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- Abstract：Neuroblastoma （NB）， the commonest extracranial solid malignant tumor in children， is an adrenergic-derived neuroendocrine tumor characterized by highly heterogeneous clinical manifestations. Children with high-risk NB exhibit poor prognosis， often experiencing recurrence or metastasis despite intensive intervention. NB cells primarily consist of two subtypes： adrenergic （ADRN） and mesenchymal （MES）. The ADRN subtype is associated with differentiation and demonstrates greater sensitivity to differentiation-inducing agents and chemotherapeutic drugs， whereas the MES subtype correlates with invasiveness and chemotherapy resistance. Studies indicate that lineage transition between ADRN and MES subtypes contributes to tumor heterogeneity， potentially triggering chemotherapy resistance or recurrence. Elucidating the molecular mechanisms underlying their interconversion is crucial for overcoming lineage-transition-induced drug resistance and targeting ADRN in high-risk NB treatment. This article comprehensively reviews the role of adrenergic signaling in NB pathogenesis and its intrinsic molecular regulatory mechanisms while summarizing recent advances in ADRN-targeted strategies for NB clinical diagnosis and treatment， with an aim to provide a theoretical basis for future clinical management and prevention of NB.Keywords：neuroblastoma;adrenergic;high risk;core regulatory circuitry;targeted therapy595|1546|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
Invited Review
- Abstract：Chronic kidney disease （CKD） is a common disease with high morbidity and mortality. Increasing evidence has indicated that programmed cell death （PCD） plays a significant role in the pathogenesis and progression of CKD. Non-coding RNA （ncRNA）， defined as a category of RNA that lacks coding potential， has emerged as a pivotal regulator of gene expression. This regulatory function of ncRNA extends to various biological processes， including PCD. This paper reviews the recent advances on the involvement of ncRNAs in the regulation of apoptosis， autophagy， pyroptosis， ferroptosis， necroptosis， and PANoptosis in CKD. It explores the crosstalk between different pathways and categorizes therapeutic strategies targeting ncRNA regulation of PCD into three main areas： the active ingredients of traditional Chinese medicine， tissue engineering technologies， and drugs. The objective of this study is to identify novel therapeutic targets and strategies for clinical treatment.Keywords：chronic kidney disease;non-coding RNA;apoptosis;autophagy;pyroptosis;ferroptosis620|1476|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：Mitophagy is an evolutionarily highly conserved selective autophagy process that maintains cellular homeostasis and mitochondrial quality control by specifically recognizing and removing damaged or superfluous mitochondria. During tumorigenesis， mitophagy eliminates damaged mitochondria and reduces the accumulation of reactive oxygen species （ROS）， thereby helping to sustain cellular homeostasis. Energy metabolism refers to the core biological process through which cells convert chemical energy from nutrients into adenosine triphosphate （ATP） via biochemical pathways such as glycolysis and oxidative phosphorylation， providing energy for cellular activities. While research on gastrointestinal tumors is advancing rapidly， a major bottleneck lies in their complex metabolic adaptations and therapeutic resistance. Targeting the interplay between mitophagy and energy metabolism has emerged as a promising therapeutic strategy for this disease. Current research on mitophagy and energy metabolism in gastrointestinal tumors， including the molecular mechanisms of their bidirectional regulatory network and applications in targeted therapies， remains to be systematically elucidated. Therefore， this review summarizes the implications of the mitophagy-energy metabolism interplay in gastrointestinal tumors， with the aim of providing insights for future research.Keywords：mitophagy;energy metabolism reprogramming;gastrointestinal tumors;tumor microenvironment;targeted therapy;review467|3911|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：Normal tension glaucoma （NTG） is recognized as a distinct subtype of primary open-angle glaucoma， characterized by normal intraocular pressure （IOP<21 mmHg） in conjunction with progressive optic neuropathy， retinal ganglion cell （RGC） apoptosis， and visual field defects. The pathogenesis of NTG