Peritoneal carcinomatosis (PC) is a common pattern of recurrence in gastric cancer patients and is associated with a poor prognosis. This study aimed to evaluate the predictive value of the albumin-fibrinogen ratio (AFR) for PC in patients with gastric cancer and to develop two preoperative prediction models.

A total of 745 gastric cancer patients were included in this study. Preoperative AFR, along with other serum markers and clinical tumor characteristics, was assessed. Univariate and multivariate logistic regression analyses were performed to determine the odds ratios (ORs) and 95% confidence intervals (CIs) of the independent variables. Propensity score matching (PSM) was used to control for potential confounders, and one-way ANOVA was conducted to evaluate differences in distribution between groups. Two prediction models incorporating the independent predictive indicators were constructed and validated via receiver operating characteristic (ROC) curves.

Poorly differentiated type (OR 2.679; P = 0.001), nondiffuse morphological type (OR 2.123; P = 0.040), BMI < 23.550 kg/m² (OR 4.635; P = 0.001), AFR < 11.275 (OR 2.895; P = 0.003) and CA199 ≥ 73.615 U/mL (OR 2.040; P = 0.037) were identified as independent risk factors for PC in patients with gastric cancer. After PSM, the AFR remained the only inflammatory marker that was independently associated with PC (P = 0.003). AFR demonstrated consistent robustness in predicting PC across multiple sample sets. Among all the independent risk factors, the AFR had the highest area under the curve (AUC) for ROC analysis (AUC 0.648; 95% CI 0.580–0.715). Two combination models incorporating the AFR demonstrated enhanced predictive ability: Combination Model 1 (AUC 0.759; 95% CI 0.699–0.820) and Combination Model 2 (AUC 0.801; 95% CI 0.744–0.859).

The preoperative AFR serves as a useful indicator for predicting PC. Two reliable prediction models based on the AFR have been developed.

To analyze the risk factors for lymph node metastasis (LNM) in patients with stage pT1 lung adenocarcinoma to select a more appropriate surgical option.

In this retrospective study, 294 patients with postoperative pathologically confirmed stage pT1 invasive lung adenocarcinoma were collected and divided into two groups according to whether they had mediastinal or hilar LNM. Patient tumor imaging, pathological features and gene mutations were analyzed, and risk factors that might predict LNM were derived via univariate and multivariate logistic analyses. LNM-related variables were screened by Boruta and least absolute shrinkage and selection operator regression analysis.

Among the 294 patients, 45 (15.3%) had positive mediastinal or hilar lymph nodes. There were no significant differences between the two groups in terms of sex, age, or underlying disease. The difference in the percentage of solidity between the two groups was significant, with the higer percentage group showing a more significant difference. The results of multivariate logistic analysis revealed that a high percentage of solid components and wild-type epidermal growth factor receptor (EGFR) were risk factors for LNM. The nomogram for predicting LNM included the consolidation tumor ratio, tumor size, micropapillary and EGFR, with an area under the curve of 93.4% (95% CI: 88.7–99.1) in the derivation cohort and 92.3% (95% CI: 84.6–99.9) in the validation cohort.

A high proportion of solid components and wild-type EGFR were risk factors for pT1 stage lung adenocarcinoma, suggesting that the choice of lung segmentectomy needs to be evaluated and selected more cautiously.

To investigate the effects of calprotectin (S100A8/A9) on the biological activity of acute myeloid leukemia (AML) cells harboring a DNA methyltransferase 3A (DNMT3A) mutation and to explore the underlying molecular mechanisms involved.

AML monoclonal cell lines harboring the DNMT3A^R882H mutation were generated via lentiviral transduction and limiting dilution. RNA sequencing was used for differential gene expression analysis, followed by bioinformatic pathway enrichment and gene correlation analyses. The biological effects of paquinimod, a selective S100A8/A9 inhibitor, on DNMT3A^R882H AML cells were assessed via Cell Counting Kit (CCK-8) proliferation assays, Annexin V/PI staining, cell cycle analysis, cell adhesion assays, and transwell migration assays.

