EUROPEAN JOURNAL OF MEDICAL RESEARCH欧洲医学研究杂志
EUROPEAN JOURNAL OF MEDICAL RESEARCH(英文缩写 EUR J MED RES),ISSN 0949-2321,eISSN 2047-783X,中文译名:欧洲医学研究杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 4.981 | Q2 |
| 2022 | 4.200 | Q2 |
| 2023 | 2.800 | Q2 |
| 2024 | 3.400 | Q2 |
| 2025 | 4.800 | Q2 |
EUROPEAN JOURNAL OF MEDICAL RESEARCH 最新收录文献
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1. MCT1 inhibition reprograms Treg metabolism via ABC transporters: implications for tumor immunity and the prognosis of acute myeloid leukemia patients.
1. MCT1抑制通过ABC转运蛋白重新编程Treg代谢：对肿瘤免疫和急性髓系白血病患者预后的影响PMID:日期:2026-03-09Glycolysis plays a critical role in regulatory T cells (Tregs), which are frequently exploited by tumor cells, as Treg survival depends on glycolytic activity to suppress antitumor immunity. However, the precise effects of glycolysis on Treg proliferation and differentiation remain incompletely understood. Monocarboxylate transporters (MCTs) are pivotal regulators of glycolytic flux. In this study, we investigated how MCT1 inhibition modulates Treg metabolism and function, and the potential implications for tumor immunotherapy. Silencing MCT1 in human primary Tregs using siRNA disrupted glycolysis, leading to G0/G1 cell cycle arrest, increased apoptosis, and ATP depletion. Integrated metabolomic and transcriptomic analyses identified the ABC transporter pathway as the most significantly altered, with coordinated changes in key genes (ABCA1, ABCB10, ABCC9, etc.) and the metabolite adenosine. Validation using The Cancer Genome Atlas (TCGA) acute myeloid leukemia cohort demonstrated that high expression of the ABC transporter gene ABCC9 is associated with improved overall survival (hazard ratio = 0.45, p < 0.001). These findings indicate that MCT1 inhibition is associated with alterations in the ABC transporter pathway, which may correlate with changes in Treg metabolism and the tumor immune microenvironment. Collectively, this work highlights metabolic reprogramming of Tregs as a novel therapeutic target for cancer immunotherapy.
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2. Delayed bedtime on workdays is associated with an increased prevalence of gallstones: a population-based study.
PMID:日期:2026-03-09The relationship between sleep and gallstones (GS) has rarely been reported. We aimed to investigate whether sleep traits are associated with the prevalence of GS. A cross-sectional study was conducted using data from the National Health and Nutrition Examination Survey 2017-2020. Participants aged ≥ 20 years with complete information on sleep and GS questionnaires were enrolled. Binary logistic regression analyses were performed to investigate the relationship between sleep traits and GS while adjusting for confounding factors. Stratified and interaction analyses were conducted to evaluate whether factors such as age, gender, race, education, marital status, body mass index, smoking, and comorbidities modified the association. A total of 7329 participants were included in this study, and 736 had a self-reported history of GS. In the fully adjusted model, we found that each hour of delay in workday bedtime was associated with an 8.60% increase in the odds of GS (OR = 1.09; 95% CI: 1.02-1.15, P = 0.026). Compared to individuals with a workday bedtime between 18:00-≦20:00, those sleeping later, between 22:00-≦24:00 faced higher odds of GS (OR = 5.82; 95% CI: 1.63-20.83, P = 0.035), while the odds were even greater for those sleeping between 24:00-≦06:00 (OR = 6.68; 95% CI: 1.76-25.36, P = 0.032). Subgroup analyses revealed that age acted as an effect modifier in the relationship between workday bedtime and GS. In participants aged > 40 years, the odds of GS increased significantly with delayed workday bedtime (OR = 1.14; 95% CI: 1.07-1.22, P = 0.009). Furthermore, the fully adjusted model found no significant association between wake-up time, sleep duration, or sleep disorders and the prevalence of GS. Delayed workday bedtime is associated with a higher prevalence of GS. Age modifies the association between workday bedtime and the prevalence of GS. Notably, for individuals aged > 40 years, the odds of GS increased significantly with delayed bedtime on workdays.
