Long non-coding RNAs (lncRNAs) play crucial roles in the onset and progression of cardiovascular disease, particularly atherosclerosis. However, the role of PARD3-AS1 in atherosclerosis remains largely uncharacterized. This study therefore aimed to investigate the impact of the PARD3-AS1/miR-668-3p axis on atherosclerosis. The expression levels of PARD3-AS1 and miR-668-3p in human umbilical vein endothelial cells (HUVECs) were quantified by quantitative real-time polymerase chain reaction (RT-qPCR). HUVEC proliferation was assessed using a Cell Counting Kit-8 (CCK-8) assay and 5-ethynyl-2′-deoxyuridine (EdU) incorporation, and migratory and invasive capacities were evaluated using wound healing and Transwell assays. The interaction between PARD3-AS1 and miR-668-3p was confirmed by bioinformatics analysis and dual-luciferase reporter assays. In addition, serum samples were collected from patients diagnosed with atherosclerosis, and ApoE⁻/⁻ C57BL/6 mice were fed a high-fat diet for 8 weeks to establish a model of atherosclerosis. PARD3-AS1 expression was significantly reduced in the serum of patients with atherosclerosis, whereas miR-668-3p levels were markedly elevated, and the two were negatively correlated. Subsequent experiments confirmed that miR-668-3p effectively reversed the promotion effects of PARD3-AS1 on HUVEC proliferation and migration. In vivo, histological staining showed that the PARD3-AS1 overexpression group exhibited improved endothelial repair. Collectively, these findings demonstrate that PARD3-AS1 directly interacts with miR-668-3p to modulate HUVEC proliferation, migration, and invasion, suggesting that PARD3-AS1 may serve as a potential therapeutic target for atherosclerosis.

Objective:To evaluate the feasibility and short-term clinical outcomes of the Kabedon technique-based endovascular aneurysm repair (EVAR) for abdominal aortic aneurysms (AAA) with severe infrarenal neck angulation (angle >60°). Methods:This retrospective cohort study was based on a single-center database. Between January 2019 and May 2023, 120 patients with AAA of hostile neck angulation underwent endovascular procedures using the Kabedon technique for abdominal aortic remodeling. A standardized protocol was followed to calculate the serial changes in the aneurysmal neck angle. The primary endpoints were proximal type Ia endoleak and stent-graft migration. The secondary endpoints were all-cause and aneurysm-related mortality, proximal neck dilatation, and re-intervention. Results:The mean age was 71.40 ± 10.69 years, and 95 (79.17%) were male. The mean AAA sac diameter and proximal neck angle were 63.71 ± 17.32 mm and 83.67 ± 18.45°, respectively. All patients underwent the Kabedon-based EVAR, with a technical success rate of 94.17% (113/120). During the operation, 7 cases of endoleak and 2 cases of endograft migration were observed, which were resolved by corresponding measures such as coil embolization and proximal cuff stent salvage. No complications were observed within 30 days. In addition, neck calcification, funnel-shaped aneurysm, intraoperative complications and corresponding treatments may be potential negative factors for technical success, but there was no statistical difference. Conclusions:Kabedon-based EVAR for AAA with a severely angulated neck provided high technical success, low mortality and complication rates during short-term follow-up. Further studies with larger sample sizes and longer follow-up periods are warranted.

Objective: The objective of this study was to develop and evaluate the effectiveness of machine learning (ML) models in predicting carotid plaque instability. Methods:A retrospective analysis was conducted on data from 449 patients with carotid plaques treated at The Affiliated Hospital of Qingdao University between July 2022 and November 2024. Patients were randomly divided into a training set and a testing set at a 7:3 ratio. Five ML algorithms were utilized to establish prediction models. The predictive performance of each model was assessed using the area under the receiver operating characteristic curve (AUC), accuracy, sensitivity, and specificity on the testing set. Results: Among the five ML algorithms, the light gradient boosting machine (LightGBM) demonstrated the best performance with an AUC of 0.921 (95% confidence interval [CI]: 0.887–0.956) and an accuracy of 0.837 in the training set, and an AUC of 0.864 (95% CI: 0.784–0.944) and an accuracy of 0.811 in the testing set. The feature importance results showed that C-reactive protein (CRP), leukocytes, high-density lipoprotein (HDL), and platelets were the four most significant contributors to carotid plaque instability. Conclusion:We developed and validated the ML models for predicting carotid plaque instability, and identified that LightGBM model with 9 relevant factors had the best performance and high levels of clinical applicability.

