Wuhan Children's Hospital

Abstract Background Pulmonary aspiration is a rare but potentially serious complication of pediatric anesthesia. Concerns regarding aspiration risk continue to influence perioperative decision-making, particularly with respect to fasting policies and airway management strategies. However, real-world clinical practice often differs from guideline recommendations [1,2]. Methods We conducted a retrospective cohort study of pediatric patients undergoing anesthesia at a tertiary pediatric hospital over a 10-year period. Data were extracted from the institutional anesthesia database and electronic medical records. Variables included patient demographics, surgical category, fasting duration, last intake type, airway management technique, and aspiration-related events. Results A total of 3230 pediatric anesthetics were included. The median age was 4.61 years (IQR 2.1–8.0) . The median fasting duration was 5.19 hours (IQR 3.91–6.47) and 65.8% of patients fasted less than 6 hours . Supraglottic airway devices were used in 2763 cases (85.6%) , while 467 cases (14.4%) underwent primary endotracheal intubation. Conversion from supraglottic airway to tracheal intubation occurred in 93 cases (3.4%) . No intraoperative pulmonary aspiration events were observed. One intraoperative regurgitation event occurred without pulmonary complications. Two aspiration events occurred in the ward several hours after postoperative feeding. With zero intraoperative aspiration events in 3230 anesthetics, the upper bound of the 95% confidence interval estimated using the rule-of-three method was approximately 0.93 per 1000 anesthetics [13]. Conclusions In this 10-year cohort of pediatric anesthetics, no intraoperative pulmonary aspiration events were observed despite relatively short fasting durations and widespread use of supraglottic airway devices . Aspiration events occurred only after postoperative feeding, suggesting that perioperative vigilance should extend beyond the operating room to the postoperative recovery period .

Megalobrama amblycephala is an economically important fish species in Chinese aquaculture, but its high sensitivity to hypoxia poses a major challenge for farming. This study aims to investigate the role of the E3 ubiquitin ligase parkin in regulating hypoxia signaling in fish. Under hypoxic stress, parkin expression was significantly upregulated in oxygen-sensitive tissues (brain and gills) and embryos of M. amblycephala, consistent with the expression of hypoxia-responsive genes. Ma-parkin was found to exhibit high conservation in its key functional domains. Mechanistically, it directly interacts with Ma-hif-α, promoting their ubiquitination and proteasomal degradation via E3 ligase activity, thereby suppressing hif-mediated transcriptional activation. Critical residues T74 and C333 were identified as essential for this activity; mutations at these sites impaired Ma-hif-α degradation and ubiquitination, as well as HRE transactivation. Furthermore, we found that Ma-hif-α can regulate the transcription of parkin, forming a negative feedback loop to fine-tune the hypoxic response. Our study demonstrates that parkin serves as a key negative regulator of the hypoxia signaling pathway in M. amblycephala, operating through a finely tuned feedback mechanism. The E3 ubiquitin ligase activity of parkin, dependent on critical residues T74 and C333, directly mediates hif-α ubiquitination and degradation. The reciprocal regulation between hif-α and parkin forms a regulatory circuit that modulates the hypoxic response. These findings not only reveal a conserved adaptive mechanism to hypoxia in fish but also identify specific molecular targets for genetic improvement of hypoxia tolerance in aquaculture species.

Neurofibromatosis type 1 (NF1) and Peutz-Jeghers syndrome (PJS) are distinct autosomal dominant disorders. Their concomitant occurrence is exceptionally rare. This report describes a unique pediatric case of this dual diagnosis. An 8-year-old boy presented with paroxysmal abdominal pain accompanied by crying. He had multiple café-au-lait macules and a family history of NF1. He experienced recurrent intussusception resistant to non-invasive reduction. Exploratory laparotomy revealed jejunal intussusception caused by hamartomatous polyps, leading to resection and anastomosis. Histopathology revealed hamartomatous polyps consistent with PJS. Subsequent genetic testing revealed a paternally inherited pathogenic NF1 variant and a de novo pathogenic STK11 variant, confirming the dual diagnosis. Comprehensive evaluation identified additional NF1-associated features, including intracranial lesions. The patient recovered well postoperatively and remained asymptomatic during one-year of follow-up. This case highlights one of the rare documented instances of concurrent NF1 and PJS. It underscores the critical importance of considering a second underlying pathology in patients with known genetic disorders who present with atypical or refractory symptoms. The diagnosis was ultimately corroborated by comprehensive genetic testing, underscoring its pivotal role in delineating complex phenotypes. A high index of suspicion is necessary for timely diagnosis. Optimal management for such complex cases requires a multifaceted approach, including appropriate surgical intervention and establishing a long-term, multidisciplinary surveillance strategy to address the cumulative cancer risks and multi-system complications associated with both syndromes.

