Advances in medical sciences最新文献_第9页

Fasting alleviates bleomycin-induced lung inflammation and fibrosis via decreased Tregs and monocytes 禁食可通过减少Tregs和单核细胞缓解博莱霉素诱导的肺部炎症和纤维化。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-07-08 DOI: 10.1016/j.advms.2024.07.004

Yuyang Zhao , Jingying Yang , Qi Zhang , Xiangming Chen , Wenting Liang , Yanling Zheng , Jijun Huang , Yue Liao , Cheng Fu , Ting Huang , Xiaomin Li , Yu Zheng , Jin Bu , Erxia Shen

Purpose

Idiopathic pulmonary fibrosis (IPF), a chronic and progressively worsening condition characterized by interstitial lung inflammation and fibrosis of unknown etiology, has a grim prognosis. The treatment options for IPF are limited and new therapeutic strategies are urgently needed. Dietary restriction can improve various inflammatory diseases, but its therapeutic effect on bleomycin (BLM)-induced pulmonary fibrosis mouse model remains unclear. This study aims to investigate whether intermittent fasting (IF) can alleviate BLM-induced pulmonary inflammation and fibrosis.

Methods

Pulmonary fibrosis mouse models were induced by BLM. The IF group underwent 24-h fasting cycles for one week prior and three weeks following BLM administration. Meanwhile, the ad libitum feeding group had unrestricted access to food throughout the experiment. The evaluation focused on lung pathology via histological staining, qPCR analysis of collagen markers, and immune cell profiling through flow cytometry.

Results

IF group significantly reduced inflammation and fibrosis in lung tissues of BLM-induced mice compared to ad libitum feeding group. qPCR results showed IF remarkably decreased the mRNA expression of Col 1a and Col 3a in the lungs of BLM-induced mouse models. IF also reduced the numbers of regulatory T cells (Tregs), T helper 17 (Th17) cells, monocytes, and monocyte-derived alveolar macrophages (MoAMs) in the lung tissues.

Conclusions

IF may improve BLM-induced pulmonary fibrosis by decreasing numbers of immune cells including Treg cells, Th17 cells, monocytes, and MoAMs in the lungs. This study offers experimental validation for dietary intervention as a viable treatment modality in IPF management.

目的：特发性肺纤维化（IPF）是一种病因不明的以肺间质炎症和纤维化为特征的慢性、进行性恶化的疾病，预后很差。IPF 的治疗方案有限，迫切需要新的治疗策略。饮食限制可改善多种炎症性疾病，但其对博莱霉素（BLM）诱导的肺纤维化小鼠模型的治疗效果仍不明确。本研究旨在探讨间歇性禁食（IF）能否减轻博莱霉素诱导的肺部炎症和纤维化：方法：用BLM诱导肺纤维化小鼠模型。方法：用BLM诱导肺纤维化小鼠模型。同时，自由进食组在整个实验过程中不受限制地进食。评估主要通过组织学染色、胶原蛋白标记物的 qPCR 分析和流式细胞术的免疫细胞谱分析来进行：qPCR结果显示，IF明显降低了BLM诱导小鼠肺部Col 1a和Col 3a的mRNA表达。IF 还降低了肺组织中调节性 T 细胞（Tregs）、T 辅助细胞 17（Th17）、单核细胞和单核细胞衍生肺泡巨噬细胞（MoAMs）的数量：IF可通过减少肺部Treg细胞、Th17细胞、单核细胞和MoAMs等免疫细胞的数量来改善BLM诱导的肺纤维化。这项研究为饮食干预作为治疗 IPF 的一种可行方法提供了实验验证。

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引用次数: 0

Characteristics of the radial peripapillary capillary network in patients with COVID-19 based on optical coherence tomography angiography: A literature review 基于光学相干断层血管造影的 COVID-19 患者桡侧毛细血管周围网络的特征：文献综述。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-07-06 DOI: 10.1016/j.advms.2024.07.001

Purpose

This review aimed to evaluate the significance of assessing radial peripheral capillary (RPC) network parameters by optical coherence tomography angiography (OCTA) in patients with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection confirmed by polymerase chain reaction.

Methods

A literature search was conducted in the PubMed database to select high-quality reviews and original articles on the use of OCTA for visualizing the RPC network and calculating RPC parameters.

