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Activation of mas restores hyperoxia-induced loss of lung epithelial barrier function through inhibition of apoptosis. 激活mas可通过抑制细胞凋亡恢复高氧诱导的肺上皮屏障功能丧失。
Pub Date : 2019-01-01 DOI: 10.15406/jlprr.2019.06.00208
A. Abdul-Hafez, Tarek Mohamed, B. Uhal
Background Neonatal therapy with a high concentration of oxygen (hyperoxia) is a known cause of bronchopulmonary dysplasia (BPD). BPD is characterized by increased pulmonary permeability and diffuse infiltration of various inflammatory cells. Disruption of the epithelial barrier may lead to altered pulmonary permeability and airways fluid accumulation. Mas receptor is a component of the renin angiotensin system and is the receptor for the protective endogenous peptide angiotensin 1-7. The activation of the Mas receptor was previously shown to have protective pulmonary responses. However, the effect of Mas receptor activation on epithelial barrier integrity has not been tested. Objective To determine the effects of hyperoxia with or without Mas receptor activation on epithelial cell barrier integrity. Design/Methods Human epithelial cell line A549 was cultured on transwell polycarbonate porous membrane to confluence and treated with 95% oxygen (hyperoxia) for 72 hours with or without the Mas receptor agonist (AVE0991), or the apoptotic inhibitors Z-VAD-FMK or aurintricarboxylic acid. The cells were then challenged with Rhodamine labeled bovine serum albumin (Rh-BSA) on one side of the membrane. Fluorescent quantitation of Rh-BSA (albumin flux) was performed on the media in the other side of the membrane 3 hours later and was compared with 21% oxygen (Normoxia) control group. A549 cells were also cultured with or without AVE0991 in hyperoxia or normoxia and used for nuclear fragmentation apoptosis assay using propidium iodide staining. Results Hyperoxia induced an increase in albumin flux that was significantly prevented by AVE0991 treatment and by the apoptosis inhibitors. AVE0991 also significantly decreased the hyperoxia-induced nuclear fragmentation. Conclusion These results suggest that hyperoxia causes a disruption in the epithelial barrier integrity, and that this disruption is inhibited by the Mas receptor agonist AVE0991 through inhibition of epithelial apoptosis. These results reveal a novel potential drug for BPD and pulmonary edema treatment.
背景:新生儿高浓度氧(高氧)治疗是支气管肺发育不良(BPD)的已知原因。BPD的特点是肺通透性增加,各种炎症细胞弥漫性浸润。上皮屏障的破坏可导致肺通透性改变和气道液体积聚。Mas受体是肾素血管紧张素系统的一个组成部分,是保护性内源性肽血管紧张素1-7的受体。Mas受体的激活先前被证明具有保护性肺反应。然而,Mas受体激活对上皮屏障完整性的影响尚未得到验证。目的探讨高氧激活或不激活Mas受体对上皮细胞屏障完整性的影响。设计/方法在transwell聚碳酸酯多孔膜上培养人上皮细胞系A549,用或不加Mas受体激动剂(AVE0991)、凋亡抑制剂Z-VAD-FMK或金三羧酸,95%氧(高氧)处理72小时。然后在膜的一侧用罗丹明标记的牛血清白蛋白(Rh-BSA)激射细胞。3小时后,在膜另一侧的培养基上荧光定量Rh-BSA(白蛋白通量),并与21%氧(normmoxia)对照组进行比较。A549细胞加入或不加入AVE0991分别在高氧或常氧条件下培养,碘化丙啶染色进行核碎裂凋亡实验。结果缺氧诱导大鼠白蛋白通量增加,而AVE0991和细胞凋亡抑制剂可明显抑制这种增加。AVE0991还能显著降低高氧诱导的核碎裂。结论高氧可导致上皮屏障完整性的破坏,而Mas受体激动剂AVE0991可通过抑制上皮细胞凋亡来抑制这种破坏。这些结果揭示了一种新的潜在药物治疗BPD和肺水肿。
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引用次数: 8
Activation of mas restores hyperoxia-induced loss of lung epithelial barrier function through inhibition of apoptosis. 激活mas可通过抑制细胞凋亡恢复高氧诱导的肺上皮屏障功能丧失。
Pub Date : 2019-01-01 Epub Date: 2019-07-18
Amal Abdul-Hafez, Tarek Mohamed, Bruce D Uhal

Background: Neonatal therapy with a high concentration of oxygen (hyperoxia) is a known cause of bronchopulmonary dysplasia (BPD). BPD is characterized by increased pulmonary permeability and diffuse infiltration of various inflammatory cells. Disruption of the epithelial barrier may lead to altered pulmonary permeability and airways fluid accumulation. Mas receptor is a component of the renin angiotensin system and is the receptor for the protective endogenous peptide angiotensin 1-7. The activation of the Mas receptor was previously shown to have protective pulmonary responses. However, the effect of Mas receptor activation on epithelial barrier integrity has not been tested.