Retrospective observational cohort study SETTING: Three hospitals in China. To elucidate the pathogenesis of pediatric acute hyperextension spinal cord injury (PAHSCI) through comprehensive analysis of acute-phase clinical outcomes and multimodal magnetic resonance imaging (MRI) characteristics. We retrospectively analyzed 49 persons with PAHSCI. Case data and MRI multimodal imaging such as MRI, magnetic resonance angiography (MRA), and diffusion tensor imaging (DTI) were collected. Pathogenesis was analyzed based on clinical outcomes, radiological characteristics, spinal anatomy, and biomechanics. The primary cause of PAHSCI was back-bending training (45/49). The American Spinal Injury Association (ASIA) impairment scale distribution at admission was grade A (n = 29), B (n = 13), C (n = 4), D (n = 3). Final follow-up revealed grade A (n = 29), B (n = 4), C (n = 1), D (n = 10), E (n = 5). The level of spinal cord injury in most cases (48/49) was located at the Th9-L1 level, and intramedullary edema was observed on MRI in 48 persons at admission. Intramedullary hemorrhage was observed in 27 cases, and sequential MRI showed progressively increasing intramedullary edema. In 22 cases, atrophy or even disappearance of the middle and lower thoracic spinal cord occurred 2-6 months after spinal cord injury. MRI of 19 cases showed same radiological changes at the conus-cauda equina junction, which manifested as an arcuate depression on the anterior side of the conus medullaris. Seventeen persons with MRA examination did not have vascular malformations, vascular embolisms, or arteriovenous fistulas. We believe that the possible pathogenesis of PAHSCI is: "axial traction (especially at conus) + transverse compression (especially at Th9-10)" of the spinal cord and the resulting microvascular damage ultimately resulting in spinal cord ischemia, edema, necrosis, and the formation of a vicious cycle, ultimately causing spinal cord atrophy.

This report describes a patient with a <i>de novo</i> missense variant in the N-terminal zinc-finger domain of <i>ZEB2</i> who presented with neurodevelopmental delay, atypical facial features, and recurrent respiratory infections, alongside a reduction in infection frequency during zinc supplementation. The variant is classified as likely pathogenic, and these observations expand the phenotypic variability potentially associated with <i>ZEB2</i> variants. Additional cases and functional studies are required to confirm any causal link between the variant, the observed phenotype, and the effects of zinc supplementation.

Chronic atrophic gastritis with accelerated progression represents a major risk factor for gastric cancer development, primarily driven by pathological processes including microbial imbalance, oxidative stress, chronic inflammation, immune dysregulation, mucin dynamics, and glycobiological disorders. Its global incidence is on the rise. Current diagnostic and therapeutic approaches under the reactive medicine paradigm demonstrate limited efficacy in controlling disease progression. Against this backdrop, supramolecular self-assembling delivery systems derived from herbal medicine offer breakthrough solutions to the current diagnostic and therapeutic challenges of chronic atrophic gastritis. Their advantages include natural origin, simple assembly, multi-target synergistic effects, high biocompatibility, and low potential toxicity. By summarizing the molecular mechanisms underlying chronic atrophic gastritis and the strengths and limitations of traditional Chinese and Western medical approaches, this study proposes the health benefits of herb-derived supramolecular self-assembling delivery systems for chronic atrophic gastritis under predictive, preventive, and personalized medicine (PPPM/3PM). This review further proposes an innovative strategy within the PPPM/3PM framework, positioning the herb-derived supramolecular self-assembling delivery system as a predictive medical approach, a cost-effective preventive measure, and a tailored optimal treatment plan for patients with chronic atrophic gastritis across primary care (protecting susceptible populations from health deterioration to disease), secondary care (protecting affected populations from disease progression), and tertiary care (enhancing patient quality of life and reducing complications). Supramolecular self-assembling delivery systems derived from natural herbal medicines enable personalized prevention and treatment of chronic atrophic gastritis with superior cost-effectiveness compared to conventional reactive medicine.

