Neopterin in patients with COPD, asthma, and ACO: association with endothelial and lung functionsRespiratory Research - Tập 25 Số 1
Yangli Liu, Fengjia Chen, Zhifan Zeng, Chengcheng Lei, Dubo Chen, Xiaoyu Zhang
Abstract Background and objective Endothelial dysfunction has been widely
recognized in chronic airway diseases, including chronic obstructive pulmonary
disease (COPD) and asthma; however, it remains unclear in asthma-COPD overlap
(ACO). Neopterin (NP), a metabolite of guanosine triphosphate, is a novel
biomarker for identifying the increased risk of adverse cardiovascular events.
This study aims ... hiện toàn bộ
Impaired cell–cell communication and axon guidance because of pulmonary hypoperfusion during postnatal alveolar developmentRespiratory Research - Tập 24 - Trang 1-17 - 2023
Debao Li, Jing Wang, Yuan Fang, Yuqing Hu, Yingying Xiao, Qing Cui, Chuan Jiang, Sijuan Sun, Hao Chen, Lincai Ye, Qi Sun
Pulmonary hypoperfusion is common in children with congenital heart diseases
(CHDs) or pulmonary hypertension (PH) and causes adult pulmonary dysplasia.
Systematic reviews have shown that some children with CHDs or PH have mitigated
clinical outcomes with COVID-19. Understanding the effects of pulmonary
hypoperfusion on postnatal alveolar development may aid in the development of
methods to improv... hiện toàn bộ
Sputum ACE2, TMPRSS2 and FURIN gene expression in severe neutrophilic asthmaRespiratory Research - Tập 22 - Trang 1-10 - 2021
Nazanin Zounemat Kermani, Woo-Jung Song, Yusef Badi, Ali Versi, Yike Guo, Kai Sun, Pank Bhavsar, Peter Howarth, Sven-Erik Dahlen, Peter J. Sterk, Ratko Djukanovic, Ian M. Adcock, Kian Fan Chung
Patients with severe asthma may have a greater risk of dying from COVID-19
disease. Angiotensin converting enzyme-2 (ACE2) and the enzyme proteases,
transmembrane protease serine 2 (TMPRSS2) and FURIN, are needed for viral
attachment and invasion into host cells. We examined microarray mRNA expression
of ACE2, TMPRSS2 and FURIN in sputum, bronchial brushing and bronchial biopsies
of the European U... hiện toàn bộ
Nitric oxide induces MUC5AC mucin in respiratory epithelial cells through PKC and ERK dependent pathwaysRespiratory Research - Tập 8 - Trang 1-12 - 2007
Jeong Sup Song, Chun Mi Kang, Moon Bin Yoo, Seung Joon Kim, Hyung Kyu Yoon, Young Kyoon Kim, Kwan Hyung Kim, Hwa Sik Moon, Sung Hak Park
Nitric oxide (NO) is generally increased during inflammatory airway diseases.
This increased NO stimulates the secretion of mucin from the goblet cell and
submucosal glands but the mechanism is still unknown precisely. In this study,
we investigated potential signaling pathways involving protein kinase C (PKC)
and mitogen-activated protein kinase (MAPK) in the NO-induced MUC5AC mucin gene
and prot... hiện toàn bộ
Uric acid, lung function, physical capacity and exacerbation frequency in patients with COPD: a multi-dimensional approachRespiratory Research - Tập 19 - Trang 1-10 - 2018
Kathrin Kahnert, Peter Alter, Tobias Welte, Rudolf M. Huber, Jürgen Behr, Frank Biertz, Henrik Watz, Robert Bals, Claus F. Vogelmeier, Rudolf A. Jörres
Recent investigations showed single associations between uric acid levels,
functional parameters, exacerbations and mortality in COPD patients. The aim of
this study was to describe the role of uric acid within the network of multiple
relationships between function, exacerbation and comorbidities. We used baseline
data from the German COPD cohort COSYCONET which were evaluated by standard
multiple... hiện toàn bộ
Enhanced endogenous bone morphogenetic protein signaling protects against bleomycin induced pulmonary fibrosisRespiratory Research - Tập 16 - Trang 1-10 - 2015
Ellen De Langhe, Frederic Cailotto, Vanessa De Vooght, Carolina Aznar-Lopez, Jeroen Alfons Vanoirbeek, Frank Prosper Luyten, Rik Jozef Urbain Lories
Effective treatments for fibrotic diseases such as idiopathic pulmonary fibrosis
are largely lacking. Transforming growth factor beta (TGFβ) plays a central role
in the pathophysiology of fibrosis. We hypothesized that bone morphogenetic
proteins (BMP), another family within the TGFβ superfamily of growth factors,
modulate fibrogenesis driven by TGFβ. We therefore studied the role of
endogenous BM... hiện toàn bộ
Analysis of body mass index, weight loss and progression of idiopathic pulmonary fibrosisRespiratory Research - Tập 21 - Trang 1-11 - 2020
Stéphane Jouneau, Bruno Crestani, Ronan Thibault, Mathieu Lederlin, Laurent Vernhet, Claudia Valenzuela, Marlies Wijsenbeek, Michael Kreuter, Wibke Stansen, Manuel Quaresma, Vincent Cottin
Nintedanib is an approved therapy for idiopathic pulmonary fibrosis (IPF). Some
patients treated with nintedanib experience weight loss. Exploratory data
suggest that low body mass index or weight loss are associated with worse
outcomes in patients with IPF. We investigated whether BMI at baseline or weight
loss over 52 weeks was associated with FVC decline, or influenced the effect of
nintedanib,... hiện toàn bộ
Influenza A virus enhances ciliary activity and mucociliary clearance via TLR3 in airway epitheliumRespiratory Research - Tập 21 - Trang 1-13 - 2020
Yosuke Kamiya, Tomoyuki Fujisawa, Mineo Katsumata, Hideki Yasui, Yuzo Suzuki, Masato Karayama, Hironao Hozumi, Kazuki Furuhashi, Noriyuki Enomoto, Yutaro Nakamura, Naoki Inui, Mitsutoshi Setou, Masahiko Ito, Tetsuro Suzuki, Koji Ikegami, Takafumi Suda
Viral respiratory tract infections, such as influenza A virus (IAV), are common
and life-threatening illnesses worldwide. The mechanisms by which viruses are
removed from the respiratory tract are indispensable for airway host defense.
Mucociliary clearance is an airway defense mechanism that removes pathogens from
the respiratory tract. The coordination and modulation of the ciliary beating of
ai... hiện toàn bộ
Erratum to: Risk factors for mortality in patients admitted to intensive care units with pneumoniaRespiratory Research - Tập 17 - Trang 1-1 - 2016
Guowei Li, Deborah J. Cook, Lehana Thabane, Jan O. Friedrich, Tim M. Crozier, John Muscedere, John Granton, Sangeeta Mehta, Steven C. Reynolds, Renato D. Lopes, Francois Lauzier, Andreas P. Freitag, Mitchell A. H. Levine