scholarly journals Idiopathic Premature Ventricular Contractions Arising From the Pulmonary Artery

2005 ◽  
Vol 69 (7) ◽  
pp. 865-869 ◽  
Author(s):  
Hiroshi Tada ◽  
Kenji Kurosaki ◽  
Sachiko Ito ◽  
Shigeto Naito ◽  
Minoru Yamada ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Premature Ventricular Contractions

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

Symptom-free T4 lung cancer with bilateral pulmonary artery infiltration

2005 ◽  
Vol 6 (1) ◽  
pp. 64-64
Author(s):  
A CESARIO ◽  
D ONORATI ◽  
V CARDACI ◽  
S MARGARITORA ◽  
V PORZIELLA ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Pulmonary Artery ◽  
Free T4 ◽  
T4 Lung Cancer

Dilatation of the entire thoracic aorta in patients with bicuspid aortic valve: a magnetic resonance angiography study

VASA ◽  
2005 ◽  
Vol 34 (3) ◽  
pp. 181-185 ◽  
Author(s):  
Westhoff-Bleck ◽  
Meyer ◽  
Lotz ◽  
Tutarel ◽  
Weiss ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Magnetic Resonance Angiography ◽  
Aortic Valve ◽  
Pulmonary Artery ◽  
Aortic Arch ◽  
Thoracic Aorta ◽  
Aortic Root ◽  
Ascending Aorta ◽  
Descending Aorta ◽  
Severe Aortic Regurgitation

Background: The presence of a bicuspid aortic valve (BAV) might be associated with a progressive dilatation of the aortic root and ascending aorta. However, involvement of the aortic arch and descending aorta has not yet been elucidated. Patients and methods: Magnetic resonance angiography (MRA) was used to assess the diameter of the ascending aorta, aortic arch, and descending aorta in 28 patients with bicuspid aortic valves (mean age 30 ± 9 years). Results: Patients with BAV, but without significant aortic stenosis or regurgitation (n = 10, mean age 27 ± 8 years, n.s. versus control) were compared with controls (n = 13, mean age 33 ± 10 years). In the BAV-patients, aortic root diameter was 35.1 ± 4.9 mm versus 28.9 ± 4.8 mm in the control group (p < 0.01). The diameter of the ascending aorta was also significantly increased at the level of the pulmonary artery (35.5 ± 5.6 mm versus 27.0 ± 4.8 mm, p < 0.001). BAV-patients with moderate or severe aortic regurgitation (n = 18, mean age 32 ± 9 years, n.s. versus control) had a significant dilatation of the aortic root, ascending aorta at the level of the pulmonary artery (41.7 ± 4.8 mm versus 27.0 ± 4.8 mm in control patients, p < 0.001) and, furthermore, significantly increased diameters of the aortic arch (27.1 ± 5.6 mm versus 21.5 ± 1.8 mm, p < 0.01) and descending aorta (21.8 ± 5.6 mm versus 17.0 ± 5.6 mm, p < 0.01). Conclusions: The whole thoracic aorta is abnormally dilated in patients with BAV, particularly in patients with moderate/severe aortic regurgitation. The maximum dilatation occurs in the ascending aorta at the level of the pulmonary artery. Thus, we suggest evaluation of the entire thoracic aorta in patients with BAV.

State-of-the-art pulmonary arterial imaging – Part 2

VASA ◽  
2018 ◽  
Vol 47 (5) ◽  
pp. 361-375 ◽  
Author(s):  
Harold Goerne ◽  
Abhishek Chaturvedi ◽  
Sasan Partovi ◽  
Prabhakar Rajiah
Keyword(s):  
Pulmonary Artery ◽  
State Of The Art ◽  
Therapy Monitoring ◽  
Pulmonary Arteries ◽  
Imaging Modalities ◽  
Cross Sectional ◽  
Multiple Imaging ◽  
Cross Sectional Imaging ◽  
Pulmonary Arterial ◽  
Arterial Imaging

Abstract. Although pulmonary embolism is the most common abnormality of the pulmonary artery, there is a broad spectrum of other congenital and acquired pulmonary arterial abnormalities. Multiple imaging modalities are now available to evaluate these abnormalities of the pulmonary arteries. CT and MRI are the most commonly used cross-sectional imaging modalities that provide comprehensive information on several aspects of these abnormalities, including morphology, function, risk-stratification and therapy-monitoring. In this article, we review the role of state-of-the-art pulmonary arterial imaging in the evaluation of non-thromboembolic disorders of pulmonary artery.

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