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Clinical Analysis of 32 Cases of Subglottic Benign Airway Stenosis Treated With Montgomery T Silicone Stent. 使用 Montgomery T 硅酮支架治疗声门下良性气道狭窄的 32 例临床分析。
IF 2.1 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-10-16 eCollection Date: 2024-01-01 DOI: 10.1155/2024/2145560
Zhenyu Yang, Xiaoli Zhou, Wenying Pan, Daxiong Zeng, Junhong Jiang

Objective: To explore the complications of long-term placement of Montgomery T silicone stent (T-tube) in the treatment of subglottic benign airway stenosis (SBAS) and the timing of successful T-tube removal. Methods: We retrospectively collected the clinical data of 32 patients with SBAS who underwent the treatment of T-tube and analyzed their placement and successful removal of the T-tube. Results: There were 22 males and 10 females, aged from 21 to 79 years (60.9 ± 13.7 years). The T-tubes were successfully placed in all 32 patients, and 6 patients (18.8%) with mild stenosis were placed by the intravenous conscious sedation. The longest follow-up period was 60.4 months, and 17 patients (53.1%) had the T-tubes for more than 12 months; 5 patients (15.6%) were changed to the tracheostomy cannula after unplanned removal of the T-tubes for various reasons; the T-tubes were successfully removed in 9 patients (28.1%), and the duration of T-tubes placement was 5.2-22.7 months (12.1 ± 6.3 months), among them anatomical stenosis in 9 patients (100%). Secretion retention was observed in 32 patients (100%), granulation tissue hyperplasia was observed in 9 patients (28.1%), and the normal ventilation was not affected in most patients by bronchoscopic treatment and follow-up; the T-tubes were removed in 3 patients due to severe complications. There was no significant difference in the incidences of secretion retention and granulation tissue hyperplasia between the time point at 1 week, 1 month, 3 months, and 12 months, p > 0.05. In patients with T-tube more than 12 months, the severity of secretion retention at 1 week, 1 month, 3 months, and 12 months was significantly different, p < 0.05, however, there was no significant difference in the severity of granulation tissue hyperplasia, p > 0.05. Conclusions: T-tube is safe and effective in the treatment of SBAS. The severity of secretion retention increased in patients with long-term placement of the T-tube. For patients with mild stenosis and anatomical stenosis, the T-tube removal can be attempted at about 1 year of follow-up.