is predominantly independent of IOP， with fundamental processes involving genetic and mitochondrial factors， including RGC degeneration， neuroinflammation， mitochondrial dysfunction， and genetic predisposition. This article systematically reviews the IOP-independent and gene-driven mechanisms underlying NTG， with a particular focus on the roles of OPTN， TBK1， FOXC1， and OPA1 in inducing RGC damage through pathways such as mitochondrial dysfunction， glial cell activation， inflammatory signaling， apoptosis， and axonal degeneration. Among these genes， OPTN and TBK1 collectively contribute to the development of NTG by disrupting autophagy-mitochondrial homeostasis， causing defects in axonal transport， and activating neuroinflammatory pathways. FOXC1 is implicated in the progression of RGC degeneration through transcriptional regulation， while mutations in OPA1 lead to mitochondria-dependent RGC apoptosis.Additionally， this article provides a comprehensive review of the epigenetic regulation of METTL23， mitochondrial DNA mutations， the role of Alcadein α in axonal transport， the correlation between genes associated with primary open-angle glaucoma （POAG） and normal-tension glaucoma （NTG）， as well as susceptibility loci identified through genome-wide association studies （GWAS）. In the realm of translational research， recent advancements in therapeutic studies encompass strategies such as targeting OPTN E50K， inhibiting CRMP2 phosphorylation， and employing gene augmentation， gene silencing， and gene editing techniques. The etiology of NTG is complex， predominantly independent of intraocular pressure （IOP）， and arises from the interplay between genetic and environmental factors. This article seeks to promote mechanism-based technological innovation， optimize neuroprotective strategies for NTG， and enhance clinical translation， ultimately aiming to achieve precise treatment and improve visual function outcomes for patients.Keywords：normal tension glaucoma;retinal ganglion cell;neuroprotective therapy;OPTN;TBK1274|1326|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：Ischemic stroke （IS） is a cerebrovascular disease caused by thrombosis or embolism that interrupts cerebral blood flow， resulting in brain tissue damage. Mitochondria serve as the primary site for energy metabolism and are also involved in key biological processes， including calcium signal regulation， reactive oxygen species generation， and apoptosis initiation. Therefore， the structural and functional integrity of mitochondrial is crucial for neuronal survival， and the mitochondrial quality control （MQC） system is fundamental for maintaining mitochondrial homeostasis. The MQC system maintains mitochondrial network homeostasis by synergistically regulating key processes such as biogenesis， dynamics balance （fusion and fission）， autophagy， oxidative stress clearance， and calcium homeostasis. However， following IS， neurons undergo pathological changes-including inflammatory responses， oxidative stress， and excitatory amino acid toxicity- due to ischemia and hypoxia. These factors collectively disrupt mitochondrial membrane potential and inhibit electron transport chain function， leading to MQC dysfunction. Recent studies have confirmed that acupuncture can restore MQC homeostasis after IS through multiple targets and pathways， specifically including promoting mitochondrial biogenesis， balancing mitochondrial fission and fusion， regulating mitochondrial autophagy， reducing oxidative stress damage， and inhibiting calcium overload. This article systematically reviews the relationship between MQC and IS， with a focus on elucidating the mechanistic basis of acupuncture-mediated IS treatment via regulating key MQC components. These findings provide a theoretical basis for the efficacy of acupuncture in IS management and offer novel perspectives for developing future stroke therapeutic strategies targeting MQC pathways.Keywords：acupuncture;mitochondrial quality control;ischemic stroke;neuroprotection;mitochondrial homeostasis253|781|1<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：Lung transplantation （LTx） is the only effective curative treatment for end-stage lung disease （ESLD）， applicable to patients with advanced lung diseases who do not respond to medical and other surgical management， and can significantly improve the prognosis. However， LTx still faces many challenges， such as ischemia-reperfusion injury （IRI） and low long-term survival. Improving lung IRI is of great significance for the