ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

Background/Aims: Liver transplantation (LT) following total hepatectomy is a life-saving treatment for hepatocellular carcinoma (HCC). The HCC recurrence after LT hinders the effectiveness of the procedure. The objective of this study is to develop a pre-operative risk stratification model based on a liquid biopsy. Methods: We conducted a comprehensive multi-omics study of 260 HCC patients from three centers, including clinical data, low-coverage whole-genome sequencing of cell-free DNA (cfDNA) from plasma, as well as whole-exome, single-nucleus RNA, and spatial transcriptomics from matched tumor and non-tumor tissues. Results: We identified cfDNA-derived copy number alteration (CNA) signatures associated with post-transplant recurrence. By integrating cfDNA-derived CNA profiles with single-cell transcriptomic data, we traced recurrence-associated cfDNA to a distinct subpopulation of malignant cells within the primary tumor. These cells were embedded in a pro-metastatic microenvironment of specialized endothelial subtypes and cancer-associated fibroblasts. Notably, most recurrence-associated lesions were detectable in cfDNA prior to liver transplantation (LT). Building on these insights, we developed the ZJU Criteria based on CNA fragments and tumor markers, a pre-LT risk prediction tool that integrates conventional clinical factors with cfDNA-derived CNA signatures, and validated it using internal and independent external cohorts. Conclusion Our findings suggest that post-transplant recurrence commonly originates from advanced subclones that emerge late during tumor evolution. The ZJU Criteria provides an accurate, non-invasive strategy that significantly improves pre-LT risk stratification and clinical decision-making for patients with HCC.

Objective To explore the injury process of retinal ganglion cells(RGCs)after glucocorticoid(GC)-in-duced ocular hypertension(OHT),as well as the protective effect and mechanism of estradiol(E2)in RGC injury in rats with OHT.Methods Atotalof36(36 eyes)12-week-old male Sprague-Dawley(SD)rats were randomly divided into the blank control group,the GC-OHT group,and the OHT-E2 group,with 12 rats in each group.Rats in the GC-OHT group and the OHT-E2 group were subconjunctivally injected with GC,while those in the blank control group were subconjuncti-vally injected with an equal volume of normal saline.Two weeks after modeling,in addition to being injected with GC,rats in the OHT-E2 group were also provided with E2 eye drops.Before modeling and 1,2,3,and 4 weeks after modeling,the intraocular pressure of rats in each group was measured.The visual acuity changes of rats in each group were detected by pattern electroretinogram(P-ERG)and flash visual evoked potential(F-VEP)4 weeks after modeling.After the eyeballs were removed,the distribution and number of RGCs in rats of each group were observed by immunofluorescence staining.Immunohistochemistry,Western blot,and real-time fluorescence-based quantitative polymerase chain reaction were used to detect the relative protein and mRNA expression levels of NOD-like receptor protein 3(NLRP3),cysteine aspartate prote-ase-1(Caspase-1),and gasdermin-D(GSDMD)in rats in each group.Results There was no statistically significant difference in the intraocular pressure of rats in each group before modeling(P＞0.05).Compared with the blank control group,the intraocular pressure of rats in the GC-OHT group increased 1,2,3,and 4 weeks after modeling,and the differ-ences were all statistically significant(all P＜0.01).Compared with the GC-OHT group,the intraocular pressure of rats in the OHT-E2 group decreased 3 and 4 weeks after modeling,and the differences were all statistically significant(all P＜0.01).The P-ERG and F-VEP results showed that compared with the blank control group,the amplitudes of P50 and P1 waves of rats in the GC-OHT group decreased,and the differences were both statistically significant(both P＜0.05).Com-pared with the GC-OHT group,the amplitudes of P50 and Pl waves of rats in the OHT-E2 group increased,and the differ-ences were both statistically significant(both P＜0.05).The immunofluorescence staining results showed that compared with the blank control group,the number of RGCs of rats in the GC-OHT group decreased,and the difference was statisti-cally significant(P＜0.001).Compared with the GC-OHT group,the number of RGCs of rats in the OHT-E2 group in-creased,and the difference was statistically significant(P＜0.001).The results of immunohistochemistry,Western blot,and real-time fluorescence-based quantitative polymerase chain reaction showed that compared with the blank control group,the relative protein and mRNA expression levels of NLRP3,Caspase-1,and GSDMD in the retina of rats in the GC-OHT group all increased,and the differences were all statistically significant(all P＜0.05).Compared with the GC-OHT group,the relative protein and mRNA expression levels of NLRP3,Caspase-1,and GSDMD in the retina of rats in the OHT-E2 group all decreased,and the differences were all statistically significant(all P＜0.01).Conclusion GC-induced OHT can cause pyroptosis of RGCs,and E2 may alleviate the injury of RGCs in rats with OHT by inhibiting the pyroptosis-related NLRP3/Caspase-1/GSDMD signaling pathway.

