As a consequence of hypertension, left ventricular (LV) structural alterations are associated with cognitive decline in the elderly. However, its role in early childhood remains unclear. We examined the relationship between blood pressure (BP), LV structure, and cognitive function in preschool-aged children. This population is free from aging-related comorbidities. We recruited 1279 4-year-old children from the Shanghai Birth Cohort (2018–2021), excluding those with birth defects or developmental delays. BP and echocardiographic assessment were conducted at follow-up. Cognitive function was evaluated using the Wechsler preschool and primary scales of intelligence-fourth edition. Elevated BP (107.4 ± 6.2 mmHg) compared to normal BP (96.0 ± 5.9 mmHg) tended towards lower full scale intelligence quotient (IQ) [adjusted mean difference (β) = − 2.95, 95

The quantitative associations of prenatal exposure to fine particulate matter (PM2.5) and its components with neonatal blood amino acid (AA) and acylcarnitine (AC) profiles, as well as the critical exposure windows, remain largely unknown. Using data from a birth cohort in Shanghai, we aimed to explore these associations in 4802 mother-infant pairs, with metabolite levels measured by liquid chromatography-tandem mass spectrometry. All neonatal metabolite levels were log-transformed and standardized. We found that per interquartile range increase in prenatal PM2.5 exposure was significantly associated with 18 neonatal metabolites. Specifically, levels of aspartic acid (β: 0.395), glycine (β: 0.364) and medium-chain ACs (C6DC (β: 0.374), C10 (β: 0.409), C12 (β: 0.378)) were increased, while levels of arginine (β: -0.465), citrulline (β: -0.355) and short-chain ACs (C2 (β: -0.376), C3 (β: -0.349), C4 (β: -0.554)) were decreased. Pathway analysis revealed four exploratory metabolic pathway signals linked to prenatal PM2.5 exposure: the urea cycle, oxidation of branched-chain fatty acids, arginine and proline metabolism, and aspartate metabolism. Organic matter, approximated as residual organic matter (estimated), was the major contributor among PM2.5 components. Mid-gestation exposure showed the strongest associations with AA metabolism and the urea cycle pathways, whereas late-gestation exposure was more strongly linked to oxidation of branched-chain fatty acids. Mediation analyses suggested that, for the associations of PM2.5 and its components with glutamine and short-chain ACs, there were possible and small mediation effects by thyroid-stimulating hormone, but results were not statistically robust. Overall, prenatal exposure to PM2.5 was significantly associated with alterations in neonatal AAs and ACs, with residual organic matter (estimated) being the most important component of PM2.5.

Metallic atrial septal defect (ASD) occluders are associated with various mid- to long-term complications. To address this, our team developed a novel biodegradable Pansy ASD occluder, and this multicenter RCT aimed to evaluate its effectiveness and safety. A prospective, multicenter, randomized controlled trial was carried out on adult and pediatric patients using the Pansy occluder with a biodegradable polydioxanone (PDO) framework. The primary efficacy endpoint of this clinical trial is the closure success rate at six months post-operation. From May 2021 to March 2023, a total of 127 patients were screened across seven research centers, with 112 patients (including 71 pediatric patients; 57 to the experimental group, 55 to the metal occluder control group) ultimately underwent occluder implantation. In these patients, the average defect size was 8.48 ± 2.86 mm in the experimental group and 10.41 ± 5.21 mm in the control group. The closure success rate at six months post-operation was 100

