Advances in medical sciences最新文献_第3页

Reducing metastasis ability of gastric cancer cell line by targeting MMP16 using miR-193a-5p and 5-FU 利用 miR-193a-5p 和 5-FU 靶向 MMP16 降低胃癌细胞株的转移能力

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-09-01 DOI: 10.1016/j.advms.2024.09.008

Tahani Ahmad Almatrafi , Natrayan Lakshmaiya , Hailah M. Almohaimeed , Srikumar Chakravarthi , Ali H. Amin , Ayman Jafer , Amany I. Almars , Ammar A. Basabrain , Youssef S. Alghamdi , Mohamed J. Saadh , Reza Akhavan-Sigari

Purpose

Co-administration of microRNAs and chemotherapy drugs effectively treats several cancers. The current study sought to investigate the function of matrix metalloproteinase 16 (MMP16) and miR-193a-5p in the pathogenesis of gastric cancer (GC).

Materials/methods

Sixty-five surgical patients, 15 receiving 5-fluorouracil (5-FU), provided GC and adjacent non-cancerous tissue. Following that, qPCR was used to assess the expression levels of MMP16 and miR-193a-5p in GC cells. The impact of miR-193a-5p and 5-FU administration on MMP16 mRNA expression was evaluated using qRT-PCR and Western blotting. MTT and Scratch tests were also conducted to assess their effects on cell viability and migration. Moreover, a rescue experiment using an MTT assay was performed. Using flow cytometry, the apoptotic rate was calculated. Finally, it was evaluated how MMP16 and miR-193a-5p related to the clinicopathological characteristics of the patients.

Results

The current study found that while MMP16 expression increased in GC patients (P < 0.0001), miR-193a-5p expression significantly decreased (P < 0.001). MMP16 down-regulation was another effect of miR-193a-5p replacement, particularly when 5-FU was added (P < 0.01). In addition, this study found that miR-193a-5p, by concentrating on MMP16, decreased the migration of GC cells brought on by MMP16. In GC cell lines, miR-193 and 5-FU induce apoptosis, with the 5-FU being more pronounced when combined with mir-193, according to flow cytometry results. A strong correlation was also found between clinicopathological traits associated with MMP16 and miR-193a-5p.

Conclusions

These findings suggest that miR-193a-5p, in conjunction with 5-FU, down-regulates MMP16 in GC, where it suppresses tumor growth.

目的：microRNAs与化疗药物联合应用可有效治疗多种癌症。本研究试图探讨基质金属蛋白酶16（MMP16）和miR-193a-5p在胃癌（GC）发病机制中的功能：65例手术患者（其中15例接受了5-氟尿嘧啶（5-FU）治疗）提供了GC和邻近的非癌组织。然后，使用 qPCR 评估 GC 细胞中 MMP16 和 miR-193a-5p 的表达水平。使用 qRT-PCR 和 Western 印迹法评估了 miR-193a-5p 和 5-FU 给药对 MMP16 mRNA 表达的影响。还进行了 MTT 和划痕试验，以评估它们对细胞活力和迁移的影响。此外，还利用 MTT 试验进行了挽救实验。使用流式细胞术计算了细胞凋亡率。最后，还评估了 MMP16 和 miR-193a-5p 与患者临床病理特征的关系：结果：目前的研究发现，虽然 MMP16 在 GC 患者（PConclusions.）中的表达增加，但 miR-193a-5p 在 GC 患者中的表达却没有增加：这些研究结果表明，miR-193a-5p 与 5-FU 联用可下调 MMP16 在 GC 中的表达，从而抑制肿瘤生长。

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引用次数: 0

LRRC45 promotes lung cancer proliferation and progression by enhancing c-MYC, slug, MMP2, and MMP9 expression LRRC45 通过增强 c-MYC、Slug、MMP2 和 MMP9 的表达，促进肺癌的增殖和进展。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-09-01 DOI: 10.1016/j.advms.2024.09.007

Qian Wang , Xin-Yan Liu , Xiao-Qi Zhang , Zheng-Xing Huo , Cheng-Yu Chen , Shi Chen , Cheng-Yong Liu , Jia Zhu , Shan-Shan Liu , Bing Lu

Background

The leucine-rich repeat-containing (LRRC) superfamily members are known for their significant roles in tumorigenesis and cellular proliferation. However, the specific regulatory role of LRRC45 in lung cancer remains unexplored. This study investigated the impact and underlying mechanisms of LRRC45 on the proliferative, migratory, and invasive capacities of lung adenocarcinoma (LUAD) cells, potentially identifying new targets for therapeutic intervention.