目的探讨长期放置蒙哥马利 T 型硅胶支架(T 型管)治疗声门下良性气道狭窄(SBAS)的并发症以及成功拔除 T 型管的时机。方法我们回顾性地收集了 32 例接受 T 型管治疗的 SBAS 患者的临床资料,并分析了他们放置和成功拔除 T 型管的情况。结果:男 22 例,女 10 例:其中男性 22 例,女性 10 例,年龄从 21 岁到 79 岁(60.9±13.7)岁。所有 32 名患者都成功置入了 T 型管,其中 6 名轻度狭窄患者(18.8%)在静脉清醒镇静的情况下置入了 T 型管。最长随访时间为 60.4 个月,17 名患者(53.1%)留置 T 型管超过 12 个月;5 名患者(15.6%)因各种原因意外拔除 T 型管后改用气管造口插管;9 名患者(28.1%)成功拔除 T 型管,留置 T 型管时间为 5.2-22.7 个月(12.1±6.3 个月),其中 9 名患者(100%)为解剖性狭窄。32 例患者(100%)出现分泌物潴留,9 例患者(28.1%)出现肉芽组织增生,通过支气管镜治疗和随访,大多数患者的正常通气未受影响;3 例患者因严重并发症而拔除 T 型管。1周、1个月、3个月和12个月时点的分泌物潴留和肉芽组织增生发生率无明显差异,P>0.05。在插管超过 12 个月的患者中,1 周、1 个月、3 个月和 12 个月时分泌物潴留的严重程度有显著差异(P < 0.05),但肉芽组织增生的严重程度无显著差异(P > 0.05)。结论T管治疗SBAS安全有效。长期放置 T 型管的患者分泌物潴留的严重程度增加。对于轻度狭窄和解剖性狭窄的患者,可在随访 1 年左右时尝试拔除 T 型管。
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引用次数: 0
Nomograms for Predicting High Hospitalization Costs and Prolonged Stay among Hospitalized Patients with pAECOPD. 预测 pAECOPD 住院患者住院费用高昂和住院时间延长的提名图。
IF 2.2 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-09-06 DOI: 10.1155/2024/2639080
Nafeisa Dilixiati,Mengyu Lian,Ziliang Hou,Jie Song,Jingjing Yang,Ruiyan Lin,Jinxiang Wang
This study aimed to develop nomograms to predict high hospitalization costs and prolonged stays in hospitalized acute exacerbations of chronic obstructive pulmonary disease (AECOPD) patients with community-acquired pneumonia (CAP), also known as pAECOPD. A total of 635 patients with pAECOPD were included in this observational study and divided into training and testing sets. Variables were initially screened using univariate analysis, and then further selected using a backward stepwise regression. Multivariable logistic regression was performed to establish nomograms. The predictive performance of the model was evaluated using the receiver operating characteristic (ROC) curve, area under the curve (AUC), calibration curve, and decision curve analysis (DCA) in both the training and testing sets. Finally, the logistic regression analysis showed that elevated white blood cell count (WBC>10 × 109 cells/l), hypoalbuminemia, pulmonary encephalopathy, respiratory failure, diabetes, and respiratory intensive care unit (RICU) admissions were risk factors for predicting high hospitalization costs in pAECOPD patients. The AUC value was 0.756 (95% CI: 0.699-0.812) in the training set and 0.792 (95% CI: 0.718-0.867) in the testing set. The calibration plot and DCA curve indicated the model had good predictive performance. Furthermore, decreased total protein, pulmonary encephalopathy, reflux esophagitis, and RICU admissions were risk factors for predicting prolonged stays in pAECOPD patients. The AUC value was 0.629 (95% CI: 0.575-0.682) in the training set and 0.620 (95% CI: 0.539-0.701) in the testing set. The calibration plot and DCA curve indicated the model had good predictive performance. We developed and validated two nomograms for predicting high hospitalization costs and prolonged stay, respectively, among hospitalized patients with pAECOPD. This trial is registered with ChiCTR2000039959.
本研究旨在开发提名图,以预测慢性阻塞性肺疾病(AECOPD)急性加重并伴有社区获得性肺炎(CAP)(又称 pAECOPD)的住院患者的高住院费用和延长住院时间。这项观察性研究共纳入了 635 名 pAECOPD 患者,并将其分为训练集和测试集。首先使用单变量分析筛选变量,然后使用后向逐步回归法进一步筛选变量。采用多变量逻辑回归建立提名图。在训练集和测试集中,使用接收者操作特征曲线(ROC)、曲线下面积(AUC)、校准曲线和决策曲线分析(DCA)对模型的预测性能进行了评估。最后,逻辑回归分析表明,白细胞计数升高(WBC>10 × 109 cells/l)、低白蛋白血症、肺性脑病、呼吸衰竭、糖尿病和入住呼吸重症监护室(RICU)是预测 pAECOPD 患者住院费用高的风险因素。训练集的 AUC 值为 0.756(95% CI:0.699-0.812),测试集的 AUC 值为 0.792(95% CI:0.718-0.867)。校准图和 DCA 曲线表明该模型具有良好的预测性能。此外,总蛋白减少、肺性脑病、反流性食管炎和入住 RICU 是预测 pAECOPD 患者住院时间延长的风险因素。训练集的 AUC 值为 0.629(95% CI:0.575-0.682),测试集的 AUC 值为 0.620(95% CI:0.539-0.701)。校准图和 DCA 曲线表明该模型具有良好的预测性能。我们开发并验证了两个提名图,分别用于预测 pAECOPD 住院患者的高住院费用和延长住院时间。本试验的注册号为 ChiCTR2000039959。
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引用次数: 0
Gentiopicroside Ameliorates Sepsis-Induced Acute Lung Injury via Inhibiting Inflammatory Response. 龙胆草甙通过抑制炎症反应改善败血症诱发的急性肺损伤
IF 2.2 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-09-05 DOI: 10.1155/2024/1068326
Mu Hu,Hangxiang Du,Yang Xu,Yan Wang
Sepsis is a systemic inflammatory reaction syndrome caused by infections. Acute lung injury (ALI) occurs first and most frequently in patients with sepsis. Gentiopicroside (GPS), which originates mostly from Gentiana, is classified as a secoiridoid glycosides. Terpenoid glycosides have various biological effects, including liver protection, blood glucose and cholesterol level management, and anti-inflammatory and antitumor effects. However, presently, the biochemical foundation and mechanism of the anti-inflammatory effects of GPS in sepsis-induced ALI have not been explained. In the present study, we established a rat model of sepsis ALI induced by cecal ligation and puncture. This enables us to observe the effects of GPS therapy, which significantly reduced the inflammatory response (TNF-α, IL-1β, and IL-6), nitrogen stress, oxidative stress, and severity of ALI at both the whole animal and molecular levels. In addition, GPS ameliorates LPS-induced ALI via regulation of inflammatory response and cell proptosis in BEAS-2B. This study provides a theoretical basis for treating sepsis-induced ALI with GPS.
败血症是一种由感染引起的全身炎症反应综合征。急性肺损伤(ALI)在败血症患者中最先发生,也最常见。龙胆草甙(Gentiopicroside,GPS)主要来源于龙胆草,属于仲萜类甙。萜类苷具有多种生物效应,包括保护肝脏、控制血糖和胆固醇水平、抗炎和抗肿瘤作用。然而,目前 GPS 在败血症引起的 ALI 中抗炎作用的生化基础和机制尚未得到解释。在本研究中,我们建立了一个由盲肠结扎和穿刺诱导的大鼠败血症 ALI 模型。GPS能在动物整体和分子水平上显著降低炎症反应(TNF-α、IL-1β和IL-6)、氮应激、氧化应激和ALI的严重程度。此外,GPS 还能通过调节 BEAS-2B 的炎症反应和细胞突眼来改善 LPS 诱导的 ALI。这项研究为利用 GPS 治疗败血症诱发的 ALI 提供了理论依据。
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引用次数: 0
Development of Prone Position Ventilation Device and Study on the Application Effect of Combined Life Support Technology in Critically Ill Patients. 俯卧位通气装置的开发及联合生命支持技术在重症患者中的应用效果研究。
IF 2.1 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-08-19 eCollection Date: 2024-01-01 DOI: 10.1155/2024/5812829
Yufeng Li, Qiaoqiao Hu, Wenjie Wang, Changhong Du, Siwen Fan, Linlin Xu, Songmei Li, Bei Chen

