Acute myeloid leukemia (AML) is a common and aggressive blood cancer characterized by the abnormal growth of primitive bone marrow cells. Genetic mutations prevent normal differentiation into blood components. Potential causes include environmental factors, radiation, and viral infections. Research on AML is essential for enhancing our understanding of the disease, facilitating the development of effective treatments, and improving early diagnostic methods to ultimately increase patient survival rates and quality of life. This study focused on the T-cell immune response and T-cell immunotherapy in AML. We collected CD8+ T cells, CD4 + T cells, Natural killer T (NKT) cells, and γδ T cells among the T cells and analyzed the roles that they play in AML. Long-term disease control in AML requires a variety of immunotherapies, including T-cell receptor-engineered T cells (TCR-T), chimeric antigen receptor T-cell therapy (CAR-T), and T-cell immune checkpoint inhibitors. We discuss these treatments and try to find better treatments for AML in the future.

Obesity is a common noncommunicable disease characterized by persistent low-grade chronic inflammation and is associated with various metabolic disturbances, including insulin resistance and diabetes. The search for effective obesity treatments has led to growing interest in the role of amino acids in metabolic regulation. Tryptophan (TRP), an essential amino acid, participates in several biological pathways, including the kynurenine, 5-hydroxytryptamine (5-HT, also known as serotonin), and indole pathways. Recent evidence underscores the significance of TRP metabolism in obesity, showing that various metabolites and enzymes in its metabolic pathways are altered in individuals with obesity. These changes influence physiological processes, mood regulation, and overall metabolic health. This review provides a comprehensive overview of TRP metabolism. It highlights the potential of targeting TRP metabolism as a therapeutic strategy for managing obesity and its related metabolic and psychological comorbidities.

This study aimed to develop a few-shot learning model for lung nodule detection in CT images by leveraging visual open-set object detection.

The Lung Nodule Analysis 2016 (LUNA16) public dataset was used for validation. It was split into training and testing sets in an 8:2 ratio. Classical You Only Look Once (YOLO) models of three sizes (n, m, x) were trained on the training set. Transfer learning experiments were then conducted using the mainstream open-set object detection models derived from Detection Transformer (DETR) with Improved DeNoising AnchOr Boxes (DINO), i.e., Grounding DINO and Open-Vocabulary DINO (OV-DINO), as well as our proposed few-shot learning model, across a range of different shot sizes. Finally, all trained models were compared on the test set.

After training on LUNA16, the precision, recall, and mean average precision (mAP) of the different-sized YOLO models showed no significant differences, with peak values of 82.8%, 73.1%, and 77.4%, respectively. OV-DINO’s recall was significantly higher than YOLO’s, but it did not show clear advantages in precision or mAP. Using only one-fifth of the training samples and one-tenth of the training epochs, our proposed model outperformed both YOLO and OV-DINO, achieving improvements of 6.6%, 9.3%, and 6.9% in precision, recall, and mAP, respectively, with final values of 89.4%, 96.2%, and 87.7%.

The proposed few-shot learning model demonstrates stronger scene transfer capabilities, requiring fewer samples and training epochs, and can effectively improve the accuracy of lung nodule detection.

Accumulating evidence suggests that transmembrane 4 L6 family member 1 (TM4SF1) is associated with the development of various cancers; yet comprehensive studies on TM4SF1 in cervical cancer are lacking. Therefore, we aimed to evaluate the prognostic value of TM4SF1 in cervical cancer, elucidate its potential oncogenic functions in this disease, and further explore its feasibility as a therapeutic target.

The expression profiles and clinical information of cervical cancer patients were obtained from The Cancer Genome Atlas (TCGA) database. The expression levels of TM4SF1 were compared between cervical cancer and normal cervical tissues using the Wilcoxon rank-sum test. Kaplan–Meier analysis was employed to assess the prognostic value of TM4SF1. Furthermore, functional enrichment analyses were performed to explore the associated signaling pathways and biological functions. The methylation status of TM4SF1 was analyzed using the UALCAN and MethSurv databases. In addition, in vitro experiments were conducted to preliminarily validate the role and mechanisms of TM4SF1 in cervical cancer.

