Abstract Objective: Prenatal ultrasound screening has been widely implemented for congenital heart disease (CHD). This study aimed to describe the prevalence and detection patterns of prenatal and postnatal screening for CHD. Methods: This retrospective cohort study was conducted at the Obstetrics and Gynecology Hospital of Fudan University between 2018 and 2020. Pregnant women with complete prenatal and postnatal follow-up data were recruited for final analysis. Prenatal and postnatal screening for CHD included mid-trimester fetal cardiac ultrasound at 20–24 gestational weeks, neonatal pulse oximetry and cardiac auscultation 6–72 hours after birth, and at a 42-day postnatal visit. Results: Of 21,920 fetuses or neonates (including 548 twin pregnancies), 318 CHD cases were identified. The annual prevalence of CHD was 14.5 per 1000 births. CHD was associated with a higher proportion of male gender in infants, preterm birth, low birth weight, and multiple pregnancy ( P < 0.001). Of the 318 CHD cases, 270 (84.9%) were simple CHD and 48 (15.1%) were complex CHD (most common was tetralogy of Fallot, coarctation of the aorta). Overall, 40.6% (129/318) of CHD cases were diagnosed prenatally, and 59.4% (189/318) were diagnosed postnatally. The prenatal diagnosis rate for complex CHD was 89.6% (43/48), whereas 68.1% (184/270) of simple CHD cases were diagnosed postnatally. The annual pattern was consistent between 2018 and 2020 ( χ 2 = 0.2245, P for trend = 0.894). Conclusion: Our findings indicate the application of a combined prenatal and postnatal screening strategy for comprehensive CHD detection. Prenatal screening for CHD achieved high levels of efficacy for complex CHD with a detection rate of 89.6%. Sequential newborn screening was crucial for identifying simple CHD with a postnatal detection rate of 68.1%. Our findings indicate that prenatal and postnatal detection pattern vary by CHD complexity.

Background:Childhood hypertension is a significant global health concern, with left ventricular hypertrophy (LVH) being its most common target organ damage. Evidence from Chinese pediatric populations remains scarce. Therefore, this study aimed to investigate the risk factors of LVH in children with primary hypertension and to develop a prediction model. Methods:In this cross-sectional study, 121 children diagnosed with primary hypertension (aged 3-17 years) admitted to Children's Hospital of Fudan University (January 1, 2019-December 31, 2024) were included. Clinical data (age, sex, height, weight, birth history, and family history of hypertension), laboratory parameters, 24-hour ambulatory blood pressure monitoring (ABPM), and echocardiography were collected. Participants were stratified into the LVH group and the non-LVH group based on left ventricular mass index (LVMI). Partial correlation analysis evaluated associations of variables with left ventricular mass and LVMI. Stepwise multivariable logistic regression was used to identify independent risk factors. Based on significant factors, a risk prediction model was constructed, with model performance assessed via receiver operating characteristic (ROC) curves [area under the curve (AUC)] and goodness-of-fit tests (Hosmer-Lemeshow χ2). Results:LVH was observed in 17.4% (21/121) of participants, predominantly concentric hypertrophy. Partial correlation analysis adjusted for age and sex revealed positive correlations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), 24-hour mean systolic blood pressure (SBP), daytime mean SBP, and morning mean SBP (the average of ambulatory SBP readings taken within 2 hours of waking up) with LVMI (r=0.26, 0.37, 0.25, 0.25, and 0.23, all P<0.05), respectively. Nocturnal hypertension was identified as an independent risk factor of LVH [odds ratio (OR) =4.07; 95% confidence interval (CI): 1.47-13.24; P=0.01]. The combined prediction model incorporating age, sex, body mass index (BMI), and nocturnal hypertension demonstrated a moderate discrimination (AUC =0.710; 95% CI: 0.593-0.827) and good calibration (Hosmer-Lemeshow χ2=5.70; P=0.68). Conclusions:This study identified nocturnal hypertension as a critical independent risk factor for LVH in pediatric primary hypertension. The prediction model may provide valuable insights for early identification of LVH.