Results

The study revealed that systemic hypoxia, hypercoagulable state, and inflammation affect the RPC network in patients with coronavirus disease 2019 (COVID-19). Reduced RPC parameters were observed early in the course of SARS-CoV-2 infection and after several months of follow-up. Additionally, there was a correlation between reduced RPC parameters and subsequent thinning of the retinal nerve fiber layer.

Conclusions

The OCTA examination of the retina and optic disc should be considered in patients with a history of COVID-19 to assess the impact of systemic hypoxia and inflammation on ocular function. Follow-up assessment of these patients is also necessary to understand the potential consequences of ischemia affecting the optic nerve, retina, and choroid.

目的：本综述旨在评估在聚合酶链反应证实感染严重急性呼吸系统综合征冠状病毒-2（SARS-CoV-2）的患者中通过光学相干断层血管成像（OCTA）评估径向外周毛细血管（RPC）网络参数的意义：方法：在PubMed数据库中进行文献检索，选择有关使用OCTA观察RPC网络和计算RPC参数的高质量综述和原创文章：研究发现，全身缺氧、高凝状态和炎症会影响2019年冠状病毒病（COVID-19）患者的RPC网络。在SARS-CoV-2感染初期和数月随访后，观察到RPC参数降低。此外，RPC参数降低与随后视网膜神经纤维层变薄之间存在相关性：结论：对于有 COVID-19 病史的患者，应考虑对视网膜和视盘进行 OCTA 检查，以评估全身缺氧和炎症对眼部功能的影响。还需要对这些患者进行随访评估，以了解缺血对视神经、视网膜和脉络膜的潜在影响。

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引用次数: 0

Bioconcentration of polycyclic aromatic hydrocarbons in the adipose tissue of women with pelvic endometriosis and idiopathic infertility: A case-control study 盆腔子宫内膜异位症和特发性不孕妇女脂肪组织中多环芳烃的生物浓缩：一项病例对照研究。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-07-06 DOI: 10.1016/j.advms.2024.07.002

Iwona Gawron , Malgorzata Wegiel , Ryszard Chrzaszcz , Robert Jach , Anna Maslanka

Purpose

Polycyclic aromatic hydrocarbons (PAHs), present in air and food, generated during energy production and waste incineration, are known for health toxicity. PAHs may activate the aryl hydrocarbon receptor, which could in turn modify estrogen-dependent inflammatory pathways in endometriosis. The possible role of PAHs in the pathogenesis of endometriosis remains unclear. The study aimed to evaluate the potential link between exposure to PAHs and the occurrence of peritoneal and ovarian endometriosis.

Methods

A prospective case-control tertiary-center study included 46 women aged 22–45 undergoing laparoscopy due to pelvic endometriosis (n = 32; arm 1) and idiopathic infertility (n = 14; arm 2). A sample of the greater omentum was collected intraoperatively for detection of 16 standard PAHs by gas chromatography-isotope dilution mass spectrometry method. PAHs concentrations were compared in both study arms. The associations between PAHs concentrations and selected variables were investigated.

Results

There were no significant differences between both arms in terms of reference PAHs concentrations, nor correlations between PAHs concentrations and the stage of endometriosis. However, notable differences were observed in specific PAHs concentrations related to certain conditions. The concentrations of acenaphthene (p = 0.016) and fluorene (p = 0.013) were significantly lower in women with peritoneal adhesions, while the concentrations of benz[a]anthracene, benzo[k]fluoranthene and indeno[1,2,3-cd]pyrene [ng/g] were higher in cigarette smokers.

Conclusions

The study showed no differences in exposure to PAHs between women with and without pelvic endometriosis. Determining the toxicity of PAHs in endometriosis requires further research.

目的：多环芳烃（PAHs）存在于空气和食物中，在能源生产和废物焚烧过程中产生，具有已知的健康毒性。多环芳烃可能会激活芳基烃受体，进而改变子宫内膜异位症中依赖雌激素的炎症途径。多环芳烃在子宫内膜异位症发病机制中可能扮演的角色尚不清楚。本研究旨在评估多环芳烃暴露与腹膜和卵巢子宫内膜异位症发生之间的潜在联系：一项前瞻性病例对照三级中心研究纳入了46名因盆腔子宫内膜异位症（32人；第一组）和特发性不孕症（14人；第二组）而接受腹腔镜检查的22-45岁女性。术中采集大网膜样本，采用气相色谱-同位素稀释质谱法检测 16 种标准多环芳烃。对两个研究组的多环芳烃浓度进行了比较。对 PAHs 浓度与选定变量之间的关系进行了研究：结果：就参考 PAHs 浓度而言，两组之间没有明显差异，PAHs 浓度与子宫内膜异位症阶段之间也没有相关性。然而，在与某些病症相关的特定 PAHs 浓度方面却发现了明显的差异。患有腹腔粘连的妇女体内苊（p=0.016）和芴（p=0.013）的浓度明显较低，而吸烟妇女体内苯并[a]蒽、苯并[k]荧蒽和茚并[1,2,3-cd]芘[纳克/克]的浓度较高：研究表明，患有和未患有盆腔子宫内膜异位症的妇女在多环芳烃暴露方面没有差异。确定多环芳烃在子宫内膜异位症中的毒性还需要进一步研究。