TM4SF1 was overexpressed in nearly all tumors, and its overexpression was associated with poor prognosis in cervical cancer. Moreover, the correlation between TM4SF1 expression and the expression of immune cell infiltration markers and immune checkpoint genes suggested that it had potential applications in cancer immunotherapy. Western blot analysis and immunohistochemistry revealed significantly elevated protein levels of TM4SF1 in cervical cancer tissues and cells. Further studies revealed that the knockdown of TM4SF1 significantly inhibited the migration, invasion, and epithelial-mesenchymal transition (EMT) of HeLa and SiHa cells, as well as promoted their apoptosis.

TM4SF1 may serve as a potential prognostic biomarker and therapeutic target for cervical cancer.

Iodinated contrast media (ICM) are widely used in medical imaging, particularly in computed tomography (CT) and magnetic resonance imaging (MRI) examinations, to increase image quality and improve diagnostic accuracy. Despite their clinical utility, ICM are associated with various adverse drug reactions (ADRs), including allergic reactions and other systemic effects. This study aimed to evaluate ICM-related ADRs through the Chinese spontaneous reporting system (SRS) and provide reference information for clinical practice.

We analyzed ADRs related to ICM on the basis of data from the SRS in Wuhan, China, from January 1, 2018, to December 31, 2023.

A total of 2,166 ADR reports related to four ICM (iodixanol, iohexol, ioversol, and iomeprol) were analyzed to assess the proportion and severity of adverse reactions. The results revealed that the majority of the ADRs were mild, with the most common symptoms being rash (54.76%) and itching (35.18%). Gastrointestinal and respiratory symptoms were also noted, although less frequently. Anaphylactic shock was documented in 48 patients, accounting for 9.69% of severe adverse reactions. The incidence of ADRs was greater in summer. Circulatory system diseases were the most prevalent underlying conditions in patients who experienced ADRs. Treatment primarily involved symptomatic management, including corticosteroids and antihistamines, with adrenaline administered in severe cases.

This study highlights the importance of monitoring high-risk patients, especially elderly patients and those with preexisting conditions, and underscores the need for timely intervention in severe reactions. Future prospective studies are necessary to facilitate the selection of more appropriate ICM for individual patients.

This study aimed to investigate the virulence characteristics of Klebsiella pneumoniae (KP) strains isolated from children to analyze the genetic relatedness between pediatric and local adult CRKP isolates and to identify clinical risk factors associated with high-risk strains.

KP strains and corresponding clinical data were collected at a tertiary provincial children's hospital in Henan province from January 2021 to May 2023. The molecular and clinical characteristics of pediatric carbapenem-resistant KP (CRKP) strains were analyzed. Genomic data from local adult isolates were integrated, and the virulence profiles of pediatric and adult isolates were compared. Clinical risk factors for isolating high-risk strains were initially screened via LASSO regression and then evaluated via multivariate binomial regression.

Among the 205 collected KP isolates, 87 (42.4%) were CRKP, and 118 (57.6%) were carbapenem-sensitive KP (CSKP). The predominant carbapenem resistance gene was bla_KPC-2 (89.7%), followed by bla_NDM-1 (5.7%) and bla_IMP-4 (4.6%). Ten sequence types (STs) were identified among the CRKP isolates, with ST11–KL47–KPC2 (52.9%) being the predominant genotype. Screening for virulence genes revealed that 55 (63.2%) CRKP isolates carried both the hypervirulence-associated genes iuc and rmpA2. Single-nucleotide polymorphism (SNP) analysis revealed that 34 of these strains had fewer than 10 SNPs. Phylogenetic and population genetic analyses revealed close genomic relatedness between pediatric and adult CRKP strains. Young age and exposure to invasive procedures were identified as independent risk factors for the isolation of iuc⁺rmpA2⁺ CRKP.

The ST11–KL47–KPC2 genotype was the predominant CRKP isolate in pediatric patients. The close genomic relatedness between pediatric and adult CRKP isolates suggests a common ancestor that has disseminated across populations. The high prevalence and clonal transmission of pediatric iuc⁺rmpA2⁺ CRKP strains warrant heightened clinical vigilance.

Patients with chronic kidney disease (CKD) without atherosclerotic cardiovascular disease (ASCVD) have high mortality rates. Guidelines indicate that statin therapy can reduce mortality in CKD patients with ASCVD; however, its benefits for CKD patients without ASCVD remain unclear. This study examined the survival benefits of statin therapy in CKD patients without ASCVD in American and Chinese cohorts.

