miR-138-5p plays a tumor-suppressing role, but its function in Wilms tumor (WT) has not yet been explored. This study aimed to investigate the role of miR-138-5p in the progression of WT. Hematoxylin‒eosin staining was used to analyze histopathological changes in WT tissues and adjacent normal tissues. qPCR was used to detect the expression of miR-138-5p in WT tissues and cells. Immunohistochemical staining and qPCR were used to detect the expression of TCF3. The interaction between miR-138-5p and TCF3 was confirmed by correlation analysis, qPCR, and dual-luciferase assays, respectively. CCK-8, colony formation, Transwell, and wound-healing assays were performed to identify the effects of miR-138-5p and TCF3 on the proliferation and migration of WiT49 cells. A murine xenograft model was used to investigate the function of miR-138-5p on WT growth in vivo. miR-138-5p was expressed at low levels in WT tissues and WiT-49 cells. Functional studies demonstrated that the upregulation of miR-138-5p markedly inhibited the proliferation, colony-formation capacity, and migratory/invasive potential of WiT-49 cells. Subsequently, the therapeutic potential of miR-138-5p overexpression was confirmed in murine xenograft models, which markedly inhibited tumor growth compared with that in the control group. TCF3 is a target of miR-138-5p, and its expression is negatively correlated with that of miR-138-5p. Furthermore, the results of rescue experiments indicated that the tumor-suppressing effects of miR-138-5p in WiT-49 cells were reversed by TCF3 overexpression. miR-138-5p could be a tumor suppressor that regulates the proliferation of WT cells by targeting and reducing TCF3 expression.
This ambispective cohort study evaluates the effectiveness of cardioprotective strategies in reducing anthracycline-induced cardiotoxicity in pediatric patients with acute lymphoblastic leukemia (ALL). We conducted a single-center, historically controlled ambispective cohort study at Kunming Children’s Hospital. Children with newly diagnosed ALL treated with the CCLG-ALL2018 protocol between May 2018 and May 2020 comprised the retrospective historical control cohort (no dexrazoxane). After institutional adoption of dexrazoxane, consecutive eligible patients treated between May 2020 and May 2022 were prospectively enrolled and followed according to a prespecified cardiac monitoring schedule. The exposure (use of dexrazoxane) was determined by calendar time rather than randomization. The combination therapy group exhibited significantly lower rates of electrocardiogram and echocardiogram abnormalities (P < 0.01 and P < 0.01, respectively), suggesting a notable cardioprotective effect. Although baseline cardiac markers did not show significant differences between the groups, post-treatment levels of cardiac troponin T were significantly improved in the combination therapy group (P < 0.05). Additionally, trends toward improved left ventricular ejection fraction and Creatine Kinase-Myocardial Band levels were observed, although these did not reach statistical significance. Importantly, the use of the cardioprotective agent did not lead to a significant increase in adverse reactions. Incorporating a cardioprotective strategy into pediatric ALL treatment protocols appears to lower the risk of anthracycline-induced cardiotoxicity without compromising safety, hence boosting patient outcomes. These findings should be interpreted in light of the historically controlled, nonrandomized design and potential time-related confounding.
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons and alpha-synuclein (α-syn) aggregation. Although current therapies alleviate symptoms, they fail to halt disease progression, and the underlying drivers remain elusive. Cellular metabolic dysfunction, particularly impaired glucose metabolism and reduced adenosine triphosphate production, considerably contributes to PD pathogenesis. This review systematically describes the core features of brain glucose metabolism and the cooperative metabolic network between neurons and astrocytes. Furthermore, it details specific alterations in glycolytic pathways observed in PD, elucidating the mechanisms by which key factors such as dopamine, α-syn, and DJ-1 contribute to this metabolic impairment. Finally, the review critically evaluates emerging therapeutic strategies targeting glycolysis to restore energy homeostasis, underscoring their potential as novel interventions to suppress disease progression. A deeper understanding of these metabolic mechanisms promises new avenues for developing effective PD treatments.
Background: With the increasing variety of pediatric diagnostic procedures, a growing number of children require sedation for diagnostic examinations. Appropriate sedation protocols guarantee the safety of children during sedation and improve its efficiency. Currently, there are significant differences in pediatric sedation practices across countries, regions, and medical institutions. Methods: The Pediatric Anesthesiology Group of the Chinese Society of Anesthesiology organized experts from multiple countries to develop the "Chinese Society of Pediatric Anesthesiology Guideline for Pediatric sedation (2025)" based on evidence-based medicine, considering the safety and efficacy, the preferences of children and parents, and drug accessibility. Results: The guideline provided 28 recommendations addressing 12 clinical issues related to pre-sedation assessment, safety measures for sedation personnel and facilities, sedation protocols, sedation monitoring, and post-sedation recovery. Conclusions: The guideline is planned to be disseminated globally through multiple channels, aiming to standardize the management of pediatric sedation and improve its safety and efficacy.
Systemic juvenile idiopathic arthritis (sJIA) is an autoinflammatory disorder that impacts children aged ≤ 16 years. This study evaluated the efficacy and safety of firsekibart, a fully human anti-IL-1β monoclonal antibody, in children with active sJIA. This multicenter, randomized, open-label, active-controlled phase 2 study (NCT05925452) enrolled participants aged 2– < 18 years with active sJIA across 14 sites in China. Participants were randomized (1:1:1) to firsekibart 3.0 mg/kg or 4.0 mg/kg subcutaneously every 4 weeks, or tocilizumab intravenously every 2 weeks, for 24 weeks. The primary endpoint was modified JIA American College of Rheumatology Pediatric criteria (ACR Pedi) 30 response at day 28. Secondary endpoints included ACR Pedi 30/50/70/90 responses, corticosteroid tapering, immunogenicity, and safety. Fifty participants were randomized (firsekibart 3.0 mg/kg: n = 17; 4.0 mg/kg: n = 16; tocilizumab: n = 17). At day 28, ACR Pedi 30 response rates were 94.1