Objective:To evaluate the clinical efficacy of Xiaoxuming Decoction combined with conventional Western medicine therapy in the treatment of patients with ischemic stroke in the recovery period.Methods:A randomized controlled clinical study was conducted. A total of the 118 patients with wind phlegm obstructing collaterlas syndrome during the recovery period of ischemic stroke in our hospital from September 2023 to July 2024 were selected as the observation subjects. They were divided into two groups using a random number table method, with 59 patients in each group. The control group was treated with conventional Western medicine therapy, while the TCM group was treated with modified Xiaoxuming Decoction on the basis of the control group. Both groups were treated for 2 months and followed up for 1 month. TCM syndrome scoring was performed before and after treatment, Barthel Index was used to evaluate daily living ability, and carotid artery ultrasound detector was used to evaluate the stability of carotid vascular plaques. Inter group comparisons were performed using t test, χ2 test, or repeated measures analysis of variance (RM-ANOVA). Results:RM-ANOVA showed that the time effect and inter group effect of TCM syndrome integration in the TCM group were significantly different from those in the control group ( Ftime=55.56, Ptime<0.001); Fbetween=18.94, Pbetween<0.001); there was no statistical significance in the interaction effect compared to the control group ( Finteraction=0.24, Pinteraction=0.866); the time effect, inter group effect, and interaction effect of Barthel Index in the TCM group were significantly different from those in the control group ( Ftime=44.57, Ptime<0.001); Fbetween=18.94, Pbetween<0.001; Finteraction=7.45, Pinteraction<0.001). The number of patients with unstable plaques in the TCM group after 3 months of treatment was lower than that in the control group ( χ2=4.52, P=0.033). Conclusion:The combination of modified Xiaoxuming Decoction and conventional Western medicine therapy can effectively improve the clinical symptoms and daily living ability of patients in the recovery period of ischemic stroke, improve the stability of cervical vascular plaques, and the clinical efficacy becomes more significant over time.

Objective:To explore the association between childhood trauma and prefrontal cortex functional networks in early adulthood using functional near-infrared spectroscopy(fNIRS).Methods:Twenty-eight individu-als with childhood trauma comprised the trauma group,while 32 without trauma formed the control group.The Childhood Trauma Questionnaire(CTQ)assessed abuse and neglect,the Ruminative Responses Scale(RRS)meas-ured repetitive thinking about negative events,and the Iowa Gambling Task(IGT)evaluated decision-making tend-encies.fNIRS data collected during the IGT were used to calculate degree centrality(DC),betweenness centrality(BC),and local efficiency(LE)in prefrontal networks.Mediation analysis explored relationships among childhood trauma,brain function(DC,BC,LE),and ruminative thinking.Results:Compared to controls,the trauma group had decreased DC in bilateral dorsolateral prefrontal cortices,increased DC,BC,and LE in the right inferior frontal gy-rus,and elevated LE in the bilateral frontal poles.BC and LE in the right inferior frontal gyrus partially mediated the relationship between CTQ sexual abuse and RRS scores(48.57％and 41.43％,respectively).Conclusion:Child-hood trauma is significantly associated with changes in prefrontal network properties in early adulthood.Sexual a-buse,in particular,may influence emotional regulation and cognitive functions by altering the network attributes of the right inferior frontal gyrus.

