Short-term influence of polytetrafluoroethylene micro/nano-plastics on the inhibition of copper and/or ciprofloxacin on the nitrifying sludge activities based on concentration addition and independent action models.

Short-term influence of polytetrafluoroethylene micro/nano-plastics (PTFE-MPs/NPs) on the inhibition of copper (Cu2+) and/or ciprofloxacin (CIP) on the nitrifying sludge activities was explored based on concentration addition (CA) and independent action (IA) models. The half maximal inhibitory concentration (IC50) of Cu2+, CIP, PTFE-MPs (3 µm), and PTFE-NPs (800 nm) on the specific ammonium oxidation rate (SAOR) of nitrifying sludge was 64.57, 51.29, 102.33 and 93.33 mg L-1, respectively, while those on the specific nitrite oxidation rate (SNOR) of nitrifying sludge were 77.62, 32.36, 104.70 and 97.72 mg L-1, respectively. Among the five binary mixtures and two ternary mixtures composed by Cu2+, CIP, and/or PTFE-MPs/NPs, it was found that the two joint inhibitory actions from ternary mixtures on the SAOR and SNOR of the sludge showed time-dependent characteristics by analyzing of CA and IA models, while the five combined inhibitory effects from different binary mixtures did not all have time-dependent features. The two joint inhibition actions from diverse ternary mixtures on the SAOR at the exposure time of 60 min and on the SNOR at 90 min showed always concentration-dependent features, while the combined inhibitions with concentration-dependent characteristics had never been observed in the binary Cu2+ and PTFE-NPs mixtures at different exposure time. The Cu2+, CIP, and PTFE-MPs mixtures (or Cu2+, CIP, and PTFE-NPs mixtures) had synergistic actions on the SAOR at 90 min and antagonistic effects on the SNOR at 60 min based on CA and IA models, and these combined inhibitions did not exhibit concentration-dependent characteristics. In contrast, the joint inhibitory effects (on the SAOR and SNOR) with concentration-dependent features were found in the binary mixtures of CIP and PTFE-MPs at different exposure time, and the join inhibition changed from synergism to antagonism as the increasing concentration of mixed CIP and PTFE-MPs. This study provides novel perspectives for understanding the combined influence of plastic particles with different sizes, antibiotics, and heavy metals on the biological wastewater treatment process.

Study on the Sliding Tribological Behavior of Oleic Acid-Modified MoS2 under Boundary Lubrication.

The effects of MoS2 and MoS2 modified by adding oleic acid (OA) on the friction properties of lithium-based grease under boundary lubrication conditions are studied by molecular dynamics (MD) simulation and experiment. A rough wall boundary lubrication MD model with peaks and grooves is established to simulate the mechanical properties and lubrication effects of three lubrication systems on rough walls for the relative shear velocity between the two solid walls of 5 m/s at 500 MPa. The stress, wear amount, friction force, normal pressure, and friction heat of the friction surface are quantitively calculated. Simultaneously, a Retc friction and wear testing machine is used to measure the friction coefficient under different concentrations of additives and different pressures. The results show that the grease added with MoS2 can reduce friction, wear, and the temperature between friction pairs. However, under high pressure and shear, MoS2 can easily agglomerate and accumulate in the pits, reducing the lubricating effect. At the same time, since OA-modified MoS2 can reduce agglomeration, the modified MoS2 is adsorbed on the metal wall surface, forming a stable lubricant film. The main contributions of this article can be found in combining MD simulation and experimentation, establishing the connection between micronano structures and macroscopic properties, exploring the mechanism of the influence of wall roughness and particle size on the friction performance of lubricating oil, and providing a theory for predicting and developing high-performance new lubricating grease.

Downregulation of TNFRSF19 and RAB43 by a novel miRNA, miR-HCC3, promotes proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma cells.