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3. Salvianolic acid B attenuates post-cardiac arrest cerebral ischemia-reperfusion injury via activation of the Nrf2 signaling pathway.
PMID:日期:2026-03-09Cerebral ischemia-reperfusion (CI/R) injury following cardiac arrest (CA) leads to profound neurological dysfunction driven by oxidative stress, inflammation, and apoptosis. Salvianolic acid B (SalB), a polyphenolic compound with reported neuroprotective activity, has not been fully evaluated in CA-related CI/R injury. A rat CA-induced cerebral ischemia-reperfusion (CA-CI/R) model was established. SalB (20 mg/kg) was administered after resuscitation. Neurological deficits were assessed at 6, 24, and 48 h using the neurological deficit score. Neuronal morphology and survival were examined by hematoxylin-eosin (HE) and Nissl staining. Oxidative stress indices included superoxide dismutase (SOD) activity and malondialdehyde (MDA) content. Inflammatory cytokines measured were interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Neuronal apoptosis was evaluated by TUNEL staining. PC12 cells were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to assess cell viability, reactive oxygen species (ROS) production, lipid peroxidation, apoptosis, and nuclear factor erythroid 2-related factor 2 (Nrf2) pathway activation. SalB significantly improved neurological outcomes and preserved cortical neuronal integrity in CA-CI/R rats. SalB enhanced SOD activity, reduced MDA accumulation, decreased IL-1β and TNF-α levels, and attenuated neuronal apoptosis. In OGD/R-treated PC12 cells, SalB increased viability, reduced ROS and lipid peroxidation, and inhibited apoptosis. Mechanistically, SalB facilitated Nrf2 release from Kelch-like ECH-associated protein 1 (Keap1) and its nuclear translocation, leading to upregulation of heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1). Immunofluorescence confirmed Nrf2 nuclear localization, and the Nrf2 inhibitor ML385 reversed these effects. SalB protects against CI/R-induced neurological injury by reducing oxidative stress, inflammation, and apoptosis through Nrf2 activation, supporting its potential as a therapeutic agent for post-CA cerebral injury.
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4. Clinical value of sputum galactomannan testing in the diagnosis of invasive pulmonary aspergillosis among chronic obstructive pulmonary disease patients.
PMID:日期:2026-03-09Diagnosing invasive pulmonary aspergillosis (IPA) in patients with chronic obstructive pulmonary disease (COPD) remains challenging due to the non-specific nature of imaging findings, the limited sensitivity of current diagnostic methods, and the difficulty of obtaining appropriate clinical specimens. To evaluate the diagnostic accuracy of sputum galactomannan (GM) testing in COPD patients with IPA. In this multicenter cross-sectional study, COPD patients with suspected IPA and patients with community-acquired pneumonia (CAP) were enrolled. GM testing was performed on sputum, serum, and bronchoalveolar lavage fluid (BALF) samples, while fungal culture was conducted on sputum samples. Diagnostic performance was assessed using the EORTC/MSGERC criteria as the reference standard. A total of 134 patients were included, comprising the COPD + IPA group (n = 43), the COPD + CAP group (n = 70), and the CAP group (n = 21). The areas under the receiver operating characteristic curve (AUCs) for GM detection in sputum, BALF, and serum were 0.833 (95% CI: 0.753-0.913), 0.884 (95% CI: 0.799-0.970), and 0.659 (95% CI: 0.552-0.766), respectively. The optimal cut-off values for sputum and BALF GM were 1.64 and 1.12, respectively. At these thresholds, sputum GM demonstrated a sensitivity of 79.1% and specificity of 75.7%, while BALF GM showed a sensitivity of 76.5% and specificity of 96.6%. Sputum GM testing demonstrates significant diagnostic value for IPA in COPD patients and provides a non-invasive alternative with reliable performance, making it a promising tool for preliminary screening and reducing the need for invasive procedures in clinical practice. ChiCTR2400089800.