<title>Abstract</title> <bold>Objective:</bold> Differentiating septic arthritis from transient synovitis in children is challenging. This study aimed to determine the diagnostic value for distinguishing these two conditions and to develop an effective clinical prediction model based on multi-center clinical data to identify and differentiate between the two diseases more comprehensively and accurately. <bold>Methods:</bold> We retrospectively analyzed data of children aged under 18 years who were hospitalized in eight specialized children's hospitals in China from 2013 to 2021. The data included age, sex, initial hospital admission temperature, history of prodromal respiratory infection, prodromal history of strenuous exercise, etc. Laboratory test results, including that of erythrocyte sedimentation rate (ESR), serum white blood cell count (WBC), C-reactive protein (CRP), platelet count (PC), pathogenic bacterial count and other information. The common sites of bone and joint infection in children are the hip and knee joints. Therefore, to ensure the prediction model's reliability, we established three clinical prediction models: one for septic hip arthritis and transient hip synovitis, one for septic knee arthritis and transient knee synovitis, and one for septic arthritis and transient synovitis in either joint which we merged all the data of the hip and knee joints into one data set to build a clinical prediction model. In addition, we conducted single-factor and multi-factor analyses on the data classified by these models. <bold>Results:</bold> This study collected data of 819 children from 8 tertiary children's hospitals, including 265 patients with septic arthritis (mean age 5.55±7.16 years) and 554 patients with transient synovitis (mean age 4.8±3.2 years). In 265 blood and joint aspirate cultures of septic arthritis, the most common causative organism was Staphylococcus aureus (59%). To ensure the quality and reliability of the prediction models, we established three clinical prediction models. For septic hip arthritis, a retrospective study based on six clinical predictors was a history of prodromal respiratory tract infection (HRTI), temperature&gt;37.5 ºC, ESR&gt;20 mm/h, CRP&gt;10 mg/L, red blood cell distribution width (RDW)&gt;50%, and WBC&gt;11×109 /L. When these six factors were present, the probability of septic hip arthritis was 99.99%. For septic knee arthritis, a retrospective study based on three clinical predictors, the predictors were ESR&gt;20 mm/h, CRP&gt;10 mg/L, and absolute monocyte count (AMONO)&gt;0.74×109/L. When these three factors were present, the probability of having septic knee arthritis was 94.68%. For septic arthritis (septic hip arthritis or septic knee arthritis), a retrospective study based on six clinical predictors, the predictors were male children, history of HRTI), temperature&gt;37.5 ºC, ESR&gt;20 mm/hr, PC &gt; 407×10 ⁹ /L and CRP&gt;10 mg/L. When these six factors were present, the probability of septic arthritis was 99.65%. <bold>Conclusion:</bold> This study used multi-center clinical data to construct a new clinical prediction model for children with septic arthritis. The clinical prediction model algorithm developed here outperformed that of previous studies in the probability of diagnosing septic arthritis. In addition to considering body temperature, WBC, ESR, and CRP, we identified new clinical predictors such as sex, history of HRTI, RDW, PC and AMONO.

Despite the persistent global threat of seasonal influenza viruses such as A(H1N1)pdm09 and A/H3N2, their epidemiological and genetic characteristics in China following the implementation of COVID-19 non-pharmaceutical interventions (NPIs) remain poorly characterized. Between September 2020 and December 2023, we conducted an integrated epidemiological and genomic analysis of influenza A viruses in children in Wuhan. The overall positivity rate for influenza A virus was markedly low at 3.43% (109/3171), reflecting a profound suppression of circulation during the pandemic. Among genotyped positives, H1N1pdm09 was predominant (52.3%), followed by H3N2 (16.5%) and untypeable strains (32.1%). Preschool children showed the highest susceptibility. Phylogenetic analysis revealed that the circulating H1N1 strains (90%) belonged to clade 6B.1A.5a.2, clustering with viruses from Hong Kong and Pakistan. In contrast, H3N2 strains (76.92%) primarily fell into clade 3C.2a1b.2a.2b, closely related to contemporary strains from Europe and North America. Notably, we identified key hemagglutinin mutations associated with antigenic drift (e.g., R240Q in H1N1; E78G, R158G in H3N2) and neuraminidase mutations potentially conferring antiviral resistance (e.g., S247N in H1N1; S245N, a putative novel glycosylation site, in H3N2). Evidence of reassortment events was also detected, underscoring the continued genomic evolution of these viruses despite their low prevalence. Our findings demonstrate that genetically diverse and antigenically drifted influenza A viruses continued to circulate and evolve in Wuhan during the COVID-19 pandemic, albeit at dramatically reduced levels. This highlights the critical need for sustained genomic surveillance and timely updates of vaccine compositions to pre-empt the resurgence of influenza in the post-pandemic era.

Non-obstructive azoospermia (NOA) is the severest form of male infertility. This study aimed to identify core genes associated with mitochondrial dysfunction and regulatory networks in NOA, providing potential diagnostic biomarkers and therapeutic targets for NOA. We identified mitochondrial dysfunction-related hub genes by analyzing three testis transcriptome datasets, and further confirmed their diagnostic value, differential expression in clinical specimens, and immune infiltration associations. For GSE108886 and GSE145467, 35 mitochondrial dysfunction-related differentially expressed genes (MD-DEGs, 10 upregulated and 25 downregulated) were obtained. And 6 common hub genes (COX7A1, COX7A2, COX7B2, MRPS15, AURKAIP1, and PDHA2) were identified. hsa-miR-12,116, hsa-miR-296-5p, and transcription factors (FOXA1, FOXC1, GATA2, SRF) simultaneously targeted two hub MD-DEGs. Diagnostic model incorporating COX7A1, COX7A2, AURKAIP1 and MRPS15 presented preliminary diagnostic efficacy with AUC value of 0.930 (95% CI [0.835-1.000]). Subsequently, RT-qPCR confirmed upregulation of COX7A1 (P < 0.05) and downregulation of COX7A2, COX7B2, MRPS15, AURKAIP1 and PDHA2 (P < 0.05 for all) in NOA patients. In addition, T cells CD8 and Mast cells resting were enriched in NOA patients. MD-DEGs including COX7A1, COX7A2, MRPS15 and AURKAIP1 may play pivotal roles in NOA pathogenesis, and could serve as a pre-biopsy screening tool to stratify patients and monitor therapeutic responses for NOA.