Postinjury restenosis is a common complication of peripheral arterial disease treated via endovascular techniques. Its pathogenesis mainly involves neointimal hyperplasia and persistent inflammation. Although antiproliferative drugs used clinically can temporarily slow restenosis, their effects are limited by short action duration and lack of precise regulation. In this investigation, tRF-49:69-chrM.Trp-TCA (tRF-Trp-TCA) was identified through sequencing data from an animal restenosis model, and its regulatory effects on endothelial cell migration and inflammation were confirmed. Additionally, we discovered that cabbage exosome-like nanoparticles (CELNs) could precisely target injured blood vessels in vivo, enhance the stability of nucleic acid therapeutics, and more effectively inhibit neointimal hyperplasia in a carotid artery balloon injury model. Our results demonstrated that tRF-Trp-TCA is crucial in restenosis induced by arterial injury and CELNs loaded with tRF-Trp-TCA effectively inhibit neointimal hyperplasia following carotid artery injury in rats, showing good biocompatibility. This study has, for the first time, identified the target tRF-Trp-TCA for treating restenosis after vascular injury and has also, for the first time, used CELNs as the delivery system. This discovery could provide new insights for noninvasive treatments or mitigation of restenosis post-endovascular therapy.

BACKGROUND AND AIMS:Endothelial-to-mesenchymal transition (EndMT) is an important reason for restenosis but the underlying mechanisms need to be further explored. Therefore, the purpose of this study is to screen significantly different microRNAs (miRNAs) and assess their functions and downstream pathways. METHODS:This study screened several miRNAs with significant differences between human arterial segments from restenosis patients and healthy volunteers using whole transcriptome resequencing and real-time quantitative reverse transcription PCR (qRT-PCR). We explored the correlation between miR-1290 and EndMT using Western blot, qRT-PCR, Pearson correlation analysis and further functional gain and loss experiments. Subsequently, we identified the direct downstream target of miR-1290 by bioinformatics analysis, RNA pull-down, double Luciferase reporter gene and other functional experiments. Finally, rat carotid artery balloon injury model demonstrated the therapeutic potential of miR-1290 regulator. RESULTS:We screened 129 differentially expressed miRNAs. Among them, miR-1290 levels were significantly higher in restenosis arteries than in healthy arteries, and as expected, EndMT was functionally enhanced with miR-1290 overexpression and comparatively weakened when miR-1290 was knocked down. In addition, fibroblast growth factor-2 (FGF2) was established as the downstream target of miR-1290. Finally, we utilized an animal model and found that low miR-1290 levels could alleviate EndMT and the progression of restenosis. CONCLUSIONS:Our study demonstrated the strong regulatory effects of miR-1290 on EndMT, endometrial hyperplasia and restenosis, which could be useful as biomarker and therapeutic target for stent implantation in patients with arterial occlusive disease of the lower extremities.

