最新刊期
卷 51 ， 期 5 ， 2026
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摘要：High-altitude deacclimatization syndrome (HADS), also known as high-altitude deadaptation syndrome, refers to a series of multi-system dysfunction syndromes occurring in individuals who have been continuously exposed to a high-altitude environment (altitude ≥2500 m) for more than 3 months after returning to plains. It results from a sharp increase in partial pressure of oxygen, as the body readapts to a relatively higher-pressure and oxygen-rich environment at low altitude. In China, more than 20 million people travel between high-altitude and plain areas annually, with the incidence of HADS ranging from 30.0% to 87.5%, which has become a major public health issue seriously affecting the health of migrants to high-altitude regions. HADS presents with diverse clinical manifestations involving multiple systems such as nervous, cardiovascular, respiratory, and digestive systems. Mild cases lead to significant declines in work efficiency and quality of life, while severe cases may develop organ injury or even a forced return to high-altitude. In view of the high incidence, severe harm and lack of standardized diagnosis and treatment protocols for HADS, the Army Health Service Training Base of Army Medical University organized a multidisciplinary expert panel to formulate the "Expert consensus on the diagnosis, treatment, and health management of high-altitude deacclimatization syndrome (2026 edition)", grounded in evidence-based medicine principles. This consensus employs the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system to appraise the quality of evidence. Guided by basic theories and cutting-edge advances in high-altitude health management, and informed by literature review and semi-structured interviews, the panel formulated 16 recommendations encompassing the pathophysiology, diagnostic classification, prevention strategies, pharmacotherapy, and rehabilitative interventions for HADS. Furthermore, based on the principle of full-cycle high-altitude health management, this consensus established a HADS health management model centered on "Prioritizing Prevention first (P), early Identification (I), graded Intervention (I), and timely Rehabilitation (R)". This model spans three critical phases-prior to descent, during descent, and following descent- and progressively establishes an integrated "prevention-treatment-rehabilitation" tripartite framework, aiming to provide scientific and standardized diagnostic and therapeutic evidence for clinicians, improve the prevention and treatment of HADS, and enhance the quality of life of affected patients.关键词：high altitude de-acclimatization syndrome;diagnosis;prevention;treatment;rehabilitation;expert consensus2104|137|0更新时间：2026-07-10
Guideline and Consensus
- 摘要：Sepsis-associated acute lung injury (SALI) is one of the common complications of sepsis, characterized by high mortality and complex pathophysiological mechanisms. Recent studies have demonstrated that gut microbiota and their metabolites participate in the progression of SALI via the gut-lung axis, influencing the local microenvironment and immune responses of lung tissue at multiple levels, through diverse targets, and across various stages. Firstly, this review systematically summarizes the multidimensional regulatory mechanisms of the gut-lung axis in SALI. Beginning with the role of the gut-lung axis in the pathophysiology of SALI, it elucidates the anatomical and functional connections of the gut-lung axis. It then focuses on analyzing the immunomodulatory effects of gut microbiota and their metabolites (such as short-chain fatty acids, bile acids, and tryptophan, etc.) in SALI, and discusses the interplay among different metabolic pathways. Secondly, the review emphasizes the roles of gut barrier dysfunction and bacterial translocation in SALI pathogenesis. Finally, it identifies key unresolved issues currently facing the field and outlines future research directions, with the aim of broadening the understanding of the SALI pathogenesis and providing a theoretical foundation and translational opportunities for developing novel effective interventions.关键词：sepsis-associated acute lung injury;gut-lung axis;gut microbiota;immune regulation1009|205|0更新时间：2026-07-10
Expert Review
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摘要：ObjectiveTo explore the expression pattern of Bcl-2 interacting killer protein (BIK) in pancreatic cancer, its relationship with tumor microenvironment and patient prognosis, and to evaluate its potential as a prognostic biomarker and therapeutic target.Methods(1) Expression profile data of pancreatic cancer were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. Differentially expressed genes were screened using bioinformatics methods, and BIK was identified as the research target based on survival analysis. Furthermore, Gene Ontology (GO) enrichment analysis and the Gene Expression Profiling Interactive Analysis (GEPIA) database were used to evaluate its potential biological function and its correlation with collagen deposition and immune cell infiltration. (2) Tissue samples from 56 pancreatic cancer patients admitted to Lanzhou University Second Hospital between December 2020 and September 2023 were retrospectively collected. Hematoxylin-eosin (HE), immunohistochemistry (IHC), and Sirius red staining were performed to assess the correlation between BIK expression and patients' clinicopathological features as well as prognosis.ResultsBIK was significantly overexpressed in pancreatic cancer tissues and associated with poor prognosis (P<0.05). It was enriched in extracellular matrix regions containing collagen and positively correlated with the expression of collagen type Ⅳ alpha 1 chain (COL4A1) and lysyl oxidase (LOX) (r=0.39, 0.23, P<0.001). BIK expression was significantly inversely correlated with M1 macrophage infiltration (r=-0.166, P<0.001), but showed a significant positive correlation with the expression