Differential gene expression analysis revealed 442 upregulated and 535 downregulated genes in DNMT3A-mutated (DNMT3A^mut) cells compared with those in DNMT3A wild-type (DNMT3A^wt) cells, with the S100A8/A9 complex recurrently enriched in Reactome pathway analysis. Compared with healthy controls, patients with AML presented increased expression of S100A8 and S100A9 and increased expression of DNMT3A^mut cells relative to DNMT3A^wt cells, which was correlated with poor prognosis in patients with AML. There were no notable differences in proliferation among the DNMT3A^mut, DNMT3A^wt, and empty vector cells under normal or starvation conditions. However, paquinimod treatment notably inhibited the proliferation, migration, and adhesion of DNMT3A^mut AML cells in a dose-dependent manner, causing G0/G1 cell cycle arrest, whereas no significant effects on apoptosis were observed. Paquinimod also downregulated key adhesion molecules, including intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), monocyte chemoattractant protein-1 (MCP-1), and matrix metalloproteinase-2 (MMP-2). Additionally, S100A8 and S100A9 expression was upregulated in a dose-dependent manner in response to cytarabine treatment.

Elevated S100A8/A9 expression contributes to the abnormal proliferation, migration, adhesion, and chemoresistance of DNMT3A^mut AML cells. Targeting S100A8/A9 alone or in combination with other treatments represents a promising therapeutic strategy for DNMT3A^mut AML.

This study aimed to investigate the neuroprotective effects of cholecalciferol cholesterol emulsion (CCE), a vitamin D (VD) precursor, in a murine model of acute cerebral infarction (ACI) and to elucidate the role of the Nrf2 signaling pathway in mediating these effects.

Forty C57BL/6J mice (male and female) were divided into five groups (n = 10 per group): control, control + CCE, ACI, ACI + CCE, and ACI + CCE + ML385 (an Nrf2 inhibitor). ACI was induced by middle cerebral artery occlusion (MCAO). CCE was administered for three weeks prior to ACI induction, and ML385 was administered intravenously to inhibit Nrf2. Neurological function, brain edema, and infarct size, as well as inflammatory and apoptotic marker levels, were assessed post-ACI. Statistical analyses were conducted via one-way ANOVA and Student's t test, with P < 0.05 considered significant.

Compared to ACI group, CCE significantly reduced neurological deficits, brain edema, and infarct size (P < 0.01). The ACI + CCE group presented improved short-term memory retention, as evidenced by shorter avoidance latency in shuttle avoidance tests (P < 0.01). CCE administration attenuated the expression of inflammatory markers (IL-6, MIF, Lp-PLA2) while increasing IL-10 levels (P < 0.001). Furthermore, CCE increased Nrf2 and HO-1 expression and reduced apoptosis by decreasing the Bax/Bcl-2 ratio in brain tissue (P < 0.001). ML385 abolished these neuroprotective effects, confirming the role of the Nrf2 pathway in mediating the benefits of VD.

VD, via VD receptor-mediated activation of the Nrf2/HO-1 pathway, reduces inflammation, apoptosis, and neurological damage following ACI. These findings support the therapeutic potential of VD in the treatment of ischemic stroke and highlight the importance of Nrf2 in mediating these effects.

The systemic immune-inflammation index (SII) has recently attracted significant interest as a new biomarker for predicting the prognosis of patients with glioblastoma (GBM). However, the predictive significance of it is still a subject of debate. This study intended to assess the clinical effectiveness of the SII in GBM and establish a nomogram.

Receiver operating characteristic (ROC) curves were utilized to determine the optimal cut-off values of the SII. Kaplan–Meier (KM) survival curves were used to analyze the median overall survival (OS). Cox regression analysis was carried out to evaluate the associations between OS and different clinical factors. Based on the SII and clinical characteristics, a nomogram was constructed, and its value in clinical application was evaluated by means of decision curve analysis.

The optimal SII cut-off value was 610.13. KM analysis revealed that GBM patients with higher SII values had shorter OS (15.0 vs. 34.0 months, P = 0.044). Multivariate analysis demonstrated that a high SII was an independent predictor of poor outcome in GBM (HR = 1.79, P = 0.029). The nomogram incorporating the preoperative SII showed good predictive accuracy for GBM patient prognosis (C-index = 0.691).

The SII is an independent predictive indicator for GBM. Patients with elevated SII levels tend to have a poorer prognosis. A nomogram combining the SII with clinical and molecular pathological features can assist clinicians in assessing the risk of death in GBM patients, providing a basis for individualized treatment decisions.

Inflammation plays a pivotal role in the progression of coronary artery disease (CAD). High-sensitivity C-reactive protein (hsCRP) serves as a well-established biomarker for assessing cardiovascular inflammation risk. However, the specific intestinal microbiota alteration contributing to increased inflammation remains unclear. Therefore, the present study investigated the correlation between the intestinal microbiota and inflammation in patients with unstable angina (UA).