recovery of lung function and the prognosis of patients after transplantation. Lung IRI is a response to tissue damage and inflammation that worsens when the blood supply to the lung tissue is restored （reperfusion） after it has undergone a disruption of blood flow （ischemia）. IRI is an important pathophysiological basis for primary graft dysfunction （PGD）， and its injury mechanisms are complex and diverse， involving the activation of multiple cell deaths. Programmed cell death （PCD） is a highly ordered process of cell self-extinction regulated by genes， mainly including apoptosis， necroptosis， autophagy， ferroptosis， pyroptosis and cuproptosis， which are of great physiological significance for maintaining biological development， homeostasis and immune defense. Recent studies have shown that the activation of multiple PCDs is closely related to the occurrence and development of lung IRI. PCD is widely involved in lung IRI through different molecular mechanisms， but its specific regulatory mechanism has not been fully elucidated. This article systematically reviews the latest progress of various types of PCD in lung IRI， analyzes the molecular mechanism and interaction of PCD in lung IRI， and explores their potential as therapeutic targets， aiming to provide new insights for the development of clinical lung protection strategies.Keywords：lung ischemia reperfusion injury;apoptosis;necroptosis;autophagy;ferroptosis;pyroptosis;cuproptosis323|764|1<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：Amyloid-β peptide （Aβ） is considered a major cause of Alzheimer's disease （AD）. However， current researches emphasize that Aβ can activate microglia and astrocytes， which causes neuroinflammation. Neuroinflammation plays a crucial role in the neuronal mortality process， and can be considered the underlying cause of AD. In addition， vascular damage was proposed to play an important role in the pathogenesis of AD more than two decades ago， but few researchers have focused on the positive role of cerebrovascular damage in AD. In recent years， a growing body of evidence has supported that brain microvascular injury causes the occurrence of AD. Moreover， recent research indicated that inflammation caused by brain microvascular injury is also a significant risk factor for the development of AD. In damaged microvessels， C-reactive protein （CRP） is a non-specific inflammatory marker， which can activate the complement and enhance phagocytosis of immune cells， and help to eliminate pathogenic microorganisms from the body. The plenty of evidence indicated that CRP penetrated brain tissue and participated in neuroinflammation during brain microvascular injury， thereby influencing the pathogenesis of AD. Therefore， the negative effects of CRP and Aβ on the pathogenesis of AD are equally important. At present， few researchers have established a link between the effects of CRP and Aβ on AD and conducted in-depth analysis. This article firstly and deeply analyzed and summarized the significant function and connection of Aβ and CRP in AD， which provided support for the theory that neuronal cerebrovascular injury is the cause of AD.Keywords：C-reactive protein;amyloid-β peptide;Alzheimer' disease;inflammation;microvascular injury225|853|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：Cataract remains a cause of growing blind worldwide， and phacoemulsification is currently the preferred surgical technique due to its minimal invasiveness and rapid recovery. However， the intraoperative parameters setting of phacoemulsification remains crucial due to their potential impact on ocular tissues， particularly the corneal endothelium and retina. This review systematically examines the effects and interactions of these critical parameters during phacoemulsification， including ultrasonic frequency， infusion bottle height， and ultrasound energy. High-frequency ultrasound enhances emulsification efficiency and reduces operation time but significantly increases localized thermal effects， especially when combined with high-energy output， exacerbating the risk of thermal damage to the corneal endothelium. While a high bottle height stabilizes the anterior chamber， it simultaneously elevates mechanical shear stress and turbulence， further damaging endothelial cells. Conversely， low bottle height combined with low vacuum settings protects endothelial cells but may compromise chamber stability， increasing surgical difficulty. Additionally， oxidative stress and inflammatory cytokines， such as reactive