Objective: This study aims to evaluate a novel prone position ventilation device designed to enhance patient safety, improve comfort, and reduce adverse events, facilitating prolonged tolerance in critically ill patients.

Methods: A randomized controlled trial was conducted on 60 critically ill patients from January 2020 to June 2023. Of which, one self-discharged during treatment and another was terminated due to decreased oxygenation, leaving an effective sample of 58 patients. Patients were allocated to either a control group receiving traditional prone positioning aids (ordinary sponge pads and pillows) or an intervention group using a newly developed adjustable prone positioning device. A subset of patients in each group also received life support technologies such as extracorporeal membrane oxygenation (ECMO) and continuous renal replacement therapy (CRRT). We assessed prone position ventilation tolerance, oxygen saturation increments postintervention, duration of prone positioning, CRRT filter lifespan, and the incidence of adverse events.

Results: The intervention group exhibited significantly longer average tolerance to prone positioning (16.6 hours vs. 8.3 hours, P < 0.001 with a difference of 8.3 (4.4, 12.2) hours), higher increases in oxygen saturation postventilation (9% vs. 6%, P < 0.001 with a difference of 3.0 (1.5, 4.5)), and reduced time required for medical staff to position patients (11.7 min vs. 21.8 min, P < 0.001 with a difference of -10.1 (-11.9, -8.3)). Adverse events, including catheter displacement or blockage, facial edema, pressure injuries, and vomiting or aspiration, were markedly lower in the intervention group, with statistical significance (P < 0.05). In patients receiving combined life support, the intervention group demonstrated improved catheter blood drainage and extended CRRT filter longevity.

Conclusion: The newly developed adjustable prone ventilation device significantly improves tolerance to prone positioning, enhances oxygenation, and minimizes adverse events in critically ill patients, thereby also facilitating the effective application of life support technologies.

研究目的本研究旨在对一种新型俯卧位通气装置进行评估,该装置旨在提高患者安全性、改善舒适度并减少不良事件,从而延长危重症患者的耐受时间:2020年1月至2023年6月,对60名重症患者进行了随机对照试验。其中,一名患者在治疗期间自行出院,另一名患者因氧合下降而终止治疗,因此有效样本为 58 名患者。患者被分配到接受传统俯卧定位辅助工具(普通海绵垫和枕头)的对照组或使用新开发的可调节俯卧定位装置的干预组。每组的一部分患者还接受了体外膜氧合(ECMO)和持续肾脏替代疗法(CRRT)等生命支持技术。我们评估了俯卧位通气耐受性、干预后血氧饱和度增量、俯卧位持续时间、CRRT 过滤器寿命和不良事件发生率:结果:干预组患者对俯卧位通气的平均耐受时间明显更长(16.6 小时 vs. 8.3 小时,P < 0.001,差异为 8.3 (4.4, 12.2) 小时),通气后血氧饱和度的升高幅度更大(9% vs. 6%,P < 0.001,差异为 8.3 (4.4, 12.2) 小时)。6% ,P < 0.001,差异为 3.0 (1.5, 4.5)),医护人员为患者定位所需的时间缩短(11.7 分钟对 21.8 分钟,P < 0.001,差异为 -10.1 (-11.9, -8.3))。干预组的不良事件明显减少,包括导管移位或堵塞、面部水肿、压伤、呕吐或吸入,差异有统计学意义(P < 0.05)。在接受联合生命支持的患者中,干预组改善了导管排血,延长了 CRRT 过滤器的使用寿命:结论:新开发的可调式俯卧位通气装置可显著提高重症患者对俯卧位的耐受性,增强氧合,并将不良事件降至最低,从而促进生命支持技术的有效应用。
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引用次数: 0
IL-17 Mildly Rescued the Impaired Proliferation of Alveolar Epithelial Cells Induced by LCN2 Overexpression. IL-17可轻度修复LCN2过表达引起的肺泡上皮细胞增殖障碍
IF 2.1 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-08-06 eCollection Date: 2024-01-01 DOI: 10.1155/2024/9284430
Tingting Lv, Ziliang Hou, Kaiyuan Yang, Jinxiang Wang

Introduction: The impaired proliferative capacity of alveolar epithelial cells after injury is an important factor causing epithelial repair dysfunction, leading to the occurrence of idiopathic pulmonary fibrosis (IPF). Alveolar type 2 (AT2) cells as the stem cells of alveolar epithelium participate in the repair process after alveolar injury. Lipocalin-2 (LCN2) participates in multiple processes regulating the pathological process of alveolar epithelial cells, but the mechanisms involved are still unclear.

