Hangzhou Children's Hospital

Abstract Objective To analyze the epidemiological characteristics and macrolide resistance profile of Mycoplasma pneumoniae (MP) infections among children in Hangzhou during the post-COVID-19 period (2024–2025), providing evidence for precise clinical management. Methods We conducted a retrospective analysis of 12,380 respiratory specimens from patients at Hangzhou Children’s Hospital (March 2024 to December 2025). MP nucleic acid and the 23S rRNA A2063G/A2064G resistance mutations were detected using quantitative PCR. Positivity and resistance rates were analyzed across gender, age, care setting (inpatient/outpatient), and time. Results The overall MP positivity rate was 19.98% (2,473/12,380). Among positive cases, 86.94% (2,150/2,473) carried resistance mutations. Positivity rates did not differ significantly by gender (19.58% vs 20.41%, P > 0.05). However, outpatients had a significantly higher positivity rate than inpatients (29.96% vs 18.96%; χ²=74.32, P < 0.01), and a higher resistance rate (92.13% vs 86.10%; χ²=11.89, P < 0.01). Infection rates exhibited a unimodal age distribution, peaking in children aged 6–12 years (27.90%-39.08%). Resistance rates exceeded 78% across all age groups. In 2024, the monthly resistance rate fluctuated between 74.89% and 94.20%. Conclusion During 2024–2025, MP infections in children showed distinct age clustering, with school-aged children at highest risk. Macrolide resistance was alarmingly prevalent (> 85%) and particularly prominent in outpatients. These findings underscore the need for enhanced resistance surveillance and optimized antibiotic stewardship in pediatric and outpatient settings.

The complement system constitutes a critical component of innate immunity against fungal pathogens. Complement component 9 (C9), an essential constituent of the membrane attack complex (MAC), plays a pivotal role in pathogen elimination. However, isolated C9 deficiency has not been previously reported in association with fungal esophagitis. We present the case of a nearly 7-year-old girl who suffered from progressive dysphagia, nausea, and vomiting for more than two months. Esophagogastroduodenoscopy revealed esophageal stricture, and histopathological examination of mucosal biopsies confirmed Candida albicans infection. Despite multiple endoscopic dilations, symptomatic recurrence occurred monthly. Whole-exome sequencing identified a pathogenic variant confirming isolated C9 deficiency. Combined systemic antifungal therapy with fluconazole and repeated endoscopic dilatation achieved sustained symptomatic resolution. Isolated C9 deficiency may represent a susceptibility factor for recurrent fungal esophagitis with stricture formation in children. Complement screening should be considered in unexplained recurrent cases. Combined antifungal therapy and endoscopic intervention achieved sustained remission in this patient.

To investigate the potential role of the environmental pollutant tris(2-butoxyethyl) phosphate (TBOEP) in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) and to elucidate its underlying molecular mechanisms. We employed an integrated multi-omics approach. First, a multidatabase strategy identified overlapping targets between TBOEP and MASLD, which were subjected to functional enrichment and protein-protein interaction (PPI) network analysis. Molecular docking was then used to predict binding affinities. Second, transcriptomic profiling (RNA sequencing (RNA-seq)) was performed on TBOEP-treated AML-12 hepatocytes to identify differentially expressed genes and pathways. Finally, key findings were validated in vitro using Oil Red O staining, triglyceride quantification and western blot analysis. We identified 154 common targets between TBOEP and MASLD, with enrichment analysis pointing to pathways in non-alcoholic fatty liver disease and insulin resistance. PPI analysis highlighted ACTB, IL6, PPARG and PPARA as pivotal hub proteins. RNA-seq revealed 326 differentially expressed genes, with significant alterations in metabolic pathways. Cross-referencing pathways predicted from target genes with RNA-seq data revealed 10 pathways potentially impacted by TBOEP, emphasising its multifaceted effects on hepatocyte function. In vitro studies showed that TBOEP promotes lipid accumulation in hepatocytes by increasing PPARγ expression. Our study provides evidence that TBOEP acts as a potential environmental risk factor for MASLD. We demonstrate that TBOEP promotes hepatocyte steatosis, likely through the dysregulation of metabolic pathways centred on PPARγ signalling. These findings provide new insights into the pathogenesis of MASLD.