Material and methods

The importance of LRRC45 in lung cancer was analyzed using the online databases of UCSC Xena, TCGA, TISIDB, and UALCAN, whereas to detect target gene expression, we used the qRT-PCR, Western blot, and immunofluorescence confocal. The cell growth was monitored by colony formation assay and migration was examined by cell migration assay. Finally, a xenograft mouse tumor model using A549 cells was used to explore the in vivo effect of LRRC45 in lung cancer.

Results

Inhibition of LRRC45 expression led to a notable decrease in proliferation, migration, and invasion of A549 and H1299 cells. LRRC45 silencing significantly reduced the tumor volume and improved the mice's survival. Additionally, inhibition of LRRC45 expression dramatically suppressed c-MYC, Slug, MMP2, and MMP9 expression. Overexpression of c-MYC and/or Slug in the LRRC45-deficient cells can partially or totally restore the LRRC45 deficiency-suppressed growth. Moreover, the overexpression of MMP2 and/or MMP9 could partially or totally restore LRRC45 deficiency-reduced cell metastasis.

Conclusions

LRRC45 could promote the proliferative, migrative, and invasive capacities of lung cancer cells by increasing c-MYC, Slug, MMP2, and MMP9 expression, indicating the therapeutic implications and potential significance of these pathways in lung cancer.

背景：众所周知，含亮氨酸丰富重复序列（LRRC）超家族成员在肿瘤发生和细胞增殖中发挥着重要作用。然而，LRRC45在肺癌中的具体调控作用仍未得到探索。本研究探讨了 LRRC45 对肺腺癌（LUAD）细胞增殖、迁移和侵袭能力的影响及其内在机制，从而为治疗干预寻找新的靶点：利用UCSC Xena、TCGA、TISIDB和UALCAN在线数据库分析了LRRC45在肺癌中的重要性，并利用qRT-PCR、Western印迹和免疫荧光共聚焦技术检测了靶基因的表达。通过集落形成试验监测细胞生长，通过细胞迁移试验检测细胞迁移。最后，利用 A549 细胞异种移植小鼠肿瘤模型来探讨 LRRC45 在肺癌中的体内效应：结果：抑制 LRRC45 的表达可显著减少 A549 和 H1299 细胞的增殖、迁移和侵袭。沉默 LRRC45 能显著减少肿瘤体积，提高小鼠存活率。此外，抑制 LRRC45 的表达还能显著抑制 c-MYC、Slug、MMP2 和 MMP9 的表达。在LRRC45缺陷细胞中过表达c-MYC和/或Slug可以部分或完全恢复LRRC45缺陷抑制的生长。此外，MMP2和/或MMP9的过表达可部分或完全恢复LRRC45缺陷抑制的细胞转移：结论：LRRC45可通过增加c-MYC、Slug、MMP2和MMP9的表达来促进肺癌细胞的增殖、迁移和侵袭能力，表明了这些通路在肺癌中的治疗意义和潜在重要性。

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引用次数: 0

Changes in hematopoietic stem cell numbers following acute exercise in non-athlete marathon runners 非马拉松运动员急性运动后造血干细胞数量的变化

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-09-01 DOI: 10.1016/j.advms.2024.09.003

Özgür Günaştı , Çiğdem Özdemir , Kerem T. Özgünen , Gizem Çiftdal , Ertuğrul Gezgin , Selcen Korkmaz Eryılmaz , Ömer Cumhur Boyraz , Abdullah Kılcı , Ümüt Adaş , Bülent Antmen , Sanlı Sadi Kurdak

Purpose

Hematopoietic stem cell (HSC) transplant is one of the curative methods for some patients with hematological malignancies. Granulocyte colony-stimulating factor (G-CSF) is the most common drug used to mobilize CD34⁺ cells, generally found in small numbers. Recent evidence showed that exercise causes transient mobilization in HSC. However, the type and intensity of exercise have not been fully revealed. We aimed to detect a significant increase in stem cell levels following 60 min of running at a personalized running pace.

Materials/methods

Eighteen runners, 48.2 ± 1.9 years with peak oxygen consumption of 46.2 ± 1.4 ml/kg/min, were enrolled in the study. The cardiopulmonary exercise test was performed to determine the individual running pace, and the participants ran 60-min on a treadmill at an intensity close to their ventilatory threshold (VT). The blood sampling for HSC count was performed before, immediately after, at the 1st, 4th and 24th hour after the 60-min running.