Lineage-committed precursors are essential yet rarely identified in mammalian organogenesis, as they lack definitive molecular signatures required for conventional marker-based approaches. Herein, we developed iCommitted, an integrated multi-omics computational pipeline for precise identification of these precursors. iCommitted first reconstructs in vivo organogenesis by modeling the in vitro differentiation trajectory spanning naïve to terminally differentiated cells. It then integrates epigenomic (ATAC-seq/DNase-seq) and transcriptomic (RNA-seq) data to achieve standardized developmental staging and precursor identification. Applied to mammalian hematopoiesis, iCommitted robustly identified hematopoietic progenitors as the hematopoietic lineage-committed precursors. Subsequent cis-regulatory annotation generated a high-confidence atlas of 16 774 hematopoietic cis-regulatory elements. Functional analysis of the atlas further pinpointed a 218-bp hematopoietic enhancer (chr6:145 855 899-145 856 116) that regulates Bhlhe41 expression during lineage commitment. This study establishes a valuable approach for identifying lineage-committed precursors and elucidating regulatory mechanisms in mammalian organogenesis, offering broad utility in developmental biology.

BACKGROUND:To examine the association of maternal cardiovascular health (CVH) in early-to-mid pregnancy with offspring cardiovascular phenotypes in early childhood. METHODS:A total of 980 mother-offspring pairs were included. Maternal CVH was composed of body mass index (BMI), blood pressure (BP), total cholesterol level, glucose level, and smoking status. Each metric was categorized into ideal, intermediate, or poor according to corresponding guidelines. Childhood BP measurement and transthoracic echocardiography were performed at age of 4. RESULTS:Compared to offspring from mothers with all ideal metrics, those from mothers with ≥2 poor metrics had higher BP (systolic: p = 0.01; diastolic: p < 0.01). Higher maternal CVH score was negatively associated with offspring mean BP (systolic: β: -0.38; 95% CI: -0.70, -0.06; diastolic: β: -0.36; 95% CI: -0.64, -0.08), while positively associated with offspring ventricular chamber diameter (LVEDD: β: 0.58; 95% CI: 0.03, 1.14; LVESD: β: 0.40; 95% CI: 0.04, 0.76), ventricular chamber volume (LVEDV: β: 1.06; 95% CI: 0.16, 1.97; LVESV: β: 0.41; 95% CI: 0.08, 0.74) and stroke volume (β: 0.58; 95% CI: 0.04, 1.11). CONCLUSIONS:There is a potential link between multifactorial maternal CVH during early-to-mid pregnancy and offspring early cardiovascular phenotypes, including differences in offspring BP, cardiac structure and function. IMPACT:Maternal cardiovascular health (CVH) is increasingly recognized as a key indicator of long-term cardiometabolic outcomes in offspring. This study indicates maternal CVH during early-to-mid pregnancy is associated with offspring blood pressure, cardiac structure and function at age 4. Findings suggest the potential value of multifactorial prenatal health assessment for identifying early-life cardiovascular risk, extending existing DOHaD and CVH literature.

A sustained decline in fertility in China has reshaped pedi-atric service needs but has not solved structural weaknesses[1].

Congenital heart disease (CHD) is a leading cause of neonatal morbidity and mortality, whose underlying pathogenesis remains largely unclear, and lacks reliable biomarkers or therapeutic targets for early detection and treatment during pregnancy. In this study, we investigated the role of endogenous peptide ELABELA (ELA) in fetal CHD. Our findings reveal that ELA levels are significantly reduced in human fetal cardiac tissues with CHD. In mouse models, ELA deletion in cardiac progenitor cells disrupted mitochondrial function, directly contributing to cardiac malformations. Mechanistically, ELA deficiency caused mitochondrial swelling by inhibiting the APJ-AKT-BCL2/BAX signaling pathway. Notably, exogenous ELA administration reduced both CHD severity and incidence in mice. Furthermore, plasma ELA levels were markedly down-regulated in human pregnancies with fetal CHD. These findings establish ELA as a crucial regulator of cardiac development and highlight its potential as both a biomarker and therapeutic target for the prevention and management of fetal CHD during gestation.