Tumor necrosis factor receptor superfamily 19 (TNFRSF19) is a transmembrane protein involved in tumorigenesis. RAB43 is a small molecule GTP-binding protein contributing to the occurrence and development of tumors. However, TNFRSF19/RAB43 dysregulation and their role in hepatocellular carcinoma cells are unknown. Herein, we found that TNFRSF19 and RAB43 were downregulated in hepatocellular carcinoma tissues. TNFRSF19/RAB43 overexpression suppressed, whereas TNFRSF19/RAB43 knockdown promoted cell proliferation and epithelial-mesenchymal transition (EMT) of hepatocellular carcinoma cells. Previously, using deep sequencing technology, a new miRNA, miR-HCC3, was identified and found to suppress the expression of TNFRSF19 and RAB43 by binding to their 3'untranslated regions (3'UTRs) directly. miR-HCC3 was upregulated in hepatocellular carcinoma (HCC) tissues compared with adjacent noncancerous tissues and promoted proliferation and epithelial-mesenchymal transition in HCC cells. Furthermore, TNFRSF19/RAB43 suppressed but miR-HCC3 promoted tumor growth in vivo. Collectively, our results indicated that downregulation of TNFRSF19 and RAB43 by miR-HCC3 contributes to oncogenic activities in HCC, which sheds light on tumorigenesis and might provide potential therapeutic targets for HCC.

Exposure to Low-Dose Ionizing Radiation From Cardiac Procedures and Malignancy Risk in Adults With Congenital Heart Disease.

BACKGROUND: Adults with congenital heart disease (CHD) are exposed to increasing amounts of low-dose ionizing radiation (LDIR) from cardiac procedures. Cancer prevalence in this population is higher than in the general population. This study estimates the association between LDIR exposure from cardiac procedures and incident cancer in adult patients with CHD. METHODS: The study population derived from the Quebec Congenital Heart Disease Database. We measured cumulative numbers of LDIR-related cardiac procedures for each patient until 1 year before the time of cancer diagnosis or administrative censoring. To assess the association between LDIR exposure and cancer risk, we conducted a nested case-control study and matched cancer cases with controls on sex, CHD severity, birth year, and age. RESULTS: The study included 24 833 adult patients with CHD aged 18 to 64 years from 1995 to 2009. In >250 791 person-years of follow-up, 602 cancer cases were observed (median age, 55.4 years). The cumulative incidence of cancer estimated up to 64 years of age was 15.3% (95% confidence interval [CI], 14.2-16.5). Cases had more LDIR-related cardiac procedures than controls (1410 versus 921 per 1000 adult patients with CHD, P<0.0001). Cumulative LDIR exposure was independently associated with cancer (odds ratio [OR], 1.08 per procedure; 95% CI, 1.04-1.13). Similar results were obtained by using dose estimates for LDIR exposure (OR, 1.10 per 10 mSv; 95% CI, 1.05-1.15) with a possible dose-related response. The effect measure was in the same direction, and the association was persistent for exposure from ≥6 procedures in all sensitivity analyses: after excluding most smoking-related cancer cases (OR, 1.10 per procedure; 95% CI, 1.05-1.16 and OR when exposure from ≥6 procedures, 3.08; 95% CI, 1.77-5.37), and after applying a 3-year lag period (OR, 1.09 per procedure; 95% CI, 1.03-1.14 and OR when exposure from ≥6 procedures: 2.58; 95% CI, 1.43-4.69). CONCLUSIONS: To our knowledge, this is the first large population-based study to analyze and document the association between LDIR-related cardiac procedures and incident cancer in the population of adults with CHD. Confirmations of these findings by prospective studies are needed to reinforce policy recommendations for radiation surveillance in patients with CHD where no regulation currently exists. Physicians ordering and performing cardiac imaging should ensure that exposure is as low as reasonably achievable without sacrificing quality of care.

Flexible Modeling of the Association Between Cumulative Exposure to Low-Dose Ionizing Radiation From Cardiac Procedures and Risk of Cancer in Adults With Congenital Heart Disease.