of immunosuppressive markers TGFB1 and TGFB2 (r=0.53, 0.26, P<0.001). High BIK expression was an independent risk factor affecting the overall survival (OS) in pancreatic cancer patients (P=0.0014), and it was closely correlated with the proportion of collagen regions (R²=0.5375, P<0.001) and the number of CD86-positive cells (R²=0.4345, P<0.001). Receiver operating characteristic (ROC) curve analysis demonstrated that the expression of BIK protein had certain predictive value for the survival prognosis of pancreatic cancer patients (AUC=0.7288, P=0.0034). In addition, BIK expression level was significantly correlated with lymph node metastasis (N stage) (P=0.001).ConclusionsBIK is upregulated in pancreatic cancer and may promote tumor progression by promoting collagen deposition and inhibiting M1 macrophage infiltration, it is expected to be a promising prognostic biomarker and therapeutic target.关键词：pancreatic cancer;Bcl-2-interacting killer protein;prognosis;extracellular matrix;immune infiltration1371|18|0更新时间：2026-07-10 -
摘要：ObjectiveTo analyze the epidemic trend, etiological characteristics, and genetic variation and evolution of Mycoplasma pneumoniae (MP) in Nanyang, thereby providing evidence for the assessment of clinical laboratory MP detection capabilities and epidemic prevention and control.MethodsRetrospective collection was performed on MP detection data from 117,382 febrile patients admitted to Nanyang Central Hospital from January 2011 to March 2024. The epidemiological characteristics, drug resistance trends, and methodological differences in laboratory detection of MP infection were analyzed. Based on time-series analysis in R language, the ARIMA model was used to model the positive rate of laboratory-detected MP-IgM, and the optimal prediction model for MP infection was screened according to the Bayesian Information Criterion (BIC) of goodness-of-fit statistics. MP sequences were obtained from the GenBank database of the United States, and the adhesion protein (P1) region of each isolate was intercepted with reference to the MP prototype strain to construct a phylogenetic tree and perform genetic variation analysis.ResultsMP infection remained continuously epidemic in Nanyang from 2011 to 2024. From 2011 to 2019, MP infection occurred alternately or concurrently with other respiratory pathogens; from 2020 to 2022, MP showed a single epidemic with an upward trend; while from 2023 to 2024, mixed epidemics of MP and influenza A virus (IAV) were observed. Preschool children accounted for the majority of MP-infected patients. The resistance to macrolide antibiotics in MP was consistent with the epidemic trend, showing a wave pattern, with an average resistance rate exceeding 80%, peaking in 2024. All resistance mutations were located at the A2063G locus. Fluorescent quantitative PCR and Sanger sequencing (first-generation sequencing) showed significant advantages in detecting MP-DNA from bronchoalveolar lavage fluid. MP-IAV was the most common type of mixed infection. In patients under 14 years old, other mixed infections also included MP-influenza B virus, MP-rhinovirus, MP-parainfluenza virus, MP-respiratory syncytial virus, and MP-adenovirus. The optimal MP infection prediction model was screened as ARIMA (2, 1, 3) (0, 1, 1)12, which exhibited high predictive accuracy. Compared with the MP prototype strain, MP P1 had undergone varying degrees of evolution, and the current prevalent genotype in Nanyang was MP P1 type II.ConclusionsMP infection is continuously prevalent in Nanyang. Combined detection of nucleic acid and IgM is reasonable for clinical MP testing. The high drug resistance rate and high mixed infection rate of MP necessitate widespread vaccination and rational use of clinical antibiotics.关键词：Mycoplasma pneumoniae;epidemic changes;laboratory detection37|134|0更新时间：2026-07-10 -
摘要：ObjectiveBased on the large prospective Kailuan cohort study to explore the association between remnant cholesterol (RC) inflammatory index (RCII) and the risk of cardiovascular disease (CVD), as well as its predictive value for CVD.MethodsThis study was a prospective cohort study. Participants from the Kailuan study population who participated in the 2006 physical examination were included as study subjects (n=101 510). Participants were grouped according to quartiles of RCII: Q1 group (RCII<0.925, n=21 287), Q2 group (0.925≤RCII<2.923, n=21 280), Q3 group (2.923≤RCII<9.293, n=21 293), Q4 group (RCII≥9.293, n=21 286). They were followed up every 2 years. The endpoint of the follow-up was the occurrence of CVD (including stroke and ischemic heart disease), death, or the end of observation (December 31, 2022). A Cox proportional hazards regression model was used to analyze the association between RCII and the risk of incident CVD. The predictive values of RC, high-sensitivity C-reactive protein (hs-CRP), and RCII for CVD were compared using C-index, net reclassification improvement (NRI),and integrated discrimination improvement (IDI). RC, hs-CRP, and RCII were standardized using Z-scores and their association with CVD risk was analyzed.ResultsAfter an average follow-up of (14.21±3.77) years, among 85 146 study subjects, a total of 10 105 study subjects developed incident CVD. After adjusting for confounding factors and grouping by RCII quartiles, compared with Q1 group, the HR (95%CI) of incident CVD in Q2-Q4 groups were 1.120 (1.053-1.191), 1.206 (1.136-1.282), and 1.347 (1.268-1.430), respectively, with P for trend <0.01. For each one standard deviation increase in RCII, the risk of incident CVD increased by 7.2%, and the HR (95%CI) was 1.072 (1.055-1.090). ROC curve analysis showed that RCII had the highest area under the curve (AUC) value (0.568), higher than hs-CRP (0.560) or RC (0.544), with P<0.01. The C-index, NRI, and IDI values of RCII were higher than those of RC and hs-CRP.ConclusionThe predictive value of RCII for CVD is superior to that of RC or hs-CRP, and as RCII increases, the risk of incident CVD also increases.关键词：remnant cholesterol inflammation index;cardiovascular diseases;remnant cholesterol;high sensitivity C-reactive protein2161|274|0更新时间：2026-07-10 -