BACKGROUND:Maternal obesity is a significant risk factor for liver dysfunction and metabolic dysfunction-associated steatotic liver disease (MASLD) in offspring, with oxidative stress playing a critical role in developmental programming. Understanding oxidative stress-mediated metabolic reprogramming during intrauterine overnutrition is crucial for developing MASLD preventive strategies. METHODS:Female mice were fed a Western diet to induce obesity before mating. Biochemical detection and histopathological staining were employed to assess changes in lipid metabolism and liver fibrosis. Oxidative stress indices were measured using ELISA, while metabolic profiling was conducted through liquid chromatography-tandem mass spectrometry (LC-MS) analysis. Protein expression was evaluated by western blot. RESULTS:Male offspring from obese dams (OffOb) exhibited increased activities of ALT, AST, GGT, and ALP, along with evident hepatic steatosis and fibrosis. These male offspring also showed impaired antioxidant defenses in liver. Administration of the antioxidant N-acetylcysteine during pregnancy (OffObnac) enhanced some antioxidant enzymes/substances and reversed these abnormal changes in the male offspring's liver. Notably, antioxidant treatment significantly mitigated the IL-6 increase induced by maternal obesity. According to KEGG analyses, the differential metabolites between OffOb and OffCon, as well as between OffObnac and OffOb, were primarily enriched in the forkhead box O (FoxO) signaling pathway. Protein expression results indicated that antioxidant treatment inhibited the phosphorylation activation of JAK2, STAT3, and FoxO6 in the liver of male offspring from obese mothers. CONCLUSIONS:Antioxidant management effectively alleviated oxidative stress conditions, blocked the IL-6-STAT3-FoxO6 axis, and had a robust impact on mitigating MASLD following intrauterine overnutrition-induced hepatic impairments in a mouse model.

Although it is well established that obesity is a risk factor for hypertension, the effect of distinct long-term patterns of body mass index (BMI) on blood pressure (BP) in later life is poorly understood. Based on the China Health and Nutrition Survey, we analyzed 2920 participants aged 3–17 years with initial normal BP at baseline (1991–2011), who were followed up for the development of hypertension (1993–2015). The group-based trajectory model was applied to identify BMI trajectories, and Cox regression was used to assess their associations with hypertension risk. Stratified analyses were conducted to explore differences across subgroups. During an average follow-up time of 11.20 (7.69) years for males and 7.20 (5.21) years for females, 339 males and 212 females were identified with hypertension, respectively. Three BMI trajectories were identified: low-increasing (60.58

Notch signaling activation drives an endothelial-to-mesenchymal transition (EndMT) critical for heart development, although evidence suggests that the reprogramming of endothelial cell metabolism can regulate endothelial function independent of canonical cell signaling. Herein, we investigated the crosstalk between Notch signaling and metabolic reprogramming in the EndMT process. Biochemically, we find that the NOTCH1 intracellular domain (NICD1) localizes to endothelial cell mitochondria, where it interacts with and activates the complex to enhance mitochondrial metabolism. Targeting NICD1 to mitochondria induces more EndMT compared with wild-type NICD1, and small molecule activation of PDH during pregnancy improves the phenotype in a mouse model of congenital heart defect. A NOTCH1 mutation observed in non-syndromic tetralogy of Fallot patients decreases NICD1 mitochondrial localization and subsequent PDH activity in heart tissues. Altogether, our findings demonstrate NICD1 enrichment in mitochondria of the developing mouse heart, which induces EndMT by activating PDH and subsequently improving mitochondrial metabolism. Notch signaling activation drives an endothelial-to-mesenchymal transition critical for heart development. Here, the authors investigate the role of NOTCH1 intracellular domain (NICD1) in the mitochondria of developing mouse fetal hearts.