Results

The CD34⁺ HSCs were 13.9 ± 2.3 cells/μl before and significantly increased immediately after to 19.5 ± 3.6 cells/μl (p < 0.05). The consecutive HSC counts were 15.3 ± 2.2, 19.5 ± 4.8 and 15.1 ± 3.4 cells/μl at the 1st, 4th, and 24th hour, respectively.

Conclusion

The individual data showed that some runners had higher HSC levels than the transplantation limit before and after the 60-min running trail, which was maintained for 24 h. Pre-running high CD34⁺ HSCs may reflect an adaptive response to regular exercise, with a 60-min run near the VT further elevating HSCs. Individualized exercise may be a valuable tool to mobilize the CD34⁺ HSCs in peripheral blood for donors.

目的造血干细胞（HSC）移植是治疗某些血液恶性肿瘤患者的方法之一。粒细胞集落刺激因子（G-CSF）是最常用的动员 CD34+ 细胞的药物，但其数量通常较少。最近的证据显示，运动可引起造血干细胞的短暂动员。然而，运动的类型和强度尚未完全揭示。我们的目的是检测以个性化跑步速度跑步60分钟后干细胞水平的显著增加。材料/方法18名跑步者（48.2±1.9岁，峰值耗氧量为46.2±1.4毫升/千克/分钟）参加了研究。进行心肺运动测试以确定个人的跑步速度，参与者在跑步机上以接近其通气阈值（VT）的强度跑步 60 分钟。结果跑步前，CD34+造血干细胞数量为 13.9 ± 2.3 cells/μl，跑步后立即显著增加至 19.5 ± 3.6 cells/μl（p <0.05）。在第1、4和24小时，连续的造血干细胞计数分别为15.3±2.2、19.5±4.8和15.1±3.4个细胞/μl。跑步前的高 CD34+ 造血干细胞水平可能反映了对常规运动的适应性反应，而接近 VT 的 60 分钟跑步则进一步提高了造血干细胞水平。个性化的运动可能是动员外周血中CD34+造血干细胞的重要工具。

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引用次数: 0

Pentraxin 3 as a marker of development and severity of stable coronary artery disease 作为稳定型冠状动脉疾病发展和严重程度标志物的五胜肽 3。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-09-01 DOI: 10.1016/j.advms.2024.07.010

Malgorzata Knapp, Monika Gil-Mika, Robert Sawicki, Anna Lisowska, Marcin Kaminski, Bozena Sobkowicz, Katarzyna Ptaszynska

Purpose

Inflammation plays a crucial role in the development of atherosclerotic plaques. Pentraxin 3 (PTX3) is produced at the site of inflammation and has been identified as a specific marker of atherosclerosis, vascular inflammation, and progression of the coronary artery disease (CAD).

The aim of the study was to establish if PTX3 has potential relations with classical markers of cardiovascular risk, and if PTX3 may act as an independent risk factor of CAD occurrence and advancement.

Materials and methods

The study included 98 patients with stable CAD confirmed in coronary angiography (CAD group) (median age 65 interquartile range [IQR] 61–72 years; 72 % men). The control group consisted of 40 patients without CAD.

Results

The CAD group had significantly higher PTX3 concentration compared to the control group. There was a correlation with age, male gender, lipid profile and intima-media thickness. There was no correlation between PTX3 concentration and the number of coronary vessels with significant atherosclerotic lesions and the advancement of atherosclerotic lesions on the Gensini scoring scale. The cut-off point was determined for 0.89 ng/ml for the exclusion of angiographically significant atherosclerotic lesions.

Conclusions

Patients with CAD have significantly higher concentration of PTX3. There was no correlation between PTX3 and the advancement of angiographically significant atherosclerotic lesions in coronary arteries. Low PTX3 concentration may serve as an indicator for the absence of atherosclerosis.