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引用次数: 0

Periodontal disease in patients with thyroid diseases: A systematic review with meta-analysis 甲状腺疾病患者的牙周病：系统回顾与荟萃分析。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-06-20 DOI: 10.1016/j.advms.2024.06.003

Martyna Ortarzewska , Kacper Nijakowski , Jakub Jankowski , Nadia Sawicka-Gutaj , Marek Ruchała , Anna Surdacka

Purpose

The imbalance of thyroid hormones affects the metabolic activity of various tissues, including periodontium. Also, autoimmune diseases present an increased tendency to suffer from periodontal disease. Therefore, our systematic review was designed to answer the question "Is there a relationship between thyroid diseases and periodontal disease?".

Materials and methods

Following the inclusion and exclusion criteria, 10 studies were included in this systematic review using the databases PubMed, Scopus and Web of Science (according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement guidelines).

Results

Based on the meta-analysis, patients with thyroid diseases (especially with hypothyroidism) demonstrated significantly worse periodontal status than systemically healthy controls. Moreover, according to the cross-sectional studies, 5.74 % of periodontitis patients reported the concomitance of thyroid diseases.

Conclusions

In summary, the included studies suggest a potential relationship between thyroid diseases and periodontal disease. However, further research is necessary to reliably assess the oral health in patients with hypothyroidism and hyperthyroidism.

目的：甲状腺激素失衡会影响包括牙周在内的各种组织的新陈代谢活动。此外，自身免疫性疾病也会增加患牙周病的几率。因此，我们的系统综述旨在回答 "甲状腺疾病与牙周病之间是否存在关系？按照纳入和排除标准，使用 PubMed、Scopus 和 Web of Science 数据库（根据系统综述和荟萃分析首选报告项目声明指南）将 10 项研究纳入本系统综述：根据荟萃分析，甲状腺疾病（尤其是甲状腺功能减退症）患者的牙周状况明显差于全身健康的对照组。此外，根据横断面研究，5.74%的牙周炎患者报告患有甲状腺疾病：总之，纳入的研究表明甲状腺疾病与牙周病之间存在潜在的关系。然而，要可靠地评估甲状腺功能减退症和甲状腺功能亢进症患者的口腔健康状况，还需要进一步的研究。

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引用次数: 0

Lack of Nr2e1 expression in hepatocytes impaired cell survival and aggravated palmitate-induced oxidative stress 肝细胞中缺乏 Nr2e1 的表达会损害细胞存活并加剧棕榈酸酯诱导的氧化应激。

IF 2.5 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-06-18 DOI: 10.1016/j.advms.2024.06.002

Purpose

Nuclear receptor subfamily 2 group E member 1 (Nr2e1) has been regarded as an essential regulator in neural stem cells. However, its function is still not clear in hepatocytes. This study aimed to clarify the effects of Nr2e1-deficiency in hepatocytes in lipotoxic conditions.

Materials/methods

Nr2e1-knockdown AML12 cells were generated by lentiviral vector transfection. The influences of Nr2e1-deficiency on hepatocyte survival were determined by cell cycle progression and cell apoptosis rate using flow cytometry. Real-time quantitative PCR and Western blot were used to examine the genes and protein expression related to apoptosis, lipid metabolism, and oxidative stress. Meanwhile, RNA sequencing was adopted in liver samples from Nr2e1-knockout (Nr2e1-KO) mice.