Adults with congenital heart disease are increasingly being exposed to low-dose ionizing radiation (LDIR) from cardiac procedures. In a recent study, Cohen et al. (Circulation. 2018;137(13):1334-1345) reported an association between increased LDIR exposure and cancer incidence but did not explore temporal relationships. Yet, the impact of past exposures probably accumulates over years, and its strength may depend on the amount of time elapsed since exposure. Furthermore, LDIR procedures performed shortly before a cancer diagnosis may have been ordered because of early symptoms of cancer, raising concerns about reversal causality bias. To address these challenges, we combined flexible modeling of cumulative exposures with competing-risks methodology to estimate separate associations of time-varying LDIR exposure with cancer incidence and all-cause mortality. Among 24,833 patients from the Quebec Congenital Heart Disease Database, 602 had incident cancer and 500 died during a follow-up period of up to 15 years (1995-2010). Initial results suggested a strong association of cancer incidence with very recent LDIR exposures, likely reflecting reverse causality bias. When exposure was lagged by 2 years, an increased cumulative LDIR dose from the previous 2-6 years was associated with increased cancer incidence, with a stronger association for women. These results illustrate the importance of accurate modeling of temporal relationships between time-varying exposures and health outcomes.

2-Phenyl-3-(p-aminophenyl) Acrylonitrile: A Reactive Matrix for Sensitive and Selective Analysis of Glycans by MALDI-MS.

Analysis of glycans by matrix-assisted laser desorption/ionization mass spectrometry (MALDI-MS) is usually limited by the intrinsically low abundance and low ionization efficiency of glycans. Aiming to enhance the ionization efficiency of glycans and simplify the sample preparation procedure during MALDI-MS analysis, we reported herein a novel reactive matrix, 2-phenyl-3-(p-aminophenyl) acrylonitrile (PAPAN), for sensitive and selective detection of glycans. PAPAN is a derivative of α-cyanocinnamic acid, which possesses high ionization efficiency in MALDI-MS. The PAPAN can react with the terminal aldehyde of glycans and thereby enable the significant enhancement of ionization efficiency of glycans. As a result, using PAPAN as a reactive matrix, the detection sensitivity for glycans was improved 100-fold compared with that using 2,5-dihydroxybenzoic acid (DHB) as the matrix. Meanwhile, the ionization of peptides can be significantly suppressed using PAPAN as the matrix, which allowed the selective detection of N-glycans from a deglycosylated tryptic digest of glycoprotein without any prepurification. Moreover, the PAPAN matrix also endowed the analysis of glycans with enhanced fragmentation during MS/MS analysis, which could facilitate glycan structure interpretation. Finally, PAPAN was successfully used for the analysis of N-glycome in human serum. Thus, a simple, sensitive, and selective method for the analysis of glycans has been achieved by using a novel reactive matrix, PAPAN.

miR-377-3p drives malignancy characteristics via upregulating GSK-3ß expression and activating NF-κB pathway in hCRC cells.

MicroRNA (miRNA) dysregulation has been associated with carcinogenesis in many cancers, including human colorectal cancer (hCRC). However, the effect and mechanism of miR-377-3p on CRC remains elusive. Herein, we first found that miR-377-3p was upregulated in CRC tissues and promoted tumorigenic activity by accelerating the G1 -S phase transition, promoting cell proliferation and epithelial-mesenchymal transition (EMT) while repressing apoptosis in CRC cells. Glycogen synthase kinase-3ß (GSK-3ß) was a direct target of miR-377-3p, and upregulated by miR-377-3p. Knockdown of GSK-3ß partly rescued miR-377-3p-mediated malignancy characteristics. Most importantly, we showed that miR-377-3p promoted carcinogenesis by activating NF-κB pathway. Taken together, our results first reported that miR-377-3p functions as an oncogene and promotes carcinogenesis via upregulating GSK-3ß expression and activating NF-κB pathway in hCRC cells.

Exposure to Low-Dose Ionizing Radiation From Cardiac Procedures in Patients With Congenital Heart Disease: 15-Year Data From a Population-Based Longitudinal Cohort.