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5. Integrative analysis reveals luteolin's molecular targets and mechanisms in pancreatic cancer treatment.
PMID:日期:2026-03-09Pancreatic cancer remains one of the most lethal malignancies with limited therapeutic options. Luteolin, a natural flavonoid compound, has demonstrated potential anti-cancer properties, but its specific mechanisms of action in pancreatic cancer are not fully understood. To identify potential molecular targets of luteolin in pancreatic cancer and elucidate the underlying therapeutic mechanisms through comprehensive bioinformatics and experimental approaches. We employed multiple databases including SwissTargetPrediction, GeneCards, and OMIM to predict luteolin targets and pancreatic cancer-related genes. Differential gene expression analysis was performed using the GSE32676 dataset. KEGG and GO enrichment analyses were conducted to identify key pathways. Molecular docking and dynamics simulations validated protein-ligand interactions. TCGA data analysis examined MET expression patterns and prognostic significance. In vitro and in vivo experiments confirmed luteolin's therapeutic effects. We identified 7 overlapping genes between luteolin targets and pancreatic cancer-related genes, with MET emerging as the primary target through network analysis. Molecular docking revealed stable binding between luteolin and MET (- 8.0 kcal/mol). Molecular dynamics simulations confirmed the structural stability of the MET-luteolin complex. TCGA analysis showed MET overexpression in pancreatic cancer correlating with poor prognosis. Experimental validation demonstrated that luteolin inhibited pancreatic cancer cell proliferation and tumor growth through MET/PI3K/AKT pathway modulation. This study identifies MET as a critical therapeutic target of luteolin in pancreatic cancer, providing mechanistic insights into luteolin's anti-cancer effects via the MET/PI3K/AKT signaling pathway and supporting its potential clinical application.
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6. Non-linear association between cardiometabolic index and helicobacter pylori infection: a cross-sectional study.
PMID:日期:2026-03-09Helicobacter pylori (H. pylori) infection poses a significant global public health challenge. While prior studies have examined metabolic abnormalities in relation to H. pylori infection, the association between the cardiometabolic index (CMI) and H. pylori infection remains understudied. The present cross-sectional study utilized information from the National Health and Nutrition Examination Survey (NHANES) 1999-2000, encompassing 3357 participants with complete H. pylori serology, CMI, and relevant covariate data. Multivariable regression models, smoothing curve fitting, and threshold effect analysis were implemented to examine the link between CMI and H. pylori infection, alongside subgroup analyses to confirm consistency across various populations. Increased CMI levels were associated with a higher likelihood of H. pylori infection. Each standard deviation increase in CMI was associated with a 21% higher odds of H. pylori infection (OR = 1.21, 95% CI 1.06-1.39, P = 0.005). A significant non-linear relationship was identified, with an inflection point at a CMI of approximately 2.8. Below this threshold, elevations in CMI were associated with a significant increase in infection risk (OR = 1.41, 95% CI 1.18-1.69, P = 0.0002). In contrast, increases beyond this point showed no statistically significant relationship (OR = 0.74, 95% CI 0.49-1.12, P = 0.1604). Tests for interaction indicated no significant differences across subgroups (P-interaction > 0.05). This cross-sectional study demonstrates a substantial non-linear association between the CMI and the risk of H. pylori infection. Future research should seek to confirm this association in contemporary, longitudinal cohorts to further validate these findings.
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7. ARPC1B promotes gastric cancer tumorigenesis via IGF2BP3-mediated stabilization of HK2 mRNA and glycolytic reprogramming.
