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Dose-effect and Mechanism of Uncooked Corn Starch on the Intestinal Mucosal Barrier Function in Mice
Abstract：ObjectiveTo investigate the effects of different doses of uncooked corn starch （UCCS）， type 2 resistant starch， on intestinal mucosal barrier function in mice and to explore the potentional underlying mechanisms.MethodsTwenty C57BL/6 mice were randomly assigned to four groups and fed either a standard diet （control group） or diets supplemented with low （188.8 g/kg）， medium （314.8 g/kg）， or high （440.6 g/kg） doses of UCCS for 8 weeks. Body weight and disease activity index （DAI） were monitored. At the endpoint， colon length was measured； histopathological changes in were assessed via HE staining. The expression of tight junction proteins （ZO-1， E-cadherin， and Villin） in the colonic mucosa were detected using immunofluorescence. Serum inflammatory cytokines （IL-6， TNF-α， IL-1β， MIP-1α/CCL3） and fecal calprotectin levels were measured by ELISA. Gut microbiota alterations were analyzed via 16S rRNA gene sequencing and PICRUSt2 functional prediction.ResultsCompared with the control group， UCCS intervention across all doses significantly shortened colon length （P=0.000 5） and increased colonic inflammation scores （P=0.013 3）. Immunofluorescence revealed a significantly reduction in the expression and co-localization of ZO-1 and Villin in the colonic mucosa （P＜0.05）. Systemic inflammation was evidenced by significantly elevated serum levels of IL-6 （P=0.006 4）， TNF-α （P=0.000 1）， IL-1β （P=0.001 4）， and MIP-1α/CCL3 （P＜0.000 1）. Fecal calprotectin levels were also significantly increased during the early phase （weeks 1-2， P＜0.05）. 16S rRNA sequencing showed that UCCS significantly altered the β-diversity of the gut microbiota （P＜0.05）， characterized by the enrichment of butyrate-producing Clostridia_UCG-014， and the opportunistic pathogen Desulfovibrio， alongside a decreased abundance of immunomodulatory genera Akkermansia and Dubosiella. PICRUSt2 analysis suggested that UCCS modulated metabolic pathways related to energy metabolism， glutathione metabolism， and sulfur cycling.ConclusionLong-term or high-dose intake of UCCS may disrupt gut microbiota homeostasis and trigger inflammation response， thereby damaging the intestinal mucosal barrier. These findings suggest that the clinical or dietary application of UCCS should be cautioned regarding dose-dependent risks of intestinal injury.Keywords：uncooked corn starch;gut microbiota;intestinal inflammation;intestinal mucosal barrier;resistant starch280|371|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20- Abstract：ObjectiveTo characterize the features of the gut microbiome and its association with clinical prognosis in patients with intermediate and advanced hepatocellular carcinoma （HCC） treated with transcatheter arterial chemoembolization （TACE） combined with targeted therapy and immunotherapy.MethodsThis retrospective study enrolled patients with intermediate and advanced HCC who received TACE combined with targeted therapy and immunotherapy at the First Affiliated Hospital of Sun Yat-sen University from February 2025 to July 2025. Baseline clinical data and fecal samples were collected from all enrolled patients before the index hospitalization and treatment. Patients were stratified using two independent criteria： ① a good-prognosis group and a poor-prognosis group， based on whether progression-free survival （PFS） reached 6 months； ② a response group and a non-response group， based on tumor response to the first TACE assessed by the modified Response Evaluation Criteria in Solid Tumors （mRECIST）. Metagenomic sequencing was performed on fecal samples. Bioinformatic analysis was conducted to evaluate the diversity and compositional differences of intestinal bacterial and fungal communities between groups in each stratification， and to screen for prognosis-associated characteristic microbial taxa.ResultsA total of 61 patients met the inclusion criteria. Analysis of α-diversity and β-diversity showed no statistically significant differences in bacterial and fungal diversity between groups under either stratification strategy （P＞ 0.05）. At the bacterial level， Lactobacillus johnsonii （prognosis stratification： P=0.048； response stratification： P=0.043）， Bifidobacterium dentium （prognosis stratification： P=0.004； response stratification： P=0.030） and Clostridioides difficile （prognosis stratification： P=0.017； response stratification： P=0.016） were significantly enriched in both the good prognosis group and the response group. At the fungal level， Cryptococcus decaguttatus （P=0.045）， Puccinia striiformis （P=0.002）， and Kwoniella quercicola （P=0.015） were enriched in the good‑prognosis group； Kwoniella bestiolae （P=0.037） was enriched in the response group； and Akanthomyces muscarius （P=0.024） was enriched in the non-response group. Survival analysis based on the common differential bacterial abundance in both groupings showed a significant correlation between the abundance of Bifidobacterium dentium and patient prognosis.ConclusionDifferences in the gut microbiota are associated with the prognosis of patients with intermediate and advanced HCC treated with TACE combined with targeted therapy and immunotherapy. Bifidobacterium