Objective:To investigate the clinical and endoscopic characteristics of patients with autoimmune gastritis (AIG).Methods:From January 1, 2013 to December 31, 2023, 73 AIG patients who visited Peking Union Medical College Hospital were retrospectively enrolled. The clinical data of all the patients were analyzed, including gender, age, symptoms, laboratory examination results (such as serum hemoglobin, vitamin B 12, serum iron, gastrin, anti-parietal cell antibody (APCA), anti-intrinsic factor antibody (AIFA), Helicobacter pylori ( HP) infection status; the indicators were judged based on the normal reference value), and endoscopic and histopathological examination results. Descriptive statistical methods were used for statistical analysis. Results:Among the 73 AIG patients, there were 27 males (37.0%) and 46 females (63.0%), with a median age of 57 years old (ranged from 25 to 85 years old). Among the 73 AIG patients, 68 patients received APCA test, with a positivity rate of 88.2% (60/68); 67 patients took the AIFA test, with a positivity rate of 52.2%(35/67); 62 patients underwent both APCA and AIFA tests, of which 22 patients (35.5%) showed double positive. Serum level of vitamin B 12 was detected in 59 patients, and decreased in 27 cases (median level: 0.100 ng/L, mean level: 0.102 ng/L). Gastrin level was detected in 58 patients, and increased in 55 cases (median level: 0.930 ng/L, mean level: 1.203 ng/L). The levels of serum iron and ferritin were tested in 52 patients, the level of serum iron of 5 cases decreased, and the level of ferritin of 17 cases decreased (median level: 780.0 and 26.0 μg/L, mean level: 807.8 and 76.0 ng/L, respectively).Among the 73 AIG patients, the urea breath test was performed in 12 patients, and the result was positive in 6 cases. Endoscopic rapid urease test was performed in 69 patients, and the result was positive in 11 cases (15.9%). Regular blood analysis was performed in 71 patients, 24 cases (33.8%) were diagnosed with anemia, the median age of patients with anemia was 55 years old, and male-to-female ratio was 1∶5. There were 6 cases of iron-deficiency anemia and 5 cases of pernicious anemia. The endoscopic examination results of 73 patients indicated that 65 cases (89.0%) with mucosal atrophy under endoscopy, including 47 cases (64.4%) with mucosal atrophy in the gastric fundus and body, and 18 cases (24.7%) with whole gastric atrophy, more obviously in the gastric body. The pathological examination results showed type Ⅰ gastric neuroendocrine tumor(g-NET) in 35 cases (47.9%). Conclusions:The early clinical symptoms of AIG patients are nonspecific, often present with anemia and vitamin B 12 deficiency. Close monitoring of serological markers including APCA, AIFA and gastrin is essential. For patients diagnosed or suspected with AIG, intervals of endoscopic surveillance should be shortened to prevent the genesis and development of neoplasms such as g-NET.

The intelligent development of the medical field is burgeoning,and smart healthcare has become a crucial driver for enhancing medical service efficiency and improving patient experience.However,the specific pathways through which smart healthcare improves patient experience have not been fully explained.To address this gap,this study utilizes micro-level individual data collected by the Beijing Hospitals Authority in 2023 from patients in municipal hospitals,employing the Technology Acceptance Model(TAM)to investigate the impact mechanisms of smart service construction on patient experience.The results indicate that smart services significantly improve patient experience by enhancing perceived ease of use,with this effect being particularly prominent during the treatment stage.Additionally,smart services demonstrate potential advantages in alleviating the"digital divide,"with a more pronounced optimization effect on the healthcare experience of elderly populations.Highly educated groups exhibit greater satisfaction and perceived benefits from smart services.