A cohort of 92 patients with UA was recruited for this study. The plasma hsCRP level was measured via a CardioPhase hsCRP assay, fecal samples were collected after admission, and 16S rRNA sequencing was conducted to identify the fecal microbial profile. The participants were classified into two groups according to the median hsCRP level (1.11 mg/L). The composition of the fecal microbiota was compared between patients with hsCRP ≥ 1.11 mg/L and those with hsCRP < 1.11 mg/L. Additionally, the correlations between the fecal microbiota and clinical characteristics were analyzed.

A notable reduction in the relative abundance of Akkermansia was observed in patients with hsCRP ≥ 1.11 mg/L, whereas the diversity of the fecal microbiota was not significantly different between patients with hsCRP ≥ 1.11 mg/L and those with hsCRP < 1.11 mg/L. Furthermore, the abundance of Akkermansia was negatively correlated with hsCRP levels.

This study suggested a significant association between decreased levels of Akkermansia and inflammatory risk in patients with UA. These findings underscore the potential role of the intestinal microbiota in contributing to inflammation in UA patients. Further work is needed on the mechanism by which the microbiota contributes to inflammatory risk.

The aim of this study was to examine the relationship between the sonographic hepatorenal index and stroke risk in patients with nonalcoholic fatty liver disease (NAFLD).

From December 2023 to July 2024, 72 NAFLD patients with stroke, 53 stroke-free NAFLD patients, and 54 healthy controls were enrolled in our study. The hepatorenal index was calculated as the ratio of the echo intensity of the liver to that of the renal cortex. The mean brightness values for one region of interest within the right hepatic lobe and the other size-matched region at the same depth of field within the right kidney were obtained with two-dimensional ultrasound and a 1- to 6-MHz convex array probe. Laboratory tests were performed with a Cobas 8000 automatic biochemical analyzer. Univariate and multivariate analyses were adopted to analyze the risk factors for stroke in NAFLD patients.

NAFLD patients had a greater hepatorenal index than healthy controls did (P < 0.05). Additionally, NAFLD patients with stroke had an even greater hepatorenal index than did those with stroke-free NAFLD (P < 0.001). Multivariate regression analysis further revealed that the hepatorenal index was independently associated with stroke risk in NAFLD patients (β = 8.897, P < 0.001) after controlling for age, body mass index, systolic blood pressure, and serum glucose, total cholesterol, alanine transaminase, and creatinine concentrations. Receiver operating characteristic curve analysis revealed a sensitivity of 62.5% and specificity of 95.3% for the hepatorenal index, with a cutoff value of 1.255 and an area under the curve of 0.80.

The increased sonographic hepatorenal index could be an independent predictor of stroke development in patients with NAFLD.

The combined use of quantitative real-time polymerase chain reaction (qPCR) and next-generation sequencing (NGS) to detect molecular measurable residual disease (mMRD) has been shown to have prognostic value for patients undergoing matched-hematopoietic stem cell transplantation (HSCT). However, there have been no related studies in the context of haploidentical HSCT (haplo-HSCT).

We included 148 acute myeloid leukemia (AML) patients who were in first complete remission (CR1) and underwent HSCT at Union Hospital (Wuhan, China) between 2019 and 2023. Among them, 28 patients were mMRD (+) before transplantation according to PCR/NGS. Then, on the basis of the 2017 European Leukemia Net (ELN) risk stratification, we randomly enrolled 56 mMRD (–) patients at a 1:2 ratio. Finally, we compared the outcomes, including overall survival (OS), cumulative incidence of relapse (CIR), leukemia-free survival (LFS), and nonrelapse mortality (NRM), between the two groups.

Persisting mMRD predicts worse long-term clinical outcomes in AML patients who received haplo-HSCT. The 2-year OS and LFS between the mMRD (+) and mMRD (–) groups were 77.1% (95%CI 62.5–95.2) versus 92.3% (95%CI 85.3–99.9) (P = 0.044) and 72.7% (95%CI 56.9–92.8) versus 90.7% (95%CI 83.2–98.8) (P = 0.003), respectively. The results of multivariate analysis revealed that mMRD (+) patients had worse OS and LFS than control patients did and that the mMRD (+) score was an independent prognostic factor for OS and LFS.

Pre-HSCT mMRD has predictive value for haplo-HSCT outcomes in AML patients. Patients who are mMRD (+) before transplantation have poorer OS and LFS. For these patients, intensified myeloablative conditioning (MAC), rapid reduction in immunosuppressive agents after 30 days, and pro-donor lymphocyte infusion (DLI) can improve post-transplant outcomes.