dentium may serve as a potential predictive biomarker for the efficacy of this combination regimen， and represents a potential intervention target to modulate treatment response. Differences in gut fungal communities are also potentially associated with the prognosis of intermediate and advanced HCC patients receiving TACE combined with targeted therapy and immunotherapy.Keywords：hepatocellular carcinoma;gut microbiota;transarterial chemoembolization;immunotherapy;targeted therapy225|360|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：The integrity of the intestinal barrier is the basis of physiological function of the intestine， which is essential for maintaining nutrient absorption， antigen exclusion， and immune homeostasis. High-altitude environments are characterized by hypobaric hypoxia and are often complicated by combined stresses such as cold， intense ultraviolet radiation， increased physical exertion， dehydration， and dietary changes. These factors may lead to synergistic dysfunction of the mechanical， chemical， immune， and biological barriers of the intestine， thereby inducing local or systemic inflammatory responses. Current evidence indicates that high-altitude-related intestinal barrier injury is not driven by a single pathway but is co-mediated by multiple factors： aberrant activation of hypoxia-inflammation signaling pathways， including hypoxia-inducible factor-1α （HIF-1α） and nuclear factor-κB （NF-κB）； synergistic enhancement of Notch and Wnt/β-catenin signaling pathways leading to goblet cell reduction and insufficient mucin 2 （MUC2） secretion； imbalance of T helper 17/regulatory T cells （Th17/Treg） and activation of the NOD-like receptor family pyrin domain containing 3 （NLRP3） inflammasome； as well as gut microbiota dysbiosis and weakened protective effects of short-chain fatty acids （SCFAs）. This article systematically reviews the molecular mechanisms underlying high-altitude-induced intestinal barrier injury， and proposes a multi-mechanism synergistic model under the “adaptation-decompensation” framework on this basis. Combined with scenarios of acute high-altitude exposure， it summarizes the evidence progress and limitations of intervention strategies of ameliorating intestinal barrier injury， aiming to provide a theoretical basis and practical reference for the prevention and intervention of high-altitude-related intestinal injury.Keywords：intestinal barrier;high-altitude environment;gut microbiota;injury mechanisms;multi-mechanism synergistic model;intervention strategies184|186|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：Chronic excessive alcohol consumption is a major global public health concern that severely endangers human health. Excessive alcohol intake disrupts the functions of multiple organs and systems in the human body through diverse mechanisms. The alcohol-sensitive microbiota-gut-brain axis plays a critical role in maintaining systemic homeostasis， immune maturation， and endocrine metabolism. Chronic excessive alcohol consumption not only alters the composition of the gut microbiota and the levels of its metabolites， but also compromises intestinal barrier integrity， increases intestinal permeability， and allows harmful metabolites to enter the systemic circulation， thereby triggering a variety of diseases including alcohol-related brain injury. Alcohol-related brain injury is one of the most severe consequences of unrecognized or inadequately treated alcohol use disorder （AUD）， which can lead to extensive neuronal damage and neurocognitive dysfunction. Although the potential role of the microbiota-gut-brain axis in alcohol-related brain injury has been proposed， the exact underlying mechanisms have not yet been fully elucidated. Therefore， in this review， we systematically analyze the associations among chronic excessive alcohol consumption， the microbiota-gut-brain axis， and alcohol-related brain injury， and explore the potential mechanisms underlying alcohol-induced brain damage via this axis.Keywords：chronic excessive alcohol consumption;microbiota-gut-brain axis;alcohol-related brain injury;gut dysbiosis;interventions202|273|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
Academic Frontiers\：Gut Microbiota and Barrier Function
- Abstract：Upper limb motor impairment is a common sequela of stroke and significantly compromisses patients’ activities of daily living and quality of life . Non-invasive vagus nerve stimulation （nVNS） ，developed from conventional vagus nerve stimulation （VNS）， is a safer， more convenient， and cost-effective neuromodulation technique with the adventage of avtive regulation， It has been increasingly applied in clinical practice and neuroscience research，and its therapeutic potential in post-stroke upper limb rehabilitation has been preliminaruly demonstrated. This systematic review comprehensively examines the mechanistic basis and clinical advancements of nVNS in treating upper limb motor dysfunction following stroke， with a particular focus on the International Classification of Functioning， Disability and Health （ICF） framework. From the perspectives of body function， individual activity， and social participation， the rehabilitative effects of nVNS are analyzed in an integrated manner. Specifically， nVNS enhances neural plasticity， mitigates