Method: We used a BLM-treated mouse model to characterize the expression of LCN2 in lung fibrosis regions and analyzed the location of LCN2 in alveolar epithelial cells. Moreover, human pulmonary alveolar epithelial cells (HPAEpiCs) were transfected with the LCN2 overexpression plasmid vector in vitro. Recombinant human interleukin-17 (IL-17) protein (rhIL-17) at different concentrations was administered to intervene in HPAEpiCs, observing cell viability and analyzing the concentration-dependent effect of IL-17.

Results: LCN2 was increased in the alveolar epithelium post-BLM injury, and highly expressed LCN2 was mainly concentrated on AT2 cells in BLM-injured lungs. Meanwhile, LCN2-overexpressing HPAEpiCs showed impaired cell viability and cell growth. HPAEpiC intervention with rhIL-17 mildly rescued the impaired cell proliferation induced by LCN2 overexpression, and the effect of IL-17 intervention was partially concentration-dependent.

Conclusions: The results revealed the reversed effect of IL-17 on the impaired proliferative capacity of the alveolar epithelium induced by LCN2 overexpression. The target alveolar epithelial cells regulated by this process were AT2 cells, providing new clues for alveolar epithelium repair after injury and the treatment of lung injury diseases.

导言:肺泡上皮细胞损伤后增殖能力受损是导致上皮修复功能障碍的一个重要因素,从而导致特发性肺纤维化(IPF)的发生。肺泡2型(AT2)细胞作为肺泡上皮的干细胞,参与了肺泡损伤后的修复过程。脂褐素-2(LCN2)参与调节肺泡上皮细胞病理过程的多个过程,但其机制尚不清楚:方法:我们利用BLM处理的小鼠模型研究了LCN2在肺纤维化区域的表达特征,并分析了LCN2在肺泡上皮细胞中的位置。此外,在体外用 LCN2 过表达质粒载体转染人肺泡上皮细胞(HPAEpiCs)。给 HPAEpiCs 注射不同浓度的重组人白细胞介素-17(IL-17)蛋白(rhIL-17),观察细胞活力并分析 IL-17 的浓度依赖效应:结果:BLM损伤后肺泡上皮细胞中LCN2增高,高表达的LCN2主要集中在BLM损伤肺的AT2细胞上。同时,LCN2-表达缺失的HPAEpiC细胞显示出细胞活力和细胞生长受损。用rhIL-17干预HPAEpiC可轻度挽救LCN2过表达引起的细胞增殖受损,且IL-17干预的效果部分取决于浓度:结果表明,IL-17对LCN2过表达导致的肺泡上皮细胞增殖能力受损具有逆转作用。该过程调控的靶肺泡上皮细胞是AT2细胞,为肺泡上皮损伤后的修复和肺损伤疾病的治疗提供了新的线索。
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引用次数: 0
The Correlation between Lung Ultrasound and Pathology in Rat Model of Monocrotaline-Induced Pulmonary Hypertension. 单克隆盐碱诱发肺动脉高压大鼠模型中肺部超声波与病理学之间的相关性
IF 2.1 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-07-23 eCollection Date: 2024-01-01 DOI: 10.1155/2024/6619471
Yan-Fen Zhong, Bin-Bin Liang, Xiao-Feng Zhang, Ji-Wu

Pulmonary hypertension (PH) is a progressive and complex pulmonary vascular disease with poor prognosis. The aim of this study was to provide a new understanding of the lung pathology of disease and a noninvasive method in monitoring the establishment of animal models for basic and clinical studies of PH, indeed to explore clinical application value of lung ultrasound for patients with PH. Totally 32 male SD rats were randomly divided into control group, MCT (monocrotaline) group, PDTC (pyrrolidine dithiocarbamate) group, and NS (normal saline) group. Rats in the MCT group, PDTC group, and NS group received single intraperitoneal injection of MCT, while the control group received the same dose of NS. Then, PDTC group and NS group received PDTC and NS daily for treatment at the end of the model. Each group received lung ultrasound examination and measurement of pulmonary arterial pressure (PAP). Then, the rats were sacrificed to take the lung specimens to being observed. The ultrasound and pathological results were analyzed with a semiquantitative score. With the pulmonary artery pressure increases, the MCT group had a higher pulmonary ultrasound score and pathological score compared with the control group (p < 0.05). After PDTC treatment, the pulmonary ultrasound score and the pathological score decline (p < 0.05). We investigated both lung ultrasound scores, and the pathological scores were positively correlated with mean pulmonary artery pressure (mPAP) (both r > 0.8, p < 0.0001). Moreover, lung ultrasound scores were positively correlated with pathological scores (r > 0.8, p < 0.0001). We elucidated lung ultrasound evaluation providing more evidence for the management of PH in the rat model. Moreover, lung ultrasound provided a noninvasive method in monitoring the establishment of animal models for basic and clinical studies of PH.