The approved AAV9-based gene therapy (onasemnogene abeparvovec) extends survival and motor milestones in spinal muscular atrophy (SMA) type 1 but is administered at a high dose (1.1E14 vg/kg) and carries a boxed warning for liver injury. We engineered SKG0201, a self-complementary AAV9 vector encoding codon-optimized SMN1 under central nervous system (CNS)-selective regulatory cassette (Syn-Cbin-rGBpA), driving CNS-preferential transgene expression and minimizing acute peripheral overexpression. In SMNΔ7 mice with a median survival of 15 days, a single 1E11 vg/pup (equivalent to 6.67E13 vg/kg) injection of SKG0201 extended median survival beyond 160 days, normalized rotarod and grip performance, and ameliorated neuropathology. No aminotransferase elevations were elicited up to 4E11 vg/pup. In a phase I trial (NCT06191354), 10 symptomatic infants with SMA type 1 received 3.7-5.5E13 vg/kg SKG0201. This interim analysis reports safety and preliminary efficacy data with at least 24 weeks of follow-up. At 24 weeks post treatment, 80% remained free from permanent ventilation, 6 of 8 survivors (75%) achieved a≥4-point increase in CHOP INTEND score, and 4 of 8 survivors (50%) achieved head control. Treatment-related adverse events were largely transient and manageable, with no high-grade drug-related hepatotoxicity observed. SKG0201's design reduces the viral dose requirement while optimizing CNS target engagement, suggesting an improved therapeutic index for SMA gene therapy.

Background Prenatal exposure to individual metals has been studied, but effects of two-timepoint metal mixtures on offspring blood pressure (BP) and their mechanisms remain unclear. Methods The prospective birth cohort study (n = 541) investigated the effects of two-timepoint prenatal metal mixture exposure on offspring blood pressure (BP) and its underlying metabolic mechanisms. Measuring eight toxic metals in maternal blood during early to mid-pregnancy and umbilical cord blood at delivery, combined with neonatal metabolomics analysis, the study revealed a positive association between maternal metal mixture exposure and offspring BP. Results Using Bayesian kernel machine regression (BKMR) and weighted quantile sum (WQS) models, arsenic (As) was identified as the most significant contributor (PIP>0.8 in BKMR, weights>0.5 in WQS). Both maternal blood As and cord blood As showed significant positive associations with offspring systolic BP (SBP) [Pregnancy: β = 4.41, 95% CI 2.39-6.44, P < 0.001; Cord: β = 2.97, 95% CI 1.17-4.78, P = 0.013] and mean arterial pressure (MAP) [Pregnancy: β = 2.67, 95% CI 1.13-4.21, P < 0.001; Cord: β = 2.50, 95% CI 1.06-3.94, P < 0.001]. Metabolic pathway analysis indicated that prenatal arsenic exposure was associated with alterations in carnitine homeostasis (including acetylcarnitine [C2], suberylcarnitine [C8DC], decanoylcarnitine [C10], and decadienoylcarnitine [C12DC]), while showing little association with amino acid metabolism. These carnitine-related metabolic changes were consistent with a potential mediating role in the association between prenatal arsenic exposure and offspring blood pressure. Conclusion Early to mid-pregnancy exposure to metal mixtures, particularly arsenic, shows a stronger association with offspring BP than later-gestation exposure measures, and this association is linked to disruptions in carnitine metabolism.

Accurate segmentation of breast tumors in Dynamic Contrast-Enhanced Magnetic Resonance Imaging (DCE-MRI) is essential for the early diagnosis of breast cancer. However, existing Transformer and Mamba-based architectures suffer from either excessive computational complexity or inadequate performance, creating an urgent need for structural innovation to achieve an optimal balance between accuracy and efficiency. We propose a dual-branch Hybrid Efficient Transformer Network (HCRT) to address these challenges. HCRT employs Light Ghost Blocks for efficient feature extraction and introduces a Correlation-Aware Region Transformer Block (CART), which utilises Multi-Dconv Channel Attention (MDCA) to capture long-range dependencies efficiently; in the auxiliary branch, a similarity matrix is generated through the Position-Aware (PAC) Correlation mechanism to weight attention maps in MDCA, preserving fine-grained spatial details. This design significantly reduces computational complexity from O(N2) to O(C2). Additionally, we propose Regional Prototype Contrastive Learning (RPCL), which operates solely during training to enhance model generalisation without compromising inference efficiency. Extensive experiments on a large-scale dataset of over 1,000 cases and three additional datasets demonstrate that our method achieves superior segmentation accuracy and stronger generalisation ability. The code is available at https://github.com/ZhouL-lab/HCRT.