Non-small cell lung cancer (NSCLC) is a leading cause of cancer-associated mortality. This study aimed to investigate the role of checkpoint kinase 1 (CHEK1) in NSCLC progression and its regulatory relationship with forkhead box protein M1 (FOXM1).

Transwell assays were used to evaluate the migration and invasion capabilities of NSCLC cells with either CHEK1 overexpression or knockdown. The expression of epithelial−mesenchymal transition (EMT) markers in NSCLC cells under CHEK1 overexpression or knockdown conditions was analyzed via Western blotting. Proliferative capacity was assessed using CCK-8 assays in NSCLC cells with modulated CHEK1 expression. Additionally, real-time quantitative PCR was employed to measure CHEK1 and FOXM1 expression levels in NSCLC tissues. The effects of CHEK1 knockdown on tumor growth were further validated in animal models. The binding of FOXM1 to the CHEK1 promoter region was examined using dual-luciferase reporter assays and chromatin immunoprecipitation (ChIP) assays.

FOXM1 and CHEK1 were upregulated in NSCLC tissues. CHEK1 overexpression promoted NSCLC cell proliferation, while its knockdown suppressed proliferation, inhibited EMT, and reduced tumor growth in vivo. FOXM1 was shown to directly bind to CHEK1 promoter, thereby upregulating CHEK1 expression.

CHEK1 promotes NSCLC cell proliferation and tumor growth, and its expression is regulated by FOXM1. These findings suggest CHEK1 and FOXM1 are potential therapeutic targets for NSCLC treatment.

The geriatric nutritional risk index (GNRI) is widely used for nutritional assessment. Poor nutritional status is associated with complications and poor survival in cirrhotic patients. We aimed to investigate the value of the GNRI in predicting outcomes in cirrhotic patients.

This retrospective study included 420 cirrhotic patients from three centers between 2013 and 2017. Patients were divided into the high GNRI group (≥ 92) and low GNRI group (< 92). Overall survival (OS) in the two groups was evaluated via the Kaplan‒Meier method. Cox proportional hazards model was used to estimate the value of the GNRI in predicting outcomes. Restricted cubic spline model was used to intuitively display the dose‒response associations between the GNRI and OS. A nomogram was constructed to predict OS.

During the 2-year follow-up period, 58 (13.81%) patients died, and 262 (62.38%) patients experienced episodes of complications. Compared with patients in the low GNRI group, those in the high GNRI group had lower mortality rates (18.73% vs. 5.23%, P < 0.001). The GNRI was an independent predictor of OS (hazard ratio [HR] = 0.958, 95% confidence interval [CI] 0.929–0.988, P = 0.007). The GNRI was associated with the cumulative incidence of ascites (HR = 0. 954, 95% CI 0.940–0.969, P < 0.001), spontaneous bacterial peritonitis (HR = 0.928, 95% CI 0.891–0.966, P < 0.001), hepatic encephalopathy (HE; HR = 0.944, 95% CI 0.920–0.968, P < 0.001), and hepatorenal syndrome (HRS) (HR = 0.916, 95% CI 0.861–0.974, P = 0.005). Furthermore, 6 independent factors were included to construct the nomogram for OS prediction, including GNRI, age, total bilirubin, serum sodium, history of HE and HRS. The C statistics of our model were 0.83 (95% CI 0.75–0.90) and 0.80 (95% CI 0.73–0.86) at 1 and 2 years, respectively. Patients whose GNRI score decreased within 3 and 6 months had poorer outcomes (P < 0.001).

The lower GNRI score was associated with the higher cumulative incidence of complications and poorer OS of cirrhotic patients. The GNRI could be a helpful tool for assessing nutritional status and prognosis of these patients.

Glioma is a highly heterogeneous and malignant intracranial tumor that presents challenges for clinical treatment. ELMO domain containing 2 (ELMOD2) is a GTPase-activating protein that regulates a range of cellular biological processes. However, its specific role and prognostic value in tumorigenesis are still unknown. This study aimed to assess the prognostic relevance and signaling function of ELMOD2 in gliomas.

The Chinese Glioma Genome Atlas (CGGA) and The Cancer Genome Atlas (TCGA) databases were utilized to conduct a comprehensive analysis of the expression profile of ELMOD2 in gliomas, elucidating its associations with clinicopathological parameters and patient prognosis. Single-cell analysis was performed to characterize ELMOD2 expression across distinct glioma cell subpopulations. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, and Gene Set Variation Analysis (GSVA) were employed to evaluate the potential biological functions of ELMOD2 in gliomagenesis. Specific small interfering RNAs (siRNAs) were used to knock down ELMOD2 in the glioma cell lines U251 and A172 to assess their cellular behaviors and examine the levels of multiple key signaling molecules associated with the occurrence of gliomas.