目的：炎症在动脉粥样硬化斑块的形成过程中起着至关重要的作用。五胜肽 3（PTX3）产生于炎症部位，已被确定为动脉粥样硬化、血管炎症和冠状动脉疾病（CAD）进展的特异性标志物。该研究的目的是确定 PTX3 是否与心血管风险的经典标志物有潜在的关系，以及 PTX3 是否可能成为 CAD 发生和发展的独立风险因素：研究对象包括98名经冠状动脉造影证实患有稳定型CAD的患者（CAD组）（中位年龄65岁，四分位数区间[IQR]61-72岁；72%为男性）。对照组由 40 名无 CAD 患者组成：结果：与对照组相比，CAD 组的 PTX3 浓度明显更高。PTX3浓度与年龄、男性性别、血脂状况和血管内膜厚度相关。PTX3 浓度与有明显动脉粥样硬化病变的冠状动脉血管数量以及根西尼评分表中动脉粥样硬化病变的进展之间没有相关性。结论：CAD患者体内的PTX3浓度明显高于正常人：结论：CAD 患者的 PTX3 浓度明显更高。结论：冠状动脉粥样硬化患者的 PTX3 浓度明显较高，PTX3 与冠状动脉血管造影显着动脉粥样硬化病变的进展之间没有相关性。PTX3的低浓度可作为没有动脉粥样硬化的指标。

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引用次数: 0

Right-ventricle heart failure in PAH vs. HFrEF with secondary PH: Hemodynamic, ergospirometric, and organ function correlations PAH 与继发性 PH 的 HFrEF 中的右心室心力衰竭：血液动力学、测力和器官功能相关性。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-09-01 DOI: 10.1016/j.advms.2024.08.003

Katarzyna Krajewska, Krystian Ejdys, Klaudia Jadczak, Anna Lisowska, Karol A. Kamiński, Bożena Sobkowicz, Katarzyna Ptaszyńska

Purpose

The goal of the study was to identify markers of organ function used in daily routines that could potentially aid in the overall evaluation of the cardiovascular system in patients with right-ventricle heart failure due to pulmonary arterial hypertension (PAH) and left-ventricle heart failure. We analyzed correlations between parameters from right heart catheterization (RHC), cardiopulmonary exercise test (CPET), and selected laboratory parameters of thyroid, liver, kidneys function and iron homeostasis.

Patients and methods

A retrospective analysis included 107 patients (mean age 57.6 ± 16.2; 34.6 % women), comprising 57 patients with PAH (mean age 54.0 ± 18.2; 49.1 % women) and 50 patients with heart failure with reduced ejection fraction (HFrEF) < 40 % (mean age 61.6 ± 12.7; 18 % women). All patients underwent CPET. Each patient in the PAH group had RHC performed. Fifteen patients from the HFrEF group underwent RHC, which confirmed the suspicion of pulmonary hypertension (HFrEF-SPH).

Results

CPET and laboratory parameters’ analysis showed strong correlations between ventilation/carbon dioxide production (VE/VCO₂) slope and NT-proBNP in HFrEF without secondary PH and HFrEF-SPH groups. In the PAH group, VE/VCO₂ slope correlated with liver and thyroid function but also with morphological parameters of red-cell system.

Analysis of correlations between laboratory and hemodynamic parameters revealed significant correlations between pulmonary arterial pressure, pulmonary vascular resistance (PVR) and red-cell parameters, especially strong with fT4 in the PAH group.

Conclusions

In HFrEF-SPH patients, laboratory parameters strongly correlated with pulmonary pressures and pulmonary capillary wedge pressure (PCWP).

目的：本研究的目的是确定日常使用的器官功能标记物，这些标记物可能有助于全面评估肺动脉高压（PAH）导致的右心室心力衰竭和左心室心力衰竭患者的心血管系统。我们分析了右心导管检查（RHC）参数、心肺运动测试（CPET）参数以及甲状腺、肝脏、肾脏功能和铁平衡的部分实验室参数之间的相关性：回顾性分析纳入 107 名患者（平均年龄为 57.6±16.2；34.6% 为女性），其中包括 57 名 PAH 患者（平均年龄为 54.0±18.2；49.1% 为女性）和 50 名射血分数降低的心力衰竭患者（HFrEF）：CPET 和实验室参数分析表明，在无继发性 PH 的 HFrEF 组和 HFrEF-SPH 组中，通气/二氧化碳产生（VE/VCO2）斜率与 NT-proBNP 之间存在很强的相关性。在 PAH 组中，VE/VCO2 斜率与肝脏和甲状腺功能相关，但也与红细胞系统的形态学参数相关。实验室和血液动力学参数之间的相关性分析表明，肺动脉压、肺血管阻力（PVR）和红细胞参数之间存在显著相关性，尤其是在 PAH 组中与 fT4 的相关性更强：HFrEF-SPH患者的实验室参数与肺动脉压和肺毛细血管楔压（PCWP）密切相关。