INTRODUCTION:Organophosphate flame retardants (OPFRs) and organophosphorus pesticides (OPPs) are widely used chemicals in daily environments. Yet, evidence linking prenatal exposure to them with cardiac structure development in offspring is scarce. METHODS:Maternal urinary levels of OPFR and OPP metabolites were measured during the first and second trimesters. Left ventricular end-diastolic volume (LVEDV) and mass (LVM) were assessed by echocardiography in 4-year-old children. Multivariable linear regression and Bayesian kernel machine regression were used to evaluate individual and mixture effects, with sex-stratified and interaction analyses performed to assess potential modification. RESULTS:Among 458 mother-child pairs from the Shanghai Birth Cohort, higher maternal urinary Di-o-cresyl-phosphate (DoCP) concentrations during both trimesters were associated with lower z-scores of LVEDV (β: -0.049, 95% CI: -0.089, -0.008; and β: -0.055, 95% CI: -0.089, -0.022, respectively) and LVM (β: -0.057, 95% CI: -0.098, -0.015; and β: -0.053, 95% CI: -0.087, -0.019, respectively) in 4-year-old offspring. Similarly, higher maternal Di-phenyl phosphate (DPHP) concentration in the second trimester negatively correlated with z-scores of LVEDV (β: -0.043, 95% CI: -0.085, -0.002) and LVM (β: -0.080, 95% CI: -0.122, -0.038). Mixture analyses revealed inverted J-shape associations between maternal mixed OPFRs/OPPs exposure and offspring LVEDV and LVM. Sex-stratified analyses suggested stronger associations among girls. CONCLUSIONS:Prenatal exposure to OPFRs and OPPs was associated with smaller left ventricular structural measures in early childhood, mainly reflected by lower left ventricular volume and mass, with OPFRs emerging as main contributors and stronger associations among girls.

Rare diseases affect more than 300 million people worldwide1-3, yet timely and accurate diagnosis remains an urgent challenge1,3-5. Patients often endure a prolonged 'diagnostic odyssey' exceeding 5 years, marked by repeated referrals, misdiagnoses and unnecessary interventions, leading to delayed treatment and substantial emotional and economic burden4,5. Here we present DeepRare-a multi-agent system for rare disease differential diagnosis decision support6-8 powered by large language models, integrating more than 40 specialized tools and up-to-date knowledge sources. DeepRare processes heterogeneous clinical inputs, including free-text descriptions, structured human phenotype ontology terms and genetic testing results to generate ranked diagnostic hypotheses with transparent reasoning linked to verifiable medical evidence. Evaluated across nine datasets from literature, case reports and clinical centres across Asia, North America and Europe spanning 14 medical specialties, DeepRare demonstrates exceptional performance on 2,919 diseases. In human-phenotype-ontology-based tasks, it achieves an average Recall@1 of 57.18%, outperforming the next best method by 23.79%; in multi-modal tests, it reaches 69.1% compared with Exomiser's 55.9% on 168 cases. Expert review achieved 95.4% agreement on its reasoning chains, confirming their validity and traceability. Our work not only advances rare disease diagnosis but also demonstrates how the latest powerful large-language-model-driven agentic systems can reshape current clinical workflows.