Objective: To determine the effects of hyperoxia with or without Mas receptor activation on epithelial cell barrier integrity.

Design/methods: Human epithelial cell line A549 was cultured on transwell polycarbonate porous membrane to confluence and treated with 95% oxygen (hyperoxia) for 72 hours with or without the Mas receptor agonist (AVE0991), or the apoptotic inhibitors Z-VAD-FMK or aurintricarboxylic acid. The cells were then challenged with Rhodamine labeled bovine serum albumin (Rh-BSA) on one side of the membrane. Fluorescent quantitation of Rh-BSA (albumin flux) was performed on the media in the other side of the membrane 3 hours later and was compared with 21% oxygen (Normoxia) control group. A549 cells were also cultured with or without AVE0991 in hyperoxia or normoxia and used for nuclear fragmentation apoptosis assay using propidium iodide staining.

Results: Hyperoxia induced an increase in albumin flux that was significantly prevented by AVE0991 treatment and by the apoptosis inhibitors. AVE0991 also significantly decreased the hyperoxia-induced nuclear fragmentation.

Conclusion: These results suggest that hyperoxia causes a disruption in the epithelial barrier integrity, and that this disruption is inhibited by the Mas receptor agonist AVE0991 through inhibition of epithelial apoptosis. These results reveal a novel potential drug for BPD and pulmonary edema treatment.

背景:新生儿高浓度氧(高氧)治疗是支气管肺发育不良(BPD)的已知原因。BPD的特点是肺通透性增加,各种炎症细胞弥漫性浸润。上皮屏障的破坏可导致肺通透性改变和气道液体积聚。Mas受体是肾素血管紧张素系统的一个组成部分,是保护性内源性肽血管紧张素1-7的受体。Mas受体的激活先前被证明具有保护性肺反应。然而,Mas受体激活对上皮屏障完整性的影响尚未得到验证。目的:探讨高氧诱导或不诱导Mas受体激活对上皮细胞屏障完整性的影响。设计/方法:人上皮细胞系A549在transwell聚碳酸酯多孔膜上培养融合,95%氧(高氧)处理72小时,有或没有Mas受体激动剂(AVE0991),或凋亡抑制剂Z-VAD-FMK或金三羧酸。然后在膜的一侧用罗丹明标记的牛血清白蛋白(Rh-BSA)激射细胞。3小时后,在膜另一侧的培养基上荧光定量Rh-BSA(白蛋白通量),并与21%氧(normmoxia)对照组进行比较。A549细胞加入或不加入AVE0991分别在高氧或常氧条件下培养,碘化丙啶染色进行核碎裂凋亡实验。结果:高氧诱导的白蛋白通量增加被AVE0991和凋亡抑制剂显著阻止。AVE0991还能显著降低高氧诱导的核碎裂。结论:这些结果表明,高氧可导致上皮屏障完整性的破坏,而Mas受体激动剂AVE0991可通过抑制上皮细胞凋亡来抑制这种破坏。这些结果揭示了一种新的潜在药物治疗BPD和肺水肿。
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引用次数: 0
Presentation the new surgicaly approach in the treatment of pediatric lung hydatid disease non–captonage procedure without closure of the communication bronchial opening 介绍一种治疗小儿肺包虫病的新手术方法
Pub Date : 2019-01-01 DOI: 10.15406/jlprr.2019.06.00197
K. K, Mehic B, Guska S
Introduction: Treatment of pediatric lung hydatid disease is primarily surgical, and any suspicion on hydatid lung disease justified indication for surgical intervention. The aim of our research is to investigate efficacy and safety of treatment of residual cavity by "non-capitonage" method, without closure of communicating bronchial opening compared to the classic "capitonage" method with closure of communicating bronchial opening. Patients and Methods: The study included 80 patients of both sexes under aged 18 years, who were surgically treated at the Clinic for Child Surgery and the Department of Thoracic Surgery, Clinical Center University in Sarajevo (KCUS) and Childrens Surgical Clinic of the Institute of Children's Diseases, Clinical Center of Montenegro in Podgorica due to pulmonary echinococcosis, based on clearly defined criteria for inclusion and exclusion from the study. 