Our previous study has demonstrated that the decline in cardiomyocytes proliferation capacity induced by maternal androgen excess was mainly attributed to the accumulation of androsterone in the heart. However, the underlying mechanism by which androsterone inhibits cardiomyocytes proliferation remains unknown. In this study, pregnant mice were injected subcutaneously daily with dihydrotestosterone (DHT) from gestational day (GD) 16.5 to GD18.5. On GD18.5, fetal heart tissue was dissected and used for analyzing androgen receptor (AR) levels. H9c2 cells and primary cardiomyocytes, isolated from fetal hearts, were applied to investigate the mechanism. H9c2 cells under androsterone treatment were subjected to RNA sequencing analysis and the results showed that genes were primarily enriched in cell cycle and DNA replication pathways. Elevated AR levels were observed in fetal cardiac tissue in the maternal DHT-treated group. Androsterone treatment increased the ratio of nuclear AR and cytoplasmic AR both in H9c2 cells and primary cardiomyocytes. The ablation and overexpression of AR can mildly reverse and aggravate cell cycle arrest induced by androsterone, respectively. ChIP-qPCR analysis suggested that AR can directly repress cell cycle and DNA replication-related gene expression, which was mediated by the recruitment of retinoblastoma protein (Rb). The repression of cell proliferation in response to androsterone was alleviated partly through the downregulation of Rb by siRNA transfection. In conclusion, AR repression to cell cycle and DNA replication-related gene expression, mediated by recruitment of Rb, may be one of the potential mechanisms of cell cycle arrest in cardiomyocytes induced by androsterone.

Background: The adverse effects of a Western diet on obesity and diabetes among reproductive-aged women pose a significant threat to the cardiovascular health of their offspring. Given the crucial role of glutathione metabolism and glutathione-related antioxidant defense systems in cardiovascular diseases through scavenging ROS and maintaining redox homeostasis, further exploration of their specific influence is imperative to develop therapeutic strategies for cardiomyopathy induced by a maternal Western diet. Methods: We developed a prenatal maternal Western diet exposure model in C57/B6 mice to investigate cardiac morphology and function through histological analysis and echocardiography. RNA sequencing and analysis were utilized to elucidate the mechanisms underlying the impact of a maternal Western diet and N-acetylcysteine treatment on cardiomyopathy. Additionally, ELISAs, transmission electron microscopy, and flow cytometry were employed to assess the antioxidant defense system and mitochondrial ROS levels in progenitor cardiomyocytes. Results: N-acetylcysteine significantly mitigated cardiomyocyte hypertrophy, myocardial interstitial fibrosis, collagen type I accumulation, and left ventricular remodeling induced by a maternal Western diet, particularly in male offspring. Furthermore, N-acetylcysteine reversed the increase in apoptosis and the increase in the β/α-MyHC ratio in the myocardium of offspring that results from a maternal Western diet. RNA sequencing and GSEA revealed that the beneficial effects of N-acetylcysteine were linked to its ability to modulate oxidative phosphorylation pathways. Additionally, N-acetylcysteine treatment during pregnancy can markedly elevate glutathione levels, augment glutathione peroxidase (GPx) activity, and mitigate the accumulation of mitochondrial ROS caused by a maternal Western diet. Conclusions: N-acetylcysteine mitigated cardiomyopathy induced by a maternal Western diet by bolstering glutathione synthesis and enhancing GPx activity, thereby scavenging mitochondrial ROS and modulating oxidative phosphorylation pathways.

Maternal hyperhomocysteinemia is widely considered as an independent risk of congenital heart disease (CHD). However, whether high paternal homocysteine causes CHD remains unknown. Here, we showed that increased homocysteine levels of male mice caused decreased sperm count, sperm motility defect and ventricular septal defect of the offspring. Moreover, high levels of paternal homocysteine decrease sperm DNMT3A/3B, accompanied with changes in DNA methylation levels in the promoter regions of CHD-related genes. Folic acid supplement could decrease the occurrence of VSD in high homocysteine male mice. This study reveals that increased paternal homocysteine level increases VSD risk in the offspring, indicating that decreasing paternal homocysteine may be an intervening target of CHD.