肺动脉高压(PH)是一种进展性、复杂的肺血管疾病,预后不良。本研究的目的是提供一种对肺部病理的新认识和一种无创的监测方法,以建立肺动脉高压基础和临床研究的动物模型,并探索肺部超声对肺动脉高压患者的临床应用价值。32只雄性SD大鼠被随机分为对照组、MCT(单克隆)组、PDTC(吡咯烷二硫代氨基甲酸盐)组和NS(生理盐水)组。MCT组、PDTC组和NS组的大鼠腹腔注射一次MCT,而对照组则注射相同剂量的NS。然后,PDTC 组和 NS 组在模型结束后每天接受 PDTC 和 NS 治疗。每组大鼠均接受肺部超声波检查和肺动脉压(PAP)测量。然后,大鼠被处死,取肺标本进行观察。对超声和病理结果进行半定量评分分析。与对照组相比,随着肺动脉压力的升高,MCT 组的肺部超声评分和病理评分更高(P < 0.05)。PDTC 治疗后,肺超声评分和病理评分下降(P < 0.05)。我们研究发现,肺部超声评分和病理评分均与平均肺动脉压(mPAP)呈正相关(r 均大于 0.8,p < 0.0001)。此外,肺部超声评分与病理评分呈正相关(r > 0.8,p < 0.0001)。我们阐明了肺部超声评估,为大鼠模型中 PH 的治疗提供了更多证据。此外,肺部超声还为建立 PH 的基础和临床研究动物模型提供了一种无创的监测方法。
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引用次数: 0
Update in Noninvasive Home Mechanical Ventilation: A Narrative Review of Indications, Outcomes, and Monitoring. 无创家庭机械通气的最新进展:关于适应症、结果和监测的叙述性回顾。
IF 2.1 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-07-03 eCollection Date: 2024-01-01 DOI: 10.1155/2024/7013576
Laura Tregidgo, Prasheena Naran, Eshrina Gosal, Rebecca F D'Cruz

Hypercapnic respiratory failure arises due to an imbalance in the load-capacity-drive relationship of the respiratory muscle pump, typically arising in patients with chronic obstructive pulmonary disease, obesity-related respiratory failure, and neuromuscular disease. Patients at risk of developing chronic respiratory failure and those with established disease should be referred to a specialist ventilation unit for evaluation and consideration of home noninvasive ventilation (NIV) initiation. Clinical trials demonstrate that, following careful patient selection, home NIV can improve a range of clinical, patient-reported, and physiological outcomes. This narrative review provides an overview of the pathophysiology of chronic respiratory failure, evidence-based applications of home NIV, and monitoring of patients established on home ventilation and describes technological advances in ventilation devices, interfaces, and monitoring to enhance comfort, promote long-term adherence, and optimise gas exchange.

高碳酸血症呼吸衰竭是由于呼吸肌泵的负荷-容量-驱动关系失衡所致,通常发生在慢性阻塞性肺病、肥胖相关性呼吸衰竭和神经肌肉疾病患者身上。有患慢性呼吸衰竭风险的患者和已确诊疾病的患者应转诊至专业通气科进行评估,并考虑启动家庭无创通气(NIV)。临床试验表明,在仔细选择患者后,家庭无创通气可改善一系列临床、患者报告和生理结果。本综述概述了慢性呼吸衰竭的病理生理学、家庭无创通气的循证应用和对已建立家庭通气的患者的监测,并介绍了通气设备、接口和监测方面的技术进步,以提高舒适度、促进长期坚持和优化气体交换。
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引用次数: 0
Amelioration of Oxidative Stress in Rats with Chronic Obstructive Pulmonary Disease through Shenqi Huatan Decoction Activation of Peroxisome Proliferator-Activated Receptor Gamma-Mediated Activated Protein Kinase/Forkhead Transcription Factor O3a Signaling Pathway. 通过神气花丹煎剂激活过氧化物酶体增殖物激活受体 Gamma 介导的活化蛋白激酶/叉头转录因子 O3a 信号通路改善慢性阻塞性肺病大鼠的氧化应激反应
IF 2.1 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-07-02 eCollection Date: 2024-01-01 DOI: 10.1155/2024/5647813
Jingjing Chen, Wenxiao Qiao, Xiaoming Xue, Dian Li, Ye Zhang, Di Xie, Jinyun Wang, Yaoqin Sun, Shuo Yang, Zhuomin Yang

Background: Chronic obstructive pulmonary disease (COPD) is a common respiratory disease. Currently, no specific treatment strategy has been established; therefore, finding new treatment methods is essential. Clinically, Shenqi Huatan Decoction (SQHT) is a traditional Chinese medicinal formula for COPD treatment; however, its mechanism of action in treatment needs to be clarified.