摘要：ObjectiveTo develop and validate a nomogram-based predictive tool for postoperative restenosis in patients with Trans-Atlantic Inter-Society Consensus (TASC) Ⅱ C/D lower extremity arteriosclerosis obliterans (ASO).MethodsClinical data of 307 patients with TASC Ⅱ C/D ASO admitted to the Second Hospital of Lanzhou University from January 2018 to December 2023 were collected and analyzed, including basic information, medical history, imaging findings, treatment regimens, and follow-up outcomes. According to whether stenosis occurred within 2 years postoperatively, patients were divided into restenosis group (n=101) and patency group (n=206). A prediction model was established by univariate analysis, multivariate binary logistic regression analysis, and variables selected by least absolute shrinkage and selection operator (LASSO) regression. The area under the receiver operating characteristic (ROC) curve (AUC), calibration curve, and decision curve analysis were employed to evaluate the prediction performance of the model, and the Bootstrap method was performed for internal verification.ResultsLASSO regression, univariate analysis and multivariate binary logistic regression analyses showed that long smoking history, low transcutaneous oxygen pressure (TcPO2), decreased peripheral perfusion index (PI), TASC Ⅱ type D classification, long vascular lesion length, high degree of arterial calcification, and non-use of drug-coated balloon (DCB) during operation were independent risk factors for postoperative restenosis in ASO patients. On this basis, considering clinical importance and model performance optimization, age, lower limb capillary filling time (CRT), and whether regular dual antiplatelet therapy was administered postoperatively were further incorporated into the model. Finally, a nomogram prediction model for postoperative restenosis in patients with TASC Ⅱ C/D type ASO was established by integrating the above 10 factors. The model exhibited good discrimination ability in training set, with an AUC of 0.844 (95%CI 0.797-0.891); the AUC still reached 0.820 (95%CI 0.775-0.870) in internal validation. Hosmer-Lemeshow test of the calibration curve showed a P-value of 0.856, indicating that the prediction model had good calibration.ConclusionsPatients' age, smoking history, lower limb CRT, TcPO2, PI, TASC Ⅱ classification, vascular lesion length, degree of arterial calcification, whether DCB was used intraoperatively, and whether regular dual antiplatelet therapy was administered postoperatively are independent influencing factors for postoperative restenosis in patients with TASC Ⅱ C/D type ASO. The prediction model based on these factors has favorable predictive performance and can provide a reference basis for formulating individualized clinical treatment strategies.关键词：lower extremity arteriosclerosis obliterans (ASO);Trans-Atlantic Inter-Society Consensus (TASC) Ⅱ C/D type;postoperative restenosis;nomogram27|219|0更新时间：2026-07-10 - 摘要：ObjectiveTo investigate the clinical efficacy of powered burr-assisted percutaneous endoscopic lumbar discectomy in the treatment of calcified lumbar disc herniation (CLDH) and its impact on postoperative spinal biomechanical stability.MethodsThis study is a retrospective case-control study. A total of 92 CLDH patients admitted to the Department of Orthopedic Surgery, Mudanjiang Forestry Center Hospital in Heilongjiang Province from January 2022 to January 2025 were collected as research subjects. According to different therapeutic methods, the patients were divided into observation group (treated with powered burr-assisted PELD, n=45) and control group (treated with conventional PELD, n=47). Propensity score matching method (PSM) was used to match the baseline data of the two groups with a caliper value of 0.02 and a 1:1 matching ratio, and 40 matched pairs were successfully obtained. The clinical data, clinical efficacy, imaging indicators before and after treatment, spinal range of motion (ROM), hip joint ROM, as well as visual analog scale (VAS) scores, Japanese Orthopaedic Association (JOA) scores, and Oswestry Disability Index (ODI) scores before and after treatment were compared between the two groups. A difference-in-differences model was used to analyze the changes in JOA, ODI, and VAS scores after treatment in the two groups. Pearson correlation analysis was employed to investigate the correlation between pelvic tilt (PT), lumbar lordosis (LL), sacral slope (SS), spinal sagittal and coronal ROM, hip joint sagittal and coronal ROM, and coronal ROM with JOA, ODI, and VAS scores.ResultsThe total effective rate (92.5% vs. 75.0%, P=0.034), the complete clearance rate of calcified lesions (95.0% vs. 77.5%, P=0.023), and the complete nerve decompression rate (95.0% vs. 80.0%, P=0.043) in observation group were significantly higher than those in control group after surgery. Compared with those before treatment, the JOA scores were significantly increased, while ODI and VAS scores were significantly decreased in both groups after treatment (P<0.05). Compared with control group, observation group had significantly higher JOA scores and significantly lower ODI and VAS scores after treatment (P<0.05). The difference-in-differences model showed that there were statistically significant differences in JOA, ODI, and VAS scores for the group factor, treatment time factor, and group × treatment time interaction term (P<0.05). The increased amplitude of JOA score and the decreased amplitudes of ODI and VAS scores in observation group were significantly higher than those in control group after treatment. Compared with preoperative values, both groups showed decreased PT, increased LL and SS, and increased spinal and hip joint sagittal and coronal ROM after treatment (P<0.05). Compared with control group after treatment, observation group exhibited significantly decreased PT, increased LL and SS, and greater increases in spinal and hip joint sagittal and coronal ROM after treatment (P<0.05). Pearson correlation analysis showed that PT was negatively correlated with JOA score, and positively correlated with ODI and VAS scores (P<0.05). LL, SS, spinal sagittal ROM and coronal ROM, and hip joint sagittal ROM and coronal ROM were positively correlated with JOA score, and negatively correlated with ODI and VAS scores (P<0.05).ConclusionPowered burr-assisted percutaneous endoscopic lumbar discectomy has significant clinical advantages in the treatment of CLDH, which can effectively alleviate pain, improve functional status, and enhance quality of life without compromising spinal stability, thus being worthy of clinical promotion and application.