Results

Nr2e1 expression was observed with a significant decrease in AML12 cells after palmitic acid-stimulation. Knockdown of Nr2e1 in AML12 cells resulted in increased sensitivity to lipotoxicity, evidenced by a partial G0/G1 cell-cycle arrest and higher rates of cell apoptosis. Moreover, Nr2e1-knockdown AML12 cells presented increased gene expressions relative to lipid synthesis but decreased levels of β-oxidation related genes. Lack of Nr2e1 augmented palmitate-induced oxidative stress in hepatocytes. In vivo, differential genes in Nr2e1-KO mice liver were enriched in pathways associated with liver regeneration and cell proliferation.

Conclusions

This study indicated that hepatocytes lacking Nr2e1 were more susceptible to lipotoxic-mediated damage. Nr2e1 may serve as a potential target for the development of novel therapies for lipotoxicity-induced liver injury.

目的：核受体亚家族 2 E 组成员 1（Nr2e1）一直被认为是神经干细胞的重要调节因子。然而，它在肝细胞中的功能仍不明确。本研究旨在阐明脂肪毒性条件下Nr2e1缺失对肝细胞的影响：材料/方法：通过慢病毒载体转染产生Nr2e1敲除的AML12细胞。使用流式细胞术通过细胞周期进展和细胞凋亡率测定 Nr2e1 缺失对肝细胞存活的影响。利用实时定量 PCR 和 Western 印迹检测与细胞凋亡、脂代谢和氧化应激相关的基因和蛋白表达。同时，对 Nr2e1 基因敲除（Nr2e1-KO）小鼠的肝脏样本进行了 RNA 测序：结果：在棕榈酸刺激下，AML12细胞中的Nr2e1表达量明显下降。在 AML12 细胞中敲除 Nr2e1 会增加细胞对脂肪毒性的敏感性，表现为部分 G0/G1 细胞周期停滞和更高的细胞凋亡率。此外，Nr2e1敲除的AML12细胞中与脂质合成有关的基因表达量增加，但β氧化相关基因的表达量减少。缺乏 Nr2e1 会增加棕榈酸酯诱导的肝细胞氧化应激。在体内，Nr2e1-KO 小鼠肝脏中与肝脏再生和细胞增殖相关的通路中富含不同的基因：本研究表明，缺乏 Nr2e1 的肝细胞更容易受到脂肪毒性介导的损伤。Nr2e1可能是开发脂肪毒性诱导的肝损伤新型疗法的潜在靶点。

{"title":"Lack of Nr2e1 expression in hepatocytes impaired cell survival and aggravated palmitate-induced oxidative stress","authors":"","doi":"10.1016/j.advms.2024.06.002","DOIUrl":"10.1016/j.advms.2024.06.002","url":null,"abstract":"<div><h3>Purpose</h3><p>Nuclear receptor subfamily 2 group E member 1 (<em>Nr2e1</em>) has been regarded as an essential regulator in neural stem cells. However, its function is still not clear in hepatocytes. This study aimed to clarify the effects of <em>Nr2e1</em>-deficiency in hepatocytes in lipotoxic conditions.</p></div><div><h3>Materials/methods</h3><p><em>Nr2e1</em>-knockdown AML12 cells were generated by lentiviral vector transfection. The influences of <em>Nr2e1</em>-deficiency on hepatocyte survival were determined by cell cycle progression and cell apoptosis rate using flow cytometry. Real-time quantitative PCR and Western blot were used to examine the genes and protein expression related to apoptosis, lipid metabolism, and oxidative stress. Meanwhile, RNA sequencing was adopted in liver samples from <em>Nr2e1</em>-knockout (<em>Nr2e1</em>-KO) mice.</p></div><div><h3>Results</h3><p><em>Nr2e1</em> expression was observed with a significant decrease in AML12 cells after palmitic acid-stimulation. Knockdown of <em>Nr2e1</em> in AML12 cells resulted in increased sensitivity to lipotoxicity, evidenced by a partial G0/G1 cell-cycle arrest and higher rates of cell apoptosis. Moreover, <em>Nr2e1</em>-knockdown AML12 cells presented increased gene expressions relative to lipid synthesis but decreased levels of β-oxidation related genes. Lack of <em>Nr2e1</em> augmented palmitate-induced oxidative stress in hepatocytes. <em>In vivo</em>, differential genes in <em>Nr2e1</em>-KO mice liver were enriched in pathways associated with liver regeneration and cell proliferation.</p></div><div><h3>Conclusions</h3><p>This study indicated that hepatocytes lacking <em>Nr2e1</em> were more susceptible to lipotoxic-mediated damage. <em>Nr2e1</em> may serve as a potential target for the development of novel therapies for lipotoxicity-induced liver injury.</p></div>","PeriodicalId":7347,"journal":{"name":"Advances in medical sciences","volume":"69 2","pages":"Pages 320-330"},"PeriodicalIF":2.5,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141431128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of static magnetic field on gene expression of human umbilical cord mesenchymal stem cells by transcriptome analysis 通过转录组分析静态磁场对人脐带间充质干细胞基因表达的影响。