BACKGROUND: The burden of low-dose ionizing radiation (LDIR) exposure from medical procedures among individuals with congenital heart disease (CHD) is unknown. In this longitudinal population-based study, we sought to determine exposure to LDIR-related cardiac imaging and therapeutic procedures in children and adults with CHD. METHODS AND RESULTS: In an analysis of the Quebec CHD database, exposure to the following LDIR-related cardiac procedures was recorded: catheter-based diagnostic procedures, structural heart interventions, coronary interventions, computed tomography scans of the chest, nuclear procedures, and pacemaker/implantable cardioverter-defibrillator insertion and repair. From 1990 to 2005, there were 16 253 LDIR-exposed patients with CHD with 317 988 patient-years of available follow-up. The total number of LDIR-related procedures increased from 18.5 to 51.9 per 1000 CHD patients per year (P<0.0001). This increase was attributable to increases in rates per 1000 CHD patients in diagnostic cardiac catheterizations (11.7 to 13.7 per 1000), structural heart interventions (1.0 to 5.2 per 1000), coronary interventions (1.0 to 2.4 per 1000), pacemaker/implantable cardioverter-defibrillator insertions (1.6 to 4.4 per 1000), nuclear procedures (4.2 to 13.8 per 1000), and computed tomography scans of the chest (2.5 to 12.3 per 1000). Over time, among children with CHD, the median age at first LDIR procedure decreased from 5.0 years to 9.6 months. Severity of CHD significantly predicted extent of exposure. CONCLUSIONS: From 1990 to 2005, patients with CHD were exposed to increasing numbers of LDIR-emitting cardiac procedures. This exposure occurred at progressively younger ages. These findings provide an important perspective on longitudinal LDIR exposure in this at-risk population.

Crystal structure of PnpCD, a two-subunit hydroquinone 1,2-dioxygenase, reveals a novel structural class of Fe2+-dependent dioxygenases.

Aerobic microorganisms have evolved a variety of pathways to degrade aromatic and heterocyclic compounds. However, only several classes of oxygenolytic fission reaction have been identified for the critical ring cleavage dioxygenases. Among them, the most well studied dioxygenases proceed via catecholic intermediates, followed by noncatecholic hydroxy-substituted aromatic carboxylic acids. Therefore, the recently reported hydroquinone 1,2-dioxygenases add to the diversity of ring cleavage reactions. Two-subunit hydroquinone 1,2-dioxygenase PnpCD, the key enzyme in the hydroquinone pathway of para-nitrophenol degradation, catalyzes the ring cleavage of hydroquinone to γ-hydroxymuconic semialdehyde. Here, we report three PnpCD structures, named apo-PnpCD, PnpCD-Fe(3+), and PnpCD-Cd(2+)-HBN (substrate analog hydroxyenzonitrile), respectively. Structural analysis showed that both the PnpC and the C-terminal domains of PnpD comprise a conserved cupin fold, whereas PnpC cannot form a competent metal binding pocket as can PnpD cupin. Four residues of PnpD (His-256, Asn-258, Glu-262, and His-303) were observed to coordinate the iron ion. The Asn-258 coordination is particularly interesting because this coordinating residue has never been observed in the homologous cupin structures of PnpCD. Asn-258 is proposed to play a pivotal role in binding the iron prior to the enzymatic reaction, but it might lose coordination to the iron when the reaction begins. PnpD also consists of an intriguing N-terminal domain that might have functions other than nucleic acid binding in its structural homologs. In summary, PnpCD has no apparent evolutionary relationship with other iron-dependent dioxygenases and therefore defines a new structural class. The study of PnpCD might add to the understanding of the ring cleavage of dioxygenases.

Stroke in Adults With Congenital Heart Disease: Incidence, Cumulative Risk, and Predictors.