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引用次数: 0

The vitamin D analog EB1089 sensitizes triple-negative breast cancer cells to the antiproliferative effects of antiestrogens 维生素 D 类似物 EB1089 可使三阴性乳腺癌细胞对抗雌激素的抗增殖作用敏感。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-09-01 DOI: 10.1016/j.advms.2024.08.004

Adriana Zárate-Pérez , Alitzin Pamela Cruz-Cázares , David Ordaz-Rosado , Janice García-Quiroz , Alfonso León-Del-Rio , Euclides Avila , Edgar Milo-Rocha , Lorenza Díaz , Rocío García-Becerra

Purpose

Patients bearing estrogen receptor (ER)α-negative breast cancer tumors confront poor prognosis and are typically unresponsive to hormone therapy. Previous studies have shown that calcitriol, the active vitamin D metabolite, can induce ERα expression in ERα-negative cells. EB1089, a calcitriol analog with reduced calcemic effects, exhibits greater potency than calcitriol in inhibiting cancer cell growth. However, the impact of EB1089 on ERα expression in triple-negative breast cancer (TNBC) cells remains unexplored. This study aims to investigate whether EB1089 could induce functional ERα expression in TNBC cell lines, potentially enabling the antiproliferative effects of antiestrogens.

Materials and methods

TNBC cell lines HCC1806 and HCC1937 were treated with EB1089, and ERα expression was analyzed using real-time PCR and Western blots. The transcriptional activity of induced ERα was evaluated through a luciferase reporter assay. The antiproliferative effects of tamoxifen and fulvestrant antiestrogens were assessed using the sulforhodamine B assay in the EB1089-treated cells.

Results

Our findings indicated that EB1089 significantly induced ERα mRNA and protein expression in TNBC cells. Moreover, EB1089-induced ERα exhibited transcriptional activity and effectively restored the inhibitory effects of antiestrogens, thereby suppressing cell proliferation in TNBC cells.

Conclusion

EB1089 induced the expression of functional ERα in TNBC cells, restoring the antiproliferative effects of antiestrogens. These results highlight the potential of using EB1089 as a promising strategy for re-establishment of the antiproliferative effect of antiestrogens as a possible management for TNBC. This research lays the foundation for potential advancements in TNBC treatment, offering new avenues for targeted and effective interventions.

目的：雌激素受体（ER）α阴性乳腺癌肿瘤患者预后不良，通常对激素治疗无反应。先前的研究表明，活性维生素 D 代谢物钙三醇可诱导 ERα 阴性细胞中 ERα 的表达。EB1089 是一种降钙三醇类似物，具有较低的血钙效应，在抑制癌细胞生长方面比降钙三醇更有效。然而，EB1089 对三阴性乳腺癌（TNBC）细胞中 ERα 表达的影响仍有待探索。本研究旨在探讨EB1089是否能诱导TNBC细胞系中ERα的功能性表达，从而使抗雌激素的抗增殖作用成为可能：用 EB1089 处理 TNBC 细胞株 HCC1806 和 HCC1937，并使用实时 PCR 和 Western 印迹分析 ERα 的表达。通过荧光素酶报告实验评估了诱导的 ERα 的转录活性。在 EB1089 处理过的细胞中，使用磺基罗丹明 B 检测法评估了他莫昔芬和氟维司群抗雌激素的抗增殖作用：结果：我们的研究结果表明，EB1089能显著诱导TNBC细胞中ERα mRNA和蛋白的表达。此外，EB1089 诱导的 ERα 表现出转录活性，并能有效恢复抗雌激素的抑制作用，从而抑制 TNBC 细胞的增殖：结论：EB1089能诱导TNBC细胞中功能性ERα的表达，从而恢复抗雌激素的抗增殖作用。这些结果凸显了使用 EB1089 作为重建抗雌激素抗增殖效应的一种有前途的策略，作为 TNBC 的一种可能治疗方法的潜力。这项研究为TNBC治疗的潜在进步奠定了基础，为有针对性的有效干预提供了新途径。

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引用次数: 0

Associations between sleep disorders and clinical outcomes of patients with primary biliary cholangitis 原发性胆汁性胆管炎患者睡眠障碍与临床疗效之间的关系。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-09-01 DOI: 10.1016/j.advms.2024.08.002

Shijing Dong , Simin Zhou , Jiangpeng Liu , Nian Chen, Jiwen Li, Zongze Han, Ruiyun Liu, Chenyang Xuan, Weirong Wang, Liping Guo, Lu Zhou

Purpose

Primary biliary cholangitis (PBC) is a chronic autoimmune liver disease characterized by a range of symptoms, including sleep disturbances. The present study aimed to investigate the prevalence of sleep disorders and the associations between sleep disorders and clinical outcomes in PBC.

