European Journal of Medical Research最新文献

{"title":"Integrative analysis reveals luteolin's molecular targets and mechanisms in pancreatic cancer treatment.","authors":"Danhong Pan, Shixia Li, Peixi Zhong, Lili Chen, Binbo Fang, Yifu Feng","doi":"10.1186/s40001-026-04056-x","DOIUrl":"https://doi.org/10.1186/s40001-026-04056-x","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic 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.</p><p><strong>Objective: </strong>To identify potential molecular targets of luteolin in pancreatic cancer and elucidate the underlying therapeutic mechanisms through comprehensive bioinformatics and experimental approaches.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Baicalein attenuates sepsis-associated encephalopathy by inhibiting ASK1-JNK and NF-κB pathways.","authors":"Mingming Tan, Boyi Nan, Xiongbin Zhang, Yingwei Ou, Hengjie Li, Rongcheng An, Hao Lu, Yong Nan","doi":"10.1186/s40001-026-04169-3","DOIUrl":"https://doi.org/10.1186/s40001-026-04169-3","url":null,"abstract":"<p><strong>Background: </strong>Sepsis-associated encephalopathy (SAE) is a common and severe complication of sepsis characterized by neuroinflammation and neurological dysfunction, with limited effective therapies. Baicalein, a major flavonoid derived from Scutellaria baicalensis, exhibits anti-inflammatory and neuroprotective properties, but its role in SAE remains unclear.</p><p><strong>Methods: </strong>Network pharmacology was applied to identify potential targets and signaling pathways of Scutellaria baicalensis in SAE, followed by protein-protein interaction analysis and GO and KEGG enrichment. An LPS-induced SAE mouse model was used to validate the neuroprotective effects of baicalein through assessment of inflammatory cytokines, signaling pathway activation, neurological function, and survival.</p><p><strong>Results: </strong>Network analysis identified 71 core targets of Scutellaria baicalensis, including 6 core target genes: TNF, IL6, AKT1, JUN, PTGS2, and TP53. Given that JUN and pro-inflammatory cytokines are canonical downstream effectors of stress-activated kinases and NF-κB signaling, subsequent experimental validation focused on the ASK1-JNK and NF-κB pathways, which play central roles in oxidative stress and neuroinflammation associated with sepsis-associated encephalopathy. In vivo, baicalein significantly reduced hippocampal TNF-α and IL-6 levels, compared with the LPS group. Baicalein suppressed activation of the ASK1-JNK and NF-κB pathways, improved cognitive performance, and increased survival rate in SAE mice.</p><p><strong>Conclusions: </strong>Baicalein alleviated SAE through coordinated anti-inflammatory and neuroprotective effects by modulating stress- and inflammation-related signaling pathways, supporting its potential as a therapeutic candidate for SAE.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical spectrum, predictive biomarkers, and prognostic implications of peripheral neuropathies in primary Sjögren's syndrome: a retrospective cohort study.","authors":"Yanqing Wang, Jincheng Pu, Fang Han, Chunrui Li, Yan Chen, Yuanyuan Liang, Zhenzhen Wu, Shengnan Pan, Jun Qian, Wei Wang, Jianping Tang, Xuan Wang","doi":"10.1186/s40001-026-04192-4","DOIUrl":"https://doi.org/10.1186/s40001-026-04192-4","url":null,"abstract":"<p><strong>Objective: </strong>Primary 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.</p><p><strong>Methods: </strong>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).</p><p><strong>Results: </strong>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).</p><p><strong>Conclusions: </strong>Early identification and subtyping of pSS-PN are crucial for accurate disease assessment and guiding treatment.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ARPC1B promotes gastric cancer tumorigenesis via IGF2BP3-mediated stabilization of HK2 mRNA and glycolytic reprogramming.","authors":"Junjie Ma, Longyue Wang, Ting Liu, Rong Yang, Yongjing Chen","doi":"10.1186/s40001-026-04087-4","DOIUrl":"https://doi.org/10.1186/s40001-026-04087-4","url":null,"abstract":"<p><strong>Background: </strong>Cancer 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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between gonial angle and mandibular fracture risk: a retrospective study of traumatic and iatrogenic cases.","authors":"Jing-Ying Mu, Chun-Feng Wu, Da-Peng Jiang, Xiao-Li Xu, Bin Jin","doi":"10.1186/s40001-026-04198-y","DOIUrl":"https://doi.org/10.1186/s40001-026-04198-y","url":null,"abstract":"<p><strong>Background: </strong>The aim of this study is to investigate the association between gonial angle (GA) and the risk of mandibular fractures, including traumatic and iatrogenic cases, using panoramic radiograph measurements.