关键词：calcified lumbar disc herniation;spinal biomechanical stability;powered burr;clinical efficacy26|123|0更新时间：2026-07-10
Clinical Research
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摘要：ObjectiveTo investigate the effect and mechanism of curcumin nanoparticles (Cur-NPs) in alleviating early inflammatory responses in severe acute pancreatitis (SAP) by activating the nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf-2/HO-1) signaling pathway to regulate the polarization status of peritoneal macrophages (PMs) in SAP rats.Methods(1) Using the thin-film hydration method to prepare the Cur-NPS. (2) In vivo experiments were performed by establishing an SAP model in Sprague-Dawley (SD) rats. Animals were divided into Sham operation group, Cur-NPs control group, model group, and Cur-NPs treatment group (n=8). Pathological changes of pancreatic tissue, serum inflammatory cytokine levels, and enzymatic indicators were detected in each group. Primary PMs were isolated from SD rats, and the expression of M1/M2 markers and Nrf-2/HO-1 was assessed using flow cytometry (CD86, CD163, CD68, CD45), Western blotting, and RT-qPCR. (3) In vitro, primary PMs isolated from SD rats were co-cultured with SAP ascites and divided into control group, TBHQ (Nrf-2-specific agonist) control group, SAP ascites group, Cur-NPs treatment group, TBHQ treatment group. ELISA, immunofluorescence, and flow cytometry were used to verify the effects of Cur-NPs on PM polarization and the Nrf-2/HO-1 pathway.ResultsCur-NPs with favorable stability, sustained-release properties, and biological safety were successfully prepared in this study. In the SAP rat model, Cur-NPs effectively alleviated pancreatic tissue injury, reduced serum amylase and lipase activities, and significantly inhibited the release of pro-inflammatory cytokines TNF-α and IL-1β (P<0.05). Mechanistically, Cur-NPs drove the polarization of PMs from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype both in vivo and in vitro, as evidenced by downregulation of M1 markers (CD86, iNOS) and upregulation of M2 markers (CD163) (P<0.05). Further studies confirmed that Cur-NPs inhibited the phosphorylation levels of key proteins in the NF-κB pathway by promoting the nuclear translocation of Nrf-2, thereby significantly alleviating oxidative stress, manifested as decreased malondialdehyde (MDA) content and restored superoxide dismutase (SOD) activity (P<0.05). Treatment with the Nrf-2-specific agonist TBHQ mimicked the above effects of Cur-NPs.ConclusionsCur-NPs effectively drive the polarization of PMs from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype by activating the Nrf-2/HO-1 signaling pathway, thereby alleviating early inflammatory responses and pancreatic tissue injury in SAP. This study provides important experimental evidence for Cur-NPs as a potential therapeutic strategy for SAP.关键词：severe acute pancreatitis;peritoneal macrophages;cell polarization;curcumin;nanoparticles1447|424|0更新时间：2026-07-10 -
摘要：ObjectiveTo investigate the inhibitory effect of ultrafine Xiebai powder (UXP) on pulmonary fibrosis and its regulatory mechanisms associated with epithelial cell ferroptosis.Methods(1) Network pharmacology analysis was performed to predict potential targets and signaling pathways of four major active components of UXP. (2) Human bronchial epithelial cells (Beas-2b) were divided into control, bleomycin (BLM), BLM+1 mg/ml UXP (UXP-L), BLM+5 mg/ml UXP (UXP-H), and BLM+1 μmol/L nintedanib (NIN) groups. Except for control group, cells in all groups were treated with BLM (10 μg/ml) to establish a pulmonary fibrosis model. Cell viability, apoptosis level, reactive oxygen species (ROS), mitochondrial function, lipid peroxidation, and ferroptosis indicators were detected in each group. (3) Co-cultured Beas-2b cells and human lung fibroblasts (HLF-1) were randomly divided into control, BLM, BLM+UXP-L, BLM+UXP+H and BLM+NIN groups. Except for control group, cells in all groups were treated with BLM (10 μg/ml) to establish a pulmonary fibrosis cell model. Immunofluorescence staining was used to assess the expression levels of collagen type I alpha 1 chain (Col1a1) and α-smooth muscle actin (Acta2) in HLF-1 cells. (4) C57BL/6 mice were randomly divided into control, BLM, BLM+UXP-L, BLM+UXP-H, and BLM+NIN groups (n=8 per group). Except for control group, mice in all groups were intratracheally instilled with BLM (0.5 mg/ml) to establish a pulmonary fibrosis model. From day 7 to day 20 after modeling, mice were intragastrically administered UXP-L (100 mg/kg), UXP-H (500 mg/kg), or NIN (50 mg/kg) daily respectively; control and BLM groups were given an equal volume of normal saline by gavage. Lung index, lung wet/dry weight ratio (W/D), Masson staining and Sirius Red staining were measured to assess pulmonary edema and pathological changes. The contents of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and hydroxyproline were detected. RT-qPCR was used to detect mRNA expression of fibrosis-related factors, and Western blotting was performed to analyze the expression levels of related proteins. Transmission electron microscopy was employed to observe changes in mitochondrial ultrastructure.Results(1) A