oxygen species （ROS）， vascular endothelial growth factor（VEGF） and interleukin（IL）-6， significantly contribute to tissue injury， particularly pronounced in diabetic and ocular fundus disease patients. Based on current evidence， this article provides specific recommendations for parameter settings tailored to patients with hard nuclear cataracts， compromised corneal endothelial function， diabetes， and postoperative glaucoma. Moreover， this review highlights current research limitations， including high heterogeneity in clinical data， insufficient long-term follow-up， and inadequate mechanistic understanding. Future research should prioritize individualized parameter optimization， long-term clinical outcomes evaluation， and real-time intraoperative monitoring techniques， aiming to enhance surgical safety， reduce complications， and improve visual outcomes.Keywords：cataract;ultrasonic emulsification;ultrasonic energy;corneal endothelial cells;intraocular pressure228|985|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
Review
- Abstract：ObjectiveCardiovascular diseases pose a major public health challenge in China. The burden of cardiovascular disease associated with high low-density lipoprotein cholesterol （LDL-C） has increased steadily nationwide. A comprehensive analysis of secular trends in cardiovascular disease burden and its determinants is crucial for developing targeted interventions and evidence-based health policies.MethodsBased on data from the Global Burden of Disease Study 2021， we analyzed the trends in deaths， disability-adjusted life years （DALYs）， age-standardized mortality rates （ASMR）， and age-standardized DALY rates （ASDR） of cardiovascular diseases attributable to high LDL-C in China from 1990 to 2021 using Joinpoint regression analysis. An age-period-cohort model was applied to assess the contributions of age， period， and cohort effects to changes in the cardiovascular disease burden attributable to high LDL-C. Projections of the high LDL-C-attributable cardiovascular disease burden in China from 2022 to 2030 were generated using a Bayesian age-period-cohort model.ResultsBetween 1990 and 2021， China saw a substantial rise in both deaths and disability-adjusted life years （DALYs） from cardiovascular disease linked to high LDL-C. Joinpoint regression revealed key turning points in this trend： an overall increase continued until 2004， after which the burden began to fall starting in 2011. Throughout this period， age-standardized mortality and DALY rates were consistently higher in males than in females. Age-period-cohort analysis further indicated that mortality and DALY rates due to high LDL-C increased almost exponentially with age， while period and cohort risks generally decreased over time. Projections suggest a continued decline in age-standardized mortality rates from LDL-C-related cardiovascular disease for both Chinese men and women by 2030.ConclusionRapid population growth and accelerated ageing in China emerge as primary drivers of the escalating cardiovascular diseases burden linked to elevated LDL-C. The burden of cardiovascular diseases is higher in men compared to women. By 2030， the burden of cardiovascular disease caused by high LDL-C in China will remain severe. These findings underscore the critical need for gender-specific screening protocols， age-tailored interventions， and personalized management frameworks to mitigate this public health challenge.Keywords：disease burden;cardiovascular disease;low-density lipoprotein cholesterol;Joinpoint regression;age-period-cohort analysis310|818|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：ObjectiveTransfusion-Related Acute Lung Injury （TRALI） is a common fatal transfusion adverse reaction. Major Histocompatibility Complex （MHC） class I is an important factor involved in the pathogenesis of TRALI； however， the role of complement in itspathogenesis has not been fully elucidated. This study aims to explore the role of complement in MHC class I antibody-mediated TRALI， so as to provide a theoretical basis for clinical prevention and treatment.MethodsThis study established a murine model of transfusion-related acute lung injury （TRALI） based on the "two-hit" theory， with lipopolysaccharide （LPS） as the first hit and MHC class I antibody as the second hit. Male Balb/c mice were randomly divided into seven groups （n=5 per group per experiment）： Naive （blank control）， LPS （first hit only）， Isotype （isotype antibody control）， TRALI （model group）， C5aR1 inhi （C5aR1 antagonist