BACKGROUND: Stroke is an important cause of morbidity and mortality, although there is a lack of comprehensive data on its incidence, cumulative risk, and predictors in patients with adult congenital heart disease. METHODS AND RESULTS: This retrospective study of 29 638 Quebec patients with adult congenital heart disease aged 18 to 64 years between 1998 and 2010 was based on province-wide administrative data. The cumulative risk of ischemic stroke estimated up to age 64 years was 6.1% (95% confidence interval [CI], 5.0-7.0%) in women and 7.7% (95% CI, 6.4-8.8%) in men; the risk of hemorrhagic stroke was 0.8% (95% CI, 0.4-1.2%) and 1.3% (95% CI, 0.8-1.8%), respectively. Compared with rates reported for the general Quebec population, age-sex standardized incidence rates of ischemic stroke were 9 to 12 times higher below age 55 years and 2 to 4 times higher in the age group 55 to 64 years; hemorrhagic stroke rates were 5 to 6 times (age <55 years) and 2 to 3 times higher. Using a combination of stepwise model selection and Bayesian model averaging, the strongest predictors of ischemic stroke were heart failure (odds ratio for age group 18-49 years, 5.94 [95% CI, 3.49-10.14], odds ratio for age group 50-64 years, 1.68 [95% CI, 1.06-2.66]), diabetes mellitus (odds ratio, 2.33 [95% CI, 1.66-3.28]), and recent myocardial infarction (odds ratio, 8.38 [95% CI, 1.77-39.58]). CONCLUSIONS: Among patients with adult congenital heart disease, 1 in 11 men and 1 in 15 women experienced a stroke between ages 18 and 64 years. Stroke incidence was considerably higher than in the general population, especially at a younger age. The most important predictors of ischemic stroke were heart failure, diabetes mellitus, and recent myocardial infarction. Additional research is required to see whether advances in the management of adult congenital heart disease may reduce this substantial stroke rate.

The REC domain mediated dimerization is critical for FleQ from Pseudomonas aeruginosa to function as a c-di-GMP receptor and flagella gene regulator.

FleQ is an AAA+ ATPase enhancer-binding protein that regulates both flagella and biofilm formation in the opportunistic pathogen Pseudomonas aeruginosa. FleQ belongs to the NtrC subfamily of response regulators, but lacks the corresponding aspartic acid for phosphorylation in the REC domain (FleQ(R), also named FleQ domain). Here, we show that the atypical REC domain of FleQ is essential for the function of FleQ. Crystal structure of FleQ(R) at 2.3Å reveals that the structure of FleQ(R) is significantly different from the REC domain of NtrC1 which regulates gene expression in a phosphorylation dependent manner. FleQ(R) forms a novel active dimer (transverse dimer), and mediates the dimerization of full-length FleQ in an unusual manner. Point mutations that affect the dimerization of FleQ lead to loss of function of the protein. Moreover, a c-di-GMP binding site deviating from the previous reported one is identified through structure analysis and point mutations.

Lifetime prevalence of congenital heart disease in the general population from 2000 to 2010.

BACKGROUND: Our objective was to obtain contemporary lifetime estimates of congenital heart disease (CHD) prevalence using population-based data sources up to year 2010. METHODS AND RESULTS: The Quebec CHD database contains 28 years of longitudinal data on all individuals with CHD from 1983 to 2010. Severe CHD was defined as tetralogy of Fallot, truncus arteriosus, transposition complexes, endocardial cushion defects, and univentricular hearts. We used latent class bayesian models combining case definitions from physician claims, hospitalization, and surgical data to obtain point and interval prevalence estimates of CHD in the first year of life, in children (<18 years of age) and in adults. We identified 107 559 CHD patients from 1983 to 2010. Prevalence of CHD in the first year of life was 8.21 per 1000 live births (95% confidence interval, 7.47-9.02) from 1998 to 2005. In 2010, overall prevalence of CHD was 13.11 per 1000 (95% confidence interval, 12.43-13.81) in children and 6.12 per 1000 (95% confidence interval, 5.69-6.57) in adults. CHD prevalence increased by 11% in children and 57% in adults from 2000 to 2010. Prevalence in the severe CHD subgroup increased by 19% (95% confidence interval, 17%-21%) in children and 55% (51%-62%) in adults. By 2010, adults accounted for 66% of the entire CHD population. CONCLUSIONS: With an increase of >50% in CHD prevalence since 2000, by 2010 adults accounted for two thirds of patients with severe and other forms of CHD in the general population. Our findings should inform allocation of resources and the planning of workforce needs for the predominantly adult CHD population.

Structural insight of a concentration-dependent mechanism by which YdiV inhibits Escherichia coli flagellum biogenesis and motility.