total of 240 overlapping target genes were identified between the main active components of UXP and pulmonary fibrosis. (2) Compared with control group, BLM group exhibited significantly decreased cell viability and mitochondrial membrane potential (P<0.05), along with markedly increased apoptosis rate, ROS levels, lipid peroxidation content, and Fe2+ content (P<0.001). Compared with BLM group, BLM+UXP-L, BLM+UXP-H, and BLM+NIN groups exhibited significantly increased cell viability and mitochondrial membrane potential (P<0.001), and significantly decreased cell apoptosis rate, ROS levels, lipid peroxidation content, and Fe2+ content (P<0.001). (3) Compared with control group, the levels of Acta2 and Col1a1 in HLF-1 cells co-cultured with Beas-2b were significantly higher in BLM group (P<0.001). Compared with BLM group, BLM+UXP-L, BLM+UXP-H, and BLM+NIN groups showed significantly lower levels of Acta2 and Col1a1 in HLF-1 cells (P<0.001). (4) Compared with control group, BLM group showed significant increased lung index, W/D ratio, hydroxyproline and MDA contents, mRNA expression levels of fibrosis-related and pro-ferroptotic genes (Acta2, Col1a1, Col1a2, Fn, Acsl4, Ncoa4) and protein expression levels of Acta2, Col3a1 and p-ERK (P<0.05, P<0.01, or P<0.001), while the activities of SOD and GSH and expression levels of anti-ferroptotic gene Gpx4, Slc7a11 were significantly decreased (P<0.001). Significant collagen deposition, iron deposition, and mitochondrial ultrastructural damage were observed in lung tissues. Compared with BLM group, BLM+UXP-L, BLM+UXP-H, and BLM+NIN groups showed significantly decreased lung index, W/D ratio, hydroxyproline and MDA contents, mRNA expression levels of Acta2, Col1a1, Col1a2, Fn, Acsl4, Ncoa4, and expression levels of Acta2, Col3a1 and p-ERK protein (P<0.01 or P<0.001), while SOD and GSH activities and expression levels of Gpx4 and Slc7a11 were significantly increased (P<0.05 or P<0.001). Collagen deposition, iron deposition, and mitochondrial ultrastructural damage in lung tissues were alleviated.ConclusionUXP may inhibit pulmonary fibrosis by regulating oxidative stress, lipid peroxidation, and the ferroptosis pathway.关键词：ultrafine Xiebai powder;pulmonary fibrosis;oxidative stress;mitochondrial protection;ferroptosis24|185|0更新时间：2026-07-10 -
摘要：ObjectiveTo investigate the effects and underlying mechanisms of hawthorn-derived exosome-like nanovesicles (HDELNs) on trimethylamine N-oxide (TMAO)-induced injury in human umbilical vein endothelial cells (HUVECs).MethodsPrimary HUVECs were cultured in HUVECs-specialized medium; HDELNs were isolated from hawthorn using differential centrifugation and sucrose density gradient centrifugation, and characterized by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), Coomassie brilliant blue staining and Western blotting. (1) The following groups were established: control group (HUVECs cultured under normal conditions), TMAO concentration gradient subgroups (HUVECs treated with 150, 300, 600, 900, 1800, or 3600 μmol/L TMAO for 24 h), TMAO time gradient subgroups (HUVECs treated with 900 μmol/L TMAO for 4, 8, 12, 24, 48 h), and HDELNs concentration gradient subgroups (HUVECs treated with 1×10⁶, 1×10⁷, 1×10⁸, 1×109, 1×1010, 1×1011 particles/ml HDELNs for 24 h). Cell viability of each group was assessed using the CCK-8 assay, and the protein expression levels of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), matrix metallopeptidase 9 (MMP-9) and interleukin-1β (IL-1β) in HUVECs were determined by Western blotting. (2) Four independent groups were set up: control group, TMAO group (HUVECs treated with TMAO for 24 h), HDELNs group (HUVECs treated with HDELNs for 24 h) and TMAO+HDELNs group (HUVECs co-treated with TMAO and HDELNs for 24 h). Cell viability of each group was measured by the CCK-8 assay. The protein expression levels of ICAM-1, VCAM-1, MMP-9, IL-1β, endothelial nitric oxide synthase (eNOS), and peroxisome proliferator-activated receptor γ (PPAR-γ) in HUVECs were detected by Western blotting. The mRNA expression level of PPAR-γ in HUVECs was quantified using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Intracellular adenosine triphosphate (ATP) content was determined by luciferase assay. Intracellular superoxide dismutase (SOD) activity was evaluated using the WST-8 assay. Mitochondrial membrane potential, reactive oxygen species (ROS) and mitochondrial superoxide contents were detected by fluorescent probe assays. (3) The following groups were designed: control group, TMAO group, HDELNs group, TMAO+HDELNs group, TMAO+HDELNs+PPAR-γ inhibitor T0070907 subgroups (HUVECs co-treated with TMAO, HDELNs and 1, 3, 10, 30 μmol/L T0070907 for 24 h) and TMAO+HDELNs+PPAR-γ agonist rosiglitazone subgroups (HUVECs co-treated with TMAO, HDELNs and 20, 30, 50 μmol/L rosiglitazone for 24 h). Cell viability was assessed by the CCK-8 assay. (4) Five independent groups were established: control group, TMAO group, HDELNs group, TMAO+HDELNs group, and TMAO+HDELNs+PPAR-γ agonist/inhibitor groups (HUVECs co-treated with TMAO, HDELNs and the PPAR-γ agonist or inhibitor for 24 h). Cell viability of each group was measured using the CCK-8 assay. The protein expression levels of ICAM-1, VCAM-1, MMP-9, IL-1β and eNOS in HUVECs were detected by Western blotting. Intracellular ATP content of each group was determined by the luciferase assay. Intracellular SOD activity was measured by the WST-8 assay. Mitochondrial membrane potential, ROS and mitochondrial superoxide content in cells were examined by fluorescent probe assays.ResultsHDELNs with uniform size and double-layer membrane structure were isolated from hawthorn by differential centrifugation and sucrose density gradient centrifugation. Protein bands in HDELNs were visualized by Coomassie brilliant blue staining. CCK-8 results demonstrated that treatment with 900 μmol/L TMAO for 24 h significantly decreased HUVEC viability (P<0.01), while 1×107 particles/ml HDELNs markedly restored cell viability (P<0.01). Western