Objective To investigate the effects and mechanism of Ferrostatin-1(Fer-1),a ferroptosis inhibitor,on myocardial ischemia-reperfusion injury(MIRI).Methods Rat H9c2 cardiomyocytes were ran-domly divided into five groups:Control group,H/R medium group,H/R medium+Fer-1 group,H/R medium+Nec-1 group,and H/R medium+emricasan group.Cell morphology was observed using electron mi-croscopy.Cell proliferation activity was assessed via CCK-8 assay and lactate dehydrogenase(LDH)release.I-ron ion levels were measured using an iron detection kit.Reactive oxygen species(ROS)and mitochondrial su-peroxide levels were detected by flow cytometry and MitoSOXTM fluorescence staining,respectively.Western blot was employed to analyze the expression of glutathione peroxidase 4(GPX4),acyl-CoA synthetase long-chain family member 4(ACSL4),nicotinamide adenine dinucleotide phosphate oxidase(NOX1),and cycloox-ygenase 2(COX2).Results Compared to the Control group,the H/R medium group exhibited significantly increased cytotoxicity(LDH levels)and reduced cell viability,with statistically significant differences(P<0.05).Treatment with Fer-1,Nec-1,or emricasan in the H/R medium group increased cell adherence,reduced vacuolization,enhanced cell viability,and decreased cytotoxicity(LDH relative releasing rate)compared to the H/R medium group.Intracellular ferrous iron and total iron levels were elevated in the H/R medium group compared to the Control group,with statistically significant differences(P<0.05),while Fer-1 treatment sig-nificantly reduced these levels(P<0.05).ROS levels were higher in the H/R medium group than in the Con-trol group,and Fer-1 treatment attenuated this increase(P<0.05).Western blot analysis revealed elevated ACSL4,NOX1,and COX2 levels,alongside reduced GPX4 levels,in the H/R medium group compared to the Control group,with statistically significant differences(P<0.05).Fer-1 treatment reversed these trends,de-creasing ACSL4,NOX1,and COX2 levels while increasing GPX4 expression,with statistically significant differences(P<0.05).Conclusion Ferroptosis plays a critical role in MIRI.Fer-1 mitigates oxidative stress injury and alleviates MIRI by inhibiting ferroptosis.

Objective:To explore the differences between the Phoenix sepsis scoring system including Phoenix sepsis score (PSS) and Phoenix-8 organ dysfunction score (hereinafter referred to as Phoenix-8) and the commonly used pediatric sepsis scores in evaluating clinical characteristics and prognostic analysis of pediatric patients with severe sepsis diagnosed under traditional standards, namely the diagnostic criteria from the 2005 International Pediatric Sepsis Consensus Conference.Methods:This study was a retrospective observational study. From December 2020 to March 2023, 202 pediatric patients with severe sepsis meeting the inclusion criteria were admitted to the Children's Hospital of Nanjing Medical University. Based on the sepsis diagnostic criteria outlined in the International Consensus Criteria for Pediatric Sepsis and Septic Shock (2024), the pediatric patients were categorized into a sepsis group and a non-sepsis group. Sepsis group was further subdivided into a death subgroup and a survival subgroup based on the outcomes. The age, hospitalization costs, disease outcome indicators (e.g., mortality rate and incidence of septic shock), major organ (e.g., heart, liver, lungs, and kidneys) damage and their correlations, as well as PSS, Phoenix-8 and commonly used pediatric sepsis scores (e.g., pediatric sequential organ failure assessment (pSOFA), pediatric risk of mortality score Ⅲ (PRISM Ⅲ), pediatric logistic organ dysfunction-2 score (PELOD-2), pediatric multiple organ dysfunction score (P-MODS), pediatric critical illness score (PCIS), and pediatric early warning score (PEWS)) were collected and compared. Receiver operating characteristic (ROC) curve and