intervention）， C5aR2 inhi （C5aR2 antagonist intervention）， and Anti-C5 （anti-complement C5 antibody intervention）. Rectal temperature was monitored after MHC class I antibody injection. After sample collection， the severity of pulmonary edema was assessed by measuring the lung wet-to-dry weight ratio， histological analysis， and immunohistochemistry. Serum and bronchoalveolar lavage fluid were collected to measure cytokine and complement levels.ResultsMice in the TRALI group exhibited a significant decrease in rectal temperature， an increased lung wet-to-dry weight ratio， elevated serum cytokine levels， and markedly heightened complement C5a levels in bronchoalveolar lavage fluid （P＜0.000 1）. Histopathological examination revealed substantial infiltration of inflammatory cells， predominantly neutrophils accompanied by fewer lymphocytes， plasma cells， and monocytes， along with increased deposition of the membrane attack complex C5b-9 in lung tissues. In contrast， mice treated with anti-C5 antibody demonstrated no significant decrease in rectal temperature. The lung wet-to-dry weight ratio in this group showed no statistical difference compared to either the Naive or Isotype control groups （P＞0.05）. Furthermore， these mice displayed reduced serum cytokine levels， a significant attenuation of inflammatory cell infiltration in the lungs， and a 100% survival rate at the 2-hour time point. However， mice administered either the C5aR1 antagonist or the C5aR2 antagonist failed to be protected and subsequently developed TRALI.ConclusionComplement activation， which forms the membrane attack complex C5b-9， plays a critical role in MHC class I antibody-mediated TRALI. Blocking complement C5 activation can effectively prevent the occurrence of TRALI.Keywords：transfusion-related acute lung injury;MHC-Ⅰ antibody;complement;complement C5a receptor;membrane attack complex;cytokines211|483|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：ObjectiveTo investigate the reversal effect of Cordyceps sinensis extract on immunotherapy resistance of non-small cell lung cancer （NSCLC）.MethodsELISA， flow cytometry， and co-culture assays were performed to evaluate the effects of Cordyceps sinensis extract on cytokine secretion， proliferation， and tumor cell killing activity of Jurkat （JKT） cells. Furthermore， the therapeutic effect of Cordyceps sinensis extract on programmed cell death ligand 1 （PD-L1） resistant lung cancer was evaluated through in vivo experiments both alone and in combination with anti-PD-L1 monoclonal antibody.ResultsCordyceps sinensis extract enhanced the secretion of cytokines interferon gamma（IFN-γ）， tumor necrosis factor-alpha（TNF-α） and interleukin-2 （IL-2）in JKT cells， promoted cell proliferation （P=0.006）， and boosted their killing function against tumors （P＜0.001）. Compared with the control group， in vivo study demonstrated that Cordyceps sinensis extract monotherapy effectively inhibited the growth of PD-L1-resistant tumors ［tumor growth inhibition value （TGI）=26.1%， P=0.090］， while its combination with anti-PD-L1 antibody significantly reversed PD-L1 resistance （TGI=50.6%， P＜0.001）.ConclusionThis study provides certain data support for the activation of anti-tumor immunity by Cordyceps sinensis extract， and offers a new treatment strategy for enhancing anti-tumor immunity and reversing immune resistance in lung cancer.Keywords：Cordyceps sinensis;non-small cell lung cancer;immunotherapy;drug resistance;anti-cancer586|781|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：ObjectiveTo explore the effects of exosomal CXCL on the biological behavior of cervical cancer cells and its underlying mechanisms.MethodsChemokine CXCL was first screened through bioinformatics databases. The GEPIA database was analyze CXCL expression in cervical cancer tissues and adjacent normal cervical tissues. Western blot was performed to detect CXCL expression levels in cervical cancer cells （Caski） and normal cervical epithelial cells （H8）. The successful isolation of exosomes was confirmed by nanoparticle tracking analysis， transmission electron microscopy （TEM） and Western blot. ELISA was employed to detect the expression level of exosomes CXCL was determined by ELISA. After CXCL knockdown via siRNA transfection， cells were divided into three groups： blank control， negative control and experimental groups. Cell proliferation was evaluated using the CCK-8 assay， while cell migration and invasion were assessed by Transwell assays.ResultsExosomal CXCL expression was significantly upregulated in cervical cancer cells compared with normal cervical epithelial cells （P<0. 