</p><p><strong>Methods: </strong>A retrospective study was conducted, analyzing data from 174 patients with mandibular fractures treated at Yanbian University Hospital. A normal group comprised 104 individuals without fractures, in addition to 20 cases of impacted tooth extractions and 20 cases of iatrogenic mandibular fractures sourced from the literature, resulting in a total of 318 cases. The demographic characteristics, including patient age and sex, were thoroughly documented, and GA values were systematically measured based on the measurement methods in the literature combined with orthodontic cephalometric methods.</p><p><strong>Results: </strong>In the fracture group, the mean GA value was 124.84 ± 6.56, with females having higher values than males. In the normal group, the average GA values were 121.82 ± 7.84 on the left side and 120.36 ± 7.61 on the right side, indicating a statistically significant lateral difference (p < 0.001). Furthermore, females in this group had significantly higher GA values than males (p < 0.05). The mean GA values for the iatrogenic fracture group (124.21 ± 4.45) and the traumatic fracture group (124.84 ± 6.54) were considerably higher than those of the normal group (121.09 ± 7.47) and the impacted tooth extraction group (120.46 ± 5.58), with intergroup comparisons demonstrating statistical significance (p < 0.001).</p><p><strong>Conclusion: </strong>A higher GA is associated with an increased risk of mandibular fractures including those of traumatic and iatrogenic origin. These findings suggest that GA measurement may serve as a valuable parameter in assessing fracture susceptibility in clinical practice.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147375819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glucocorticoid monotherapy vs. immunosuppressant-combined therapy in retroperitoneal fibrosis: clinical evidence and mechanistic insights from bioinformatics.","authors":"Tong Zheng, Zhuoyi Wu, Yishan Ding, Cuiping Pan, Yuexian Shi, Hui Gao","doi":"10.1186/s40001-026-03856-5","DOIUrl":"https://doi.org/10.1186/s40001-026-03856-5","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the differences in efficacy and safety between two therapeutic approaches: glucocorticoids monotherapy and combined therapy of glucocorticoids and immunosuppressants, in patients with retroperitoneal fibrosis (RPF).</p><p><strong>Methods: </strong>Systematic searches of PubMed, EMBASE, Cochrane Library, Web of Science and ProQuest were performed. Randomized controlled trials, quasi-experimental designs and observational cohort studies that reported the efficacy or recurrence on RPF patients treated with glucocorticoid monotherapy or glucocorticoids combined with specified immunosuppressants therapy were included. Subsequently, a meta-analysis was conducted, followed by an independent bioinformatics analysis to elucidate the mechanisms by which glucocorticoids combined with immunosuppressants potentiate therapeutic effects in the treatment of RPF.</p><p><strong>Results: </strong>A total of 11 studies comprising 224 patients were identified. Compared with glucocorticoid monotherapy, combined therapy demonstrated a significant higher response rate (98.9% vs. 85.1%, P = 0.08) and a trend toward more frequent disappearance of hydronephrosis (97.1% vs. 90.0%, P = 0.29). Moreover, while recurrence rates were comparable between the two groups within the first year (5.7% vs. 4.9%, P = 0.92), recurrence in the monotherapy group surpassed that in the combined therapy group beyond 1 year of continuous follow-up (10.6% vs. 7.4% at 24 months, 21.1% vs. 10.7% at 36 months, and 26.1% vs. 12.5% overall), although without significant difference. Bioinformatic analysis revealed that prednisone targets overlapping with RPF-associated genes are mainly involved in acute inflammatory responses and cytokine regulation, whereas immunosuppressants act on a broader range of pathogenic genes implicated in key immunological and fibrotic pathways in RPF. This complementary targeting provides a mechanistic rationale for the role of immunosuppressants in promoting fibrotic tissue remodeling and alleviating mechanical obstruction in RPF. The use of immunosuppressants was associated with a low incidence of adverse events (7.2%), and no severe side effects were reported.