40 patients (group A) were subjected to non-capitonnage treatment of residual cavity that remained after the removal of parasites and partial pericystectomy without closure of orificium of bronchial opening. The control group consisted of 40 patients who had done narrowing of residual pericystic cavity with closure of bronchial opening. This is a multicenter, open-targeted clinical comparative study of safety of surgery procedures and intraoperative findings. Important aspects of these procedures being assessed included: the duration of the surgical procedure, the amount of administered blood products, drainage length, the amount of secretion, duration of drainage fistula, the time required for reexpansion of lungs, and variables of complications (such as : occurrence of empyema, atelectasis, postoperative fever, postoperative wound infection). Postoperative effectiveness (efficacy) was measured by a record of length of stay in the intensive care unit and hospital stay, as well as radiological findings of the subjects lungs six months after surgery. Results: In the control group we observed that the overall time of surgery was longer compared to the study group. Man-Vitni’s U test confirmed a statistically significant difference between the results of the test and control groups, U = 285.50, z = 4.957, p = 0.0001. Additionally, we observed a slightly larger amount of fluid drained in the control group vs. the study group. Man-Vitni’s U test revealed a statistically significant difference in the amount of drained fluid between the study and control groups, U = 325.50, z = 4.583, p = 0.0001. In the study group there were no cases of postoperative pulmonary atelectasis, while in the control group were 16 (40.0%) patients with documented atelectasis. Mean time to reexpansion of the lung using the control radiological findings was 11 days in the study group (Md = 11.000 days, n = 40) vs. 16 days in the control group of patients (MD = 16.000 days, n = 40) . We also observed that the control group of subjects had significantly longer time in the intensive care unit compared
儿科肺包虫病的治疗主要是手术治疗,任何怀疑包虫病的诊断都需要手术治疗。我们的研究目的是探讨不关闭交通支气管开口的“非资本化”方法与经典的关闭交通支气管开口的“资本化”方法治疗残余腔的疗效和安全性。患者和方法:该研究纳入80例年龄在18岁以下的男女患者,他们在萨拉热窝临床中心大学(KCUS)儿童外科诊所和胸外科以及波德戈里察黑山临床中心儿童疾病研究所儿童外科诊所接受肺棘球蚴病的手术治疗,根据明确的纳入和排除标准。40例患者(A组)在不关闭支气管开口口的情况下,对切除寄生虫和部分包皮切除术后遗留的残余腔进行非资本化治疗。对照组为40例经囊周残余腔狭窄合并支气管开口封闭的患者。这是一项多中心、开放目标的手术安全性和术中发现的临床比较研究。评估这些手术的重要方面包括:手术时间、给血量、引流长度、分泌物量、引流瘘持续时间、肺再扩张所需时间以及并发症的变量(如:发生脓胸、肺不张、术后发热、术后伤口感染)。术后有效性(疗效)通过在重症监护病房和住院时间的记录以及手术后6个月受试者肺部的放射检查结果来衡量。结果:在对照组中,我们观察到手术总时间比研究组长。Man-Vitni’s U检验证实了实验组与对照组的结果有统计学差异,U = 285.50, z = 4.957, p = 0.0001。此外,我们观察到对照组排出的液体量略大于研究组。Man-Vitni’s U检验显示,研究组与对照组的排液量差异有统计学意义,U = 325.50, z = 4.583, p = 0.0001。研究组无术后肺不张病例,对照组有16例(40.0%)记录肺不张。根据对照放射学结果,研究组肺部再扩张的平均时间为11天(Md = 11000天,n = 40),而对照组患者为16天(Md = 16000天,n = 40)。我们还观察到,对照组受试者在重症监护病房的时间明显长于实验组(U = 426.00, z = 3.654, p = 0.0003)。对照组患者住院时间明显长于实验组(U = 373.50, z = 4.112, p = 0.0001)。结论:我们在此报告了我们医疗系统中两种治疗包虫病的手术方法有意义的差异。与术后6个月的对照手术方法相比,非资本化手术方法显著缩短了手术时间,减少了分泌物引流、肺不张和胸膜脓胸事件,缩短了手术干预肺再扩张所需的时间,并改善了总体结果。根据我们的经验,非手术方法比手术方法更有利,这反映在患者术后在重症监护病房和医院的住院时间明显缩短。对于儿童肺包虫病残留的囊周腔,特别是巨大、复杂、多发包虫病,应采用“非闭合”或“非狭窄”(非capitonnage)的治疗方法,因为残留的囊周腔会被周围胸膜和肺实质的上皮细胞迅速覆盖