To enhance clinicians' understanding of Sifrim-Hitz-Weiss syndrome (SIHIWES), this study investigated the clinical phenotypes, genetic characteristics, and response to growth hormone therapy in a patient. A case of a patient with global developmental delay and distinctive facial features is presented. To identify the underlying etiology, peripheral blood samples were collected from the patient and both parents. Whole-exome sequencing (WES) and genomic copy number variation (CNV) analysis were conducted. Candidate variants were confirmed by Sanger sequencing within the family, and bioinformatics tools assessed their pathogenicity. WES identified a de novo heterozygous variant, c.3547C>T (p.Arg1183Cys), in CHD4. Both parents were wild-type at this locus, and CNV analysis revealed no pathogenic variants. Based on ACMG guidelines, this variant is classified as pathogenic. Combining clinical phenotypes with genetic findings, this study confirmed the diagnosis of Sifrim-Hitz-Weiss syndrome. Protein structure modeling indicated that the CHD4 protein harbors an Arg1183Cys variant in the α-helix. The cysteine side chain, containing a sulfur atom, may introduce new chemical interactions, potentially altering CHD4 protein function. Short-term growth-promoting effects were observed with recombinant human growth hormone (rhGH) therapy, providing new insights for managing this disorder. Long-term efficacy and safety should be evaluated in larger studies.

BackgroundMicroRNAs (miRNAs) have been verified to be involved in various biological processes through regulating their target genes, and some previous studies have revealed the antitumour role of microRNA-374b-5p (miR-374b-5p) in several tumours. Therefore, the purpose of this study was to explore the functions and potential mechanisms of miR-374b-5p in osteosarcoma (OS) progression.MethodsThe differentially expressed gene miR-374b-5p was discovered in the dataset GSE65071 from the Gene Expression Omnibus (GEO) database via bioinformatics analysis, and its expression levels in OS tissues and cell lines were confirmed by RNA fluorescence in situ hybridization (FISH) staining and quantitative real-time polymerase chain reaction (qRT-PCR). OS cell proliferation ability was evaluated by Cell Counting Kit-8 (CCK-8) assay and colony formation assay, cell migration and invasion abilities were assessed by Transwell assays, and apoptosis was detected by flow cytometry. The underlying mechanisms of miR-374b-5p in regulating OS progression were explored by qRT-PCR, dual-luciferase reporter assay and western blotting. In vivo experiments, a nude mice xenograft tumour model was performed to evaluate the effects of miR-374b-5p on tumour growth and gene expression changes.ResultsIn this study, miR-374b-5p expression was confirmed to be significantly down-regulated in OS, and miR-374b-5p overexpression could inhibit the proliferation, migration, and invasion abilities but promote apoptosis of OS cells. Mechanism studies revealed that miR-374b-5p suppressed the AKT pathway via negatively regulating the expression of phosphoinositide-dependent protein kinase 1 (PDPK1). Notably, PDPK1 were highly expressed in OS cell lines, as verified by qRT-PCR, and PDPK1-silencing considerably restrained OS progression. Moreover, the inhibitory effects of miR-374b-5p on OS progression were partially reversed by PDPK1 overexpression both in vitro and in vivo.ConclusionsMiR-374b-5p was lowly expressed in OS, and its upregulation inhibited the progression of OS by directly targeting PDPK1 to affect the activity of the AKT pathway.

Allergic asthma in children significantly impacts quality of life, and immunotherapy, including subcutaneous immunotherapy (SCIT) and sublingual immunotherapy (SLIT), has emerged as an effective treatment. However, their comparative immunological mechanisms remain unclear. This study aimed to compare the effects of SCIT and SLIT on immune response in children with allergic asthma and to explore their underlying immunological mechanisms. A total of 86 children aged 5-12 years with allergic asthma who visited Hangzhou Children's Hospital were prospectively enrolled and randomly assigned to three groups: inhaled corticosteroids (ICS) group (n = 30), SCIT group (n = 30), and SLIT group (n = 26). Clinical and immunological parameters-including Childhood Asthma Control Test (C-ACT) scores, forced expiratory volume in the first second percentage (FEV1%), Th17, Treg cells, and serum levels of IL-17, IL-9, IL-10-were assessed before treatment and after one year. After treatment, all three groups showed significant improvements in C-ACT scores and FEV1% compared to baseline (all p < 0.05). The SCIT and SLIT groups demonstrated greater improvements than the ICS group (all p < 0.05), with no significant differences between the SCIT and SLIT groups (p > 0.05). In terms of immune markers, significant differences were observed in all parameters before and after treatment in the SCIT and SLIT groups (all p < 0.05), while Treg levels in the ICS group remained unchanged (p > 0.05). No statistically significant differences in immune markers were found among the three groups post-treatment (all p >0.05). Both SCIT and SLIT, when combined with ICS, offer superior efficacy compared to ICS monotherapy. The comparable immunological changes observed in SCIT and SLIT suggest a shared mechanism of immune tolerance, potentially mediated through Treg cell induction.