</p><p><strong>Conclusions: </strong>Clinical evidence from literature and mechanistic insights from bioinformatics both suggest a potential benefit of combination therapy in RPF. However, the evidence remains associative and exploratory. Further randomized controlled trials are warranted to evaluate the potential benefits and risks associated with the addition of immunosuppressants in patients with RPF.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical features, prognosis, and influencing factors of relapse in autoimmune encephalitis associated with antibodies against cell surface antigens: a single-center retrospective study.","authors":"Pankui Li, Jing Zhou, Yixin Gu, Zhenhai Wang","doi":"10.1186/s40001-026-04111-7","DOIUrl":"https://doi.org/10.1186/s40001-026-04111-7","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to systematically analyze the clinical features, prognosis, and relapse of patients with autoimmune encephalitis associated with antibodies against cell surface antigens (AEASA), and to explore the independent risk factors for poor prognosis.</p><p><strong>Methods: </strong>A retrospective study was conducted on 91 patients diagnosed with AEASA at our hospital between 2015 and 2023. Demographic data, clinical characteristics, and follow-up information were collected and analyzed. Patients were grouped based on antibody type, modified Rankin Scale (mRS) score, relapse status, and Clinical Assessment of Autoimmune Encephalitis (CASE) score. Statistical analyses included t-tests, analysis of variance (ANOVA), chi-square tests, Spearman correlation analysis, univariate and multivariate binary logistic regression, and receiver operating characteristic (ROC) curve analysis to evaluate the predictive efficacy of risk factors.</p><p><strong>Results: </strong>Among the 91 patients, 58.3% were male, with a mean age of 47.9 ± 18.8 years. Clinical manifestations varied by antibody subtype: Anti-NMDAR encephalitis was more common in young females, with prominent neuropsychiatric symptoms, and significantly elevated CSF inflammatory markers (pressure, lymphocyte count) and systemic inflammatory indicators (CRP, CAR). Anti-LGI1 encephalitis was more prevalent in middle-aged and elderly males, often accompanied by hyponatremia, hypochloremia, and hippocampal MRI abnormalities. Anti-GABABR encephalitis had high rates of consciousness disturbance and cognitive impairment, with a significantly higher tumor comorbidity rate (37.5%) than other groups. Follow-up showed 71.4% of patients had a good prognosis, and 19.8% experienced relapse. Multivariate logistic regression analysis revealed that prolonged hospital stay (OR = 1.029, 95% CI: 1.008-1.066), elevated C-reactive protein (CRP; OR = 1.040, 95% CI: 1.032-1.058), and increased CRP/albumin ratio (CAR; OR = 1.032, 95% CI: 1.005-3.043) were independent risk factors for poor prognosis. ROC curve analysis confirmed these three factors had good predictive value for poor prognosis (AUC: 0.706, 0.697, 0.714, respectively).</p><p><strong>Conclusions: </strong>AEASA subtypes differ significantly in demographic characteristics, clinical manifestations, laboratory results, and imaging findings, forming distinct disease spectra. Hospital stay duration, CRP, and CAR are robust, independent biomarkers for predicting poor prognosis in AEASA patients, providing important guidance for clinical risk stratification and treatment decisions. Early identification and intervention for high-risk patients with relapse potential are crucial for improving long-term prognosis.