Methods: The COPD rat model was replicated by cigarette smoking and tracheal injection using the LPS method. The control group and the SQHT groups were treated with dexamethasone and SQHT by gavage, respectively. After treatment, superoxide dismutase (SOD) serum levels, total antioxidant capacity (TAOC), lipid peroxidation, and malondialdehyde (MDA) were detected by enzyme-linked immunosorbent assay (ELISA). Activated protein kinase alpha (AMPK-α), forkhead transcription factor O3a (FOXO3a), manganese SOD (MnSOD), and peroxisome proliferator-activated receptor gamma (PPARγ) were detected using reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) and Western blot. Microribonucleic acid and protein expression levels were measured, and pathological changes in lung tissue were observed using hematoxylin and eosin staining.

Results: The pathological findings suggested that SQHT substantially affects COPD treatment by enhancing alveolar fusion and reducing emphysema. ELISA results showed that SQHT could lower the blood levels of MDA and lipid peroxide and raise SOD and TAOC levels, suggesting that it could lessen oxidative stress. In the lung tissue of rats with COPD, large doses of SQHT intervention dramatically increased AMPK protein expression, AMPK-α, FOXO3a, MnSOD, and PPARγ, indicating that SQHT may reduce oxidative stress by activating the PPARγ-mediated AMPK/FOXO3a signaling pathway. Similar results were obtained using RT-qPCR.

Conclusion: SQHT is effective for COPD treatment. The mechanism of action may be related to the activation of the PPARγ-mediated AMPK/FOXO3a signaling pathway to improve oxidative stress in lung tissue.

背景:慢性阻塞性肺疾病(COPD)是一种常见的呼吸系统疾病。目前,尚无特效的治疗策略,因此,寻找新的治疗方法至关重要。临床上,神气化瘀汤是治疗慢性阻塞性肺疾病的传统中药方剂,但其治疗作用机制尚待明确:方法:通过吸烟和气管注射 LPS 法复制 COPD 大鼠模型。对照组和 SQHT 组分别灌胃地塞米松和 SQHT 治疗。治疗后,用酶联免疫吸附试验(ELISA)检测超氧化物歧化酶(SOD)血清水平、总抗氧化能力(TAOC)、脂质过氧化和丙二醛(MDA)。使用逆转录酶定量聚合酶链反应(RT-qPCR)和 Western 印迹法检测活化蛋白激酶α(AMPK-α)、叉头转录因子 O3a(FOXO3a)、锰 SOD(MnSOD)和过氧化物酶体增殖激活受体γ(PPARγ)。测定微核糖核酸和蛋白质的表达水平,并用苏木精和伊红染色观察肺组织的病理变化:结果:病理研究结果表明,SQHT 通过增强肺泡融合和减轻肺气肿对慢性阻塞性肺疾病的治疗有显著影响。酶联免疫吸附试验结果表明,SQHT 可降低血液中 MDA 和过氧化脂质的水平,提高 SOD 和 TAOC 的水平,从而减轻氧化应激。在慢性阻塞性肺病大鼠的肺组织中,大剂量 SQHT 干预可显著增加 AMPK 蛋白表达、AMPK-α、FOXO3a、MnSOD 和 PPARγ,表明 SQHT 可通过激活 PPARγ 介导的 AMPK/FOXO3a 信号通路来减轻氧化应激。使用 RT-qPCR 也得到了类似的结果:结论:SQHT 可有效治疗慢性阻塞性肺疾病。其作用机制可能与激活 PPARγ 介导的 AMPK/FOXO3a 信号通路以改善肺组织中的氧化应激有关。
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引用次数: 0
Prognostic Value of Novel CARWL Score in Stage IIIC Non-Small-Cell Lung Cancer Patients Undergoing Concurrent Chemoradiotherapy. 新型 CARWL 评分对同时接受化疗放疗的 IIIC 期非小细胞肺癌患者的预后价值
IF 2.1 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-06-28 eCollection Date: 2024-01-01 DOI: 10.1155/2024/2803044
Erkan Topkan, Ahmet Kucuk, Duriye Ozturk, Emine Elif Ozkan, Ali Ayberk Besen, Berrin Pehlivan, Ugur Selek

Objectives: We explored the prognostic utility of the unique combination of C-reactive-protein-to-albumin ratio (CAR) and significant weight loss (WL > 5%) over the preceding 6 months, namely, the CARWL score, in stage IIIC non-small-cell lung cancer (NSCLC) patients who underwent concurrent chemoradiotherapy (CCRT).

Methods: For each patient, the CAR was calculated using C-reactive protein and albumin measurements obtained on the first day of CCRT: CAR = C-reactive protein ÷ albumin. The availability of an ideal CAR cutoff that may categorize patients into two distinct progression-free (PFS) and overall survival (OS) outcomes was explored by employing receiver operating characteristic (ROC) curve analysis. Patients were additionally divided into two groups based on their status of significant WL according to the well-recognized Delphi criteria. Then, the CARWL score was created by combining all feasible combinations of the CAR and significant WL groupings. The potential links between pretreatment CARWL groups and the post-CCRT OS and PFS outcomes were determined as the primary and secondary endpoints.