IF 2.7 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-06-04 DOI: 10.1016/j.advms.2024.06.001

Fang Fang , Chunyan Liu , Qi Huang , Chao Dong , Guirong Zhang , Jinhe Jiang , Shi Lu

Purpose

Static magnetic fields (SMFs) induce various biological reactions and have been applied in the biological therapy of diseases, especially in combination with mesenchymal stem cells (MSCs) and tissue engineering. However, the underlying influence of SMFs on MSCs gene expression remains largely unclear. In this study, we aim to investigate the effects of SMFs on gene expression of human MSCs.

Materials and methods

We exposed human MSCs to two different intensities (0.35 T and 1.0 T) of SMFs and observed the effects of SMFs on cell morphology. Subsequently, RNA-sequencing was performed to explore the gene expression changes.

Results

Compared with control group cells, no significant differences in cell morphology were observed under a phase contrast inverted microscope, but the transcriptome of SMF-exposed MSCs were significantly changed in both 0.35 T and 1.0 T groups and the differential expressed genes are involved in multiple pathways, such as ubiquitin mediated proteolysis, TNF signaling pathway, NF-kappa B signaling pathway, TGF-beta signaling pathway, metabolic pathways, and apoptosis, which regulate the biological functions of MSCs.

Conclusions

SMFs stimulation could affect the gene expression of human MSCs and the biological effects vary by the different intensities of SMFs. These data offer the molecular foundation for future application of SMFs in stem cell technology as well as tissue engineering medicine.

目的：静态磁场（SMF）可诱导各种生物反应，已被应用于疾病的生物治疗，尤其是与间充质干细胞（MSCs）和组织工程相结合。然而，SMF 对间充质干细胞基因表达的潜在影响在很大程度上仍不清楚。在本研究中，我们旨在研究 SMFs 对人间质干细胞基因表达的影响：我们将人间叶干细胞暴露于两种不同强度（0.35 特斯拉和 1.0 特斯拉）的 SMFs，观察 SMFs 对细胞形态的影响。随后，进行 RNA 测序以探讨基因表达的变化：与对照组细胞相比，在相差倒置显微镜下未观察到细胞形态的显著差异，但在 0.35 特斯拉和 1.0 特斯拉组中，差异表达的基因涉及多种途径，如泛素介导的蛋白酶解、TNF 信号通路、NF-kappa B 信号通路、TGF-beta 信号通路、代谢途径和细胞凋亡，这些途径调控间充质干细胞的生物学功能：结论：SMFs刺激可影响人间叶干细胞的基因表达，且不同强度的SMFs可产生不同的生物效应。这些数据为 SMFs 未来在干细胞技术和组织工程医学中的应用提供了分子基础。

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引用次数: 0

Dexmedetomidine improves mitophagy and pyroptosis through the ALKBH5/FUNDC1 axis during epidural-related maternal fever 右美托咪定可通过 ALKBH5/FUNDC1 轴改善硬膜外麻醉相关产妇发热时的有丝分裂和嗜热症。

IF 2.7 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-05-28 DOI: 10.1016/j.advms.2024.05.002

Fei Xiao , Hanqing Yao , Jing Qian , Jiayue Huang , Guangfa Xia

Purpose

Epidural analgesia has emerged as a commonly used method for relieving labor pain. However, epidural-related maternal fever (ERMF) is characterized by a high occurrence rate and can have detrimental consequences for the well-being of both the mother and the fetus. This study aimed to investigate the functional role and underlying mechanism of dexmedetomidine (DEX) in ERMF.

Materials and methods

Ropivacaine (ROP)-induced human umbilical vein endothelial cells (HUVECs) were treated with DEX and/or transfected with ALKBH5 or FUNDC1 overexpression plasmid. qPCR and Western blot were adopted for mitophagy and pyroptosis marker protein detection. Autophagosomes were observed through electron microscopy, Caspase-1/PI double-positive cells were determined using flow cytometry. Inflammation-related factors were quantified using ELISA. The N⁶-methyladenosine (m⁶A) modification of FUNDC1 mRNA was examined using methylated RNA immunoprecipitation (MeRIP) and the binding between ALKBH5 and FUNDC1 mRNA was confirmed by RNA immunoprecipitation (RIP).