Mycoplasma pneumoniae(M.pneumoniae),primarily trans-mitted through respiratory droplets when infected individ-uals cough or sneeze,is a common cause of community-acquired pneumonia,especially among school-age children and adolescents.The infection occurs endemically with an epidemic peak every few years.

Background:In 2023, China witnessed an earlier and more widespread outbreak of Mycoplasma pneumoniae pneumonia (MPP). To address this situation, an online training program was designed to enhance the knowledge of MPP among pediatricians in Shanghai, China.Methods:An online training program on the diagnosis and treatment of MPP, guided by Kern's six-step approach, was developed by the Shanghai Pediatric Clinical Quality Control Center. A pre- and post-training survey was conducted using a 20-item self-administered questionnaire to investigate the pediatricians' knowledge of MPP. A linkage mechanism was established to match pretest/posttest questionnaires using personal identifiers. Paired t-tests and McNemar tests were performed to measure the differences, as appropriate, between pre- and post-training groups. A higher survey score indicated better knowledge.Results:There were 289 participants performed pre- and post-tests. The average age of the respondents was 38.7 years (standard deviation: 8.9). Over 80% of the participants were primary (32.5%) and intermediate (47.8%) pediatricians. Those from specialized hospitals accounted for the highest proportion (41.5%). The post-training group achieved significantly higher total scores than the pre-training group (91.3 vs. 67.7, t=22.48, P<0.001), regardless of the professional titles or hospital levels (all P<0.001). The accuracy rates of each question increased significantly in the post-training group (all P<0.001).Conclusions:The online training program effectively enhanced pediatricians' understanding of diagnosing and treating MPP. It is recommended to maintain continuous education and training targeting all healthcare providers.

Background Intravenous immunoglobulin (IVIG)-resistant Kawasaki disease (KD) poses a considerable challenge to patients and their families due to its severe complications. Previous researches have highlighted the critical role of immune disorders in its pathogenesis. However, fragmented studies based on isolated cases hinder a comprehensive understanding of this deadly illness. This study aimed to explore the overall landscape of peripheral blood mononuclear cells (PBMCs) in IVIG-resistant KD patients using single-cell RNA sequencing (scRNA-seq). Methods The scRNA-seq was used to characterize the transcriptomic profiles of IVIG-resistant KD patients, IVIG-responsive KD patients, and healthy controls. Data quality control (QC) and subsequent analysis were conducted using various R packages. These included DoubletFinder and Harmony for QC, Seurat and SingleR for identifying and annotating major cell types, ggpubr for calculating and visualizing the percentages of each cell type, Seurat for characterizing differentially expressed genes (DEGs) between groups, pheatmap for visualizing the DEGs, clusterProfiler for performing Gene Ontology (GO) enrichment analysis of DEGs, scRepertoire for TCR and BCR data analysis, Monocle for assessing cell differentiation trajectories, and CellChat for intercellular interaction evaluation. Results High-quality single-cell transcriptome data from 12 participants were analyzed, including five with IVIG-resistant KD, four with IVIG-responsive KD, and three healthy controls. We identified 10 major cell types and observed that the differentiation of CD8+ effector T cells was impeded in IVIG-resistant KD patients with coronary artery lesion (CAL) according to cell differentiation trajectory analysis. Subsequent cell communication analysis demonstrated that myeloid cluster with high expression of LCN2, S100P, and LTF played a key role, potentially signaling through MIF-CD74/CXCR4 and MIF-CD74/CD44 ligand-receptor pairs. Conclusion Complex immunopathological changes occur during the development of CAL in IVIG-resistant KD. Stunted differentiation of CD8+ effector T cells is noted in KD-CAL. Interactions between myeloid cells and T cells activates multiple inflammatory signaling pathways, with ligand-receptor pairs, including MIF-CD74/CXCR4 and MIF-CD74/CD44, potentially playing crucial roles.