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calcium channel blockers affect angiogenesis by modulating inflammatory factors: a meta-analysis of randomized controlled trials.","authors":"Jianwei Ge, Menglin Sun, Shuo Yang, Bo Yang, Yuxia Wang, Tao Wang, Bo Liu, Xiaoyong Wei, Lijuan Wang, Lihua Jiang","doi":"10.1186/s40001-025-03781-z","DOIUrl":"https://doi.org/10.1186/s40001-025-03781-z","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Neovascularization is balanced by various factors that stimulate and inhibit angiogenesis, thus ensuring the physiological formation of blood vessels. Pathological angiogenesis also occurs in the development of the disease. Calcium ions play an important role in the human body, and can participate in various functions in cell physiology, such as gene expression, control of the cell cycle, cell motility, apoptosis, and autophagy. Selective activation of transcription factors that can be used for gene transcription, cell proliferation, and migration (have deleted). Studies have found that calcium channel blockers have the effect of inhibiting angiogenesis, which plays an important role in the synthesis and release of inflammatory chemical mediators, calcium channel blockers can play an anti-inflammatory role by reducing the production of inflammatory factors, such as IL-1, IL-6, TNF-α and other substances; thereby, inhibiting angiogenesis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;In this meta-analysis, we searched eight major databases-CNKI, Wanfang Medical, VIP, CBM, Cochrane, Embase, PubMed and Web of Science-from their inception to June 2024. After screening eligible literature, randomized controlled methods were used to compare the subjects of angiogenesis and inflammation research into experimental and control groups, and whether there was any difference between IL-1, IL-6 and TNF-αbefore and after treatment.(original text: After screening eligible literature, randomized controlled methods were used to compare the infected subjects into experimental group and control group, and whether there was any difference between IL-1, IL-6 and TNF-αbefore and after treatment.) After statistical analysis, the results were verified to be statistically significant.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;A total of nine trials were included. The statistical results showed that there was no heterogeneity in the baseline period difference of IL-1 between the experimental group and the control group before treatment (I&lt;sup&gt;2&lt;/sup&gt; = 0% &lt; 50%, P = 0.69 &gt; 0.1 in Q test), no heterogeneity in the baseline period difference of IL-6 (I&lt;sup&gt;2&lt;/sup&gt; = 0% &lt; 50%, P = 0.99 &gt; 0.1 in Q test), and no heterogeneity in the baseline period difference between TNF-α(I&lt;sup&gt;2&lt;/sup&gt; = 0% &lt; 50%, P = 0.97 &gt; 0.1 in Q test). The effect size after Meta merger in IL-1 group was -23.26 (-25.39 ~ -21.14), and the effect size was significant (Z = 21.46, P &lt; 0.05). The effect size after Meta merger in IL-6 group was -37.19 (-42.56 ~ -31.83), and the effect size was significant (Z = 13.58, P &lt; 0.05). The effect size after Meta merger in the TNF-αgroup was -55.51 (-57.60 ~ -53.42), and the effect size was particularly significant (Z = 52.05, P &lt; 0.05). The IL-1 treated with calcium channel blocker was significantly lower than that of the control group by 23.26, IL-6 was significantly lower than that of the control group by 37.19, and TNF-αwas significantly lower than that of t","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between HAR (hemoglobin-to-age ratio) and unplanned cardiovascular readmission risk in patients with non-valvular AF: a retrospective cohort study.","authors":"Jing Li, LeiLei Guo, ChunChang Qin","doi":"10.1186/s40001-026-04182-6","DOIUrl":"https://doi.org/10.1186/s40001-026-04182-6","url":null,"abstract":"<p><strong>Background: </strong>Evidence links hemoglobin levels to atrial fibrillation prognosis, but hemoglobin is also known to change with age. The hemoglobin-to-age ratio (HAR) integrates age and hemoglobin. Its impact on the prognosis of non-valvular AF (NVAF) remains uncertain. Our aim is to investigate the relationship between HAR and clinical outcomes in NVAF patients.