Cardiovascular disease (CVD) remains the leading cause of global mortality, with a concerning trend toward younger onset. This shift highlights the urgent need to advance the window of attention and intervention for cardiovascular health (CVH). The Developmental Origins of Health and Disease (DOHaD) hypothesis proposes that adverse intrauterine exposures can program long-term alterations in offspring CVH, underscoring the significance of early-life origins. Maternal health conditions during pregnancy, environmental exposures, and lifestyle factors are consistently associated with adverse cardiovascular outcomes in children, including elevated blood pressure, structural and functional abnormalities, and impaired cardiometabolic profiles. These associations are mediated through pathways involving placental dysfunction, inflammation, oxidative stress, and hormonal imbalance, which collectively reshape fetal cardiovascular development and increase susceptibility to CVD later in life. From a management perspective, adverse intrauterine exposures should be integrated into pediatric CVH risk assessment, and preventive strategies should be shifted to the preconception and prenatal periods. This review highlights intrauterine environment as a critical determinant of intergenerational cardiovascular risk and emphasizes the necessity of implementing precision prevention strategies beginning from the earliest stages of life.

N-acetylated amino acids systemically accumulate in the circulatory system in patients with chronic kidney disease (CKD), raising questions about their roles in peripheral tissues1,2. Here, targeted metabolomics in patients with CKD identified that circulating N-acetylaspartate (NAA) as the metabolite most closely linked to early cardiac dysfunction. In mice, both CKD and exogenous NAA administration induced pronounced cardiac NAA accumulation, resulting in systolic dysfunction and pathological hypertrophy. Activity-based protein profiling identified cytosolic malate dehydrogenase 1 (MDH1) and sirtuin 2 (SIRT2) as direct targets of NAA. NAA acts as a substrate analogue that occupies the MDH1 substrate-binding pocket, competitively inhibits its enzymatic activity, and disrupts the malate–aspartate shuttle, thereby lowering cytosolic and mitochondrial NAD⁺/NADH ratios, suppressing tricarboxylic acid cycle flux, and compromising cardiomyocyte energy metabolism. Notably, we identified SIRT2 as a previously unrecognized NAA hydrolase that specifically binds and hydrolyzes NAA in an NAD⁺-dependent manner, thereby mitigating NAA-induced metabolic stress. Cardiomyocyte-specific restoration of SIRT2 activity in mice reduced cardiac NAA levels, improved systolic dysfunction, and attenuated hypertrophy. These findings expand sirtuins from protein deacylases to direct regulators of small-molecule metabolites and establish NAA as a kidney–heart metabolic mediator, revealing an amino acid acetylation-dependent layer of energy homeostasis.

The association of secondhand smoke exposure during pregnancy with childhood cardiac alterations remains insufficiently elucidated. This study aims to explore the correlation between maternal passive smoking during gestation with cardiac structure and function of offspring. 1089 mother-offspring pairs from the Shanghai Birth Cohort were included. Information on secondhand smoke exposure during each trimester of pregnancy and baseline characteristics was documented during pregnancy via structured questionnaire. Subsequent follow-up assessments, encompassing anthropometric information and echocardiographic evaluation, were conducted from 2018 to 2021, when the children were 4 years old. Multiple linear regressions models were used to explore the association of secondhand smoke exposure during pregnancy with left ventricular measurements in early childhood. Secondhand smoke exposure during pregnancy was correlated with increased left ventricle (LV) internal diameter in diastole [LVIDd; β = 0.38, 95