BackgroundThe rising burden of pediatric allergic diseases underscores parental intentions and behaviors as critical to allergic prevention and management. This study aims to develop and validate a Protection Motivation Theory (PMT) based scale for parents of children with allergic diseases, and to examine the associations between parental protection motivation, their management intentions and behaviors, and pediatric health outcomes.MethodsWe conducted a cross-sectional study among parents of children with allergic diseases at Hangzhou Children’s Hospital, Zhejiang Province, China, from July to December 2022. The PMT scale was developed using data from a pilot survey (N = 440) and validated in an empirical study (N = 443). Structural equation modeling mapped interconnections between parental protective motivation, intention, and behavior. Multiple linear regression explored PMT dimensions’ association with parental intentions and behaviors, while machine learning models evaluated their clinical relevance to children’s disease outcomes.ResultsThe PMT scale demonstrated good reliability (Cronbach’s α coefficient = 0.844) and validity (χ2/df = 2.918, RMSEA = 0.066, GFI = 0.906, CFI = 0.937, NFI = 0.908, IFI = 0.937, TLI = 0.919). In structural equation model, protection motivation showed significant overall interconnections with parental intention (0.78, p < 0.001). PMT dimensions were associated to 48.2% and 45.5% of the variance in parental intention and behavior related to allergic diseases in multiple linear regressions, with self-efficacy and perceived susceptibility being the most strongly associated factors. Random forest models demonstrated good discrimination in identifying associations between PMT dimensions and children’s atopic severity and attacks, achieving AUC of 0.84 and 0.88 respectively, with all six PMT dimensions among the top-15 related variables.ConclusionsOur findings reveal the relevance of measuring parental protective motivation as captured by the developed PMT scale. It had significant associations with key parental intentions and behaviors in managing childhood atopy. This implies the necessity of refined PMT-based interventions to support outcomes in childhood allergic disease management.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12889-025-24580-5.

BackgroundAsthma is the most common chronic respiratory disease in children. Although conventional treatments such as inhaled corticosteroids and long-acting β2-receptor agonists can effectively control symptoms, some children still face the problem of frequent attacks and drug side effects. As a potential etiological treatment, allergen-specific immunotherapy aims to induce immune tolerance by gradually increasing exposure to specific allergens, thereby relieving asthma symptoms in the long term. This meta-analysis aims to synthesize the existing high-quality evidence and systematically review the efficacy of allergen-specific immunotherapy for childhood asthma.MethodsWe performed literature search, screening, and data extraction according to the Cochrane Collaboration guidelines. A computerized search of PubMed, Embase, Web of Science, Cochrane Central, and CNKI databases was performed, and 10 randomized controlled clinical trials (RCTs) were included. Two independent reviewers screened the literature, extracted data, and assessed the risk of bias according to predefined criteria. The main outcome measures included TASS, TMS, VAS scores, and FEV1%.ResultsA total of 10 RCT studies were included, and all met the inclusion criteria. Meta-analysis results showed that allergen-specific immunotherapy showed a positive effect in improving the symptoms of childhood asthma and reducing the need for medication. Specifically, immunotherapy significantly reduced the total asthma symptom score (TASS, SMD=-1.05, 95% CI [-2.09; -0.01]) and total medication score (TMS, SMD=-1.32, 95%CI [-2.21; -0.43]). However, no significant difference was found in VAS score and FEV1% (SMD=-1.77, 95% CI [-3.76;0.22]; SMD = 0.51, 95% CI [-0.38;1.40]). All indicators had high heterogeneity.ConclusionAllergen-specific immunotherapy showed a positive effect in improving the symptoms of childhood asthma and reducing the need for medication, but there was significant heterogeneity among different studies. More high-quality RCTs are needed in the future to further explore the safety and long-term efficacy of immunotherapy to optimize its application in the management of childhood asthma.