Results

In ROP-induced HUVECs, there was a significant upregulation in ALKBH5 and FUNDC1, resulting in a notable increase in inflammation, pyroptosis, and mitophagy. The administration of DEX demonstrated the ability to alleviate ROP-induced pyroptosis and promote protective mitophagy. Interestingly, DEX treatment significantly reduced the interaction between ALKBH5 and FUNDC1 mRNA, while simultaneously increasing the m⁶A level of FUNDC1 mRNA in ROP-treated cells. Moreover, the overexpression of FUNDC1 partially reversed the effects of ALKBH5 overexpression on mitophagy and pyroptosis in HUVECs.

Conclusions

DEX can promote mitophagy and inhibit pyroptosis through the ALKBH5/FUNDC1 axis in ERMF, indicating its potential as a therapeutic strategy for clinical ERMF treatment.

目的：硬膜外镇痛已成为缓解分娩疼痛的常用方法。然而，硬膜外相关产妇发热（ERMF）的发生率很高，可能对产妇和胎儿的健康造成不利影响。本研究旨在探讨右美托咪定（DEX）在ERMF中的功能作用和潜在机制：采用qPCR和Western blot技术检测有丝分裂和裂解标志蛋白。电子显微镜观察自噬体，流式细胞仪测定 Caspase-1/PI 双阳性细胞。用酶联免疫吸附法对炎症相关因子进行量化。用甲基化 RNA 免疫沉淀（MeRIP）检测了 FUNDC1 mRNA 的 N6-甲基腺苷（m6A）修饰，用 RNA 免疫沉淀（RIP）证实了 ALKBH5 与 FUNDC1 mRNA 的结合：结果：在ROP诱导的HUVECs中，ALKBH5和FUNDC1明显上调，导致炎症、热噬和有丝分裂显著增加。服用DEX能缓解ROP诱导的热蛋白沉积，促进保护性有丝分裂。有趣的是，在ROP处理的细胞中，DEX处理明显减少了ALKBH5和FUNDC1 mRNA之间的相互作用，同时提高了FUNDC1 mRNA的m6A水平。此外，FUNDC1的过表达部分逆转了ALKBH5过表达对HUVECs中有丝分裂和嗜热的影响：结论：DEX可通过ALKBH5/FUNDC1轴促进ERMF的有丝分裂和抑制脓毒症，有望成为临床治疗ERMF的一种治疗策略。

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引用次数: 0

Cefiderocol – An effective antimicrobial for MDR infections but a challenge for routine antimicrobial susceptibility testing 头孢羟氨苄--治疗耐药菌感染的有效抗菌药，但对常规抗菌药敏感性检测是一项挑战。

IF 2.7 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-05-21 DOI: 10.1016/j.advms.2024.05.001

Małgorzata Brauncajs , Filip Bielec , Anna Macieja , Dorota Pastuszak-Lewandoska

Purpose

Cefiderocol is a novel cephalosporin–siderophore conjugate antibiotic that holds promise to thwart infections caused by multi-drug-resistant gram-negative bacilli. Its antibacterial activity against normally susceptible species is not affected by most β-lactamases, including metallo-β-lactamases. Due to the siderophore-mediated entry into the cell, the activity of cefiderocol is less affected by porin loss or active efflux resistance than many other β-lactam antibiotics. The aim of this study was to assess in vitro susceptibility to the cefiderocol of carbapenemase-producing gram-negative bacilli from clinical samples of hospitalized patients.

Materials and methods

We analyzed 102 clinical strains of carbapenemase-producing Enterobacterales and non-fermentives from hospital centers in Łódź, Poland. Antimicrobial susceptibility to cefiderocol was tested by the minimum inhibitory concentration test strips and disc diffusion methods.

Results

The obtained results turned out to be ambiguous, and the area of technical uncertainty made their interpretation very difficult.

Conclusions

The cost of therapy with this antibiotic, and difficulties in interpreting the drug susceptibility are the limitations to the use of cefiderocol. Intensive work should be carried out to finally standardize an easily accessible and reliable method for the determination of susceptibility to cefiderocol.