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引用次数: 1
PM2.5, PM2.5-related air pollutants, health hazards and impacts on respiratory and cardiovascular disorders and diseases: systematic review and meta-analysis PM2.5、PM2.5相关空气污染物、健康危害及其对呼吸和心血管疾病的影响:系统综述和荟萃分析
Pub Date : 2019-01-01 DOI: 10.15406/jlprr.2019.06.00205
A. Cheepsattayakorn, R. Cheepsattayakorn
The objective of the study is to perform a critical review, exploration, and strong summary of the relationships between personal and ambient concentrations of mainly particulate matter with diameter of 2.5µm or less with the measures of cardiopulmonary health. A comprehensive search was carried out in mainstream bibliographic databases or Medical Subject Headings, including Scien Direct, PubMed, Scopus, and ISI Web of Science. The search was applied to the articles that were published between 2017 and early 2019. Needed article information was extracted from each article by: direct information including journal (research article, review article, meeting abstract, conference abstract, correspondence, author index, editorial board meeting abstract, discussion), book chapter, title, authors, abstract, full text documents of candidate studies, publishing year. Study period, Research (study) method used, types of air pollutants variables studied; Types of organ system disorder or disease studied The conclusions made about the health hazards, impacts on humans or animal models, novel therapeutics, and economic loss. With strict literature search and screening processes, it yielded 140 articles (2017=45; 2018=61; and early 2019=34 articles) from 3,968 articles of initial literature database (1952-early 2019). The main compositions of air pollutants are PM, particularly PM2.5 and PM10, O3, CO, SO2, and NOx. Exposure to O3 is frequently associated with respiratory tract inflammation, whereas exposure to PM, CO, No2, and SO2 is related to pulmonary edema, respiratory and cardiovascular hospitalizations, and cardiopulmonary mortality. Any compromise to endothelial cells, the key components of lung barrier integrity contributes to vascular leakage and inflammation. Endothelial cells could be the target of PM exposure. The various effects on various disease entities contribute to hypothesize that Melatonin might protect the lung integrity against PM2.5-induced acute lung injury. Bufei Huoxue (BFHX) could reduce secretory immunoglobulin A (sIgA) and collagen fibers deposition in lung, thus, improved pulmonary function. In conclusion, identification of various crucial signaling pathway involving PM-induced cardiopulmonary disorders and diseases may assist in the development of effective therapeutics, including clean energy use, clean industrialization, proper agriculture, high land use diversity, and proper urbanization for reduction of the air pollution.