YdiV is a negative regulator of cell motility. It interacts with FlhD(4)C(2) complex, a product of flagellar master operon, which works as the transcription activator of all other flagellar operons. Here, we report the crystal structures of YdiV and YdiV(2)-FlhD(2) complex at 1.9 Å and 2.9 Å resolutions, respectively. Interestingly, YdiV formed multiple types of complexes with FlhD(4)C(2). YdiV(1)-FlhD(4)C(2) and YdiV(2)-FlhD(4)C(2) still bound to DNA, while YdiV(3)-FlhD(4)C(2) and YdiV(4)-FlhD(4)C(2) did not. DNA bound FlhD(4)C(2) through wrapping around the FlhC subunit rather than the FlhD subunit. Structural analysis showed that only two peripheral FlhD subunits were accessible for YdiV binding, forming the YdiV(2)-FlhD(4)C(2) complex without affecting the integrity of ring-like structure. YdiV(2)-FlhD(2) structure and the negative staining electron microscopy reconstruction of YdiV(4)-FlhD(4)C(2) suggested that the third and fourth YdiV molecule bound to the FlhD(4)C(2) complex through squeezing into the ring-like structure of FlhD(4)C(2) between the two internal D subunits. Consequently, the ring-like structure opened up, and the complex lost DNA-binding ability. Thus, YdiV inhibits FlhD(4)C(2) only at relatively high concentrations.

Portable hydroxyl-functionalized coal gangue-based cordierite porous ceramics sheets for effective adsorption of fluorine-containing wastewater.

Monolithic adsorbent removal of fluoride from water is considered an effective and non-secondary pollution method. Here, a portable hydroxyl-functionalized coal gangue-based cordierite porous ceramic sheet (ACGC-Fe) is prepared by using coal gangue solid waste with a specific silicon-aluminum-rich composition ratio and a small amount of magnesium oxide as a raw material through powder compression molding and mild chemical modification. The prepared ACGC-Fe can be used to treat fluorine-containing wastewater and the maximum adsorption of fluorine can reach 18.69 mg g-1. The Langmuir (Freundlich) adsorption isotherm model and pseudo-second-order kinetic model here provided a satisfactory description of the fluoride removal operating mechanism, and it is confirmed that the adsorption mechanism of ACGC-Fe is mainly attributed to the chemisorption of hydrogen bonds (with hydroxyl group) and ionic bonds (with metal), and physical adsorption based on cordierite porous ceramic pores. This research will provide a new idea for designing high-performance materials by mining and analyzing the composition and structure characteristics of coal gangue solid waste itself and broaden the application range of high-value-added coal gangue solid waste.

Label-free and highly sensitive detection of aflatoxin B1 by Ag IANPs via surface-enhanced Raman spectroscopy.

Aflatoxin B1 (AFB1), a pernicious constituent of the aflatoxin family, predominantly contaminates cereals, oils, and their derivatives. Acknowledged as a Class I carcinogen by the World Health Organization (WHO), the expeditious and quantitative discernment of AFB1 remains imperative. This investigation delineates that aluminum ions can precipitate the coalescence of iodine-modified silver nanoparticles, thereby engendering hot spots conducive for label-free AFB1 identification via Surface-Enhanced Raman Spectroscopy (SERS). This methodology manifests a remarkable limit of detection (LOD) at 0.47 fg/mL, surpassing the sensitivity thresholds of conventional survey techniques. Moreover, this method has good anti-interference ability, with a relative error of less than 10% and a relative standard deviation of less than 6% in quantitative results. Collectively, these findings illuminate the substantial application potential and viability of this approach in the quantitative analysis of AFB1, underpinning a significant advancement in food safety diagnostics.

Revealing Distance-Dependent Synergy between MnCo2O4 and Co-N-C in Boosting the Oxygen Reduction Reaction.