A total of 4369 patients diagnosed with CKD without concurrent ASCVD were included from the American Medical Information Mart for Intensive Care (MIMIC)-IV database (n = 1786) and the Chinese Multicenter Registry Cohort for Cardiorenal Improvement II (CIN-II, n = 2583). Participants were grouped by statin use (treated and untreated). The two groups were compared for key indicators, including: (1) statin use rate; (2) 4-year all-cause mortality; (3) 4-year cardiovascular mortality (assessed in the CIN-II cohort). Statistical analyses included Kaplan–Meier survival curves (with log-rank test for group differences) and Cox proportional hazard models (adjusted for confounders) to estimate the association between statin use and mortality.

In the MIMIC-IV cohort, 37.6% of CKD patients received statins, with a 4-year all-cause mortality of 36.3%. After adjustment, statin therapy was associated with lower all-cause mortality (adjusted hazard ratio [aHR]: 0.61; 95% confidence interval [CI]: 0.51–0.72; P < 0.001). In the CIN-II cohort, 33.9% of patients received statins; the 4-year all-cause and cardiovascular mortalities were 10.5% and 5.3%, respectively. Adjusted analyses demonstrated that statin therapy reduced both all-cause mortality (aHR: 0.74; 95% CI: 0.56–0.99; P = 0.037) and cardiovascular mortality (aHR: 0.64; 95% CI: 0.42–0.97; P = 0.031).

Approximately two-thirds of CKD patients without ASCVD in both the American (MIMIC-IV) and Chinese (CIN-II) cohorts did not receive statins. However, statin therapy reduced 4-year all-cause mortality by 26% and 39% in the American and Chinese cohorts, respectively. These findings highlight a clear survival benefit of statin therapy and warrant future randomized controlled trials.

Cardiovascular-kidney-metabolic (CKM) syndrome involves complicated interactions among cardiovascular integrity, metabolic disorders, and chronic kidney disease, significantly impacting global morbidity and mortality. This study aimed to investigate the effect of an inflammatory diet on CKM syndrome progression.

This study included 10,387 adults aged 20 years and older with complete data on CKM syndrome diagnosis and dietary inflammatory index (DII) scores. The DII score was derived on the basis of a 2-day dietary recall interview, and CKM syndrome stages were categorized according to clinical criteria. Multinomial logistic regression, restricted cubic spline (RCS) model, and mediation analysis were used to assess the associations between food components, DII scores, and CKM syndrome stages.

A higher DII score was significantly associated with advanced CKM syndrome stages, with odds ratios increasing from 1.35 (1.10, 1.65) to 3.76 (2.76, 5.12) as the DII score rose from the 1st quartile to the 4th quartile (all P < 0.05). The RCS model presented a linear relationship between the DII score and the CKM stage. Mediation analysis revealed that biological age acceleration partially mediated the association between DII score and CKM syndrome, accounting for 21.43%–40.00% of the effect.

Inflammatory diets are associated with increased risk and progression of CKM syndrome. Biological age acceleration is a critical mediating factor, highlighting the importance of dietary interventions in managing CKM syndrome and its associated complications. Future research should focus on longitudinal studies to confirm these findings and explore additional mechanisms through which dietary patterns influence CKM syndrome.

Rho guanine nucleotide exchange factor 15 (ARHGEF15) is a member of the RhoGEF family that activates the Rho protein. High ARHGEF15 expression is associated with poor prognosis in patients with pancreatic cancer. Although ARHGEF15 is abundantly expressed in endothelial cells, its detailed functions remain unknown. This study aimed to elucidate the effects of ARHGEF15 on endothelial cells and the underlying molecular mechanisms involved.

The ARHGEF15 gene was overexpressed or knocked down in human umbilical vein endothelial cells (HUVECs), and the results were validated via qRT-PCR and Western blotting. CCK8 and MTT assays were used to evaluate cell proliferation. Wound healing and transwell assays were used to assess cell migration. The activation of STAT3 signaling was examined by Western blotting, and STATTIC was used to inhibit STAT3 signaling.