blotting results showed that TMAO treatment significantly increased the protein levels of ICAM-1, VCAM-1, MMP-9 and IL-1β (P<0.05), and decreased the expression level of eNOS (P<0.01), whereas HDELNs reversed these abnormal protein expression (P<0.05). Luciferase assay results indicated that TMAO significantly reduced intracellular ATP content (P<0.0001), while HDELNs restored the ATP content (P<0.0001). WST-8 assay results revealed that TMAO treatment significantly decreased SOD activity (P<0.01), while HDELNs restored SOD activity (P<0.001). Fluorescence probe assays showed that TMAO increased the ROS and mitochondrial superoxide contents and decreased the mitochondrial membrane potential (P<0.01), and these effects were reversed by HDELNs (P<0.001). Western blotting and RT-qPCR results showed that TMAO significantly downregulated PPAR‑γ expression in HUVECs (P<0.01), while HDELNs restored PPAR‑γ expression (P<0.05). CCK-8, luciferase assay, WST-8 assay, Western blotting and fluorescence probe method results showed that 30 μmol/L PPAR‑γ antagonist T0070907 antagonized the protective effect of HDELNs on TMAO-induced HUVECs' injury (P<0.05), while 50 μmol/L PPAR-γ agonist rosiglitazone enhanced the protective efficacy of HDELNs (P<0.05).ConclusionHDELNs can significantly alleviate TMAO-induced injury in HUVECs, and the underlying mechanism may be associated with the activation of the PPAR-γ signaling pathway.关键词：atherosclerosis;plant-derived exosome-like nanovesicle;peroxisome proliferator activated receptor γ30|306|0更新时间：2026-07-10 -
摘要：ObjectiveTo explore the mechanism by which silent information regulator 6 (SIRT6) deletion induces oxidative stress injury in the intestinal mucosa.MethodsAn intestinal villus epithelium-specific SIRT6 knockout mouse model was established. After the progeny mice were genetically identified, they were divided into SIRT6FL group and SIRT6IEC-KO group, with 8 mice in each group. The small intestine (jejunal segment) and colon tissues were collected. HE staining was used to observe the pathological morphology of the mouse intestinal mucosa. Transcriptome sequencing was used to analyze changes in transcriptional profiles of the jejunal tissue. The activities of superoxide dismutase (SOD), catalase (CAT), and the content of malondialdehyde (MDA) in the jejunal tissue were detected using kits. Western blotting was used to detect the expression levels of oxidative stress injury-related factors [nuclear factor E2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), SOD2] and inflammatory factors [tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, IL-10] in the intestinal mucosa. Cells of mouse intestinal epithelial cell line 6 (IEC-6) were divided into control group (without any treatment) and model group (treated with 450 μmol/L SIRT6 inhibitor OSS_128167 for 48 h). Cell viability was detected using the MTT method, and apoptosis rate was detected using flow cytometry. Western blotting was used to detect the expression levels of proteins related to the phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) signaling pathway [p-PI3K, phosphorylated glycogen synthase kinase 3β (p-GSK-3β), p-Akt, homologous phosphatase-tensin protein (PTEN)], Nrf2, HO-1, and apoptosis-related proteins (Bax, Bcl-2, Cleaved caspase-3). The level of reactive oxygen species (ROS) was detected using a kit.ResultsThe jejunal mucosa of mice in SIRT6FL group showed good growth status, with regular and tight arrangement of crypts and villi. In contrast, the jejunal mucosa of mice in SIRT6IEC-KO group presented poor growth, with significantly reduced villus height and significantly shallower crypt depth (P<0.001), while the morphology of the colon mucosa showed no significant change. Transcriptome analysis of the jejunal tissue revealed that redox processes were the main enriched biological processes for differentially expressed genes. Compared with SIRT6FL group, the activities of SOD and CAT, and the expression levels of Nrf2, HO-1, and SOD2 proteins in the jejunal tissue of SIRT6IEC-KO mice were significantly decreased, while the MDA content and protein expression levels of TNF-α, IL-1β, and IL-6 were significantly increased (P<0.05). However, there was no statistically significant difference in the protein expression level of IL-10 between the two groups (P>0.05). Compared with control group, the cell viability of IEC-6 cells of model group significantly decreased (P<0.05), the protein expression levels of p-PI3K, p-GSK-3β, p-Akt, Nrf2, HO-1, and Bcl-2 in IEC-6 cells of model group were significantly decreased, while the protein expression levels of Bax and Cleaved caspase-3, the cell apoptosis rate, and the ROS level were significantly increased (P<0.05). There was no statistically significant difference in the protein expression level of PTEN between the two groups (P>0.05).ConclusionSIRT6 deletion exacerbates the inflammatory response and oxidative stress injury of the intestinal mucosa. The mechanism is related to the inhibition of the PI3K/Akt and Nrf2 signaling pathways in intestinal epithelial cells and the promotion of cell apoptosis.关键词：silent information regulator protein 6;oxidative stress;intestinal mucosal renewal;apoptosis;PI3K/Akt signaling pathway24|133|0更新时间：2026-07-10 -