Synergistic effects have been applied to a variety of hybrid electrocatalysts to improve their activity and selectivity. Understanding the synergistic mechanism is crucial for the rational design of these types of catalysts. Here, we synthesize a MnCo2O4/Co-N-C hybrid electrocatalyst for the oxygen reduction reaction (ORR) and systematically investigate the synergy between MnCo2O4 nanoparticles and Co-N-C support. Theoretical simulations reveal that the synergy is closely related to the distance between active sites. For a pair of remote active sites, the ORR proceeds through the known 2e- + 2e- relay catalysis while the direct 4e- ORR occurs on a pair of adjacent active sites. Therefore, the formation of the undesired byproduct (H2O2) is inhibited at the interface region between MnCo2O4 and Co-N-C. This synergistic effect is further verified on an anion-exchange membrane fuel cell. The findings deepen the understanding of synergistic catalysis and will provide guidance for the rational design of hybrid electrocatalysts.

The impact of hollow core-shell nanozymes in biosensing: A case study of p-Fe3O4@PDA@ZIF-67.

BACKGROUND: Nanozymes, a new class of nanomaterials, have emerged as promising substitutes for enzymes in biosensor design due to their exceptional stability, affordability, and ready availability. While nanozymes address many limitations of natural enzymes, they still face challenges, particularly in achieving the catalytic activity levels of their natural counterparts. This indicates the need for enhancing the sensitivity of biosensors based on nanozymes. The catalytic activity of nanozyme can be significantly improved by regulating its size, morphology, and surface composition of nanomaterial. RESULTS: In this work, a kind of hollow core-shell structure was designed to enhance the catalytic activity of nanozymes. The hollow core-shell structure material consists of a nanozymes core layer, a hollow layer, and a MOF shell layer. Taking the classic peroxidase like Fe3O4 as an example, the development of a novel nanozyme@MOF, specifically p-Fe3O4@PDA@ZIF-67, is detailed, showcasing its application in enhancing the sensitivity of sensors based on Fe3O4 nanozymes. This innovative nanocomposite, featuring that MOF layer was designed to adsorb the signal molecules of the sensor to improve the utilization rate of reactive oxygen species generated by the nanozymes catalyzed reactions and the hollow layer was designed to prevent the active sites of nanozymes from being cover by the MOF layer. The manuscript emphasizes the nanocomposite's remarkable sensitivity in detecting hydrogen peroxide (H2O2), coupled with high specificity and reproducibility, even in complex environments like milk samples. SIGNIFICANCE AND NOVELTY: This work firstly proposed and proved that Fe3O4 nanozyme@MOF with hollow layer structure was designed to improve the catalytic activity of the Fe3O4 nanozyme and the sensitivity of the sensors based on Fe3O4 nanozyme. This research marks a significant advancement in nanozyme technology, demonstrating the potential of structural innovation in creating high-performance, sensitive, and stable biosensors for various applications.

CanCHD Study of Hematopoietic Cancers in Children With and Without Genetic Syndromes.

BACKGROUND: Individuals with genetic syndromes can manifest both congenital heart disease (CHD) and cancer attributable to possible common underlying pathways. To date, reliable risk estimates of hematopoietic cancer (HC) among children with CHD based on large population-based data remain scant. This study sought to quantify the risk of HC by the presence of genetic syndrome among children with CHD. METHODS AND RESULTS: Data sources were the Canadian CHD database, a nationwide database on CHD (1999-2017), and the CCR (Canadian Cancer Registry). Standardized incidence ratios were calculated for comparing HC incidences in children with CHD with the general pediatric population. A modified Kaplan-Meier curve was used to estimate the cumulative incidence of HC with death as a competing risk. A total of 143 794 children (aged 0-17 years) with CHD were followed up from birth to age 18 years for 1 314 603 person-years. Of them, 8.6% had genetic syndromes, and 898 HC cases were observed. Children with known syndromes had a substantially higher risk of incident HC than the general pediatric population (standardized incidence ratio, 13.4 [95% CI, 11.7-15.1]). The cumulative incidence of HC was 2.44% (95% CI, 2.11-2.76) among children with a syndrome and 0.79% (95% CI, 0.72-0.87) among children without a syndrome. Acute myeloid leukemia had a higher cumulative incidence during early childhood than acute lymphoblastic leukemia. CONCLUSIONS: This is the first large population-based analysis documenting that known genetic syndromes in children with CHD are a significant predictor of HC. The finding could be essential in informing risk-stratified policy recommendations for cancer surveillance in children with CHD.