</p><p><strong>Methods: </strong>In this retrospective cohort study, we conducted an analysis of clinical data from patients with NVAF who were hospitalized at the cardiology inpatient department (January 2023-July 2024). The exposure variable was the HAR, while the outcomes were unplanned cardiovascular readmission. Multivariate logistic regression evaluated HAR's independent association with unplanned cardiovascular readmission risk, with predictive accuracy assessed via ROC curves and subgroup consistency through stratified analyses. Smooth curve fitting was utilized to investigate the linear relationship, and a series of sensitivity analyses were conducted to validate the robustness of the findings.</p><p><strong>Results: </strong>This study included 985 participants (50.3% male, mean age 73.0 ± 11.9 years). This study showed that each unit increase in HAR was associated with a 39% reduction at 30-day unplanned cardiovascular readmission risk (OR = 0.61, 95% CI 0.40-0.95, P = 0.027). Compared with the low HAR group, the high HAR group (HAR > 1.94) showed a significantly lower 30-day unplanned cardiovascular readmission risk (OR = 0.49, 95% CI 0.28-0.87, P = 0.014). Similar results were observed for 90-day and 180-day unplanned cardiovascular readmission risks. There were no significant interactions found in the subgroup analysis. A linear association was identified between HAR and unplanned cardiovascular readmission risks. The optimal HAR cutoff value for predicting 30-day unplanned cardiovascular readmission risk was 1.40 (sensitivity 81.1%, specificity 42.1%, AUC = 0.618), 90-day unplanned cardiovascular readmission risk was 1.57 (sensitivity 67.8%, specificity 52.1%, AUC = 0.610), while for 180-day unplanned cardiovascular readmission risk, it was 1.56 (sensitivity 69.9%, specificity 48.9%, AUC = 0.603). Sensitivity analyses corroborated the robustness of our findings.</p><p><strong>Conclusions: </strong>The HAR has a linear negative correlation with 30-day, 90-day, and 180-day unplanned cardiovascular readmission risks in patients with NVAF, a higher HAR was significantly associated with a lower risk of 30-day, 90-day, and 180-day unplanned cardiovascular readmission in patients with NVAF.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The LINC01094 drives atherosclerosis endothelial injury and inflammation via the miR-218-5p/SP1 axis and servers as a clinical biomarker.","authors":"Shuxia Yao, Wenqi Yang","doi":"10.1186/s40001-026-04060-1","DOIUrl":"https://doi.org/10.1186/s40001-026-04060-1","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis (AS) stems from endothelial injury and inflammation. This study clarified LINC01094's clinical implication and its role in endothelial damage and inflammation.</p><p><strong>Methods: </strong>GEO databases screened differential lncRNAs in tissue samples from ruptured, unstable, and advanced human carotid atherosclerotic plaques. 118 patients with AS and 100 controls was enrolled, with oxidized low-density lipoprotein (ox-LDL)-stimulated Human aortic endothelial cells (HAECs) were used. Real-time quantitative reverse transcription PCR detected LINC01094 levels in serum and HAECs. Receiver operating characteristic curve analysis LINC01094's predictive value for AS, and logistic regression identified AS risk factors. CCK-8 and flow cytometry assessed cell viability and apoptosis. Commercial kits and Enzyme-linked immunosorbent assay were used to quantify LDH adhesion molecules, chemokines, and inflammatory factors. DLR and RIP assays assessed miR-218-5p's binding to LINC01094 or SP1.</p><p><strong>Results: </strong>LINC01094 was upregulated in the GSE28829, GSE120521, and GSE21545 datasets, with notably higher expression observed in AS patients' serum and ox-LDL-stimulated HAECs. It predicted AS occurrence with 81.36% sensitivity and 90.00% specificity, and was identified as a risk factor (OR: 8.401, 95%CI 4.175-16.907). Silencing LINC01094 countered ox-LDL-induced suppression of HAECs viability, elevation of apoptosis, LDH levels, adhesion molecules, chemokines, and inflammation. However, low miR-218-5p expression partially mitigated these effects. Overexpression of SP1 hindered the ability of miR-218-5p to alleviate ox-LDL-triggered endothelial damage and inflammation. Notably, LINC01094 positively modulated SP1 expression by sponging miR-218-5p.</p><p><strong>Conclusions: </strong>LINC01094 is a promising biomarker for predicting AS. Moreover, silencing LINC01094 may decelerate AS progression via regulating the miR-218-5p/SP1 axis, thus alleviating endothelial injury and inflammation.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}