Limited evidence was available on ambient air pollution and pediatric atopic dermatitis (AD). The study aimed to evaluate the associations between short-term exposure to air pollutants and outpatient visits for pediatric AD. From 2016-2018, we collected data on six criteria air pollutants (PM2.5, PM10, NO2, SO2, CO and O3) and daily outpatient visits for pediatric AD in 66 hospitals, covering all districts in Shanghai, China. The over-dispersed Poisson generalized additive model (GAM) was applied to fit the associations of criteria air pollutants with hospital visits. Two-pollutant models were fitted and stratified analyses by sex, age and season were conducted. We identified 477,833 outpatient visits for pediatric AD. Each interquartile range (IQR) increase in PM2.5 (IQR: 30.9 μg/m3), PM10 (8.9 μg/m3), NO2 (25.5 μg/m3), SO2 (5.8 μg/m3) and CO (0.283 mg/m3) on the concurrent day was significantly associated with increments of 2.08 % (95 % CI: 0.53 %, 3.65 %), 2.53 % (95 % CI: 0.87 %, 4.22 %), 8.14 % (95 % CI: 6.24 %, 10.08 %), 5.67 % (95 % CI: 3.58 %, 7.80 %), and 2.27 % (95 % CI: 0.70 %, 3.87 %) in pediatric AD outpatient visits, respectively. The effects of NO2 remained robust after adjustment for other air pollutants. The exposure-response curves for PM2.5 and PM10 were steeper for moderate-lower concentrations, with a flatten curves at high concentration; nearly linear relationships were found for NO2. Higher associations of NO2 exposure on AD were detected in children under 6 years old (p=0.01); and we observed larger effect of air pollutants in cool seasons (p<0.001 for PM2.5, PM10, NO2 and CO; p=0.043 for SO2). This study indicated that short-term exposure to air pollution could increase risk of outpatient visits for pediatric AD.

AIMS:Folic acid (FA) supplementation during pregnancy aims to protect foetal development. However, maternal over-supplementation of FA has been demonstrated to cause metabolic dysfunction and increase the risk of autism, retinoblastoma, and respiratory illness in the offspring. Moreover, FA supplementation reduces the risk of congenital heart disease. However, little is known about its possible adverse effects on cardiac health resulting from maternal over-supplementation. In this study, we assessed the detrimental effects of maternal FA over-supplementation on the cardiac health of the offspring. METHODS AND RESULTS:Eight-week-old C57BL/6J pregnant mice were randomly divided into control and over-supplemented groups. The offspring cardiac function was assessed using echocardiography. Cardiac fibrosis was assessed in the left ventricular myocardium by histological analysis. Proteomic, protein, RNA, and DNA methylation analyses were performed by liquid chromatography-tandem mass spectrometry, western blotting, real-time quantitative PCR, and bisulfite sequencing, respectively. We found that maternal periconceptional FA over-supplementation impaired cardiac function with the decreased left ventricular ejection fraction in the offspring. Biochemical indices and tissue staining further confirmed impaired cardiac function in offspring caused by maternal FA over-supplementation. The combined proteomic, RNA expression, and DNA methylation analyses suggested that key genes involved in cardiac function were inhibited at the transcriptional level possibly due to increased DNA methylation. Among these, superoxide dismutase 1 was down-regulated, and reactive oxygen species (ROS) levels increased in the mouse heart. Inhibition of ROS generation using the antioxidant N-acetylcysteine rescued the impaired cardiac function resulting from maternal FA over-supplementation. CONCLUSIONS:Our study revealed that over-supplementation with FA during mouse pregnancy is detrimental to cardiac function with the decreased left ventricular ejection fraction in the offspring and provides insights into the mechanisms underlying the association between maternal FA status and health outcomes in the offspring.