ARHGEF15 overexpression promoted the migration of HUVECs, and ARHGEF15 knockdown inhibited the migration of HUVECs. Neither the overexpression nor the knockdown of ARHGEF15 affected HUVEC proliferation.

Furthermore, ARHGEF15 increased STAT3 phosphorylation in HUVECs. STATTIC treatment prevents ARHGEF15 overexpression-induced STAT3 phosphorylation and HUVEC migration.

ARHGEF15 increases HUVEC migration by regulating STAT3 signaling.

Uric acid (UA) to high-density lipoprotein (HDL) ratio (UHR) has recently been proposed as a novel biomarker of inflammation. This study aimed to investigate the association between the UHR and carotid atherosclerosis (CAS) in patients with type 2 diabetes mellitus (T2DM).

In this single-center, retrospective cross-sectional study, 379 patients with T2DM were enrolled and categorized into two groups: 259 T2DM patients with CAS (T2DM-CAS) and 120 T2DM patients without CAS (T2DM-WCAS). Carotid intima‒media thickness (CIMT) and carotid atheromatous plaques (CAPs) were assessed via Doppler ultrasound. UHR values were compared between the groups, and receiver operating characteristic (ROC) curve analysis was employed to evaluate their diagnostic performance.

The UHR was significantly greater in the T2DM-CAS group than in the T2DM-WCAS group (P < 0.001). Multivariate logistic regression analysis identified the UHR as an independent risk factor for T2DM-CAS (P < 0.001). The area under the ROC curve (AUC) for UHR to detect CAS was 0.750, with an optimal cut-off value of 0.35.

The UHR is an independent risk factor for CAS in patients with T2DM and may serve as a valuable biomarker for predicting CAS in this population.

Brown and beige adipocytes dissipate energy through thermogenesis, and the impaired thermogenic function of these adipocytes is a key driver of obesity and related metabolic disorders. However, the molecular mechanisms governing adipocyte thermogenesis are not fully understood. This study investigated the role of inorganic pyrophosphatase 1 (PPA1) in regulating adipocyte thermogenesis and assessed its potential as a therapeutic target for obesity and metabolic disorders.

To investigate the function of PPA1 in adipose tissue thermogenesis, we generated adipose-specific heterozygous PPA1 knockout mice via the Cre-loxP system and established cold exposure models. PPA1 deletion effects were assessed by hematoxylin and eosin (H&E) staining, immunofluorescence, quantitative polymerase chain reaction (qPCR), and immunoblotting. Mitochondrial changes during browning were further characterized via transmission electron microscopy (TEM), mitochondrial DNA (mtDNA) quantification, qPCR, and Western blotting. The molecular mechanisms involved were subsequently dissected via mass spectrometry, coimmunoprecipitation (Co-IP), and immunofluorescence colocalization.

Adi-PPA1^fl/+ mice presented impaired adipose tissue thermogenesis upon cold exposure. Mechanistically, PPA1 deficiency impaired adipose browning in an enzyme activity-independent manner. PPA1 knockdown promoted the aberrant translocation and accumulation of fused in sarcoma (FUS) to mitochondria, which triggered mitochondrial dysfunction and suppressed browning. Crucially, silencing FUS effectively rescued the mitochondrial defects caused by PPA1 depletion.

PPA1 functions as a nonenzymatic positive regulator of adipocyte thermogenesis by interacting with FUS to prevent its mitochondrial mislocalization, thereby maintaining mitochondrial function and promoting adipose browning. These findings highlight PPA1 as a potential therapeutic avenue for obesity and metabolic disorders.

Previous studies have yielded contradictory conclusions on the relationship between intermittent exotropia (IXT) and the magnitude of myopia, especially in children. The aim of this study was to determine the clinical characteristics of IXT in children with myopia and myopic anisometropia.

We retrospectively evaluated the clinical data of patients (4–15 years of age) with convergence insufficiency (CI)-IXT and basic IXT who underwent surgery between 2022 and 2023. All patients underwent cycloplegia before the examinations and surgery. The degree of strabismus was measured when the patient viewed from the center of the glasses. Ocular dominance was routinely tested in children with IXT via the “hole-in-card test” after best-corrected visual acuity was obtained. Children were subsequently grouped into 2 groups (anisometropia and nonanisometropia) according to the difference in binocular spherical equivalent (SE) values (≥ 1.0 diopters [D]).