PMID:日期:2026-03-09Cancer cells improve survival through metabolic reprogramming, predominantly shifting to glycolysis. Actin-related protein 2/3 complex subunit 1B (ARPC1B) is abnormally overexpressed in multiple malignancies and significantly associated with the poor prognosis of patients. However, the role of ARPC1B in gastric cancer (GC) remains poorly characterized. ARPC1B expression in GC and its association with clinicopathological features were assessed using bioinformatics (TCGA, GEPIA), western blotting, and immunohistochemical staining. The functional impact of ARPC1B on glycolysis (ECAR, OCR, glucose uptake, lactate/ATP production) and tumorigenesis (proliferation, migration, invasion, in vivo xenografts) was evaluated following ARPC1B knockdown or overexpression. ARPC1B-IGF2BP3 interaction was validated by co-immunoprecipitation and confocal microscopy. IGF2BP3-dependent stabilization of hexokinase 2 (HK2) mRNA was examined via RNA immunoprecipitation and actinomycin D assays. ARPC1B was significantly upregulated in GC tissues and cell lines, with elevated expression correlating positively with advanced tumor stage and pathological grade. ARPC1B depletion suppressed glycolytic activity (reduced ECAR, increased OCR, glucose consumption, lactate/ATP production), inhibited proliferation, migration, and invasion in vitro, and attenuated tumor growth and metastasis in vivo. Mechanistically, ARPC1B bound to IGF2BP3, impeding its degradation and ubiquitination, thereby enhancing HK2 mRNA stability. Consequently, ARPC1B increased HK2 protein expression, while HK2 overexpression rescued the anti-glycolytic and anti-tumorigenic effects of ARPC1B knockdown. ARPC1B drives GC progression by stabilizing HK2 mRNA through IGF2BP3 binding, thereby potentiating glycolytic reprogramming to facilitate tumor growth and metastasis. Targeting the ARPC1B-IGF2BP3-HK2 axis may represent a novel therapeutic strategy for GC.
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8. Prognostic and predictive value of a novel immuno-proliferative biomarker signature for targeted therapy efficacy in non-small cell lung cancer.
PMID:日期:2026-03-09Non-small cell lung cancer (NSCLC) is a prevalent and lethal malignancy. Although targeted therapies have improved clinical outcomes for patients with driver gene mutations, significant variability in treatment efficacy and the frequent development of acquired resistance remain significant challenges. There is an urgent need to identify reliable predictive biomarkers. This study aimed to evaluate the association between key molecular indicators-interferon-γ (IFN-γ), Ki-67, driver gene mutation abundance (MA), and lung cancer-specific combined tumor markers (LCTM)-and response to targeted therapy in advanced NSCLC, to develop a predictive model for personalized treatment. In this retrospective study, 132 patients with advanced or locally advanced NSCLC harboring driver gene mutations (confirmed by NGS) and receiving targeted therapy were enrolled. Demographic and clinical data were collected, including serum levels of five tumor markers (CEA, NSE, SCCA, CYFRA21-1, Pro-GRP), Ki-67 expression, IFN-γ levels, and MA. Radiographic responses were assessed at 1, 3, and 6 months according to RECIST criteria. Statistical analyses included chi-square tests, Kaplan-Meier survival analysis, and multivariate Cox regression to evaluate associations between biomarkers and treatment response. The overall response rate was 52.5%. Response rates were significantly higher in patients with ≤ 2 LCTM components (76.8% vs. > 2, p < 0.001) and low Ki-67 expression (< 5%, 72.4% vs. high, p = 0.013). Multivariate analysis confirmed LCTM (HR = 1.849, p = 0.026) and Ki-67 (HR = 1.768, p = 0.016) as independent predictors. Higher IFN-γ and lower MA were associated with favorable trends in responders. High IFN-γ expression, low Ki-67 and MA levels, and ≤ 2 elevated LCTM components constitute a favorable biomarker profile for predicting response to targeted therapy in advanced NSCLC. These biomarkers could aid in predicting early response and therapeutic stratification. The proposed "driver-clone-dependent clone" co-regulation mechanism underscores the clinical value of multi-biomarker evaluation. Further multi-center prospective studies are warranted for validation.