Kawasaki disease(KD)is a disorder of immune responses.The prevalence of KD among 100,000 children aged 0-4 years was 71.9-110.0 in China,170.9-194.9 in Korea,and 18.1-21.3 in the USA[1].The most severe complication of KD is coronary artery lesions(CALs),including coronary dilatation and coronary aneurysms,which may even lead to myocardial ischemia,myocardial infarction,and sudden death.

Background: The development of the pediatric care system is uneven in China. Limited research has been conducted on pediatric care in Shanghai, which is a well-developed region in China, in which the National Children's Medical Centers are located. Methods: In November 2021, under the commission of the Shanghai Center for Medical Quality Control, a city-wide questionnaire designed to examine the provision of medical services to children in Shanghai in 2020 was conducted at 86 hospitals providing pediatric care. The overall characteristics and disparities between the general hospitals and children's hospitals and suggestions for future developments were explored. Results: In 2020, there were 86 hospitals providing pediatric care, covering all 16 municipal districts of Shanghai, with an average distribution of 1.4 hospitals per 100 km(2). The hospitals were mainly public (94.2%) and general (96.5%) hospitals. With a response rate of 90.7%, the questionnaire results revealed that there were 2,683 in-service pediatricians in Shanghai, with an average of 1.1 pediatrician per 1,000 children aged 0-14 years in Shanghai. The pediatricians were mainly women (71.8%), aged 40 years or younger (60.6%), who held a bachelor's degree or higher (99.5%). The total number of pediatric outpatient and emergency visits was approximately 8 million, with an average of 2,973 visits per pediatrician in 2020. There were >370,000 visits to fever clinics. The number of pediatric inpatient visits exceeded 160,000, with an average hospital stay length of 5.8 days. The uneven development between the children's hospitals and general hospitals represents a major challenge facing Shanghai's pediatric care system, and the close links between the 2 types of hospitals need to be further strengthened. Conclusions: Shanghai provides an overall superior medical service to children in China. The close link between the children's hospitals and general hospitals should be further strengthened to optimize the distribution of high-quality resources and greatly improve the overall provision of pediatric medical services.

Increasing evidence shows that maternal hyperglycemia inhibits cardiomyocyte (CM) proliferation and promotes cell apoptosis during fetal heart development, which leads to cardiac dysplasia. Accumulating evidence suggests that the overexpression of miR-21 in CMs has a protective role in cardiac function. Therefore, we investigated whether miR-21 can rescue CM injury caused by high glucose. First, we performed biological function analysis of miR-21-5p overexpression in H9c2 cells treated with high glucose. We found that the proliferation of H9c2 cells treated with high glucose decreased significantly and was rescued after overexpression of miR-21-5p. CCK-8 and EdU incorporation assays were performed to assess cell proliferation. The cell proliferation of the miR-21-5p mimic transfection group was improved compared with that of the NC mimic group (* p < 0.05, miR-21-5p mimics vs. NC mimics) when the proliferation of H9c2 cells was reduced by high glucose (**** p < 0.0001, high glucose (HG) vs. normal glucose (NG)). Then, we verified the targeted and negative regulation of miR-21-5p on Rhob using a dual-luciferase activity assay and RT-qPCR, respectively. We further demonstrated that miR-21-5p regulates Rhob to rescue the inhibition of CM proliferation induced by high glucose. The CCK-8 results showed that the cell proliferation of the siRNA-Rhob group was higher than that of the NC mimic group (*** p < 0.001) and that of the cotransfection group with Up-Rhob plasmids and miR-21-5p mimics was lower than that of the miR-21-5p mimic group (* p < 0.05). Conclusion: Overexpression of miR-21-5p rescues the inhibition of high glucose-induced CM proliferation through regulation of Rhob .