01）， and also markedly elevated in cervical cancer tissues compared with adjacent normal tissues. After low expression of CXCL knockdown significantly reduced CXCL expression in both cancer cells and their derived exosomes（P<0. 05）. Low expression markedly inhibited the proliferation， invasion and migration abilitiesConclusionSilencing exosomal CXCL may inhibit the malignant biological behavior of cancer cells.Keywords：cervical cancer;exosomes;C-X-C chemokine ligand 1;proliferation;invasion;migration248|244|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：ObjectiveTo investigate the potential value of thyroid hormones in cerebrospinal fluid in predicting autism-like behaviors induced by hypothyroidism in pregnant rats.MethodsTwelve pregnant Wistar rats were randomly divided into a control group and a hypothyroidism group （hypothyroidism model group）. Offspring from both groups had serum and cerebrospinal fluid levels of thyroid-stimulating hormone （TSH）， total triiodothyronine （TT3）， total thyroxine （TT4）， free triiodothyronine （FT3）， and free thyroxine （FT4） levels in serum and cerebrospinal fluid. Ultrasonic vocalization tests were conducted on postnatal day 2 （P2）， day 7 （P7）， and day 14 （P14）， while behavioral tests using the three-box social interaction test were performed on day 21（P21）.ResultsCompared with the control group， free T4 （FT4） levels in the cerebrospinal fluid of the hypothyroidism group were significantly reduced during the developmental period （P0-P21； P2： P<0.05； P7： P<0.05； P14： P<0.01； P21： P<0.01）， with no statistical difference between the two groups only at P0 （P>0.05）. In the ultrasonic vocalization （USV） tests， the number and duration of USVs in offsprings from the hypothyroidism group were significantly reduced compared with those of the control group on P2， P7 and P14： for USV counts （P2： P<0.05； P7： P<0.001； P14： P<0.01）； for USV duration （P2： P<0.05； P7： P<0.001； P14： P<0.001）. In the three-box social tests， offsprings of the hypothyroidism group showed significantly reduced sniffing time with unfamiliar rats at P21 compared to the control group （all P<0.001）. The FT4 levels in cerebrospinal fluid had a significantly positive correlation with USV counts （P7： r=0.883， P<0.05； P14： r=0.902， P<0.05） and sniffing time with unfamiliar rats （r=0.814， P<0.01）.ConclusionMeasuring free T4 in cerebrospinal fluid can predict autism-like behaviors in offsprings of rats induced by hypothyroidism during pregnancy.Keywords：hypothyroidism;autism;cerebrospinal fluid;free thyroxine;predictive indicator190|372|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
Preclinic Research
- Abstract：ObjectiveOur study seeks to investigate the connection between systemic immune inflammatory index and renal function， as well as to assess its predictive capacity for the deterioration of renal function in chronic kidney disease patients with non-dialysis.MethodsAdult non-dialyzing patients diagnosed with CKD were included. The computation of SII was calculated as the product of the peripheral blood neutrophil count （×10⁹/L） and platelet count （×10⁹/L）， divided by the lymphocyte count （×10⁹/L）. The logistic and Cox regression models were employed to scrutinize the linkage between SII levels and CKD.ResultsOut of the cohort， a significant portion of patients， numbering 244， which constitutes 17.2%， experienced progression of CKD. A notable upsurge in SII corresponded with an increased prevalence of advanced CKD and its progression， with significant difference. This trend was mirrored by a decline in the estimated glomerular filtration rate and hemoglobin levels， while serum creatinine， C-reactive protein， and lipoprotein（a） levels were on the rise. After adjusting for multiple variables， the natural logarithm of SII exhibited an independent association with advanced CKD ［OR=1.85 95% CI（1.46，2.35），P＜0.01］. Furthermore， Cox proportional hazards model analysis revealed that SII acted as an independent predictor for CKD progression ［adjusted HR= 1.35， 95% CI（1.09，1.67）， P＜ 0.01］. Subgroup analysis indicated a significant interaction among SII， gender， and hypertension concerning CKD progression.ConclusionOur findings underscore the robust relationship between SII and renal function， positioning SII as a potential forecaster for the progression of CKD.Keywords：systemic immune inflammatory index;chronic kidney disease;non-dialysis;progression;predictive