Ischemic strokes are primarily caused by intracranial and extracranial atherosclerotic stenosis. Nontraditional lipid parameters broaden traditional lipid profiles, better reflect the metabolism and interaction between different lipid components, and optimize the predictive ability of lipid profiles for atherosclerotic diseases. This research was carried out to investigate the predictive value of nontraditional lipid parameters for intracranial or extracranial atherosclerotic stenosis. The investigation collected data from inpatients who underwent cervical vascular ultrasonography, carotid CTA, cerebral artery CTA or MRA, and brain MRI or CT from December 2014 to December 2021. The nontraditional lipid parameters were calculated by collecting traditional lipid parameters. To evaluate the predictive power of nontraditional lipid parameters, logistic regression and receiver operating characteristic curve (ROC) analyses were performed. Based on the inclusion and exclusion criteria, 545 patients were included. According to the imaging results, inpatients were divided into two groups, including no intracranial or extracranial atherosclerotic stenosis (n = 250) and intracranial or extracranial atherosclerotic stenosis (AS, n = 295). Among them, AS was further divided into three subgroups: intracranial atherosclerotic stenosis (ICAS), extracranial atherosclerotic stenosis (ECAS) and combined intracranial and extracranial atherosclerotic stenosis (IECAS). Logistic regression analysis showed that nontraditional lipid parameters, including the atherogenic index of plasma (AIP), TG/HDL-C, remnant cholesterol (RC), nonhigh-density lipoprotein cholesterol (non-HDL-C), lipoprotein combine index (LCI), atherogenic coefficient (AC), Castelli’s index-I (CRI-I) and Castelli’s index-II (CRI-II), were significantly correlated with intracranial or extracranial atherosclerotic stenosis (P < 0.05). Compared with other nontraditional lipid parameters, regardless of adjusting for potential confounding factors, AIP had a greater OR value in ICAS (OR = 4.226, 95

Preparation of CTU microspheres and scheme of thrombolysis.

An abdominal aortic aneurysm is a frequently encountered clinical condition, which necessitates prompt and effective remediation to avoid rupture. Surgeons must meticulously select an appropriate method of repair and assess the long-term surgical prognosis when dealing with patients with complex abdominal aortic aneurysms. In this case report, a 74-year-old man was hospitalized due to acute abdominal pain. Upon further examination, it was discovered that he was suffering from a complex abdominal aortic aneurysm. The thoracoabdominal aorta CTA showed that the aneurysm involved both renal arteries, the part below the kidney was severely twisted, the neck of the aneurysm was short, and it was accompanied by bilateral common iliac and internal iliac aneurysms, and there were considerable thrombus attached to the vessel wall. In this case, our team used 3D technology to simulate the spatial structure of the aneurysm and comprehensively evaluate the patient's condition. Ultimately, we decided to perform a quadruple fenestration aortic stent implantation and endovascular repair of aortic aneurysm, combined with right IBE and internal iliac artery stent implantation, right internal iliac artery reconstruction, and left internal iliac artery aneurysm embolization on this patient. This is an innovative surgical method. The operation was successful and the patient recovered well after the operation.

下肢慢性静脉功能不全(chronic venous insufficiency, CVI)的发病率越来越高,严重影响患者的生活质量.目前,CVI的主要病理生理机制为静脉反流、静脉回流障碍或者两者同时存在[1-2].CVI的治疗方式仍以压力治疗为主,但对于临床表现-病因学-解剖学-病理生理学(clinical etiology anatomy pathophysiology,CEAP)分级为C3级以上的病变[3],特别是存在髂股静脉闭塞的病变,腔内血管成形术和支架植入术已成为公认的首选治疗方法[4-5].目前,国内获批的静脉专用支架有Zilver Vena支架和Venovo支架,而青岛大学附属医院暂时无此两款支架,因此,对于髂股静脉全程闭塞性病变,基于静脉的特殊病理生理学特点及解剖位置,青岛大学附属医院尝试组合应用另外两种支架进行治疗.本研究对复合支架在髂股静脉闭塞性病变中的应用效果进行探讨,现报道如下.