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9. Clinical spectrum, predictive biomarkers, and prognostic implications of peripheral neuropathies in primary Sjögren's syndrome: a retrospective cohort study.
PMID:日期:2026-03-09Primary Sjögren's syndrome-associated peripheral neuropathy (pSS-PN) represents a clinically heterogeneous complication linked to significant morbidity. This study aims to characterize its prevalence, clinical phenotypes, predictive factors, and prognosis. In this retrospective cohort study conducted at Shanghai Tongji Hospital, 553 consecutive pSS patients (2002 American-European Consensus Group criteria) were evaluated. After applying the exclusion criteria, 320 eligible patients completed the full assessment protocol and constituted the final analytical cohort. Based on the diagnostic criteria for peripheral neuropathy (PN), 59 patients were diagnosed with pSS-PN, while the remaining 261 were classified as pSS without PN (pSS-nPN). The prevalence of pSS-PN was 18.4% (59/320) in the final cohort. The predominant subtype was distal axonal sensory polyneuropathy (33.9%). Independent predictors included fatigue (OR 2.27, 95% CI 1.27-4.06; p = 0.005), Schirmer's test ≤ 2 mm/5 min (OR 2.78, 95% CI 1.62-4.76; p < 0.001), elevated creatine kinase (OR 3.78, 95% CI 1.92-7.45; p < 0.001), ischemic electrocardiogram (ECG) changes (OR 2.17, 95% CI 1.29-3.64; p = 0.003), and pulmonary involvement (OR 6.46, 95% CI 3.70-11.39; p < 0.001). Early identification and subtyping of pSS-PN are crucial for accurate disease assessment and guiding treatment.
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10. Development of a novel rabbit auricle xenograft model of human PC3 prostate cancer.
10. 一种新型人前列腺癌（PC3）兔耳廓异种移植模型的建立PMID:日期:2026-03-09Therapeutic management of prostate cancer remains challenging. Prostatic artery chemoembolization (PACE), an advanced minimally invasive technique derived from prostatic artery embolization (PAE), has shown promising potential in controling tumor growth and alleviating symptoms such as hematuria and lower urinary tract obstruction in prostate cancer, and has garnered widespread attention in recent research. However, preclinical progress is hindered by the limitations of existing animal models, and the development of a simple and reliable animal model to better understand the endovascular interventional treatment of prostate cancer is necessary. To develop and characterize a novel xenograft model of human prostate cancer in the rabbit auricle as a practical platform for experimental research on endovascular embolization techniques. Fresh human PC3 cell suspension (0.1 ml containing ~ 9 × 10 cells) was injected subcutaneously into each auricle of 15 immunosuppressed New Zealand white rabbits. Tumor growth was measured periodically, and volume doubling time (VDT) was calculated. Digital subtraction angiography was performed via the central auricular artery when tumors were greater than 150 mm. Subsequently, histopathological and immunohistochemical analyses were conducted. Repeated-measures ANOVA was used to assess the significance of differences in the VDT of auricle tumors within-rabbits and between rabbits. The model achieved a high tumor take-rate of 86% (26/30 auricles). Angiography revealed distinct tumor-feeding vessels and uniform ring-like staining. Histopathology confirmed invasive growth of poorly differentiated, atypical tumor cells with high mitotic activity and no obvious necrosis. Immunohistochemistry showed high Ki67 expression (82.43 ± 3.68)%, indicating active proliferation. During the exponential growth stage, the mean VDT was 6.4 ± 1.8 days. Repeated-measures ANOVA revealed significant variations in VDT among the rabbit subjects (P < 0.05); moreover, the VDT did not significantly differ between the left and right ears of each rabbit (P > 0.05), thereby reinforcing the consistency of the model employed. The rabbit auricle PC3 xenograft model is a valuable preclinical platform. It effectively simulates human prostate cancer with high reproducibility and clear vasculature, providing a foundational tool for subsequent investigations into the efficacy of endovascular therapies, such as PAE and PACE.