effect347|632|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：ObjectiveTo explore the distribution patterns and correlations of pet-related cat/dog dander allergens and mold allergens in patients with allergic diseases， providing evidence for individualized diagnosis， treatment， and prevention strategies.MethodsA retrospective analysis was conducted on 798 patients diagnosed with allergic diseases at the Third Affiliated Hospital of Sun Yat-sen University between April 2021 and October 2023. All patients underwent UniCAP platform testing for specific immunoglobulin E （sIgE） levels against cat dander， dog dander， and mold mix （mx1/mx2）， alongside total IgE （tIgE） quantification. Descriptive statistics， Mann-Whitney U tests， and chi-square analyses were employed to evaluate allergen distribution and interrelationships.ResultsAmong the 798 patients （395 males， 403 females， ratio 1∶1.02）， their ages ranged from 0.67 to 69 years （median 14 years， IQR 6-29）. A total of 63.2% （504/798） had a single allergic disease， with allergic rhinitis （AR， 49.2%） being the most common. The remaining 36.8% （294/798） had ≥2 allergic diseases， with AR combined with atopic dermatitis （AD， 10.7%） as the predominant comorbidity. The positivity rate for cat/dog dander sIgE was 24.1% （192/798）， with a significantly higher prevalence in females （30.8%） than males （16.7%， P＜0.05）. Cat dander sensitization increased with age in patients under 18 years. Among positive cases， cat dander sIgE level 2 was most frequent （25.9%）， while dog dander sIgE level 1 predominated （55%）. Patients with cat dander sIgE levels 4-6 had significantly higher tIgE than those with levels 1-3 （P＜0.05）. The positivity rate for mold mix （mx1/mx2） sIgE was 7.4% （59/798）， with mx2 as the primary sensitizer and level 2 being the most common. In mx2-positive patients， the cat/dog dander sIgE positivity rate （44.8%） was significantly higher than that in mx2-negative patients （17.9%， P＜0.05）， and tIgE levels were also higher （P＜0.05）.ConclusionCat dander sensitization increases with age in children. Cat/dog dander and mold allergens are closely linked to AR and AR combined with AD. Synergistic correlations exist between cat/dog dander sIgE and mold mx2 sIgE. Combined detection of these allergens is critical for precision diagnosis and management of pet-related allergic diseases.Keywords：cat dander allergen;dog dander allergen;mold allergen;specific immunoglobulin E;allergic rhinitis452|1158|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：ObjectiveTo investigate the role of sphingosine-1-phosphate （S1P） in abnormal ossification in ankylosing spondylitis （AS）， clarify the relationship between S1P and “angiogenesis-osteogenesis” coupling， and provide new strategies for AS treatment.MethodsFemoral heads from AS patients and patients undergoing routine hip replacement were collected for immunohistochemical （IHC） staining to evaluate osteogenesis and H-type vessel formation. In vitro， ELISA was used to quantify the synthesis of S1P and analyze the expression changes of S1P signaling pathway-related molecules during the osteogenic differentiation of mesenchymal stem cells derived from patients with ankylosing spondylitis （ASMSCs） and those from healthy donors （HDMSCs）， to evaluate the activation status of S1P pathway during osteogenesis. Sphingosine kinase 1 （SK1） expression was knocked down in MSCs， and the S1P receptor inhibitor FTY720 was applied to block S1P signaling. Alkaline phosphatase （ALP） activity and Alizarin Red S （ARS） quantification were used to assess the effect of S1P on ASMSCs osteogenesis. Conditioned medium from osteogenically induced MSCs was used to treat human umbilical vein endothelial cells （HUVECs） to evaluate the effect of S1P on angiogenesis. An AS mouse model （SKG mice） was treated with FTY720 or the SK1 inhibitor PF-543 citrate. IHC staining and micro-CT scanning were used to assess abnormal ossification and spinal fusion， and immunofluorescence was used to evaluate H-type vessel formation.ResultsCompared with Osteonecrosis of the Femoral Head（ONFH） patients， AS patients exhibited excessive osteogenesis and H-type vessel formation （OCN P＜0.001， CD31 P＜0.001， EMCN P＜0.001）. During osteogenic differentiation， S1P expression and secretion were significantly higher in ASMSCs than in HDMSCs （P=0.0179）. Inhibition of S1P signaling with FTY720 or SK1 knockdown significantly suppressed osteogenic differentiation （compared with ASMSC， ARS： HDMSC P=0.001 8， FTY720 P＜0.001， si-SK1 P＜0.001； ALP： HDMSC P=0.032 