ELMOD2 was overexpressed in gliomas, and this upregulation was correlated with tumor grade, isocitrate dehydrogenase mutation, and 1p/19q codeletion status. Notably, ELMOD2 expression was elevated in classical and mesenchymal subtypes, and single-cell resolution analysis revealed predominant enrichment within malignant cells. Functionally, ELMOD2 regulated cell cycle progression, and its overexpression was related to independent adverse outcomes. In vitro experiments revealed that ELMOD2 was located in the cytoplasm and nucleoplasm. Furthermore, ELMOD2 knockdown reduced proliferation, migration, and invasion and increased apoptosis in U251 and A172 cell lines. Finally, ELMOD2 knockdown significantly decreased p-Erk1/2.

ELMOD2 expression in glioma is positively correlated with tumorigenesis and is a crucial independent prognostic marker. Thus, ELMOD2 is a promising biomarker and therapeutic target for glioma treatment.

Electromagnetic navigation technology has demonstrated significant potential in enhancing the accuracy and safety of neurosurgical procedures. However, traditional electromagnetic navigation systems face challenges such as high equipment costs, complex operation, bulky size, and insufficient anti-interference performance. To address these limitations, our study developed and validated a novel portable electromagnetic neuronavigation system designed to improve the precision, accessibility, and clinical applicability of electromagnetic navigation technology in cranial surgery.

The software and hardware architecture of a portable neural magnetic navigation system was designed. The key technologies of the system were analysed, including electromagnetic positioning algorithms, miniaturized sensor design, optimization of electromagnetic positioning and navigation algorithms, anti-interference signal processing methods, and fast three-dimensional reconstruction algorithms. A prototype was developed, and its accuracy was tested. Finally, a preliminary clinical application evaluation was conducted.

This study successfully developed a comprehensive portable electromagnetic neuronavigation system capable of achieving preoperative planning, intraoperative real-time positioning and navigation, and postoperative evaluation of navigation outcomes. Through rigorous collaborative testing of the system’s software and hardware, the accuracy of electromagnetic neuronavigation has been validated to meet clinical requirements.

This study developed a portable neuroelectromagnetic navigation system and validated its effectiveness and safety through rigorous model testing and preliminary clinical applications. The system is characterized by its compact size, high precision, excellent portability, and user-friendly operation, making it highly valuable for promoting navigation technology and advancing the precision and minimally invasive nature of neurosurgical procedures.

Angiopoietin-2 (Ang-2) is a promising biomarker and therapeutic target for gastrointestinal angiodysplasia (GIAD). We hypothesized that the lncRNA-HIF1A-AS2/miR-153-3p/HIF-1α/Ang-2 axis plays a critical role in small bowel angiodysplasia (SBAD)-associated angiogenesis, which can be blocked by rifaximin. The purpose of this study was to investigate the expression and pro-angiogenic effects of the lncRNA-HIF1A-AS2/miR-153-3p/HIF-1α/Ang-2 in SBAD and to evaluate the therapeutic potential of rifaximin on SBAD by targeting this axis.

The expression and pro-angiogenic effects of lncRNA-HIF1A-AS2/miR-153-3p/HIF-1α/Ang-2 were analysed in SBAD tissues and human umbilical vein endothelial cells (HUVECs). The anti-angiogenic effect of rifaximin and its impact on the lncRNA-HIF1A-AS2/miR-153-3p/HIF-1α/Ang-2 axis were evaluated in HUVECs.

Increased expression of lncRNA-HIF1A-AS2 and decreased expression of miR-153-3p were detected in SBAD tissues. LncRNA-HIF1A-AS2/miR-153-3p /HIF-1α were upstream regulators of Ang-2, and this axis was involved in angiogenesis in HUVECs. Rifaximin exerted antiangiogenic effects on HUVECs by blocking this axis.

The lncRNA-HIF1A-AS2/miR-153-3p/HIF-1α/Ang-2 axis is critically involved in SBAD-associated angiogenesis. Rifaximin is a potential therapeutic option for SBAD via blockade of this axis.