Results: This retrospective cohort study comprised a total of 651 stage IIIC NSCLC patients. ROC curve analysis indicated that rounded 3.0 was the ideal CAR cutoff (area under the curve (AUC): 70.1%; sensitivity: 67.8%; specificity: 65.9%), which categorized the patients into CAR < 3.0 (N = 324) and CAR ≥ 3.0 (N = 327) groups. There were 308 (47.3%) and 343 (52.7%) patients without and with significant WL, respectively. The created CARWL groups were CARWL-0: CAR < 3.0 and WL ≤ 5.0%; CARWL-1: CAR < 3.0 and WL > 5.0%, or CAR ≥ 3.0 and WL ≤ 5.0%; and CARWL-2: CAR > 3.0 and WL > 5.0%. The Kaplan-Meier curves showed that the PFS (14.2 vs. 11.4 vs. 7.5 months; P < 0.001) and OS (37.3 vs. 23.6 vs. 12.8 months; P < 0.001) durations were gradually and significantly lowered from the CARWL-0 to CARWL-2 groups. The CARWL score's significant impacts on PFS and OS outcomes were found to be independent of the other variables in the multivariate analysis (P < 0.001, for each).

Conclusions: Our findings indicate that the novel CARWL score, which accounts for pretreatment CAR and significant WL during the preceding 6 months, can reliably stratify newly diagnosed stage IIIC NSCLC patients into three groups with significantly different PFS and OS after definitive CCRT.