Patients and methods

We enrolled 177 patients with PBC and 165 healthy controls (age- and sex-matched). Sleep quality was assessed by the Pittsburgh Sleep Quality Index (PSQI). Demographic and clinical data were collected from comprehensive clinical records to investigate whether sleep disorder was correlated with disease severity, therapeutic response and liver cirrhosis.

Results

The prevalence of sleep disorders in patients with PBC (50.8 %) was significantly higher than healthy controls (18.2 %). Patients with sleep disorders presented with higher levels of laboratory parameters including globulin (GLO), aspartate aminotransferase (AST), alkaline phosphatase (ALP), glutamyl transpeptidase (GGT), total bilirubin (TBIL), direct bilirubin (DBIL) and immunoglobulin M (IgM), as well as higher ratio of poor therapeutic response and liver cirrhosis (p < 0.05). There was a positive correlation between global PSQI score and AST, ALP, GGT, TBIL, DBIL and IgM in patients with PBC. Patients with poor therapeutic response and liver cirrhosis in PBC had a higher proportion of sleep disorders and more chaotic sleep patterns, whereas a stronger correlation between sleep quality and laboratory parameters was found in patients with liver cirrhosis.

Conclusions

Sleep disorders were prevalent and manifested as adverse effects in PBC. Assessment of sleep quality and intervention were essential to the overall clinical management of patients with PBC.

目的：原发性胆汁性胆管炎（PBC）是一种慢性自身免疫性肝病，以包括睡眠障碍在内的一系列症状为特征。本研究旨在调查睡眠障碍的患病率以及睡眠障碍与 PBC 临床结果之间的关系：我们招募了 177 名 PBC 患者和 165 名健康对照者（年龄和性别匹配）。睡眠质量通过匹兹堡睡眠质量指数（PSQI）进行评估。从全面的临床记录中收集了人口统计学和临床数据，以研究睡眠障碍是否与疾病严重程度、治疗反应和肝硬化相关：结果：PBC 患者的睡眠障碍发生率（50.8%）明显高于健康对照组（18.2%）。睡眠障碍患者的实验室指标水平较高，包括球蛋白（GLO）、天冬氨酸氨基转移酶（AST）、碱性磷酸酶（ALP）、谷氨酰转肽酶（GGT）、总胆红素（TBIL）、直接胆红素（DBIL）和免疫球蛋白M（IgM），治疗反应差和肝硬化的比例也较高（P < 0.05）。PBC 患者的 PSQI 总分与 AST、ALP、GGT、TBIL、DBIL 和 IgM 呈正相关。治疗反应差和肝硬化的 PBC 患者睡眠障碍的比例更高，睡眠模式更混乱，而肝硬化患者的睡眠质量与实验室指标之间的相关性更强：结论：睡眠障碍在 PBC 患者中普遍存在，并表现为不良反应。睡眠质量评估和干预对于PBC患者的整体临床管理至关重要。

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引用次数: 0

Differentiation of solid and friable tumour thrombus in patients with renal cell carcinoma: The role of MRI apparent diffusion coefficient 肾细胞癌患者实性和易碎肿瘤血栓的鉴别：磁共振成像表观弥散系数的作用。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-09-01 DOI: 10.1016/j.advms.2024.09.002

Paweł Kowal , Krzysztof Ratajczyk , Wiktor Bursiewicz , Maciej Trzciniecki , Karolina Marek-Bukowiec , Joanna Rogala , Vasyl Kowalskyi , Jozef Dragasek , Andrea Botikova , Peter Kruzliak , Yulian Mytsyk

Purpose

Inferior vena cava (IVC) involvement by renal cell carcinoma (RCC) is associated with a higher disease stage and is considered a risk factor for poor prognosis. This study aimed to investigate the role of the apparent diffusion coefficient (ADC) of MRI 3D texture analysis in the differentiation of solid and friable tumour thrombus in patients with RCC.

Materials and methods

The study involved 27 patients with RCC with tumour thrombus in the renal vein or IVC, surgically treated with nephrectomy and thrombectomy and in whom preoperatively abdominal MRI including the DWI sequence was conducted. For 3D texture analysis, the ADC map was used, and the first-order radiomic features were calculated from the whole volume of the thrombus. All tumour thrombi were histologically classified as solid or friable.