Great obstetrical syndrome (GOS) represents a group of pregnancy-related diseases that result in inadequate placentation. Most GOS cases end in preterm, either spontaneously or indicatively, and the use of antenatal corticosteroids (ACS) is inevitably discussed. The placenta is an important, transient fetal-derived organ and is the embodiment of maternal or fetal well-being. However, few studies provide histological evidence of the placenta in GOS. This study aims to address these issues.

A total of 831 pregnant women were prospectively recruited. Placenta tissue was collected immediately and fixed with 4% paraformaldehyde solution for future H&E analysis. A novel checklist was devised to evaluate maternal vascular malperfusion sections on the basis of the commonly accepted Amsterdam placental workshop group consensus statement.

A total of 131 patients were classified as having GOS. Comparisons between those with and without GOS revealed significant differences, including higher levels of distal villous hypoplasia, increased syncytial knots, accelerated villous maturation, and higher total scores in GOS. We found significant negative associations between GOS and neonatal weight, neonatal height, head circumference, placental surface area, placental volume, and placenta gross examination score. GOS neonates were 1.25 times more likely to have hyperbilirubinemia. Regarding the effect of ACS, a significant reduction in birthweight, height, and head circumference was observed, along with an increased risk of hyperbilirubinemia.

This study provides histological evidence of the GOS that supports the defective deep placentation hypothesis. Our research also contributes to benefit-risk consultation in the GOS, such as in cases of PE and FGR, where a balance between fetal lung maturation and short-term neonatal outcomes is crucial.

Heat wave exposure significantly impacts human health. Nevertheless, studies on the long-term effects of heat wave exposure during adolescence on adverse pregnancy outcomes (APOs) are rare. This study aimed to investigate the relationship between the long-term effects of heat wave exposure during adolescence and APOs.

We analyzed data from 3,376 female and 3,013 male participants across 31 provinces in China. All adolescents (10–19 years old), early adolescents (10–14), and late adolescents (15–19) were chosen as exposure windows. Heat waves were defined as periods lasting 2‒4 consecutive days with the daily temperature exceeding the 75th, 90th, and 92.5th percentiles. We employed multivariate logistic regression models to assess the associations between exposure to heat waves during adolescence and APOs.

The results revealed significant associations between male exposure to heat wave events during late adolescence and spontaneous abortion (P < 0.05), which was more pronounced in South China. In contrast, no statistically significant associations were detected between males’ exposure to heat wave events during adolescence and their partners’ preterm birth (P > 0.05 for all comparisons). The exposure of females to heat waves during adolescence was not significantly associated with subsequent spontaneous abortion or preterm birth (P > 0.05 for all comparisons).

This study demonstrates that spontaneous abortion in females is associated with heat wave exposure in their male partner during adolescence.

Liver cancer is the sixth most prevalent cancer globally and the third leading cause of cancer-related mortality, with more than three-quarters of a million deaths. This has presented a significant challenge and imposed considerable strain on global public health systems. Therefore, evaluating the updated global burden of liver cancer and its recent trends in incidence and mortality is highly important, as it provides valuable insights for shaping public health policies and improving clinical practices.

The data in our article were obtained from the Global Burden of Disease Study 2021 (GBD 2021), which is available at https://vizhub.healthdata.org/gbd-results/. In this study, liver cancer mortality and incidence were estimated via the cause of death ensemble (CODEm) model for every combination of sex, age, location, and year. The incidence was modelled with DisMod-MR 2.1, a Bayesian meta-regression tool. A linear regression model was employed to explore the temporal trend of these rates, formulated as y = α + βx + ε, where x represents the calendar year and y signifies the natural logarithm of the rate. For both incidence and mortality, the estimated annual percentage change (EAPC) was computed via the formula 100 × (e^β − 1), accompanied by a 95% confidence interval (CI).

First, 529,000 cases were newly diagnosed, with an age-standardized incidence rate (ASIR) of 6.15 per 100,000 people. In terms of etiology, the incidence of liver cancer caused by metabolic factors has tended to increase. Additionally, the incidence of liver cancer was greater in males and older populations. Several specific regions presented liver cancer burdens that overwhelmingly surpassed the expected age-standardized rates (ASRs) each year from 1990 to 2021, regardless of their respective sociodemographic index (SDI) scores.

Our findings reveal that liver cancer continues to pose a significant public health challenge. These findings suggest that targeted interventions are needed to address both the infectious and non-infectious drivers of liver cancer in different socioeconomic settings. Hence, continued efforts in prevention through vaccination, antiviral therapies, and strategies to combat metabolic diseases are crucial for reducing the global burden of liver cancer in the coming decades.