该研究的目的是对个人和环境中直径为2.5微米或更小的主要颗粒物浓度与心肺健康指标之间的关系进行批判性审查、探索和强有力的总结。在主流书目数据库或医学主题词中进行了全面的检索,包括Scien Direct、PubMed、Scopus和ISI Web of Science。该搜索应用于2017年至2019年初发表的文章。从每篇文章中提取所需的文章信息:直接信息包括期刊(研究文章、综述文章、会议摘要、会议摘要、通信、作者索引、编委会会议摘要、讨论)、图书章节、标题、作者、摘要、候选研究全文文件、出版年份。研究期限、采用的研究(研究)方法、研究的空气污染物类型变量;所研究的器官系统紊乱或疾病的类型,对健康的危害,对人类或动物模型的影响,新的治疗方法和经济损失的结论。经过严格的文献检索和筛选过程,共获得140篇文献(2017=45;2018 = 61;初始文献数据库(1952- 2019年初)3968篇,2019年初=34篇)。大气污染物的主要成分是PM,特别是PM2.5和PM10、O3、CO、SO2和NOx。暴露于臭氧通常与呼吸道炎症有关,而暴露于PM、CO、No2和SO2则与肺水肿、呼吸道和心血管住院以及心肺死亡率有关。任何损害内皮细胞,肺屏障完整性的关键组成部分,有助于血管渗漏和炎症。内皮细胞可能是PM暴露的目标。褪黑素对各种疾病实体的各种影响有助于假设褪黑素可能保护肺完整性免受pm2.5诱导的急性肺损伤。补肺活血(BFHX)可降低肺组织分泌性免疫球蛋白A (sIgA)和胶原纤维沉积,改善肺功能。总之,识别涉及pm诱导的心肺紊乱和疾病的各种关键信号通路可能有助于开发有效的治疗方法,包括清洁能源使用、清洁工业化、适当农业、高度土地利用多样性和适当城市化,以减少空气污染。
{"title":"PM2.5, PM2.5-related air pollutants, health hazards and impacts on respiratory and cardiovascular disorders and diseases: systematic review and meta-analysis","authors":"A. Cheepsattayakorn, R. Cheepsattayakorn","doi":"10.15406/jlprr.2019.06.00205","DOIUrl":"https://doi.org/10.15406/jlprr.2019.06.00205","url":null,"abstract":"The objective of the study is to perform a critical review, exploration, and strong summary of the relationships between personal and ambient concentrations of mainly particulate matter with diameter of 2.5µm or less with the measures of cardiopulmonary health. A comprehensive search was carried out in mainstream bibliographic databases or Medical Subject Headings, including Scien Direct, PubMed, Scopus, and ISI Web of Science. The search was applied to the articles that were published between 2017 and early 2019. Needed article information was extracted from each article by: direct information including journal (research article, review article, meeting abstract, conference abstract, correspondence, author index, editorial board meeting abstract, discussion), book chapter, title, authors, abstract, full text documents of candidate studies, publishing year. Study period, Research (study) method used, types of air pollutants variables studied; Types of organ system disorder or disease studied The conclusions made about the health hazards, impacts on humans or animal models, novel therapeutics, and economic loss. With strict literature search and screening processes, it yielded 140 articles (2017=45; 2018=61; and early 2019=34 articles) from 3,968 articles of initial literature database (1952-early 2019). The main compositions of air pollutants are PM, particularly PM2.5 and PM10, O3, CO, SO2, and NOx. Exposure to O3 is frequently associated with respiratory tract inflammation, whereas exposure to PM, CO, No2, and SO2 is related to pulmonary edema, respiratory and cardiovascular hospitalizations, and cardiopulmonary mortality. Any compromise to endothelial cells, the key components of lung barrier integrity contributes to vascular leakage and inflammation. Endothelial cells could be the target of PM exposure. The various effects on various disease entities contribute to hypothesize that Melatonin might protect the lung integrity against PM2.5-induced acute lung injury. Bufei Huoxue (BFHX) could reduce secretory immunoglobulin A (sIgA) and collagen fibers deposition in lung, thus, improved pulmonary function. In conclusion, identification of various crucial signaling pathway involving PM-induced cardiopulmonary disorders and diseases may assist in the development of effective therapeutics, including clean energy use, clean industrialization, proper agriculture, high land use diversity, and proper urbanization for reduction of the air pollution.","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80435812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
A comprehensive review study on pneumococcal pneumonia and its association with global mortality and morbidity 肺炎球菌性肺炎及其与全球死亡率和发病率的关系的综合综述研究
Pub Date : 2018-12-11 DOI: 10.15406/jlprr.2018.05.00190
Mohammed Alsaleh, Mohammed Aljeshi, Yazid A Alghamdi, Abdulaziz Althumair, Ali Alghareeb, Saleh Aldeailj, Hussain Alsadah, S. Mohiuddin