BACKGROUND:Congenital heart disease (CHD) is the most common anatomical malformation among live-born infants and has been linked to various prenatal factors. Maternal sleep disturbances, a common issue during pregnancy, have been associated with adverse pregnancy outcomes and neonatal health problems. However, epidemiological evidence on the association between maternal sleep disturbances and the risk of CHD in offspring remains limited and inconclusive. OBJECTIVE:This study aimed to evaluate the association between maternal sleep disturbances during pregnancy and the risk of CHD in offspring. METHODS:A total of 8514 mother-child pairs from the Early Life Plan cohort were included in this study. The Pittsburgh Sleep Quality Index (PSQI) was used to assess sleep characteristics during the first trimester of pregnancy. CHD was diagnosed through ultrasound. Logistic regression models were employed to analyze the association between maternal sleep problems during pregnancy and the risk of CHD in offspring. RESULTS:Poor maternal sleep quality (OR = 1.58, 95 % CI: 1.04-2.40) and short sleep duration (OR = 1.59, 95 % CI: 1.06-2.38) were both significantly associated with an increased risk of CHD in offspring. Subgroup analysis revealed that poor sleep quality was significantly associated with a higher risk of CHD in male offspring (OR = 1.75, 95 % CI: 1.04-2.96), but this association was not significant in female offspring. Among mothers with a habit of daytime napping, shorter sleep duration (<7 h) was significantly associated with a higher risk of CHD (OR = 1.82, 95 % CI: 1.06-3.14). When examining sleep duration as a continuous parameter, longer sleep duration was associated with lower risk of CHD (OR = 0.81, 95 % CI: 0.66-0.98) in daytime napping group. CONCLUSIONS:Poor sleep quality and short sleep duration during pregnancy were associated with an increased risk of CHD in offspring, while the observed relationships appeared more pronounced in male offspring and among mothers who engaged in daytime napping. Daytime napping might have a potential protective effect in reducing the risk of CHD in offspring. As this is an observational study, a causal relationship cannot be established, and further validation is needed in future research.

BACKGROUND:Endogenous retroviruses (ERVs) occupy >8% of the human genome. Aberrant resurgence of ERVs has been implicated recently in several critical pathologies. However, the possible incidence and role of ERV resurgence in heart failure (HF), a leading cause of global morbidity and mortality, remain unexplored. METHODS:We established a total RNA sequencing analyzing pipeline to assess the ERV occurrence in human and murine HF models. We generated 2 myocardium-specific mouse lines by crossing Myh6-MerCreMer (Myosin heavy chain 6 promoter driving MerCreMer recombinase) with TRIM28f/f and SETDB1f/f mice to identify the molecular regulators of ERV resurgence and the downstream pathways in the heart. We evaluated ERV expression by total RNA sequencing, reverse transcription-quantitative polymerase chain reaction and RNA fluorescence in situ hybridization. We restrained ERV activation by overexpressing TRIM28 (tripartite motif-containing 28) using adeno-associated virus serotype 9. The therapeutic potential of the ERV-mediated inflammatory pathway was tested in a myocardial ischemia/reperfusion model. RESULTS:ERVs, particularly class I ERVs, were prominently activated in multiple cross-species models of HF. Depletion of TRIM28, an epigenetic repressor, attenuated the epigenetic surveillance of trimethylation at lysine 9 of histone H3 and N6-methyladenosine, leading to the activation of ERVs in the failing heart. This ERV activation stimulated the antiviral innate immune pathways of TLR7/9 (Toll-like receptor 7/9) and NF-κB and lead to myocarditis and acute HF. Furthermore, restraining ERV activation and ERV-mediated innate immune responses by either adeno-associated virus serotype 9-mediated TRIM28 expression or a small-molecule TLR7/9 inhibitor improved heart function and alleviated HF in an ischemia/reperfusion model. CONCLUSIONS:ERV resurgence is a specific molecular trait of HF, driven by TRIM28 depletion in cardiomyocytes. ERV resurgence activates the innate immune TLR7/9-NF-κB pathway and induces myocarditis and HF. Inception of ERVs and the ERV-mediated immune pathway confers cardiac protection. These results identify TRIM28-ERV-TLR7/9-NF-κB as a target for therapeutic management of myocarditis and HF.