A total of 197 patients were included in the study. The preoperative deviation at near was significantly lower in the basic IXT group than in the CI-IXT group, whereas the distance exodeviation was significantly greater in the basic IXT group than in the CI-IXT group (P < 0.05). Patients with anisometropia were older than those without anisometropia (P < 0.001). The dominant eyes had significantly less myopia than the nondominant eyes did in the CI-IXT and anisometropia groups (P = 0.049 and P = 0.003, respectively). High myopia was more prevalent in middle school students with IXT (16.67%) than in preschool students (4.55%) and primary schoolchildren (3.18%). The percentage of individuals with anisometropia (≥ 3.0 D) varied in the low (1.68%), moderate (8.7%), and high myopia groups (22.22%). Binomial logistic regression analysis revealed that age and SE of the dominant eye were independent factors related to anisometropia in children with IXT (P < 0.001 and P < 0.001, respectively).

Patients with IXT, especially those with anisometropia and CI-IXT, were shown to have less myopia in the dominant eye. Age and SE of the dominant eye were found to be independent factors related to anisometropia in children with IXT.

Long non-coding RNAs (lncRNAs) are critical in the pathogenesis of hematological malignancies, including acute myeloid leukemia (AML). However, the specific role and underlying mechanisms of the lncRNA chromosome 9 open reading frame 139 (C9orf139) in AML remain unclear. This study aimed to investigate the role and molecular mechanism of C9orf139 in AML development.

AML-related sequencing and microarray data were retrieved from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Significant lncRNAs and mRNAs influencing AML progression were identified and analyzed. A competing endogenous RNA network involving lncRNA–microRNA (miRNA)3–mRNA interactions was subsequently constructed. The expression levels of C9orf139, miR-24-3p, and human TAO kinase 1 (TAOK1) were assessed via real-time fluorescent quantitative polymerase chain reaction (PCR). Cell proliferation was evaluated via the Cell Counting Kit-8 (CCK8) assay, whereas Transwell assays were used to assess cell invasion and migration. Apoptosis was measured by Annexin V Fluorescein Isothiocyanate (FITC) double staining. Tumor formation in nude mice was assessed to examine the effect of C9orf139 on in vivo tumor growth. The C9orf139-miR-24-3p-TAOK1 regulatory axis was validated via dual luciferase reporter assays and RNA-binding protein immunoprecipitation (RIP). Western blot assays were used to assess the expression and phosphorylation of key proteins in the mitogen-activated protein kinase (MAPK) signaling pathway.

Bioinformatics analysis identified C9orf139 and TAOK1 as differentially expressed genes that play key roles in AML pathogenesis. The C9orf139-miR-24-3p-TAOK1 axis was tightly linked to AML development, as confirmed by clinical sample analysis. In vitro, C9orf139 downregulation resulted in reduced proliferation, invasion, and migration and enhanced the apoptosis of AML cells. In vivo, the inhibition of C9orf139 significantly impaired tumor growth in nude mice. The regulatory axis was further validated. C9orf139 knockdown reduced the phosphorylation levels of the key MAPK pathway proteins, including Raf, mitogen-activated protein kinase kinase (MEK), and extracellular regulated protein kinase (ERK).

C9orf139 regulates AML progression by activating the MAPK signaling pathway through the C9orf139-miR-24-3p-TAOK1 axis.

This study aimed to systematically evaluate the application of the Cavitron Ultrasonic Surgical Aspirator (CUSA) system in epilepsy surgery and summarize associated surgical experiences.

In this retrospective analysis, 70 patients with refractory epilepsy underwent CUSA-assisted resection, while 20 controls underwent conventional surgical resection. Patients were categorized according to surgical scenarios for CUSA application, including lesion-related epilepsy resections, mesial temporal lobe procedures, neocortical resections within eloquent areas, and cases requiring preservation of critical vascular structures. Detailed operative metrics were analyzed for each category. Comparative assessments between the CUSA and conventional groups included surgical efficiency, complication rates, and postoperative seizure outcomes on the basis of the modified Engel classification.