目的 分析上海市市级医院儿内科卫生资源配置和医疗服务供给现况,为优化儿内科医疗资源配置、提高医疗服务能力提供依据.方法 依托上海市市级医院临床能力促进与提升儿内科联盟,采用问卷调查方法,调查上海市4家公立市级儿童专科医院、15家综合性医院儿科及3家妇产科医院新生儿科,收集2020年儿内科医师和护士人数、儿内科床位数、儿内科门急诊人次数、儿内科出院人次数等数据.比较不同类型医院数据,并与本市医护总体人力资源进行比较,描述和分析上海市市级医院儿内科卫生资源配置和医疗服务供给现状,提出儿内科医疗资源配置的对策和建议.结果 本次调研的市级医院中,儿内科医师1253人,占全市医师的1.68％,儿内科护士2029人,占全市护士的2.09％;儿内科医护比为1:1.62.儿内科医师以硕士学历为主(占50.84％),儿内科护士以本科学历为主(占55.89％).儿内科医师以中级职称为主(占39.43％);儿内科护士以初级职称为主(占54.02％),仅1.28％为高级职称.儿童专科医院在市级医院儿内科设备配置和医疗服务供给中占绝对优势,基本设备配置占81.71％,床位资源配置占75.60％,门急诊人次占74.04％,发热门诊人次数占83.58％,出院人次数占80.42％.结论 上海市儿童专科医院资源配置优势明显,但儿童专科医院医师年均负担出院人次负荷高于全市医师的平均水平.通过市级儿童专科医院对儿科联合体的技术支撑和辐射,帮助综合性医院儿内科进一步加强自身建设,将有助于提升本市综合医院儿内科门急诊服务能力,提高区域内儿内科医疗服务同质化水平.

Objective: To investigate the epidemiology and hospitalization costs of pediatric community-acquired pneumonia (CAP) in Shanghai. Methods: A retrospective case summary was conducted on 63 614 hospitalized children with CAP in 59 public hospitals in Shanghai from January 2018 to December 2020. These children's medical records, including their basic information, diagnosis, procedures, and costs, were extracted. According to the medical institutions they were admitted, the patients were divided into the children's hospital group, the tertiary general hospital group and the secondary hospital group; according to the age, they were divided into <1 year old group, 1-<3 years old group, 3-<6 years old group, 6-<12 years old group and 12-18 years old group; according to the CAP severity, they were divided into severe pneumonia group and non-severe pneumonia group; according to whether an operation was conducted, the patients were divided into the operation group and the non-operation group. The epidemiological characteristics and hospitalization costs were compared among the groups. The χ2 test or Wilcoxon rank sum test was used for the comparisons between two groups as appropriate, and the Kruskal-Wallis H test was conducted for comparisons among multiple groups. Results: A total of 63 614 hospitalized children with CAP were enrolled, including 34 243 males and 29 371 females. Their visiting age was 4 (2, 6) years. The length of stay was 6 (5, 8) days. There were 17 974 cases(28.3%) in the secondary hospital group, 35 331 cases (55.5%) in the tertiary general hospital group and 10 309 cases (16.2%) in the children's hospital group. Compared with the hospitalizations cases in 2018 (27 943), the cases in 2019 (29 009) increased by 3.8% (1 066/27 943), while sharply declined by 76.2% (21 281/27 943) in 2020 (6 662). There were significant differences in the proportion of patients from other provinces and severe pneumonia cases, and the hospitalization costs among the children's hospital, secondary hospital and tertiary general hospital (7 146 cases(69.3%) vs. 2 202 cases (12.3%) vs. 9 598 cases (27.2%), 6 929 cases (67.2%) vs. 2 270 cases (12.6%) vs. 9 397 cases (26.6%), 8 304 (6 261, 11 219) vs. 1 882 (1 304, 2 796) vs. 3 195 (2 364, 4 352) CNY, χ2=10 462.50, 9 702.26, 28 037.23, all P<0.001). The annual total hospitalization costs of pediatric CAP from 2018 to 2020 were 110 million CNY, 130 million CNY and 40 million CNY, respectively. And the cost for each hospitalization increased year by year, which was 2 940 (1 939, 4 438), 3 215 (2 126, 5 011) and 3 673 (2 274, 6 975) CNY, respectively. There were also significant differences in the hospitalization expenses in the different age groups of <1 year old, 1-<3 years old, 3-<6 years old, 6-<12 years old and 12-18 years old (5 941 (2 787, 9 247) vs. 2 793 (1 803, 4 336) vs. 3 013 (2 070, 4 329) vs. 3 473 (2 400, 5 097) vs. 4 290 (2 837, 7 314) CNY, χ2=3 462.39, P<0.001). The hospitalization cost of severe pneumonia was significantly higher than that of non-severe cases (5 076 (3 250, 8 364) vs. 2 685 (1 780, 3 843) CNY, Z=109.77, P<0.001). The cost of patients who received operation was significantly higher than that of whom did not (10 040 (4 583, 14 308) vs. 3 083 (2 025, 4 747) CNY, Z=44.46, P<0.001). Conclusions: The number of children hospitalized with CAP in Shanghai decreased significantly in 2020 was significantly lower than that in 2018 and 2019.The proportion of patients from other provinces and with severe pneumonia are mainly admitted in children's hospitals. Hospitalization costs are higher in children's hospitals, and also for children younger than 1 year old, severe cases and patients undergoing operations.