Prenatal exposure to indoor volatile organic compounds (VOCs) poses a substantial yet underestimated threat to fetal brain development. We developed a realistic mouse model to investigate how gestational exposure to such formaldehyde-free paint VOCs mixture disrupts synaptic maturation and cognitive function in postnatal offspring, revealing a novel role for retinol metabolism. Pregnant C57BL/6 J mice inhaled filtered air (control; 0.15 ± 0.01 ppm) or VOCs (0.68 ± 0.06 ppm) from embryonic day 0-21. Exposed postnatal offspring showed deficits in exploratory behavior, recognition memory, and spatial learning, alongside neurodegeneration, reduced dendritic complexity, and lower levels of synaptic proteins (PSD-95, synaptophysin). We identified through transcriptomic and biochemical analyses significant retinol metabolism pathway enrichment, with downregulation of key genes (Aldh1a2, Crabp2) and their protein products. Our findings reveal that prenatal VOCs exposure disrupts synaptic development and cognition by interfering with retinol metabolism. This challenges the assumed safety of "low-VOCs" or "green" building materials in real-world scenarios. These results underscore the critical need to minimize maternal exposure to indoor air pollutants and to consider retinoid pathways as potential targets for intervention.

BACKGROUND:Since 1998, the Shanghai Kawasaki Disease Research Group has systematically conducted four epidemiological surveys on Kawasaki disease (KD) once every 5 years. This study aimed to to analyze the epidemiological trends of KD and the potential impacts of the COVID-19 pandemic in Shanghai from 2018 through 2022. METHODS:Medical records of patients with KD diagnosed from January 2018 through December 2022 were retrospectively analyzed. Data were based on the Shenkang Kawasaki Disease Specific Database established by Shanghai Shenkang Hospital Development Center. Additional data were collected through questionnaires distributed to 48 hospitals providing pediatric medical care via the Shanghai Kawasaki Disease Research Group Network. The primary outcomes were the number and incidence of children with KD. The secondary outcomes included clinical features and changes observed during the COVID-19 pandemic. RESULTS:A total of 5791 cases were enrolled including 3549 permanent residents of Shanghai. The incidence of KD was 61.07 to 94.84 per 100,000 children aged <5 years from 2018 to 2022, with an average annual incidence of 80.7 per 100,000. The incidence decreased compared to the last survey (94.7 per 100,000), with pronounced declines in 2020 (62.74 per 100,000) and 2022 (61.07 per 100,000), which coincided with the implementation of COVID-19 containment measures. The male-to-female ratio was 1.58:1.00. The median age at onset was 25.3 months (interquartile range:14.1, 46.1 months). Of the 3654 cases with treatment information, 3310 were treated with intravenous immunoglobulin (IVIG), of which 317 (9.58%) were IVIG non-response. Out of the 4099 echocardiogram reports, 553 (13.49%) developed coronary artery lesions, and 191 (4.87%) had medium to large coronary artery aneurysms. No deaths were reported in this survey. CONCLUSIONS:The incidence of KD in Shanghai showed a downward trend during 2018-2022 compared to 2013-2017. The containment measures implemented during the COVID-19 pandemic, such as citywide suspension of work and school closures, may have affected the incidence of KD.

This study aimed to develop a new ultrasonographic dating formula to estimate gestational age (GA) based on fetal crown–rump length (CRL) in a Chinese population, evaluate model accuracy and compare its performance with established dating formulas. A prospective, multicenter study was conducted across mainland China. Participants included healthy, low-risk women with spontaneously conceived singleton pregnancies and a regular menstrual cycle in the preceding year. Ultrasonography was performed between 11 and 14 weeks of gestation, with GA determined based on the last menstrual period. Participants were randomly assigned to a development or validation cohort in a 7:3 ratio. A best-fit regression model was constructed for GA estimation based on CRL in the development cohort. For validation, mean differences between the new estimated GA and menstrual age were calculated and compared with those obtained using five established CRL-based dating formulas in the validation cohort. All participants were followed through to delivery. The study recruited 4,710 women with singleton pregnancies, with 3,297 in the development cohort and 1,413 women in the validation cohort. The mean and standard deviation values of CRL changed linearly with GA during 11–14 weeks. CRL demonstrated a linear relationship with GA between 11 and 14 weeks, yielding the regression equation GA = 59.590085 + 0.458539×CRL (R2 = 0.8042). The mean difference between estimated GA and menstrual age was 0.32 days (95