8， FTY720 P=0.001 6， si-SK1 P＜0.001） of ASMSCs and the angiogenesis of HUVEC（compared with ASMSC， cell-covered area， total loops， total tube length and total branch points P＜0.001）. Treatment with FTY720 or PF-543 markedly inhibited abnormal ossification and spinal fusion（compared with Curdlan， arthritis index score， P＜0.001； OCN：control P=0.002， PF-543 P=0.010 7， FTY720 P=0.015 9 ） in AS mice and reduced H-type vessel formation （CD31+EMCN+： compared with curdlan， control P＜0.001， PF-543 P=0.001 7， FTY720 P=0.002 1）.ConclusionIncreased S1P synthesis in ASMSCs promotes osteogenic differentiation via autocrine mechanisms and further enhances ossification by facilitating H-type angiogenesis. Inhibiting S1P secretion in ASMSCs significantly suppresses abnormal ossification in AS.Keywords：sphingosine-1-phosphate;type H vessels;angiogenesis-osteogenesis coupling;ankylosing spondylitis;mesenchymal stem cells293|654|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：ObjectiveTo investigate and explore the characteristics and influencing factors of glucose metabolism in children with β-thalassemia major （β-TM） after allogeneic hematopoietic stem cell transplantation （allo-HSCT）.MethodsThe follow-up data of 41 patients with β-TM who underwent HSCT at Hematopoietic Stem Cell Transplantation Department of Children's Medical Center of Sun Yat-sen Memorial Hospital， Sun Yat-sen University were retrospectively analyzed. Their glucose metabolism characteristics were evaluated through laboratory tests and the related influencing factors were analyzed.ResultsIn the study， 41.46% （17/41） of patients developed abnormal glucose homeostasis after HSCT. Among them， 82.35% （14/17） characterized by insulin resistance， but no cases of diabetes mellitus were found. The results of insulin releasing test and oral glucose tolerance test（OGTT） showed that 45.00% （9/20） of patients had abnormal insulin releasing curve and 40.0% （8/20） had delayed serum glucose peak. The average age of HSCT in abnormal glucose homeostasis group was significantly older than that in the normal glucose homeostasis group ［（8.8±3.9） years old vs （6.0±3.1） years old， P=0.015］.ConclusionsPatients with β-TM after HSCT may develop abnormal glucose homeostasis， consists largely of insulin resistance. The elder age of HSCT （≥7 years old） is a risk factor for abnormal glucose homeostasis in β-TM patients after HSCT. It is recommended to regularly monitor glucose metabolism indicators in β-TM children after HSCT， especially in elderly transplant recipients.Keywords：allogeneic hematopoietic stem cell transplantation;β- thalassemia major;pedia;age of HSCT;abnormal glucose metabolism279|584|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
- Abstract：ObjectiveTo sum up the clinical features of 5α-reductase type 2 deficiency （5α-RD2） complicated by central precocious puberty （CPP）， and provide experience for clinicians.MethodsA retrospective review was conducted of child patients with 5α-RD2 followed up to puberty at a single tertiary pediatric center， in whom 6 cases developed CRP. Clinical characteristics and treatment history of them were analyzed. A literature review was also performed to investigate possible mechanisms underlying the co-occurrence of 5α-RD2 and CPP.ResultsThe median age at initial presentation was 5.55 years （IQR 3.50-7.20）. Common clinical features included micropenis and hypospadias. Median stretched penile length （SPL） was 2.25 cm （IQR 1.8-2.8）， with an SPL-SDS of -4.5 （IQR -3.1 to -5.8）. Median external masculinization score （EMS） and Prader scores were 8.5 （IQR 5.0-9.0） and 4.5 （IQR 3.0-5.0）， respectively. Pubertal onset occurred at a median age of 8.70 years （IQR 7.80-9.00）. Three patients were overweight or obese. Five had received 2.5% dihydrotestosterone （DHT） gel prior to pubertal onset， with a median cumulative dose of 205.5 mg/kg （IQR 72.0-660.3 mg/kg） with DHT gel therapy. Notably， one patient with normal body mass index （BMI） and no history of androgen or gonadotropin therapy also exhibited early pubertal onset at 8.4 years.ConclusionCPP in children with 5α-RD2 may be associated with prior dihydrotestosterone （DHT） gel therapy and elevated BMI； however， a potential intrinsic link to the underlying disorder cannot be excluded. Further studies are needed to elucidate the pathophysiological mechanisms.Keywords：5α-reductase type 2 deficiency;central precocious puberty;obesity;overweight;disorders of sex development348|1555|0<HTML><L-PDF> <Meta-XML>Updated：2025-11-20
Clinical Research