CUSA was used for the following procedures: resection of epileptic lesions (n = 26), mesial temporal structures (n = 32), the epileptogenic neocortex (n = 28), and the rolandic cortex (n = 17). Additionally, it was utilized in 6 cases requiring vascular protection during insular resection and in 18 cases involving preservation of cortical dangerous veins. Although the overall surgical efficiency was comparable between the CUSA and conventional groups (68.0 ± 18.2 vs. 61.1 ± 14.7 min, P = 0.180), the CUSA group demonstrated superior efficiency in resecting low-grade tumors (58.6 ± 14.9 vs. 68.1 ± 11.2 min, P = 0.034). Furthermore, the CUSA group presented significantly fewer permanent complications (5.7% vs. 10%, P < 0.0001) and a higher rate of Engel Class I outcomes (82.9% vs. 70.0%, P = 0.278).

The CUSA system represents a suitable and promising surgical tool for resective epilepsy surgery, potentially serving as a valuable option for epilepsy surgeons. Further studies are warranted to validate these findings.

To compare the impact of different reconstruction algorithms on the image quality of 60 kVp head and neck CT angiography (CTA) using subjective and objective metrics, with a focus on vessel edge sharpness.

This prospective study enrolled 45 patients who underwent ultra-low-voltage (60 kVp) head and neck CTA. Image datasets were reconstructed with filtered back-projection (FBP), ClearView (CV) and ClearInfinity (CI) algorithms at low (30%), medium (50%), and high (70%) strengths. Image quality was assessed subjectively and objectively via the Kruskal‒Wallis test for multiple comparisons. Objective parameters, including edge rise slope (ERS) and edge rise distance (ERD), were analyzed via the Friedman test of multiple comparisons statistics.

Subjective assessments favored the CI50 reconstruction algorithm, demonstrating superior or satisfactory results compared to the other algorithms, with significantly better vessel delineation, edge definition and diagnostic confidence (all P < 0.05). Objective analysis revealed that the CV50 and CV70 algorithms significantly reduced ERS and/or elevated ERD (both P < 0.05). However, the CI50 algorithm maintained comparable vessel edge sharpness (P > 0.05) across all evaluated head and neck vascular segments when compared with the FBP algorithm.

The CI50 reconstruction algorithm optimizes image quality in 60 kVp head and neck CTA. It provides vessel edge sharpness comparable to FBP while offering superior vessel delineation, edge definition, and diagnostic confidence compared to FBP and CV algorithm. These findings suggest that CI50 has the potential to improve diagnostic accuracy in low-dose vascular imaging.

Sepsis, a life-threatening condition caused by a dysregulated host response to infection, continues to be a major cause of mortality in critical care despite medical advancements. This study aimed to investigate the therapeutic effects and neuroimmune mechanisms of electroacupuncture (EA) at the Shenshu (BL23) acupoint combined with antibiotic therapy in sepsis management.

A cecal ligation and puncture (CLP)-induced murine sepsis model was used to evaluate the combined therapy. The study employed enzyme-linked immunosorbent assays (ELISA) and histological analysis to assess systemic inflammation and intestinal damage. Three-dimensional immunolabeling of c-Fos neurons and chemogenetic modulation of hypothalamic paraventricular nucleus (PVN) neurons were performed to investigate neural mechanisms. Additionally, serum catecholamine levels were measured using ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS).

The combination of EA and antibiotics significantly improved survival rates and reduced sepsis-induced weight loss. The therapy lowered systemic levels of proinflammatory cytokines (TNF-α and IL-6) and mitigated intestinal inflammatory infiltration. EA at BL23 suppressed neuronal activation in the PVN by reducing c-Fos expression. Chemogenetic inhibition of corticotropin-releasing hormone (CRH) neurons replicated the anti-inflammatory effects of the therapy, while their activation diminished therapeutic benefits. Conversely, activation of oxytocin (OXT) neurons reproduced the anti-inflammatory effects, and their inhibition reversed these benefits. The combined therapy also elevated serum catecholamine levels, indicating sympathetic-mediated immunomodulation.

This study demonstrates that EA at BL23 enhances antibiotic efficacy in sepsis by modulating PVN activity—suppressing CRH neurons and activating OXT neurons—leading to increased catecholamine secretion and systemic inflammation control. These findings reveal a novel neuroimmunological pathway for acupuncture’s therapeutic role in sepsis, supporting its potential as a noninvasive adjunctive therapy in critical care.