摘要：ObjectiveTo investigate the effect of Alpinetin on neurological function recovery in rats with spinal cord injury (SCI) and its underlying mechanism.MethodsA modified Allen's striking method was used to establish an SCI rat model. The successfully modeled rats were randomly divided into SCI group, bpV [phosphatase and tensin homolog (PTEN) inhibitor] group, Alpinetin low-dose (Alpinetin-L) group, Alpinetin high-dose (Alpinetin-H) group, and Alpinetin-H+LY294002 [phosphatidy linositol 3-kinase (PI3K) inhibitor] group, with 12 rats in each group. Additionally, 12 healthy Sprague-Dawley (SD) rats were selected as control group. After the end of administration, the Basso-Beattie-Bresnahan (BBB) score, Reuter score, inclined plate angle and latency of cortical somatosensory evoked potential (CSEP) were detected. ELISA was performed to detect the levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α. HE staining was performed to observe the pathological changes in spinal cord tissue. Nissl staining was performed to examine the morphology and quantity of anterior horn motor neurons in spinal cord tissue. TUNEL staining was applied to detect neuronal apoptosis. Immunohistochemistry was applied to measure the expression of autophagy-related proteins. Western blotting was used to detect the expression of apoptosis-related proteins and proteins associated with the PTEN/PI3K/protein kinase B (Akt) signaling pathway.ResultsCompared with control group, SCI group exhibited severe destruction of spinal cord tissue structure, obvious cavities with necrotic tissue and focal hemorrhage, massive inflammatory cell infiltration, and significant pyknosis and necrosis of nerve cell nuclei, leading to sparse and disordered arrangement of neurons, shallow Nissl body staining, and reduced number of neurons. The BBB score, inclined plate angle, and the ratios of p-PI3K/PI3K and p-Akt/Akt were decreased, while the CSEP latency was prolonged, and the Reuter score, levels of IL-1β, IL-6 and TNF-α, neuronal apoptosis rate, expression levels of caspase-3, cleaved-caspase-3 (C-caspase-3), Beclin1, and autophagy-related protein 5 (Atg5) and the ratios of p-PTEN/PTEN were increased (P<0.05). Compared with SCI group, bpV group, Alpinetin-L group, and Alpinetin-H group showed significant improvement in pathological damage of spinal cord tissue, relatively regular tissue structure, gradually reduced cavities, alleviated inflammatory cell infiltration, deeper Nissl body staining and increased number of neurons. The BBB score, inclined plate angle, and the ratios of p-PI3K/PI3K and p-Akt/Akt were increased, while the CSEP latency was shortened, and the Reuter score, levels of IL-1β, IL-6 and TNF-α, neuronal apoptosis rate, expression levels of caspase-3, C-caspase-3, Beclin1 and Atg5, and the ratios of p-PTEN/PTEN were decreased (P<0.05). Compared with Alpinetin-H group, Alpinetin-H+LY294002 group presented aggravated pathological damage of spinal cord tissue, with decreased BBB score, inclined plate angle, and the ratios of p-PI3K/PI3K and p-Akt/Akt, prolonged CSEP latency, as well as increased Reuter score, levels of IL-1β, IL-6 and TNF-α, neuronal apoptosis rate, expression levels of caspase-3, C-caspase-3, Beclin1 and Atg5, and the ratios of p-PTEN/PTEN (P<0.05).ConclusionAlpinetin can promote neurological function recovery in SCI rats, which may be associated with the inhibition of the PTEN/PI3K/Akt signaling pathway.关键词：Alpinetin;PTEN/PI3K/Akt signaling pathway;spinal cord injury (SCI);neurological function recovery23|182|0更新时间：2026-07-10
Basic Research
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摘要：Cardiovascular disease (CVD) poses a serious threat to global population health, with inflammatory responses closely associated with its pathogenesis and progression. The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling pathway is a key component of the innate immune system. By recognizing cytoplasmic DNA, cGAS-STING activates interferon regulatory factor 3 (IRF3) and nuclear factor-kappa B (NF-κB), thereby inducing the production of type Ⅰ interferon (IFN-Ⅰ) and various inflammatory factors, which orchestrate immune responses. This pathway not only serves as a key regulatory component in inflammation, infections, cancers and autoimmune diseases, but also has been implicated in cellular processes, including apoptosis, autophagy, cellular senescence, and metabolic regulation. Notably, the cGAS-STING signaling pathway plays an important regulatory role in various CVDs (including atherosclerosis, myocardial infarction, heart failure, etc.). Moreover, inhibition of the cGAS-STING pathway attenuates inflammation and ameliorates CVD progression, highlighting its potential as a therapeutic target for CVD. This review systematically summarizes the regulatory mechanisms of the cGAS-STING pathway in various CVDs and the latest research progress, and discusses the therapeutic promise of inhibitors of cGAS and STING, aiming to provide new theoretical bases and strategic directions for CVD treatment.关键词：cyclic GMP-AMP synthase-stimulator of interferon genes;cardiovascular disease;inflammatory responses31|428|0更新时间：2026-07-10 -
Research progress in the application of natural polysaccharide-based composite hemostatic sponges AI导读
摘要：Hemorrhage is one of the most common complications in trauma and surgery, where excessive blood loss can increase mortality risk. Physiological hemostasis - a critical biological mechanism for hemorrhage control - involves cascade reactions of coagulation factors and proteins that ultimately form blood clots to achieve hemostasis. However, during surgery and emergencies, physiological hemostasis alone proves insufficient for hemorrhage control, necessitating auxiliary hemostatic materials to accelerate the process. Currently, no ideal clinical hemostatic material can simultaneously balance hemostatic efficiency, biocompatibility, and production cost. Consequently, developing safe, effective, and convenient hemostatic materials holds significant clinical significance. Hemostatic sponges, characterized by unique porous structures, exhibit strong fluid absorption capacity that effectively concentrates coagulation components, red blood cells, and platelets to promote blood clot formation, representing a vital research direction in hemostatic materials. Particularly, natural polysaccharide composite hemostatic sponges have become a research focus due to their dual advantages of hemostatic performance and excellent biocompatibility. Nevertheless, single-component polysaccharide sponges rarely achieve optimal hemostatic efficacy. Current research therefore focuses on utilizing polysaccharide macromolecules as matrix materials combined with other natural polymers, synthetic polymers, inorganic materials, or metal-containing materials. This approach was used to develop multifunctional hemostatic sponges with enhanced hemostatic capability and biocompatibility while endowing them with additional properties like antibacterial effects and wound healing promotion. This review summarizes preparation methods and hemostatic applications of various natural polysaccharide composite sponges and discusses their future prospects.