2,500 years ago, stated by Hippocrates [460BC–370BC]1 “When pneumonia is at its height, the case is beyond remedy if he is not purged.” In Pre-antibiotic era “Pneumonia has become captain of the men of death.” Stated by Dr. William Osler, the founder of modern medicine In 1928: The Greatest Discovery in the Medical Field took place by the discovery of penicillin by Alexander Fleming and the subsequent widespread use of antibiotics, penicillin revolutionized the treatment of patients with pneumococcal pneumonia, which previously had been limited to watchful waiting. Today availability of vaccination reduced the frequency of pneumonia. Many diagnostic methods and procedures are used. Despite all the advances, pneumonia remains a huge issue. Even after the introduction of fist-generation antibiotics, the mortality rate for pneumonia has not changed noticeably in the last 50 years.1
2500年前,希波克拉底(公元前460 - 370年)说:“当肺炎最严重的时候,如果不清除,就无法治愈。”在前抗生素时代,“肺炎已经成为人类死亡的首领。”1928年,现代医学的创始人威廉·奥斯勒博士说:医学领域最伟大的发现发生在亚历山大·弗莱明发现青霉素和随后抗生素的广泛使用,青霉素彻底改变了肺炎球菌肺炎患者的治疗,以前这种治疗仅限于观察等待。如今,疫苗接种减少了肺炎的发生频率。使用了许多诊断方法和程序。尽管取得了这些进展,但肺炎仍然是一个巨大的问题。即使在引进了第一代抗生素之后,肺炎的死亡率在过去的50年里也没有明显的变化
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引用次数: 0
Epidemioclinical, etiological and evolutionary aspects of neoplastic pleurisy in the pneumo-phtisiology department of the University Hospital Sylvanus Olympio of Lomé (Togo) 多哥洛莫雷大学希尔瓦努斯·奥林匹奥医院肺生理科肿瘤性胸膜炎的流行临床、病因学和进化
Pub Date : 2018-12-03 DOI: 10.15406/jlprr.2018.05.00189
Kuire Marcel
Neoplastic pleurisy (NP) is defined by the presence of tumor cells in the pleural fluid or pleural tissue.1 They are due either to a primary lesion of the pleura (mesothelioma) or to a secondary location of a bronchopulmonary or extrathoracic tumor. In sub-Saharan Africa, with better explorations (pleural biopsy) in the case of exudative pleurisy and histopathological examination of pleural fragments, we have been witnessing an increase in the proportion of cancer etiologies in recent years.
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引用次数: 0
Bronchial foreign body-presentation of a case 支气管异物1例报告
Pub Date : 2018-11-19 DOI: 10.15406/jlprr.2018.05.00187
Dulvis Amanda Almeida Arias, William Mauricio Lopez Andino, Rene Elejalde Angel Larrinaga, K. Ramirez Fajardo
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引用次数: 0
Diffuse lung disease caused by cotton dust exposure 棉尘暴露引起的弥漫性肺病
Pub Date : 2018-11-19 DOI: 10.15406/jlprr.2018.05.00188
B. Menon, P. Mrigpuri, M. Tiwari, P. Raj
In India, 20million workers are involved in the manufacturing of textiles.1 Byssinosis is caused by the inhalation of cotton, jute, flax and hemp fibers. It is a type of hypersensitivity pneumonitis. Byssinosis is characterized by acute breathlessness, cough, and wheeze, typically on Monday mornings following a weekend away from the workplace; symptoms decrease during the work week despite continued exposure. The prevalence and severity of symptoms and functional impairment are proportional to the duration and intensity of exposure.2 Although the pathogenesis of Byssinosis is unclear, the disorder shares some features with hypersensitivity pneumonitis: Both frequently occur after exposure to dust, and affected patients improve rapidly without therapy.2,3 There have been only a few reports of pulmonary fibrosis and pneumoconiosis due to cotton dust.4
在印度,2000万工人从事纺织品制造业螺旋体病是由吸入棉花、黄麻、亚麻和大麻纤维引起的。这是一种过敏性肺炎。螺旋体病的特征是急性呼吸困难、咳嗽和喘息,通常发生在周末离开工作场所后的周一早晨;尽管持续接触,但在工作周内症状会减轻。症状和功能损害的发生率和严重程度与暴露的持续时间和强度成正比虽然螺旋体病的发病机制尚不清楚,但该疾病与超敏性肺炎有一些共同特征:两者都常在接触粉尘后发生,患者无需治疗即可迅速好转。由于棉尘引起肺纤维化和尘肺病的报道很少
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引用次数: 1
Paraquat poisoning and the lung pathology; vascular injury leading to thrombotic microangiopathy is the primary pathological event 百草枯中毒与肺部病理;血管损伤导致血栓性微血管病变是主要的病理事件
Pub Date : 2018-11-16 DOI: 10.15406/JLPRR.2018.05.00185
H. Daisley, A. Rampersad, O. Acco, D. Meyers
Paraquat is an agent that is used in suicide in many agricultural societies.1‒3 Its ingestion is almost always fatal. Respiratory failure plays a significant role in the demise of these victims as pulmonary fibrosis ultimately occurs. The literature abounds with theories as to the pathogenesis of paraquat toxicity, most of which focuses on the inflammatory infiltrates and the pneumocytes’ response in the lung in paraquat poisoning. As a result immunosuppressive and anti-fibrosis therapies have been tailored against these latter pathophysiological mechanisms,4,5 needless to say these therapies have been met with little success.