inflammatory responses， and improves cerebral perfusion in ischemic regions by modulating the secretion of neurotransmitters such as norepinephrine， acetylcholine， and γ-aminobutyric acid， thereby promoting neurological recovery at the body function level. Moreover， the synergistic application of nVNS with rehabilitative training has been shown to sustainably improve motor function and activities of daily living， yielding functional benefits that extend to the levels of individual activity and social participation.Building upon this foundation， the present study examines the technical challenges confronting nVNS and proposes future research trajectories focusing on parameter optimization， multimodal neuromodulation integration， and rehabilitation for lower limb dysfunction. These directions aim to facilitate precision personalized therapeutics for stroke patients.Keywords：stroke;vagus nerve stimulation;non-invasive;upper limb motor dysfunction;rehabilitation128|106|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：Parkinson’s disease （PD） is a central neurodegenerative disorder with insidious onset and slow progression. It is pathologically characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta and the abnormal aggregation of α-synuclein （α-Syn）， resulting in the formation of Lewy bodies. These pathological changes give rise to motor dysfunction， sleep disturbances， cognitive impairment， and other symptoms， thereby markedly reducing patients’ quality of life. Current treatments remain largely symptomatic， including dopaminergic replacement therapy and deep brain stimulation （DBS）， while long-term adverse effects and declining efficacy in advanced stages remain unresolved. Therefore， the development of disease-modifying therapies capable of delaying or reversing disease progression is of critical importance. Aquaporin-4 （AQP4） is the most abundant water channel in the brain and is predominantly expressed in astrocytic endfeet， where it plays a key role in maintaining cerebral water homeostasis， blood–brain barrier integrity， and glymphatic waste clearance. Recent studies have demonstrated that both the expression level and polarization of AQP4 are altered in PD animal models and in brain tissues from patients with PD， and these alterations are closely associated with glymphatic dysfunction， impaired α-Syn clearance， disruption of central nervous system homeostasis， and activation of neuroinflammation. Following the cascade of “AQP4 alteration – impaired glymphatic clearance-α-Syn deposition-neuroinflammation-PD progression”， this review outlines the basis of AQP4 polarization and glymphatic function， summarizes the potential mechanisms by which AQP4 abnormalities promote α-Syn accumulation and inflammatory amplification， and synthesizes current clinical evidence and therapeutic advances. Nevertheless， inconsistencies across experimental models and PD subtypes remain， and the causal role of AQP4 as well as population heterogeneity has yet to be fully elucidated. Future large-scale， long-term， subtype-stratified studies are warranted to explore precise regulatory strategies targeting AQP4 and to validate its safety and efficacy as a novel disease-modifying therapeutic target for PD.Keywords：Parkinson's disease;aquaporin-4;α-synuclein;glymphatic system;neuroinflammation;disease-modifying therapy95|38|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
Review
- Abstract：ObjectiveTo investigate the role and related mechanisms of mast cells （MCs） in alcoholic cardiomyopathy （ACM）.MethodsAn ACM model was established in C57BL/6 mice by feeding them with alcohol liquid diet， and some model mice were intervened with cromolyn sodium， a mast cell stabilizer. Cardiac function， myocardial remodeling and the expression of related proteins were evaluated by echocardiography， tissue staining and Western blot. In vitro， neonatal rat ventricular cardiomyocytes （NRVCs） were stimulated with mast cell granules （MCGs） and/or alcohol， and pathway inhibitors were used to explore the underlying mechanisms.ResultsLong-term alcohol feeding caused significant cardiac dysfunction and mast cells activation in mice， accompanied by increased expressions of chymase， NOX2， NOX4 and apoptosis-related protein cleaved Caspase-3 （c-Caspase3） in myocardial tissues （P＜0.05）. Pretreatment with cromolyn sodium improved cardiac function， inhibited mast cell activation， and reduced the expressions of the above proteins. In vitro experiments showed that treatment with MCGs or alcohol alone up-regulated the expressions of c-Caspase3， NOX2， NOX4 and phosphorylated PKCβ1 （p-PKCβ1） in cardiomyocytes， and the combined stimulation of the two had a synergistic effect. Protease-activated receptor 2 （PAR2） inhibitor down-regulated the MCG-induced expressions of the above proteins. PKCβ1 inhibitor also inhibited the MCG-induced expressions of c-Caspase3， NOX2 and NOX4. Chymase inhibitor exerted a partial inhibitory effect on MCG-induced cardiomyocyte apoptosis.ConclusionDuring the development of ACM， mast cells are activated， and the released MCGs may promote cardiomyocyte apoptosis through the PAR2-PKCβ1-NOX2/NOX4 signaling pathway， in which chymase plays an important role.Keywords：mast cell;alcoholic cardiomyopathy;cardiac remodeling;chymase;apoptosis90|28|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：ObjectiveTo