single-stranded DNA aptamers targeting CTGF through a protein-based SELEX procedure. The structurally optimized variant AptW2-1-39-PEG was characterized thoroughly for its high-affinity (KD 7.86 nM), sensitivity (minimum protein binding concentration, 2 ng), specificity (negative binding to other biomarkers of RA), and stability (viability-maintaining duration in human serum, 48 h) properties using various biochemical and biophysical assays. Importantly, we showed the antiproliferative and antiangiogenic activities of the aptamers obtained using functional experiments and further verified the therapeutic effect of the aptamers on joint injury and inflammatory response in collagen-induced arthritis (CIA) mice, thus advancing this study into actual therapeutic application. Furthermore, we revealed that the binding within AptW2-1-39-PEG/CTGF was mediated by the thrombospondin 1 (TSP1) domain of CTGF using robust bioinformatics tools together with immunofluorescence. In conclusion, our results revealed a novel aptamer that holds promise as an additive or alternative approach for CTGF-targeting diagnostics and therapeutics for RA.