To investigate the combined effects of thymidine phosphorylase (TYMP) and sine oculis homeobox homologue 1 (Six1) on the tumor microenvironment and their role in promoting metastasis in gastric cancer (GC).

A total of 674 GC patients who underwent surgical resection were enrolled. Correlations between TYMP/Six1 expression and the clinicopathological characteristics and overall survival of patients were analysed. The expression of TYMP, Six1 and vascular endothelial growth factor C (VEGFc) was quantified via immunohistochemistry and quantitative real-time polymerase chain reaction. Cell transfection, wound-healing assays and bioinformatics analyses were used to explore the potential underlying mechanisms involved.

Compared with the other groups, the Six1+ /TYMP+ patients exhibited poor differentiation, advanced tumor stage, a higher rate of lymphatic vessel invasion and shorter survival. Additionally, the protein expression of TYMP and Six1 was positively correlated with the VEGFc level. A significant increase in VEGFc expression was observed in cells transfected with TYMP, Six1, and TYMP/Six1 vectors. The results of the wound-healing assay indicated that the synergistic effect of TYMP and Six1 enhanced the migratory ability of GC cells. Furthermore, bioinformatics analysis revealed that TYMP and Six1 were positively correlated with immunosuppressive immune cell subsets and elevated the expression of inhibitory immune checkpoints in GC.

The combination of TYMP and Six1 is a good predictive and prognostic biomarker for GC. This combination enhances the expression of VEGFc, facilitates the invasion of GC cells, and may be linked to inhibitory immune cells and the tumor immune microenvironment.

Th17 cell-mediated immune injury is a crucial factor contributing to tubulointerstitial fibrosis in patients with IgA nephropathy (IgAN). However, the exact mechanisms by which Th17 cells induce tubulointerstitial fibrosis remain to be fully elucidated.

An IgAN mouse model was established and validated. Transcriptome sequencing, combined with bioinformatics analysis, was carried out to explore the immune injury pathways in renal tissues and the activation pathways in Th17 cells that were co-cultured with tubular epithelial cells. In subsequent experiments, small interfering RNA (siRNA) and overexpression plasmids were used to manipulate cellular targets. Validation was conducted through quantitative real-time polymerase chain reaction (qPCR), Western blotting, and immunofluorescence assays.

Compared with the control mice, IgAN mice exhibited elevated serum creatinine levels and increased urine protein-to-creatinine ratios. Renal pathological examination revealed the characteristic features of IgAN. Transcriptomic analysis of the kidney tissues from the model mice showed the activation of Th17 differentiation pathways, which was further confirmed by immunofluorescence analysis showing increased expression of interleukin-17A (IL-17A). These findings indicate an increased abundance of Th17 cells with potential pathogenic significance. When Th17 cells were co-cultured with tubular epithelial cells, the level of interleukin-9 (IL-9) in the system increased. This increase in IL-9 activated the Janus kinase 1-signal transducer and activator of transcription 3 (JAK1-STAT3) pathway through the IL-9 receptor (IL-9R) and upregulated the signature transcription factor retinoic acid-related orphan receptor gamma (ROR-γ), thus promoting Th17 cell differentiation. When IL-9R was silenced using siRNA or when the activity of STAT3 was inhibited, both the levels of phosphorylated STAT3 (p-STAT3) and ROR-γ decreased. Moreover, IL-17A secreted by Th17 cells promoted the nuclear translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in tubular epithelial cells by activating the IL-17 receptor A (IL-17RA)–adaptor protein Act1–tumor necrosis factor receptor-associated factor 6 (TRAF6) complex. This process regulated the production of inflammatory cytokines and drove the initiation and progression of fibrosis. Treatment with a STAT3 inhibitor in IgAN mice led to a reduction in the number of renal Th17 cells and alleviated the fibrotic phenotype.

This study demonstrated that the interaction between Th17 cells and tubular epithelial cells triggers excessive extracellular matrix deposition in the tubulointerstitium, thereby exacerbating the fibrotic phenotype and accelerating the progression of IgAN.

Atherosclerosis involves not only the narrowing of blood vessels and plaque accumulation but also changes in plaque composition and stability, all of which are critical for disease progression. Conventional imaging techniques such as magnetic resonance angiography (MRA) and digital subtraction angiography (DSA) primarily assess luminal narrowing and plaque size, but have limited capability in identifying plaque instability and inflammation within the vascular muscle wall. This study aimed to develop and evaluate a novel imaging approach using ligand-modified nanomagnetic contrast (lmNMC) nanoprobes in combination with molecular magnetic resonance imaging (mMRI) to visualize and quantify vascular inflammation and plaque characteristics in a rabbit model of atherosclerosis.