ObjectiveThe occurrence of Brucella-induced abdominal aortic aneurysms is an exceedingly rare phenomenon, yet it stands as one of the most severe complications within this context. The combined utilization of serological testing and imaging diagnostics has been validated as an effective approach for the identification of Brucella-induced abdominal aortic aneurysms. Presently, the predominant therapeutic strategies encompass antibiotic treatment and surgical intervention. Nonetheless, ongoing controversies persist concerning the establishment of diagnostic criteria, the optimal timing and selection of antibiotic regimens, and the nuanced decision between open surgical procedures and endovascular interventions. Through a meticulous analysis of cases originating from our institution as well as a comprehensive review of previously documented instances, we aim to engage in a detailed discourse on the salient diagnostic and therapeutic facets surrounding Brucella-induced abdominal aortic aneurysms.MethodsWe conducted a retrospective summary of three cases involving Brucella-induced abdominal aortic aneurysms treated within our institution. Furthermore, we performed a comprehensive PubMed search, without imposing restrictions on language or publication year, to identify pertinent literature pertaining to Brucella-induced abdominal aortic aneurysms. The selection criteria primarily focused on case reports delineating occurrences of abdominal aortic aneurysms attributed to Brucella infection.ResultsWe present three distinct cases of Brucella-induced abdominal aortic aneurysms managed at our institution, providing comprehensive insights into the employed diagnostic and therapeutic approaches. Additionally, over the past five decades, a total of 24 cases in 23 publications of Brucella-induced abdominal aortic aneurysms have been reported on PubMed. The earliest report dates back to 1976.ConclusionOur analysis suggests that Brucella-induced abdominal aortic aneurysm is characterized by a remarkably low incidence but is associated with a substantial risk of life-threatening complications. The integration of serological and imaging assessments assumes pivotal importance in facilitating prompt diagnosis of this condition. The prompt initiation of targeted antibiotic therapy is recommended, and the selection of appropriate surgical strategies should be guided by considerations including aneurysm dimensions and morphological attributes. The timely identification and intervention carry utmost significance in retarding disease advancement and ameliorating unfavorable clinical outcomes.

The study was designed to discuss the effect of stratification factors in the Mayo staging on the prognosis of hilar cholangiocarcinoma (HCCA) patients, and to evaluate the predictive value of the Mayo staging on the prognosis. The Kaplan-Meier survival curve and Log-rank test were used to perform univariate analysis on each index and obtain statistically significant influencing factors. The Kaplan-Meier survival curve and Log-rank test were used to analyze the correlation between the two staging systems and the survival period. The receiver operating characteristic (ROC) curves were used for each single staging system trend analysis, and comparison of their curve area to determine prognosis prediction ability for patients with HCCA. According to Kaplan-Meier survival curve changes and Log-rank test results, it was found that both staging systems were correlated with the survival time of the patients (P < .001). Through a pairwise comparison within the stages, it was found that the heterogeneity between the stages within the Mayo staging is very good, which was better than the TNM staging. A single trend analysis of the prognostic assessment capabilities of the two systems found that the area under the ROC curve of Mayo staging system (AUC = 0.587) was the largest and better than the TNM staging system (AUC = 0.501). Mayo staging can be used for preoperative patient prognosis assessment which can provide better stratification ability based on a single-center small sample study, and the predictive value is better than TNM staging.

腹主动脉瘤是最常见的主动脉疾病,危害性极大,一旦破裂病死率极高.目前主要治疗方式有腔内修复和外科开放手术.近年来,腔内修复因其微创、高效等特点迅速发展及被推广,已经成为治疗腹主动脉瘤的主要手段.然而,腔内修复术后会出现一系列并发症,如内漏、支架移位、支架感染等,继发瘤体破裂是腔内修复术后死亡的主要原因 [1].目前鲜有支架置入后覆膜破裂的相关报道.本文旨在通过对1列腹主动脉瘤腔内修复术后覆膜破裂患者的临床资料进行分析,探讨腹主动脉瘤术前治疗方案的选择及术后并发症的认识及紧急处置总结经验,现报告如下.