characterize the features of etomidate-related criminal cases in Guangxi after its formal scheduling as a controlled substance in China.MethodsWe collected judicial documents of etomidate-related criminal cases in Guangxi， published on China Judgments Online from October 2023 to July 2025. Demographic， criminological， and forensic toxicological characteristics were extracted. We analyzed the differences in demographic characteristics between the offenders and the baseline of the general population in Guangxi， and examined the associations of age， educational attainment， prior criminal conviction， and employment status with offense types.ResultsA total of 51 adjudicated cases were included， involving 174 individuals. The offenders were predominantly male， young adults， with low educational attainment， prior criminal convictions， and unemployed status. Statistically significant differences were observed between the offenders and the baseline of the general population in Guangxi across four dimensions： gender， age， educational attainment， and employment status （all P values＜0.01）. The primary offense types were the crime of providing shelter for others to use drugs and drug trafficking offenses. The majority of cases involved joint offenses committed by multiple perpetrators， with e-cigarettes and related products as the main drug delivery vehicles. Forensic toxicological testing confirmed concurrent polydrug use of etomidate and ketamine among the involved individuals. Prior criminal conviction status was statistically associated with the choice of offense type （Fisher's P = 0.006）. Offenders with prior convictions predominantly committed single-type offenses， while those without prior convictions accounted for a significantly higher proportion of multiple concurrent offenses relative to the former group.ConclusionAfter the scheduling of etomidate， the offender population in etomidate-related criminal cases in Guangxi is characterized by low educational attainment， low employment rate， and high prevalence of prior criminal convictions. The offenses exhibited covert modus operandi， group-based offending patterns， and a growing trend of polydrug use. We recommend strengthening the monitoring of high-risk populations and upgrading the technical system of forensic toxicological testing to address the challenges posed by emerging illicit drugs.Keywords：etomidate;e-cigarettes;forensic toxicology;criminal case;characteristics analysis77|19|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：ObjectiveThis study aimed to investigate the therapaeutic effects of rabies virus glycoprotein （RVG）-modified mesenchymal stem cell-derived exosomes （MSC-EXO） in a mouse model of obsessive-compulsive disorder （OCD）， and to explore the underlying mechanisms.MethodsPrimary mouse adipose-derived MSCs were isolated and characterized by adipogenic and osteogenic differentiation assays and flow cytometry. RVG-overexpressing MSCs were generated， and the derived exosomes were characterized by nanoparticle size analysis， Western blotting， and transmission electron microscopy. An OCD mouse model was established using quinpirole， and the mice were divided into five groups： control， model， clomipramine（CMI）， MSC-EXO， and RVG-MSC-EXO. Compulsive-like behaviors and cognitive function were evaluated using the compulsive checking test， open field test， marble-burying tes， and Morris water maze. The levels of inflammatory cytokines in the mouse prefrontal cortex were measured by qPCR and ELISA. Microglial polarization in the prefrontal cortex was assessed by immunofluorescence staining. The brain-targeting ability of RVG-MSC-EXO was verified using an in vivo imaging system （IVIS）.ResultsRVG-modified MSC-derived exosomes exhibited significant brain-targeting ability in mice. Exosome treatment significantly reduced compulsive checking and marble-burying behaviors in mice. Exosome treatment decreased pro-inflammatory cytokines and increased anti-inflammatory cytokines. Exosome treatment promoted a shift in microglial polarization from the M1 phenotype to M2 phenotype.ConclusionRVG-modified mesenchymal stem cell-derived exosomes can target the mouse brain， alleviate neuroinflammation by promoting microglial polarization towards the M2 phenotype， and ultimately reduce compulsive-like behaviors in OCD mice.Keywords：rabies virus glycoprotein;microglia;obsessive-compulsive disorder;exosomes;mesenchymal stem cell77|34|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：ObjectiveTo identify key ligand-receptor axes that may improve immunotherapeutic strategies for hepatocellular carcinoma with portal vein tumor thrombus （PVTT）.MethodsSingle-cell RNA sequencing （scRNA-seq） data from normal tissues （Norm） and PVTT cells were downloaded from the gene expression omnibus （GEO） database， integrated， and annotated. CellChat was used to infer intercellular communication and compare pathway activities to screen significantly differential candidate ligand-receptor axes. Multiplex immunofluorescence （mIF） was then performed to evaluate the spatial distribution of signals related to candidate axes at the tissue level. The expression of key ligands and receptors was validated by qPCR and flow cytometry in peripheral blood-derived CD8+ T cells and the