目的：Cefiderocol 是一种新型头孢菌素-嗜苷酸盐共轭抗生素，有望挫败由多重耐药革兰氏阴性杆菌引起的感染。它对正常易感菌种的抗菌活性不受大多数β-内酰胺酶（包括金属β-内酰胺酶）的影响。与许多其他 β-内酰胺类抗生素相比，头孢羟氨苄通过苷元介导进入细胞，其活性较少受到孔蛋白缺失或主动外流抗性的影响。本研究的目的是评估住院患者临床样本中产碳青霉烯酶革兰阴性杆菌对头孢羟氨苄的体外敏感性：我们分析了波兰罗兹各医院中心的 102 株产碳青霉烯酶肠杆菌和非发酵菌临床菌株。采用最小抑菌浓度试纸法和盘扩散法检测了对头孢菌素的抗菌敏感性：结果：得到的结果并不明确，技术上的不确定性使解释这些结果非常困难：结论：使用这种抗生素治疗的成本和药物敏感性的解释困难是头孢克肟使用的局限性。应开展深入细致的工作，以最终统一一种易于使用且可靠的方法，用于测定对头孢克洛的药敏性。

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引用次数: 0

The intriguing role of IL33/ST2 axis signaling in oral diseases - A systematic review IL33/ST2 轴信号在口腔疾病中的奇妙作用--系统综述。

IF 2.7 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-05-03 DOI: 10.1016/j.advms.2024.04.007

Mala Kamboj , R. Keerthika , Anjali Narwal , Ambika Gupta , Anju Devi , Adarsh Kumar , Gitika Sharma

Purpose

Oral diseases act as a silent epidemic, and the pathogenetic role of interleukin-33/suppression of tumorigenicity-2 axis (IL-33/ST2) remains unclear due to a lack of literature. This review has attempted to highlight the importance of this axis in oral diseases, which may be helpful in developing therapeutic modalities required to halt disease progression.

Materials and methods

A thorough search was conducted using various databases. Original research articles that assessed both IL-33 and ST2 levels in oral diseases using different techniques were included in the review. The risk of bias for each study was analyzed using the Quality Assessment of Diagnostic Accuracy Studies 2 (QUADAS-2) tool and Review Manager 5.4 was used to output the results.

Results

In the qualitative data synthesis we included 13 published articles. The most commonly used method was serum estimation, while methods with optimistic results were saliva, real-time quantitative polymerase chain reaction and immunohistochemistry. The predominant mechanism of action was nuclear factor kappa B signaling and type 2 immune response. However, salivary gland epithelial cell activation, activation of mast cells, type 1 immune response, and upregulated angiogenesis are crucial in mediating IL-33/ST2 signaling in oral diseases.

Conclusions

Accumulating evidence demonstrates that the IL-33/ST2 axis is a fundamental pathogenetic mechanism of oral diseases of inflammatory, autoimmune, or neoplastic origin.

目的：口腔疾病是一种无声的流行病，由于缺乏文献，白细胞介素-33/抑制肿瘤生成-2轴（IL-33/ST2）的致病作用仍不清楚。本综述试图强调该轴在口腔疾病中的重要性，这可能有助于开发阻止疾病进展所需的治疗方法：使用各种数据库进行了全面搜索。综述包括使用不同技术评估口腔疾病中 IL-33 和 ST2 水平的原创研究文章。使用诊断准确性研究质量评估2（QUADAS-2）工具分析了每项研究的偏倚风险，并使用Review Manager 5.4输出结果：在定性数据综合中，我们纳入了 13 篇已发表的文章。最常用的方法是血清估计，而结果乐观的方法是唾液、实时定量聚合酶链反应和免疫组化。最主要的作用机制是核因子卡巴 B 信号转导和 2 型免疫反应。然而，唾液腺上皮细胞活化、肥大细胞活化、1型免疫反应和血管生成上调是介导口腔疾病中IL-33/ST2信号转导的关键：越来越多的证据表明，IL-33/ST2 轴是炎症性、自身免疫性或肿瘤性口腔疾病的基本致病机制。