Results

The solid and friable thrombus was detected in 51.9 % and 48.1 % of patients, respectively. No differences in mean values of range, 90th percentile, interquartile range, kurtosis, uniformity and variance were found between groups. Equal sensitivity and specificity (93 % and 69 %, respectively) of ADC mean, median and entropy in differentiation between solid and friable tumour thrombus, with the highest AUC for entropy (0.808), were observed. Applying the skewness threshold value of 0.09 allowed us to achieve a sensitivity of 86 % and a specificity of 92 %.

Conclusions

In patients with RCC and tumour thrombus in the renal vein or IVC, the 3D texture analysis based on ADC-map allows for precise differentiation of a solid from a friable thrombus.

目的：肾细胞癌（RCC）累及下腔静脉（IVC）与较高的疾病分期有关，被认为是预后不良的危险因素。本研究旨在探讨磁共振成像三维纹理分析的表观扩散系数（ADC）在区分RCC患者实性和易碎肿瘤血栓中的作用：该研究涉及27名肾静脉或IVC内有肿瘤血栓的RCC患者，他们均接受了肾切除术和血栓切除术，术前进行了腹部磁共振成像（包括DWI序列）。在进行三维纹理分析时，使用了 ADC 图，并根据血栓的整个体积计算了一阶放射学特征。所有肿瘤血栓在组织学上分为实性和易碎两种：结果：51.9%和48.1%的患者分别发现了实性和易碎血栓。各组间的平均值范围、第90百分位数、四分位间范围、峰度、均匀度和方差均无差异。在区分实性和易碎肿瘤血栓方面，ADC 平均值、中位数和熵的敏感性和特异性相同（分别为 93% 和 69%），其中熵的 AUC 最高（0.808）。应用0.09的偏度阈值使我们的灵敏度达到86%，特异度达到92%：结论：对于肾静脉或内静脉中存在肿瘤血栓的RCC患者，基于ADC图的三维纹理分析可精确区分实体和易碎血栓。

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引用次数: 0

Analysis of Spermine Oxidase gene and proinflammatory cytokines expression in gastric cancer patients with and without Helicobacter pylori infection – A pilot study in Polish population 分析幽门螺旋杆菌感染和未感染幽门螺旋杆菌的胃癌患者体内精胺氧化酶基因和促炎细胞因子的表达--一项在波兰人群中开展的试点研究。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-09-01 DOI: 10.1016/j.advms.2024.09.005

Magdalena Dzikowiec , Sandra Galant , Przemysław Lik , Katarzyna Góralska , Dariusz Nejc , Janusz Piekarski , Alicja Majos , Ewa Brzeziańska-Lasota , Dorota Pastuszak-Lewandoska

Purpose

Many types of cancer have infectious origins. Gastric cancer patients can demonstrate high seroprevalence of Helicobacter pylori (H. pylori). The aim of the present study was to assess the expression of SMOX gene in the group of Polish patients with gastric cancer. SMOX is believed to promote H. pylori-induced carcinogenesis via inflammation, DNA damage and activation of β-catenin signaling. We also assessed the mRNA expression of selected pro-inflammatory cytokines, i.e. IL-2, IFN-γ, TNF-α, and antimicrobial peptide, cathelicidin.

Materials/methods

The study material consisted of gastric tissue samples collected during total gastrectomy from three different places in stomach: from primary tumor, 3 cm away from the primary lesion, and from the wall opposite to the primary tumor. After RNA isolation, qPCR reactions were performed for the relevant genes.

Results

The obtained results confirmed an increased level of SMOX expression in gastric cancer patients with the history of H. pylori infection. And, as far as we know, this is the first study on SMOX gene expression conducted on tissue taken from a patient, not on a cell line. The levels of pro-inflammatory cytokines, i.e. IL-2, IFN-γ, TNF-α, were also increased, thus indicating their contribution to the specific inflammatory microenvironment of the tumor. Interestingly, the levels of CAMP, encoding antimicrobial peptide, were reduced in all tissue types.

Conclusions

The findings confirm that SMOX plays a role in gastric carcinogenesis. However, further research is needed on the role of inflammatory and other factors involved in this process to identify targets for cancer immunotherapy.