研究目的我们探讨了在接受同期化疗(CCRT)的IIIC期非小细胞肺癌(NSCLC)患者中,C反应蛋白与白蛋白比值(CAR)和前6个月体重显著下降(WL > 5%)的独特组合,即CARWL评分的预后效用:方法:每位患者的 CAR 分值均根据 CCRT 第一天获得的 C 反应蛋白和白蛋白测量值计算得出:CAR = C 反应蛋白 ÷ 白蛋白。通过接收器操作特征曲线(ROC)分析,探讨了是否有一个理想的CAR分界线,可将患者分为两种不同的无进展(PFS)和总生存(OS)结果。此外,根据公认的德尔菲(Delphi)标准,根据患者的显著 WL 状态将其分为两组。然后,结合 CAR 和显著 WL 分组的所有可行组合,得出 CARWL 评分。将治疗前CARWL分组与CCRT后OS和PFS结果之间的潜在联系作为主要和次要终点:这项回顾性队列研究共纳入了 651 例 IIIC 期 NSCLC 患者。ROC曲线分析表明,圆形 3.0 是理想的 CAR 临界值(曲线下面积 (AUC):70.1%;灵敏度:67.0%):70.1%;灵敏度:67.8%;特异性:65.9%),将患者分为 CAR N = 324 组和 CAR ≥ 3.0 组(N = 327)。无明显 WL 和有明显 WL 的患者分别为 308 人(47.3%)和 343 人(52.7%)。创建的 CARWL 组为 CARWL-0:CAR 5.0%,或 CAR ≥ 3.0 且 WL ≤ 5.0%;CARWL-2:CAR > 3.0 且 WL > 5.0%。Kaplan-Meier曲线显示,从CARWL-0组到CARWL-2组,PFS(14.2个月 vs. 11.4个月 vs. 7.5个月;P < 0.001)和OS(37.3个月 vs. 23.6个月 vs. 12.8个月;P < 0.001)持续时间逐渐显著缩短。在多变量分析中发现,CARWL评分对PFS和OS结果的显著影响与其他变量无关(P<0.001):我们的研究结果表明,新的CARWL评分考虑了治疗前的CAR和前6个月的显著WL,可以可靠地将新诊断的IIIC期NSCLC患者分为三组,三组患者在接受明确的CCRT治疗后的PFS和OS显著不同。
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引用次数: 0
Ferroptosis Mediates Pulmonary Fibrosis: Implications for the Effect of Astragalus and Panax notoginseng Decoction 铁蛋白沉积介导肺纤维化:黄芪和三七煎剂疗效的启示
IF 2.2 4区 医学 Q3 RESPIRATORY SYSTEM Pub Date : 2024-03-29 DOI: 10.1155/2024/5554886
Jing Wen, Cui Wang, Li-yun Song, Yin-ying Wang, Peng-tao Liang, Wen-lin Pang, Wen Yin, Qiang Zhang, Wei-tian Zhao, Xue-ping Sun, Jin-yuan Yan, Zhong-shan Yang
Context. Ferroptosis is known to influence the pathogenesis of pulmonary fibrosis. Astragalus and Panax notoginseng are used to treat pulmonary fibrosis; however, the therapeutic mechanisms require further elucidation. Objective. To investigate the mechanism through which Astragalus and Panax notoginseng decoction (APD) facilitates the treatment of ferroptosis-mediated pulmonary fibrosis. Materials and Methods. First, the electromedical measurement systems were used to measure respiratory function in mice; the lungs were then collected for histological staining. Potential pharmacologic targets were predicted via network pharmacology. Finally, tests including immunohistochemistry, reverse transcription-quantitative polymerase chain reaction, and western blotting were used to evaluate the relative expression levels of collagen, transforming growth factor β, α-smooth muscle actin, hydroxyproline, and ferroptosis-related genes (GPX4, SLC7A11, ACSL4, and PTGS2) and candidates involved in the mediation of pathways associated with ferroptosis (Hif-1α and EGFR). Results. APD prevented the occurrence of restrictive ventilation dysfunction induced by ferroptosis. Extracellular matrix and collagen fiber deposition were significantly reduced when the APD group compared with the model group; furthermore, ferroptosis was attenuated, expression of PTGS2 and ACSL4 increased, and expression of GPX4 and SLC7A11 decreased. In the APD group, the candidates related to the mediation of ferroptosis (Hif-1α and EGFR) decreased compared with the model group. Discussion and Conclusions. APD may ameliorate restrictive ventilatory dysfunction through the inhibition of ferroptosis. This was achieved through the attenuation of collagen deposition and inflammatory recruitment in pulmonary fibrosis. The underlying mechanisms might involve Hif-1α and EGFR.
背景。众所周知,铁蛋白沉积会影响肺纤维化的发病机制。黄芪和三七可用于治疗肺纤维化,但其治疗机制尚需进一步阐明。研究目的研究黄芪三七水煎剂(APD)促进治疗铁蛋白沉积介导的肺纤维化的机制。材料与方法。首先,使用电子医学测量系统测量小鼠的呼吸功能;然后采集肺部进行组织学染色。通过网络药理学预测潜在的药理靶点。最后,使用免疫组化、逆转录-定量聚合酶链反应和 Western 印迹等检测方法,评估胶原蛋白、转化生长因子 β、α-平滑肌肌动蛋白、羟脯氨酸、铁变态反应相关基因(GPX4、SLC7A11、ACSL4 和 PTGS2)和参与铁变态反应相关途径调解的候选基因(Hif-1α 和表皮生长因子受体)的相对表达水平。结果APD阻止了铁中毒诱导的限制性通气功能障碍的发生。与模型组相比,APD组细胞外基质和胶原纤维沉积明显减少;此外,铁变态反应减弱,PTGS2和ACSL4表达增加,GPX4和SLC7A11表达减少。与模型组相比,APD 组中与介导铁变态反应相关的候选因子(Hif-1α 和表皮生长因子受体)减少。讨论与结论APD 可通过抑制铁变态反应改善限制性通气功能障碍。这是通过减少肺纤维化中的胶原沉积和炎症招募实现的。其潜在机制可能涉及 Hif-1α 和表皮生长因子受体。
{"title":"Ferroptosis Mediates Pulmonary Fibrosis: Implications for the Effect of Astragalus and Panax notoginseng Decoction","authors":"Jing Wen, Cui Wang, Li-yun Song, Yin-ying Wang, Peng-tao Liang, Wen-lin Pang, Wen Yin, Qiang Zhang, Wei-tian Zhao, Xue-ping Sun, Jin-yuan Yan, Zhong-shan Yang","doi":"10.1155/2024/5554886","DOIUrl":"https://doi.org/10.1155/2024/5554886","url":null,"abstract":"<i>Context</i>. Ferroptosis is known to influence the pathogenesis of pulmonary fibrosis. <i>Astragalus</i> and <i>Panax notoginseng</i> are used to treat pulmonary fibrosis; however, the therapeutic mechanisms require further elucidation. <i>Objective</i>. To investigate the mechanism through which <i>Astragalus</i> and <i>Panax notoginseng</i> decoction (APD) facilitates the treatment of ferroptosis-mediated pulmonary fibrosis. <i>Materials and Methods</i>. First, the electromedical measurement systems were used to measure respiratory function in mice; the lungs were then collected for histological staining. Potential pharmacologic targets were predicted via network pharmacology. Finally, tests including immunohistochemistry, reverse transcription-quantitative polymerase chain reaction, and western blotting were used to evaluate the relative expression levels of collagen, transforming growth factor <i>β</i>, <i>α</i>-smooth muscle actin, hydroxyproline, and ferroptosis-related genes (GPX4, SLC7A11, ACSL4, and PTGS2) and candidates involved in the mediation of pathways associated with ferroptosis (Hif-1<i>α</i> and EGFR). <i>Results</i>. APD prevented the occurrence of restrictive ventilation dysfunction induced by ferroptosis. Extracellular matrix and collagen fiber deposition were significantly reduced when the APD group compared with the model group; furthermore, ferroptosis was attenuated, expression of PTGS2 and ACSL4 increased, and expression of GPX4 and SLC7A11 decreased. In the APD group, the candidates related to the mediation of ferroptosis (Hif-1<i>α</i> and EGFR) decreased compared with the model group. <i>Discussion and Conclusions</i>. APD may ameliorate restrictive ventilatory dysfunction through the inhibition of ferroptosis. This was achieved through the attenuation of collagen deposition and inflammatory recruitment in pulmonary fibrosis. The underlying mechanisms might involve Hif-1<i>α</i> and EGFR.","PeriodicalId":9416,"journal":{"name":"Canadian respiratory journal","volume":"4281 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140325059","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
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Canadian respiratory journal
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