{"title":"The intriguing role of IL33/ST2 axis signaling in oral diseases - A systematic review","authors":"Mala Kamboj , R. Keerthika , Anjali Narwal , Ambika Gupta , Anju Devi , Adarsh Kumar , Gitika Sharma","doi":"10.1016/j.advms.2024.04.007","DOIUrl":"10.1016/j.advms.2024.04.007","url":null,"abstract":"<div><h3>Purpose</h3><p>Oral diseases act as a silent epidemic, and the pathogenetic role of interleukin-33/suppression of tumorigenicity-2 axis (IL-33/ST2) remains unclear due to a lack of literature. This review has attempted to highlight the importance of this axis in oral diseases, which may be helpful in developing therapeutic modalities required to halt disease progression.</p></div><div><h3>Materials and methods</h3><p>A thorough search was conducted using various databases. Original research articles that assessed both IL-33 and ST2 levels in oral diseases using different techniques were included in the review. The risk of bias for each study was analyzed using the Quality Assessment of Diagnostic Accuracy Studies 2 (QUADAS-2) tool and Review Manager 5.4 was used to output the results.</p></div><div><h3>Results</h3><p>In the qualitative data synthesis we included 13 published articles. The most commonly used method was serum estimation, while methods with optimistic results were saliva, real-time quantitative polymerase chain reaction and immunohistochemistry. The predominant mechanism of action was nuclear factor kappa B signaling and type 2 immune response. However, salivary gland epithelial cell activation, activation of mast cells, type 1 immune response, and upregulated angiogenesis are crucial in mediating IL-33/ST2 signaling in oral diseases.</p></div><div><h3>Conclusions</h3><p>Accumulating evidence demonstrates that the IL-33/ST2 axis is a fundamental pathogenetic mechanism of oral diseases of inflammatory, autoimmune, or neoplastic origin.</p></div>","PeriodicalId":7347,"journal":{"name":"Advances in medical sciences","volume":"69 2","pages":"Pages 264-271"},"PeriodicalIF":2.7,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140847042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The oxidative stress-associated long non-coding RNAs in pancreatic cancer 胰腺癌中与氧化应激相关的长非编码 RNA

IF 2.7 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences

Pub Date : 2024-04-25 DOI: 10.1016/j.advms.2024.04.006

Setayesh Baradaran-Bagherian , Mahdieh Mehrab Mohseni , Roya Sharifi , Roya Amirinejad , Zeinab Shirvani-Farsani

Purpose

A lot of people are dying from pancreatic cancer (PC) annually. The early detection of this cancer is particularly challenging due to the fact that symptoms tend to appear in advanced stages. It has been suggested that oxidative stress may play a role in the development of PC. Several genes regulate this process, including long noncoding RNAs (lncRNAs). There is no comprehensive study on the expression pattern of lncRNAs related to oxidative stress in PC patients. In the present case-control study, we quantified levels of oxidative stress-associated lncRNAs in PC patients versus healthy controls.

Patients and methods

In the present study, we investigated the expression levels of lincRNA-p21, LUCAT, RMST, FOXD3-AS1, and MT1DP lncRNAs in the peripheral blood mononuclear cells (PBMCs) of 53 PC patients and 50 healthy controls. The association between lncRNA expression and clinical and pathological characteristics was also evaluated.

Results

The expression of lincRNA-P21 and rhabdomyosarcoma 2-associated transcript (RMST) lncRNAs in PC patients has significantly decreased. Expression of lncRNA RMST was significantly higher in TNM stage III-IV patients in comparison to TNM stage I-II patients. In addition, a significant positive association was recognized between candidate lncRNA expression, and finally, the AUC values of the expression levels of lincRNA-p21 and RMST were 0.60 and 0.61, respectively.

Conclusions

Altogether, our study suggests a possible role of lincRNA-p21 and RMST lncRNAs in the etiology of PC pathobiology, and their biomarker role may be understood in future studies.

目的每年都有许多人死于胰腺癌（PC）。由于症状往往出现在晚期，因此早期发现这种癌症尤其具有挑战性。有研究表明，氧化应激可能在胰腺癌的发病过程中起作用。有多个基因可调控这一过程，包括长非编码 RNA（lncRNA）。目前还没有关于 PC 患者中与氧化应激相关的 lncRNA 表达模式的全面研究。在本病例对照研究中，我们量化了PC患者与健康对照组中氧化应激相关lncRNAs的表达水平。结果PC患者中lincRNA-P21和横纹肌肉瘤2相关转录本（RMST）lncRNA的表达明显下降。与TNM I-II期患者相比，lncRNA RMST在TNM III-IV期患者中的表达明显升高。此外，候选lncRNA的表达之间存在明显的正相关，最后，lincRNA-p21和RMST表达水平的AUC值分别为0.60和0.61。

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引用次数: 0