目的：许多类型的癌症都有传染源。胃癌患者的幽门螺旋杆菌（H. pylori）血清阳性率很高。本研究旨在评估波兰胃癌患者中 SMOX 基因的表达情况。SMOX被认为可通过炎症、DNA损伤和β-catenin信号激活促进幽门螺杆菌诱导的癌变。我们还评估了部分促炎细胞因子（即 IL-2、IFN-γ、TNF-α 和抗菌肽 cathelicidin）的 mRNA 表达：研究材料包括全胃切除术时从胃部三个不同位置采集的胃组织样本：原发肿瘤、距离原发病灶 3 厘米处和原发肿瘤对面的胃壁。分离 RNA 后，对相关基因进行 qPCR 反应：结果：研究结果证实，在有幽门螺杆菌感染史的胃癌患者中，SMOX 的表达水平升高。据我们所知，这是首次在患者组织而非细胞系上进行的 SMOX 基因表达研究。促炎细胞因子（即 IL-2、IFN-γ、TNF-α）的水平也有所上升，这表明它们对肿瘤的特定炎症微环境起了作用。有趣的是，编码抗菌肽的 CAMP 水平在所有组织类型中都有所降低：结论：研究结果证实了 SMOX 在胃癌发生中的作用。结论：研究结果证实了 SMOX 在胃癌发生过程中的作用，但还需要进一步研究参与这一过程的炎症和其他因素的作用，以确定癌症免疫疗法的靶点。

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引用次数: 0

Evolution of splenomegaly in liver cirrhosis: Simulation using an electronic circuit 肝硬化脾肿大的演变：利用电子电路进行模拟。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-08-06 DOI: 10.1016/j.advms.2024.08.001

Jae Cheol Jung, Shin-Young Park, Kyeong Deok Kim, Woo Young Shin, Keon-Young Lee

Purpose

The evolution of splenomegaly in patients with liver cirrhosis remains largely unknown. In this study, we followed the changes in splenic volume and established the natural course of splenomegaly. We developed an electronic circuit that simulated splenoportal circulation and identified the underlying hemodynamic mechanisms.

Materials and methods

This retrospective observational study included 93 patients with cirrhosis. Splenic volumes were measured in imaging studies at 6-month intervals and normalized by the ratio of each patient's maximum volume during follow-up (%Vmax). An electronic simulation model was constructed using software and realized on a breadboard.

Results

Overall, the %Vmax increased from 0.77 ± 0.21 to a maximum of 1.00 ± 0.00 (p < 0.001) during a median follow-up of 23 (3–162) months and then decreased to 0.84 ± 0.18 (p < 0.001) during the next 9 (3–132) months. No interventional radiology procedure was performed to improve hepatic fibrosis and portal hypertension. The evolution of %Vmax showed single-peaked symmetry. An electronic simulation model showed that the upslope of the evolution curve was dependent on the increased intrahepatic vascular resistance and portal hypertension, whereas the downslope was dependent on the decreased portosystemic shunt (PSS) resistance.

Conclusions

Splenomegaly in cirrhotic patients aggravated over a period of 23 months and then regressed spontaneously to its initial volume. Electronic simulation of splenoportal circulation showed that splenic enlargement was due to the advancement of liver cirrhosis and portal hypertension, whereas its regression was due to the development of a PSS.

目的：肝硬化患者脾脏肿大的演变过程在很大程度上仍不为人所知。在这项研究中，我们跟踪了脾脏体积的变化，并确定了脾脏肿大的自然病程。我们开发了模拟脾门循环的电子电路，并确定了潜在的血液动力学机制：这项回顾性观察研究包括 93 名肝硬化患者。每隔 6 个月通过影像学检查测量脾脏体积，并以随访期间每位患者最大体积的比率（%Vmax）进行归一化。使用软件构建了一个电子模拟模型，并在面包板上实现了该模型：总体而言，在 23（3 - 162）个月的中位随访期间，最大容积百分比从 0.77 ± 0.21 增加到最大值 1.00 ± 0.00（p < 0.001），然后在接下来的 9（3 - 132）个月期间降至 0.84 ± 0.18（p < 0.001）。没有进行介入放射学手术来改善肝纤维化和门静脉高压。Vmax%的变化呈现单峰对称性。电子模拟模型显示，演变曲线的上坡取决于肝内血管阻力和门静脉高压的增加，而下坡则取决于门静脉分流（PSS）阻力的降低：结论：肝硬化患者的脾肿大在 23 个月内不断加重，然后自然消退至初始体积。对脾门静脉循环的电子模拟显示，脾脏肿大是由于肝硬化和门静脉高压的发展所致，而脾脏肿大的消退则是由于 PSS 的发展所致。

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引用次数: 0