百草枯是一种在许多农业社会用于自杀的药剂。它的摄入几乎总是致命的。随着肺纤维化的最终发生,呼吸衰竭在这些患者的死亡中起着重要作用。关于百草枯中毒的发病机制,文献中有丰富的理论,但多集中在百草枯中毒时肺内的炎症浸润和肺细胞的反应。因此,免疫抑制和抗纤维化治疗已经针对这些后一种病理生理机制进行了定制,不用说,这些治疗几乎没有成功。
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引用次数: 3
A case report-a subcutaneous sarcoidosis mimicking tumour 皮下结节病模拟肿瘤1例报告
Pub Date : 2018-11-16 DOI: 10.15406/JLPRR.2018.05.00186
P. Kumar, S. Basu
Sarcoidosis is a multisystem granulomatous disorder of unknown aetiology that affects individuals worldwide and is characterized pathologically by the presence of non-caseating granulomas in involved organs and tissues.1 Jonathan Hutchinson described the first case in 1869.2 It involves skin, lung, lymph nodes, eyes, joints, brain, kidneys, and heart. Skin involvement is the second most following pulmonary sarcoidosis. Nodular Muscle involvement in sarcoidosis was first reported by Licharew in 1908. 25% patients of sarcoidosis presents with cutaneous lesions, it varies in morphologies, including papules, nodules, plaques, and infiltrated scars3 versus subcutaneous sarcoidosis occurs in 1.4 to 6 % patients of systemic sarcoidosis. Subcutaneous sarcoidosis affects women commonly, in their fifth and sixth decades. Lesions could be multiple, bilateral, asymmetrical, asymptomatic hard indurate mobile subcutaneous nodule/nodules located in upper extremities, commonly involves forearm, without any changes in overlying epidermis.4 Nodular muscular sarcoidosis often mimics a tumour .To rule out this confusion MRI and muscle biopsy are useful investigations.5,6 Biopsy and histopathological examination is the gold standard method of diagnosis which shows “naked” granuloma formation which has sparse lymphocytes at margin with epithelioid cells with little or no necrosis. Diagnosis is confirmed after ruling out differentials which cause granulomatous lesion.7 Initial treatment option is steroid. Immunosuppressive agents have been used in corticosteroid resistant form.8 Here, we report the case of asymptomatic nodular sarcoidosis with pulmonary involvement showing bilateral hilar lymphadenopathy and small pulmonary nodules on imaging which was initially thought to be fibro-sarcoma.
结节病是一种病因不明的多系统肉芽肿性疾病,影响世界各地的个体,其病理特征是受累器官和组织中存在非干酪化肉芽肿1869.2年,乔纳森·哈钦森(Jonathan Hutchinson)描述了第一个病例,它涉及皮肤、肺、淋巴结、眼睛、关节、大脑、肾脏和心脏。皮肤受累是仅次于肺结节病的第二大疾病。结节性肌肉累及结节病是1908年由Licharew首次报道的。25%的结节病患者表现为皮肤病变,其形态各异,包括丘疹、结节、斑块和浸润性瘢痕,而系统性结节病患者的皮下结节病发生率为1.4%至6%。皮下结节病常见于五六十岁的妇女。病变可为多发、双侧、不对称、无症状、坚硬、硬化、可移动的皮下结节/结节,位于上肢,常累及前臂,上覆表皮无任何改变结节性肌肉结节病常与肿瘤相似。为了排除这种混淆,MRI和肌肉活检是有用的检查。5,6活检和组织病理学检查是诊断的金标准方法,显示“裸”肉芽肿形成,边缘有稀疏的淋巴细胞,上皮样细胞很少或没有坏死。排除引起肉芽肿病变的鉴别后确诊最初的治疗选择是类固醇。免疫抑制剂已用于皮质类固醇耐药形式在此,我们报告一例无症状结节性结节病累及肺部,表现为双侧肺门淋巴结病变和小肺结节,最初被认为是纤维肉瘤。
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引用次数: 1
期刊
Journal of lung, pulmonary & respiratory research
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