Effect of Soyasaponin on Pulmonary Tissue Apoptosis of Silicotic Fibrosis Rats

Author(s):  
Houjun Xu ◽  
Yu Su ◽  
Qingzhao Li ◽  
Jianhui Wu ◽  
Yulan Hao ◽  
...  
Keyword(s):  
Author(s):  
Kyoung Ah Kim ◽  
Young Lim ◽  
Dong Won Lee ◽  
Heung Nam Kim ◽  
Hwang Sin Chang ◽  
...  

Author(s):  
Savvas Lampridis ◽  
Sofoklis Mitsos ◽  
David R. Lawrence ◽  
Nikolaos Panagiotopoulos

Lung decortication for the treatment of chronic pleural empyema remains a technically challenging procedure that is associated with bleeding and air leak. The recent advent of pure argon plasma has provided thoracic surgeons with an electrically neutral energy source for dissection and coagulation of pulmonary tissue with minimal depth of necrosis. In this article, we describe the technique of lung decortication with argon plasma energy (PlasmaJet, Plasma Surgical, Roswell, GA, USA) for the treatment of chronic pleural empyema. With appropriate application, the PlasmaJet can facilitate the removal of fibrous cortex with satisfactory hemostasis and aerostasis. Argon plasma energy can potentially be a useful adjunct in lung decortication. Controlled trials are needed to determine its role in the surgical management of advanced pleural empyema.


Author(s):  
Davide Ventura ◽  
Amy L Carr ◽  
R Duane Davis ◽  
Scott Silvestry ◽  
Linda Bogar ◽  
...  

Abstract It has been established SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2), a membrane-bound regulatory peptide, for host cell entry. Renin-angiotensin-aldosterone system (RAAS) inhibitors have been reported to increase ACE2 in type 2 pneumocytes pulmonary tissue. Controversy exists for the continuation of ACE inhibitors, angiotensin II receptor blockers (ARBs), and mineralocorticoid receptor antagonists (MRAs) in the current pandemic. ACE2 serves as regulatory enzyme in maintaining homeostasis between proinflammatory Angiotensin II and anti-inflammatory Angiotensin 1,7 peptides. Derangements in these peptides are associated with cardiovascular disease and are implicated in the progression of acute respiratory distress syndrome (ARDS). Augmentation of the ACE2/Ang1,7 axis represent a critical target in the supportive management of COVID-19 associated lung disease. Observational data describing the use of RAAS inhibitors in the setting of SARS-CoV-2 have not borne signals of harm to date. However, equipoise persists requiring an analysis of novel agents including recombinant human-ACE2 and existing RAAS inhibitors while balancing ongoing controversies associated with increased coronavirus infectivity and virulence.


2012 ◽  
Vol 13 (1) ◽  
pp. 726-736
Author(s):  
Dennis G. Hooper ◽  
Vincent E. Bolton ◽  
John S. Sutton ◽  
Frederick T. Guilford ◽  
David C. Straus ◽  
...  

2021 ◽  
Vol 39 ◽  
pp. 101069
Author(s):  
Ivo M.B. Francischetti ◽  
Kevin Toomer ◽  
Yifan Zhang ◽  
Jayesh Jani ◽  
Zishan Siddiqui ◽  
...  

2005 ◽  
Vol 18 (1) ◽  
pp. 28-34 ◽  
Author(s):  
James F. Dillman ◽  
Christopher S. Phillips ◽  
Linda M. Dorsch ◽  
Matthew D. Croxton ◽  
Alison I. Hege ◽  
...  

1994 ◽  
Vol 20 (3) ◽  
pp. 169-184 ◽  
Author(s):  
Maria B. Lucia Garcia ◽  
Paulo S. O. Paiva ◽  
Marisa Dolhnikoff ◽  
Sonia Jancar ◽  
Paulo H. N. Saldiva ◽  
...  

PEDIATRICS ◽  
1990 ◽  
Vol 86 (4) ◽  
pp. 620-623
Author(s):  
BEVERLEY NEWMAN

Pulmonary sequestrations are congenital masses of aberrant, nonfunctioning pulmonary tissue that usually do not connect with the bronchial tree and derive their arterial blood supply from systemic vessels, most often the distal thoracic or upper abdominal aorta. The majority of sequestrations are intralobar and contained within the visceral pleura of the normal lung; these usually have their venous drainage to the pulmonary venous system. Extralobar sequestrations have a separate pleural covering and usually drain to systemic veins or the portal venous system.1-3 Patients most often come to clinical attention with repeated respiratory infections.2 The sequestered segment is usually visualized radiographically as a nonaerated opacity at the medial lung base, more often left-sided.


Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Allan K Alencar ◽  
Sharlene L Pereira ◽  
Arthur E Kummerle ◽  
Sharon S Langraf ◽  
Celso Caruso-Neves ◽  
...  

Pulmonary arterial hypertension (PAH) is characterized by enhanced pulmonary vascular resistance with subsequent remodeling and right ventricular hypertrophy. Vascular reactivity and ventricular function were investigated in rats with monocrotaline-induced PAH and treated with a new N-acylhydrazone derivative named as LASSBio-1359. METHODS: Protocols were approved by Animal Care and Use Committee at Universidade Federal do Rio de Janeiro. Male Wistar rats received a single i.p. injection of monocrotaline (MCT) (60 mg/kg) for PAH induction and were randomly divided in groups which were treated with: saline, vehicle and LASSBio-1359 (50 mg/kg p.o.). After 14 days of treatment, some parameters were evaluated: pulmonary acceleration time (PAT); right ventricular systolic pressure (RVSP); vascular reactivity to acetylcholine; expression of iNOS in pulmonary tissue; wall thickness of pulmonary artery (PAWT). Results: PAT (ms) was increased from 26.2 ± 2.8 to 41.3 ± 3.9 in PAH group treated with vehicle (n=8, p<0.05) and was reduced to 24.2 ± 1.7 when PAH group was treated with LASSBio-1359. RVSP (mmHg) increased from 26.0 ± 2.0 to 55.2 ± 2.3 in PAH group (p<0.05) but was similar to control after treatment with LASSBio-1359 (31.8 ± 2.3 mm Hg). Ratio of right ventricle and body weight (mg/g) was 0.66 ± 0.02, 1.63 ± 0.16 and 0.87 ± 0.10 for control, vehicle- and LASSBio-1359-treated PAH groups, respectively. PAH promoted ventricular dysfunction which was reduced by LASSBio-1359. The pulmonary artery maximum relaxation (%) was 57.3 ± 5.5, 43.6 ± 1.2 and 61.4 ± 8.4 for control, vehicle and LASSBio-1359-treated groups indicating that PAH promoted endothelium injury which was recovered by LASSBio-1359. iNOS expression in pulmonary tissue was increased from 0.48 ± 1.31 to 0.98 ± 3.14 in PAH group and reduced to 0.53 ± 1.83 in rats treated with LASSBio-1359. The PAWT (%) were increased from 74.1 ± 1.3 to 90.2 ± 2.7 in PAH group (p<0.05) but was 74.4 ± 1.3 when treated with LASSBio-1359. This compound showed an in vitro vasodilatory activity mediated by activation of adenosinergic A2A receptor. Conclusion: LASSBio-1359 reduced ventricular and vascular dysfunction in monocrotaline-induced PAH in rats indicating a possible new alternative to treat PAH.


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