human hepatic stellate cell line LX-2. Functional effects were further assessed in vitro using recombinant proteins and antagonists or neutralizing blockers.ResultsThe analysis revealed strong bidirectional communication between CD8+ T cells and activated hepatic stellate cells （aHSCs） in PVTT. The SPP1-CD44 axis was the most prominent in the direction from CD8+ T cells to aHSCs， whereas the MIF-（CD74+ CD44） axis was strongly supported in the opposite direction. These axes were consistently supported by bioinformatic screening， tissue spatial analysis， and cellular or functional validation.ConclusionThe SPP1-CD44 and the MIF-（CD74+ CD44） axes may collectively shape the immunosuppressive tumor microenvironment （ITME） of PVTT through stromal activation and T-cell functional reprogramming， suggesting potential targets for improving immunotherapeutic responsiveness in patients with PVTT.Keywords：portal vein tumor thrombus;tumor microenvironment;intercellular communication;CD8+ T cells;activated hepatic stellate cells79|38|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：ObjectiveTo investigate the protective effect of ellagic acid （EA） against bleomycin （BLM）-induced pulmonary fibrosis and associated pulmonary function impairment in mice， and to elucidate its relationship with the regulation of the interleukin（IL）-17/ nuclear factor （NF）-κB/ matrix metalloproteinase （MMP）9 signaling axis.MethodsA pulmonary fibrosis model was established in male C57BL/6J mice via intratracheal BLM injection. Interventions included IL-17 neutralizing antibody， Ixekizumab， SB-3CT， PDTC， or EA were used to modulate the IL-17/NF-κB/MMP9 signaling axis. Pathological changes in lung tissue were observed via HE， Masson， and Sirius red staining. Pulmonary function was assessed using a pulmonary function test （PFT）. Western blot and qRT-PCR were employed to detect related protein and gene expression. Network pharmacology was utilized to predict the potential targets of EA. A protein-protein interaction （PPI） network was constructed using the STRING database and Cytoscape. Molecular docking was performed to validate the binding capability of EA to core targets.ResultsBLM successfully induced obvious pulmonary fibrosis and lung dysfunction in mice， significantly elevating the level of the pro-inflammatory cytokine IL-17. This was associated with the activation of the transcription factor NF-κB p65， leading to the upregulation of the pro-fibrotic factor MMP9. Inhibition of the IL-17/NF-κB/MMP9 signaling axis markedly alleviated the degree of pulmonary fibrosis. EA intervention significantly suppressed the BLM-induced increase in IL-17， blocked the activation of the NF-κB/MMP9 pathway， and consequently reduced lung fibrotic lesions and improved pulmonary function.ConclusionEA may effectively ameliorate BLM-induced pulmonary fibrosis and lung dysfunction in mice， likely by inhibiting the inflammatory and fibrotic responses mediated through the IL-17/NF-κB/MMP9 signaling pathway.Keywords：pulmonary fibrosis;ellagic acid;bleomycin;interleukin-17;signaling pathway142|620|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：ObjectiveTo explore the application effects of environmentally friendly reagents versus traditional reagents in tissue processing， paraffin sectioning， hematoxylin-eosin （HE） staining， special staining， and immunohistochemistry.MethodsPancreatic， renal， splenic， hepatic， pulmonary， skeletal muscle， and cardiac tissues were collected from mice and New Zealand rabbits， and randomly divided into a traditional group （Group A）， an environmentally friendly reagent I group （Group B）， and an environmentally friendly reagent Ⅱ group （Group C）. The processed tissue sections from all three groups were subjected to paraffin sections， HE staining， phosphotungstic acid-hematoxylin staining， and Mallory trichrome staining. The pancreatic tissue sections were subjected to immunohistochemical detection of insulin protein. Evaluation criteria included tissue morphological integrity， embedding operability， section quality， and staining effects.ResultsNo significant differences were observed among the three groups of samples in terms of fixation efficacy， embedding operations， and section quality. After HE staining， all groups exhibited bright nuclear and cytoplasmic staining with clear contrast， with excellent-and-good rates of 98%， 99%， and 97% for Groups A， B， and C， respectively， showing no statistically significant differences （A vs. B， P=0.561； A vs. C， P=0.651）. In phosphotungstic acid-hematoxylin staining， Groups A and C showed clear structural contrast and bright staining for striated muscle and collagen fibers， whereas Group B exhibited uneven staining. The excellent-and-good rates were 100%， 10%， and 95% for Groups A， B， and C， respectively， with significant differences between Group A and Group B （P＜0.01） but no statistical difference between Group A and Group C （P=0.311）. In Mallory trichrome staining， Groups A and B outperformed Group C. The excellent-and-good rates were 95%， 90%， and 15% for Groups A， B， and C， respectively， with significant differences between Group A and Group C （P＜0.01）， but no statistical difference between Group A and Group B （P=0.548）. Immunohistochemical results showed that Group A had a clean background with no non-specific