A rabbit model of atherosclerosis was established and underwent mMRI before and after administration of lmNMC nanoprobes. Radiomic features were extracted from segmented images using discrete wavelet transform (DWT) to assess spatial frequency changes and gray-level co-occurrence matrix (GLCM) analysis to evaluate textural properties. Further radiomic analysis was performed using neural network-based regression and clustering, including the application of self-organizing maps (SOMs) to validate the consistency of radiomic pattern between training and testing data.

Radiomic analysis revealed significant changes in spatial frequency between pre- and post-contrast images in both the horizontal and vertical directions. GLCM analysis showed an increase in contrast from 0.08463 to 0.1021 and a slight decrease in homogeneity from 0.9593 to 0.9540. Energy values declined from 0.2256 to 0.2019, while correlation increased marginally from 0.9659 to 0.9708. Neural network regression demonstrated strong convergence between target and output coordinates. Additionally, SOM clustering revealed consistent weight locations and neighbor distances across datasets, supporting the reliability of the radiomic validation.

The integration of lmNMC nanoprobes with mMRI enables detailed visualization of atherosclerotic plaques and surrounding vascular inflammation in a preclinical model. This method shows promise for enhancing the characterization of unstable plaques and may facilitate early detection of high-risk atherosclerotic lesions, potentially improving diagnostic and therapeutic strategies.

To investigate the clinical predictors of malperfusion in patients with acute type A aortic dissection (ATAAD) and to construct a diagnostic model to identify high-risk individuals.

A retrospective analysis of 553 ATAAD patients from Tongji Hospital divided into malperfusion and non-malperfusion groups was conducted. Logistic regression was used to identify independent predictors of the outcome. Model performance via the Hosmer–Lemeshow test, decision curve analysis (DCA), the area under the receiver operating characteristic curve (AUC), sensitivity, specificity, and predictive values.

Malperfusion was observed in 28.4% of ATAAD patients. Significant predictors included elevated lactate dehydrogenase (LDH) (OR: 1.0019, 95% CI: 1.0002–1.0036, P = 0.027), alanine aminotransferase (ALT) (OR: 0.9936, 95% CI: 0.987–1.000, P = 0.046) and estimated glomerular filtration rate (eGFR) (OR: 0.9877, 95% CI: 0.977–0.998, P = 0.021), suggesting roles for tissue ischemia and impaired renal or hepatic function. Other variables, such as D-dimer, uric acid, creatinine, and NT-proBNP, showed trends toward significance but did not reach the 0.05 threshold. The model demonstrated good calibration (Hosmer–Lemeshow P = 0.318), moderate discriminatory power (AUC = 0.725), high specificity (93.62%), and low sensitivity (26.75%).

The model based on routine biochemical markers provides a practical approach for the early identification of malperfusion in ATAAD patients. It shows strong specificity and clinical utility, although its limited sensitivity highlights the need for further refinement. Future improvements should focus on incorporating additional clinical or imaging data to increase diagnostic accuracy.

Histamine N-methyltransferase (HNMT) is involved primarily in histamine metabolism, but emerging evidence suggests its potential role in cancer progression. This study investigated the role of HNMT in nasopharyngeal carcinoma (NPC) and its impact on interferon (IFN) signaling, thioredoxin-interacting protein (TXNIP), and p53 tumor suppressor pathways.

HNMT expression in NPC tissues and cell lines was analyzed via qPCR and Western blotting. Functional assays, including cell proliferation, migration, invasion, and apoptosis, were performed after HNMT knockdown or overexpression. Transcriptomic sequencing was used to identify differentially expressed genes (DEGs). In addition, we examined the relationship between HNMT and the IFN/TXNIP/p53 axis via rescue experiments in vitro and in vivo models via qPCR and Western blotting.

HNMT knockdown reduced cell proliferation, migration, and invasion, and promoted apoptosis in NPC tissues and cell lines. TXNIP was the most significantly upregulated gene following HNMT knockdown. Inhibition of the IFN pathway reversed these effects, confirming the role of HNMT in downregulating the IFN/TXNIP/p53 pathway. An in vivo study revealed that HNMT overexpression correlated with reduced expression of TXNIP and p53 in NCG mice.

In NPC, HNMT promotes tumor growth and progression by inhibiting the IFN/TXNIP/p53 axis. These findings suggest that targeting the HNMT axis or restoring its function could provide new therapeutic strategies for NPC.