关键词：natural polysaccharides;battlefield rescue;hemostasis;hemostatic sponges28|400|0更新时间：2026-07-10 - 摘要：Hepatocellular carcinoma (HCC) represents a primary malignancy of the digestive system, characterized by high incidence and mortality. A hallmark of this disease is its profound tumoral heterogeneity. During the processes of proliferation and differentiation, HCC tumor cells undergo substantial alterations at the molecular, biological, and genetic levels, driven by a complex interplay of intrinsic and extrinsic factors. These alterations result in notable variations in proliferative capacity, invasive potential, and sensitivity to therapeutic agents. This inherent heterogeneity poses a critical challenge to clinical management, serving as a primary obstacle to accurate diagnosis and successful treatment. In recent years, radiomics has emerged as a cutting-edge field at the intersection of medical imaging and artificial intelligence. Specifically, MRI-based radiomics offers a novel paradigm for the accurate diagnosis and therapy of HCC. Extracting and analyzing high-dimensional quantitative features from medical images, researchers can deeply interrogate the spatio-temporal and molecular heterogeneity of HCC. This approach allows for a comprehensive, non-invasive characterization of its structural and functional properties, thereby providing crucial decision support for clinical precision medicine. This review focuses on the latest advances of MRI-based radiomics in key clinical applications for HCC, including histopathological evaluation, the stratification of metastatic risk, and prognostic prediction. Furthermore, the current research landscape of existing bottlenecks and challenges was analyzed, aiming to provide a reference for future studies in individualized clinical management.关键词：hepatocellular carcinoma;magnetic resonance imaging;radiomics;artificial intelligence;heterogeneity22|138|0更新时间：2026-07-10
- 摘要：Rapidly progressive interstitial lung disease (RPILD) is a highly fatal pulmonary disorder associated with a poor prognosis. As a life-threatening complication in patients with dermatomyositis and antisynthetase syndrome, RPILD features challenging early recognition and rapid disease progression, and may rapidly progress to respiratory failure and even death. At present, there is a lack of therapeutic strategies for RPILD based on high-quality evidence-based medical evidence. Therefore, early prediction of disease progression, identification of high-risk patients, and formulation of individualized treatment regimens are the key to improving prognosis. This review systematically outlines the research progress on predictive indicators for RPILD, including clinical characteristics, serological markers, and imaging findings. It further evaluates the clinical application value of relevant predictive models and integrates existing therapeutic strategies, aiming to provide a reference for risk stratification and clinical management of RPILD.关键词：rapidly progressive interstitial lung disease;dermatomyositis;antisynthetase syndrome;predictive factors;therapeutic strategies34|225|0更新时间：2026-07-10
- 摘要：Neuropathic pain (NP) is a chronic pain disorder caused by injury to the central or peripheral nervous systems. The role of oligodendrocytes (OLs) in neuronal support and axonal insulation has been extensively studied; however, research on their involvement in pain modulation remains an emerging field. This review summarizes recent progress in understanding the mechanisms by which OLs contribute to NP, focusing on three key aspects: (1) disruption of myelin homeostasis resulting from OL apoptosis and aberrant differentiation of oligodendrocyte precursor cells (OPCs); (2) activation of inflammatory cascades driven by OL-secreted pro-inflammatory cytokines such as interleukin (IL)-33, IL-24); and (3) intercellular crosstalk between OLs and other glial cells. Potential therapeutic targets and novel treatment strategies are also discussed, aiming to provide theoretical insights and new perspectives for research on NP mechanisms and to promote the development of relevant therapeutic approaches.关键词：oligodendrocytes;neuropathic pain;myelination;inflammation24|118|0更新时间：2026-07-10
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Research advances in dysfunction and repair of blood-spinal cord barrier after spinal cord injury AI导读
摘要：Disruption of the blood-spinal cord barrier (BSCB) is one of the central events that amplifies secondary injury after spinal cord injury (SCI) by exacerbating inflammation, edema and neuronal death. Emerging pathophysiological insights indicate that abnormal hemodynamics, leukocyte transmigration, endothelial senescence and deleterious autoimmunity collectively compromise BSCB integrity. This review summarizes advances on treatment regimens of nano-medicine and molecular intervention strategy designed to restore BSCB function in recent years, such as delivering microRNAs or antioxidants to re-establish endothelial tight junctions by engineered exosomes, achieving efficient drug penetration and controlled release by reactive oxygen-responsive and lesion-targeted nanocarriers, interrupting inflammatory and oxidative cascades through pathway-specific blockade of NF-κB, etc. The aim is to provide a reference for research on early BSCB functional recovery and personalized therapies after SCI.关键词：spinal cord injury;blood-spinal cord barrier;nanomedicine;exosomes;molecular intervention24|140|0更新时间：2026-07-10
Review
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