precision-recall curve were plotted to evaluate the predictive ability of PSS, Phoenix-8, and commonly used pediatric sepsis scores for mortality risk in pediatric patients with severe sepsis under traditional standards. Predictive performance was quantified using the area under the ROC curve (AUROC). Univariate logistic regression analysis was employed to quantify the odds ratios of PSS and Phoenix-8 for predicting mortality risk. Patients with severe sepsis under traditional standards were further stratified into subgroups based on complications and comorbidities, including central nervous system (CNS) diseases, multiple infections, cardiovascular system diseases, shock, and malignancies. The Hosmer-Lemeshow goodness-of-fit test was used to assess calibration of PSS and Phoenix-8, and the DeLong test was used to compare whether there were statistically significant differences in the AUROC of PSS and Phoenix-8 for predicting mortality risk among different subgroups of pediatric patients. Results:Compared with those in non-sepsis group, pediatric patients in sepsis group were significantly older ( Z=-2.92, P<0.05) with higher incidences of septic shock and mortality, hospitalization costs, PRISM Ⅲ, PEWS, pSOFA, PELOD-2, PSS, and Phoenix-8 (with χ2 values of 21.28 and 13.64, respectively, Z values of -1.99, -5.33, -5.10, -8.55, -6.91, -10.98, and -9.93, respectively, P<0.05), and lower PCIS ( Z=-3.34, P<0.05). Compared with those in survival subgroup, hospitalization costs, PSS, Phoenix-8, PRISM Ⅲ, PEWS, pSOFA, PELOD-2, and P-MODS of pediatric patients in death subgroup was significantly higher (with Z values of -2.50, -3.50, -2.47, -5.11, -3.84, -2.94, -3.61, and -3.04, respectively, P<0.05). Compared with those in survival subgroup, the incidences of lung damage and liver damage of pediatric patients in death subgroup were also significantly higher (with χ2 values of 6.20 and 10.94, respectively, P<0.05), and 64.7% (97/150) of patients exhibited two or more concurrent organ damage. For predicting mortality risk in pediatric patients with severe sepsis under traditional standards, the AUROC values for PRISM Ⅲ, PCIS, PEWS, pSOFA, PELOD-2, P-MODS, PSS, and Phoenix-8 were approximately 0.70, with optimal cutoff values of 17.5, 91.0, 5.5, 4.5, 2.5, 4.5, 3.5, and 4.5, respectively; PELOD-2 demonstrated the highest sensitivity (0.83); while PRISM Ⅲ, PSS, and Phoenix-8 showed high specificity (>0.80). Univariate logistic regression analysis showed that for every 1-point increase in the PSS within 24 hours of pediatric intensive care unit admission, the relative risk of mortality increased by 63.7% (with odds ratio of 1.64, 95% confidence interval of 1.34-1.99, P<0.05). Similarly, for every 1-point increase in the Phoenix-8, the relative risk of mortality increased by 37.5% (with odds ratio of 1.38, 95% confidence interval of 1.18-1.60, P<0.05). The AUROC values (around 0.80) of PSS and Phoenix-8 for predicting mortality risk in pediatric patients with severe sepsis combined with CNS diseases, multiple infections, and cardiovascular system diseases were relatively high. In contrast, the AUROC values (0.60-0.80) for predicting mortality risk in pediatric patients with severe sepsis combined with shock or malignant tumors were moderate. All models passed the Hosmer-Lemeshow goodness-of-fit test ( P>0.05). The DeLong test indicated no statistically significant differences in predictive ability between PSS and Phoenix-8 across subgroups of pediatric patients ( P>0.05). Conclusions:PSS and Phoenix-8 exhibited higher specificity than most of the commonly used pediatric sepsis scores in predicting mortality risk under traditional standards. Both scores performed much better in predicting the mortality risk in pediatric patients with severe sepsis combined with CNS diseases, multiple infections, and cardiovascular system diseases.