staining， while Groups B and C exhibited significant non-specific staining， with statistically significant differences in non-specific staining rates between the groups （A vs. B， 5% vs. 100%， P＜0.01； A vs. C， 5% vs.100%， P＜0.01）.ConclusionIn HE staining， environmentally friendly reagents demonstrated effective tissue fixation and staining results comparable to traditional reagents， meeting the teaching requirements. For special staining， Group B and Group C performed better in Mallory trichrome staining and phosphotungstic acid-hematoxylin staining， respectively. However， environmentally friendly reagents exhibited non-specific staining issues in immunohistochemistry， where further optimization is required.Keywords：environmentally friendly reagents;paraffin section;HE staining;special staining;immunohistochemistry69|26|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
Preclinic Research
- Abstract：ObjectiveTo compare the differences between clinical and environmental sources of Acinetobacter baumannii （AB） at a tertiary hospital in Guangzhou in terms of molecular epidemiological characteristics， antimicrobial resistance， disinfectant tolerance， virulence and the distribution of related genes， as well as plasmid epidemiological characteristics； and to assess the association between environmental and clinical strains and the potential transmission risks associated with environmental contamination.MethodsA total of 118 clinical and 102 environmental AB isolates were collected from a tertiary hospital in Guangzhou between 2024 and 2025. Species identification was performed using mass spectrometry and 16S rRNA sequencing； minimum inhibitory concentrations （MICs） for eight antimicrobial agents were determined using the agar dilution method； biofilm formation capacity was assessed using the crystal violet staining method； A Galleria mellonella infection model was used to evaluate the virulence； whole-genome sequencing was employed for multilocus sequence typing （MLST）， phylogenetic analysis， and studies on the distribution of resistance， disinfectant resistance and virulence genes， and plasmid screening.ResultsA total of 38 known ST types were identified among the 220 AB strains， with ST2 and ST40 being the predominant lineages. Antimicrobial susceptibility testing revealed that the clinical infection group exhibited resistance to minocycline， imipenem and other antibiotics， as well as the tolerance levels to the disinfectants triclosan and benzalkonium bromide， were generally higher than those in the environmental group （P＜0.001）， and the detection rates of drug resistance genes such as blaOXA-23 and adeB all exceeded 70.0%. Statistical analysis confirmed that the MIC values of TCS and BAB were significantly positively correlated with various antibiotic resistance phenotypes （P＜0.05）. In biofilm experiments， the proportion of strong biofilm-forming strains in the environmental group （64.7%） was significantly higher than that in the clinical infection group （11.9%；χ²=69.06， df=2， P＜0.000 1）， and the mortality rate of the strains increased with enhanced biofilm-forming ability. Furthermore， a total of 41 plasmid lineages and 219 insertion sequences were detected； ISs such as IS1006 and IS1007 were frequently co-occurring with resistance and virulence genes including blaOXA-23 and katA.ConclusionsThe predominant lineages of AB in this tertiary hospital were ST2 and ST40. The clinical infection group generally exhibits higher levels of antibiotic resistance and tolerance to disinfectants compared to the environmental group， while biofilm-forming ability differs ： the environmental group dominates in strong biofilm formation， and the clinical group dominates in weak to moderate biofilm formation. Plasmids and ISs may be involved in the co-occurrence and dissemination control strategies and for the molecular epidemiological surveillance of multidrug-resistant bacteria.Keywords：Acinetobacter baumannii;molecular epidemiology;antimicrobial resistance;virulence;disinfectant tolerance86|24|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：ObjectiveThis study aimed to construct a neural network model integrating readily available clinical data and two-dimensional （2D） conventional ultrasound images to evaluate the severity of steatotic liver disease （SLD）.MethodsClinical data and ultrasound images were retrospectively collected from 649 patients who underwent ultrasound attenuation imaging （ATI）. Using ATI as the reference standard， patients were divided into four groups： normal （S0）， mild （S1）， moderate （S2）， and severe （S3） SLD. Data were randomly divided into training and validation sets at an 8∶2 ratio. A contrastive language-image pre-training （CLIP） model was utilized to extract features from both clinical and imaging data， which were then used to train random forest （RF） and multilayer perceptron （MLP） models. The diagnostic performance of these multimodal models was compared their single-modal counterparts in the validation set.ResultsThe MLP model outperformed the RF model （AUC［95%CI］： S0 = 0.96 ［0.93-0.99］， S1 = 0.99 ［0.96-1.00］， S2 = 0.75 ［0.64-0.82］， S3 = 0.88 ［0.81-0.93］）. Furthermore， the multimodal fusion model demonstrated significantly superior performance compared to single-modal models （clinical data only： AUC［95%CI］ of 0.89 ［0.81-0.95］， 