目的:探讨SUMO活化酶亚单位2(SAE2)在胆管癌组织中的表达及其临床意义.方法:采用免疫组化法检测60例胆管癌及20例正常胆管组织中SAE2的表达,并分析SAE2的表达与胆管癌患者临床病理因素及预后的关系.结果:SAE2在胆管癌组织中的阳性表达率明显高于正常胆管组织为(71.67％vs.30.00％,x2=10.972,P＜0.001);SAE2的表达与胆管癌的病理分化程度、TNM分期有关(均P＜0.05);SAE2阳性表达患者的中位生存时间明显短于阴性表达患者为(13.0个月vs30.7个月,x2=13.805,P＜0.001).单因素生存分析显示,患者的预后与SAE2的表达和TNM分期有关(均P＜0.001);Cox多因素回归分析显示,SAE2的表达水平和TNM分期是胆管癌患者预后的独立影响因素(均P＜0.01).结论:SAE2在胆管癌组织中高表达,且与患者的不良预后有关,提示其可能参与了胆管癌的发生、发展过程.

Lycopene (lyc) has an effect on preventing cancer, yet its effects on hypoxia/reoxygenation (H/R) injury remained obscure. The study aimed at discovering its role in preventing hepatic cells against H/R injury. Hepatic cells were incubated in hypoxia incubator to simulate ischemia/reperfusion injuryin vitro. Cell viability was detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay after Lycopene treatment with or without ML385 (nuclear factor erythroid 2-related factor 2 [Nrf2] inhibitor). Lactate dehydrogenase (LDH) and malondialdehyde (MDA) content were detected. Cellular cytokine (tumor necrosis factor-alpha, TNF-alpha; interleukin-6, IL-6) levels were measured using enzyme-linked immunosorbent assay (ELISA). Hepatic cell apoptosis and cellular reactive oxygen species (ROS) content was detected by flow cytometry. Nrf2 transfer was observed using immunofluorescence staining. Nrf2 and heme oxygenase-1 (HO-1) expressions were detected with quantitative real-time polymerase chain reaction and western blot as needed. In hepatic cells, after H/R, the viability was dropped, TNF-alpha and IL-6 levels and LDH and MDA content were increased, with high apoptosis rate and ROS content. Lycopene led to a reversed effect, with promotion on Nrf2 transfer from cytoplasm into nucleus and Nrf2/HO-1 pathway activation. Further experiments showed that ML385 could reverse the effects of Lycopene. Lycopene could activate Nrf2/HO-1 pathway to protect hepatic cells against H/R injury.

Atherosclerosis (AS) is a cardiovascular disease with a relatively high incidence rate. Krüppel‑like factor 15 (KLF15) has a role in numerous pathological processes, including nephropathy, abnormal glucose metabolism and myocardial injury. The aim of the present study was to investigate the function of KLF15 in vascular endothelial dysfunction. MTT analyses, nitric oxide (NO) detection and cell adhesion detection kits were used to investigate the viability and adhesion of, and quantity of NO released by Eahy926 cells induced by tumor necrosis factor (TNF)‑α, respectively. Reverse transcription‑quantitative polymerase chain reaction and western blot analyses were performed to determine the expression levels of KLF15, endothelial nitric oxide synthase, monocyte chemoattractant protein‑1 (MCP‑1), intercellular adhesion molecule‑1 (ICAM‑1), transforming growth factor‑β1 (TGF‑β1), phosphorylated (p‑)transcription factor p65 (p65) and nuclear factor erythroid 2‑related factor 2 (Nrf2). The results of the present study demonstrated that TNF‑α was able to induce vascular endothelial dysfunction in Eahy926 cells at an optimum concentration of 10 ng/ml. Overexpression of KLF15 markedly enhanced cell viability in addition to the quantity of released NO of TNF‑α‑induced Eahy926 cells, and increased the expression levels of eNOS and Nrf2. Furthermore, overexpression of KLF15 markedly suppressed the rate of cellular adhesion, and downregulated levels of MCP‑1, ICAM‑1, TGF‑β1 and p‑p65 in TNF‑α induced Eahy926 cells. In conclusion, the results of the present study suggested that overexpression of KLF15 in Eahy926 cells exhibited a protective effect against TNF‑α induced dysfunction via activation of Nrf2 signaling and inhibition of nuclear factor κB signaling.