目的 构建基于真实临床情景下的提升上海市儿科医护人员急诊急救能力的培训方案.方法 在复旦大学附属儿科医院门急诊电子病例系统中获取2019年1月—2021年12月进入急诊抢救室的病历,提取急诊诊疗活动名称及具体内容,结合专家访谈及德尔菲法形成儿科急诊急救可信赖专业活动(entrustable professional activities,EPAs)清单;由急诊专业领域权威专家对儿科急诊急救可信赖专业活动及内容就相关性及重要性进行评分;在前述工作的基础上,形成《儿科医护人员急诊急救能力提升培训方案》,邀请急诊医疗、护理、管理及教学相关专业专家进行两轮函询并进行专家论证.结果 《儿科医护人员急诊急救能力提升培训方案》包括理论和技能两大核心板块,并根据课程内容设置不同培训方式.经专家论证该方案契合临床真实情境,具有较强的科学性和实用性.结论 《儿科医护人员急诊急救能力提升培训方案》成功构建,可为临床实施有针对的培训继而提升儿科急诊医务人员的急救能力提供参考.

Maternal obesity affects the risk of cardiovascular disease and inflammatory response in offspring. However, the impact of maternal obesity on offspring with Kawasaki disease (KD), the leading cause of childhood acquired heart disease, is still an understudied area. This study aimed to elucidate the impact of maternal obesity on offspring in KD-like vasculitis and the underlying mechanisms. Offspring of obese female mice and normal diet dams were randomly divided into two subgroups. The pups were injected intraperitoneally with either Candida albicans water-soluble fraction (CAWS) or phosphate buffered saline (PBS) to establish the obesity (OB)-CAWS group, OB group, wild type (WT)-CAWS group, and WT group. Their weight was monitored during the study. After four weeks, echocardiography was applied to obtain the alternation of cardiac structures. Mouse cytokine panel, Hematoxylin-Eosin (HE) staining, western blot, and real-time qPCR were used to study the pathological changes and protein and RNA expression alternations. Based on the study of pathology, serology and molecular biology, maternal obesity lead to more severe vasculitis and induced altered cardiac structure in the offspring mice and promoted the expression of pro-inflammatory cytokines through activating the NF-κB signaling pathway. Maternal obesity aggravated the inflammatory response of offspring mice in KD-like vasculitis.