0.69 ［0.52-0.79］， 0.64 ［0.43-0.67］ and 0.80 ［0.73-0.90］ for S0-S3， respectively； image data only： AUC［95%CI］ of 0.91 ［0.86-0.96］， 0.89 ［0.67-0.89］， 0.69 ［0.58-0.78］ and 0.86 ［0.82-0.94］）. Metrics including precision， recall， F1-score， F2-score， confusion matrices， and loss function learning curves further confirmed that multimodal data fusion significantly improved the predictive capability.ConclusionThe proposed CLIP-based MLP multimodal model can effectively and automatically grade SLD severity. This demonstrates the significant advantage of integrating clinical and ultrasound data， providing an accurate and reliable adjunctive tool for the clinical management of chronic SLD.Keywords：steatotic liver disease;ultrasound images;clinical data;deep learning;attenuation imaging76|62|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：ObjectiveTo evaluate the predictive value of six surrogate indices of insulin resistance （IR） for cardiovascular disease （CVD） risk in adults with cardiovascular-kidney-metabolic syndrome （CKM） stages 0-3.MethodsRelated data of 6 813 participants from the China health and retirement longitudinal study （CHARLS） were analyzed. Cox proportional hazards models and restricted cubic spline （RCS） analyses were performed to evaluate the associations between six insulin resistance surrogate indices （TyG， TyG-BMI， TyG-WC， TyG-WHtR， TyG-CVAI， CVAI） and CVD incidence. Predictive performance of 6 indices was comprehensively compared from 3 dimensionalities， using receiver operating characteristic （ROC） curves for discriminative ability， net reclassification improvement （NRI） for incremental predictive value， and decision curve analysis （DCA） for clinical utility.ResultsAll six IR surrogate indices significantly predicted CVD in the CKM population. RCS analysis revealed linear associations between each index and CVD incidence. ROC analysis showed that CVAI had the highest AUC （0.628，95%CI： 0.611-0.646）， significantly outperforming the single TyG index （P=0.001 6）. NRI analysis indicated significant reclassification improvement for the event group with CVAI （event NRI=0.042 8）. DCA demonstrated that CVAI achieved the highest net benefit across most thresholds. Subgroup analysis confirmed stronger associations between CVAI and CVD risk in CKM stages 2-3.ConclusionsThese six IR surrogate indices serve as valuable tools for predicting CVD incidence in individuals with CKM stages 0-3. Among them， CVAI exhibits optimal predictive value for future CVD risk in adults with CKM stages 1-3.Keywords：cardiovascular-kidney-metabolic syndrome;insulin resistance;triglyceride-glucose;cardiovascular disease;risk prediction;cohort study90|35|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：ObjectiveTo summarize the incidence and clinical features of drug hypersensitivity reactions in children treated with sustained-releasing gonadotropin-releasing hormone agonists （GnRHa）， aiming to provide guidance for the safe clinical application of GnRHa in children.MethodsThe medical data of children diagnosed with central precocious puberty （CPP） or early and fast puberty （EFP） were retrospectively analyzed， who received GnRHa treatment at the Children's Growth Center of the First Affiliated Hospital of Sun Yat-sen University between January 1990 and July 2023. The occurrence of GnRHa-related drug hypersensitivity reactions were summarized， including the incidence and clinical features of systemic reactions and sterile abscesses.ResultsAmong the 1 684 children treated with GnRHa for CPP/EFP， the female-to-male ratio was 3.8∶1. A total of nine children （0.53%） developed 44 occurrences of drug hypersensitivity reactions. Four children （0.24%） presented with sterile abscesses （21 occurrences）， and five children （0.30%） experienced systemic hypersensitivity reactions （14 occurrences）. Four children were hypersensitive to triptorelin acetate， three were hypersensitive to leuprorelin acetate， and two were hypersensitive to both triptorelin acetate and leuprorelin acetate. The predominant hypersensitivity reactions to leuprorelin acetate were sterile abscesses， observed in four cases （4/277， 1.44%）， whereas the main reactions to triptorelin acetate were systemic hypersensitivity reactions， affecting five cases （5/1 501， 0.33%）. Case one presented with a severe and complex condition， exhibiting hypersensitivity to multiple GnRHa preparations （sustained-releasing triptorelin， sustained-releasing leuprorelin， and short-acting triptorelin）， and presenting with diverse manifestations， including induration， sterile abscesses， systemic hypersensitivity reactions， and even loss of suppression of the hypothalamic-pituitary-gonadal axis， leading to treatment failure.ConclusionsThe proportion of children experiencing drug hypersensitivity reactions to sustained-releasing GnRHa is relatively low at 0.53%， with diverse manifestations. The reactions primarily manifest as sterile abscesses and systemic hypersensitivity reactions， and in severe cases， may lead to treatment failure due to loss of suppression of the hypothalamic-pituitary-gonadal axis.Keywords：gonadotropin-releasing hormone agonists;central precocious puberty;drug hypersensitivity reaction;sterile abscess;failure to suppress the hypothalamic-pituitary-gonadal axis112|25|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：ObjectiveTo investigate the clinicopathological features， molecular profile， treatment response， and prognosis of SMARCA4 （BRG-1） and SMARCB1 （INI-1）-deficient undifferentiated tumors of the digestive system， aiming to enhance the understanding of this rare and highly aggressive molecular subtype.MethodsThis study is a single-center retrospective analysis. We included 9 cases of malignant digestive system tumors with loss of BRG-1 expression and 3 cases with loss of INI-1 expression， all pathologically confirmed at Sun Yat-sen University Cancer Center between April 2022 and December 2025. By reviewing clinical data， histological morphology，immunohistochemistry and next-generation sequencing （NGS） results from partial cases， we systematically summarized their clinicopathological and molecular characteristics， treatment strategies， and survival outcomes.Results Among the 12 patients， 6 were male and 6 were female， with a median age of 62 （44-70） years. 9 cases exhibited SMARCA4 deficiency， and 3 cases exhibited SMARCB1 deficiency. Tumors originated in the stomach （5 cases）， colon （3 cases）， pancreas （1 case）， with the primary site unknown in 3 cases. The histology predominantly showed undifferentiated carcinoma， with 1 case of poorly differentiated carcinoma. The tumor cells were epithelioid with significant atypia. Epithelial markers （e.g. CKpan） were often lost or markedly decreased， while vimentin could be positive. All 9 cases tested for MMR status were mismatch repair proficient （pMMR）， and the Ki-67 proliferation index was high ［median 80% （60%-90%）］. A discordance was observed between IHC findings and NGS results in the 6 sequenced cases. The NGS profiling revealed frequent co-occurring mutations， including TP53， KRAS， and NRAS， with no germline mutations identified.The median follow-up time was 277 （55-867） days. 9 of the 12 patients presented with stage Ⅳ disease at the time of initial diagnosis. Among 3 newly diagnosed patients without metastasis who received treatment， 2 achieved prolonged recurrence-free survival. Patients with advanced disease at initial diagnosis primarily underwent platinum-based chemotherapy or combination regimens， yet their prognosis was generally poor， with a median overall survival of 60 （45-541） days， ranging from 16 to 867 days. Notably， several patients who received chemotherapy combined with targeted therapy and immunotherapy achieved extended survival.ConclusionSMARCA4/SMARCB1-deficient undifferentiated tumor of the digestive system is a distinct molecular subtype characterized by high aggressiveness and poor prognosis， predominantly affecting middle-aged and elderly individuals. Diagnosis relies on the immunohistochemical loss of BRG-1 or INI-1 proteins. While no standard of care currently exists， treatment often refers to regimens for adenocarcinoma of the primary site. Combined immunotherapy and targeted therapy may offer potential benefits， warranting further validation in large-scale prospective studies.Keywords：BRG-1;INI-1;SWI/SNF complex;undifferentiated tumor of the digestive system;clinicopathological features190|431|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
- Abstract：ObjectiveTo investigate the chromosomal characteristics of blastocysts and pregnancy outcomes in patients with polycystic ovary syndrome （PCOS）， and to analyze the impact of PCOS on embryonic aneuploidy rate and the risk of miscarriage.MethodsThe retrospective cohort study was conducted on the preimplantation genetic testing（PGT） in the First Affiliated Hospital of Sun Yat-sen University， including cycles of PGT for aneuploidy（PGT-A） and PGT for monogenic disorders（PGT-M）. The 191 PCOS cycles（PCOS group） were matched with 564 control cycles（control group） using propensity score matching. The oocyte and embryo viability， chromosomal testing results of blastocysts， and cumulative clinical outcomes were compared between two groups. Subgroup analysis was performed by stratifying PCOS patients based on oocyte retrieval （＞20 vs. ≤20）. And the pregnancy outcomes after euploid embryo transfer were compared under different levels of ovarian response.ResultsPCOS group showed a significantly higher rate of aneuploidy per blastocyst compared to control group （21.8% vs. 19.0%， P=0.044）. Clinically， the overall miscarriage rate in the PCOS group was significantly higher than control group （17.2% vs. 10.3%， P=0.024）， even after euploid embryo transfer （17.2% vs. 10.0%， P=0.019）. In the PCOS subgroup with ＞ 20 oocytes ， the miscarriage rate following euploid embryo transfer was dramatically increased compared to control group （21.4% vs. 6.7%， P=0.001）， accompanied by higher risks of early miscarriage （15.7% vs. 5.7%， P=0.011）. Conversely， the PCOS subgroup with ≤ 20 oocytes showed outcomes comparable to control group.ConclusionsPatients with PCOS exhibit a significantly higher rate of blastocyst aneuploidy compared to the control group. Furthermore， PCOS is associated with a marked increase in miscarriage rates following blastocyst transfer， even with euploid embryos， particularly among patients with high ovarian response.Keywords：polycystic ovary syndrome;preimplantation genetic testing;aneuploid embryo;embryo transfer;miscarriage185|227|0<HTML><L-PDF> <Meta-XML>Updated：2026-05-20
Clinical Research
