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https://www.readbyqxmd.com/read/28633205/advancing-the-science-of-myocardial-recovery-with-mechanical-circulatory-support-a-working-group-of-the-national-heart-lung-and-blood-institute
#1
EDITORIAL
Stavros G Drakos, Francis D Pagani, Martha S Lundberg, Timothy J Baldwin
The medical burden of heart failure (HF) has spurred interest in clinicians and scientists to develop therapies to restore the function of a failing heart. To advance this agenda, the National Heart, Lung, and Blood Institute (NHLBI) convened a Working Group of experts from June 2 to 3, 2016, in Bethesda, Maryland, to develop NHLBI recommendations aimed at advancing the science of cardiac recovery in the setting of mechanical circulatory support (MCS). MCS devices effectively reduce volume and pressure overload that drives the cycle of progressive myocardial dysfunction, thereby triggering structural and functional reverse remodeling...
July 2017: Journal of Thoracic and Cardiovascular Surgery
https://www.readbyqxmd.com/read/28627661/altered-expression-of-ppar%C3%A2-%C3%AE-and-trpc-in-neonatal-rats-with-persistent-pulmonary-hypertension
#2
Yanna Du, Jianhua Fu, Li Yao, Lin Qiao, Na Liu, Yujiao Xing, Xindong Xue
Persistent pulmonary hypertension of the newborn (PPHN) is a life‑threatening disease that is commonly observed in the neonatal intensive care unit. PPHN is pathologically characterized by pulmonary vascular remodeling and, in particular, pulmonary artery smooth muscle cell (PASMC) proliferation. Decreased expression levels of peroxisome proliferator‑activated receptor γ (PPAR‑γ), which is a member of the nuclear receptor hormone superfamily, in combination with elevated expressions of transient receptor potential cation channel, subfamily C, member 1 (TRPC1) and TRPC6 contributes to the PASMC proliferation and excessive pulmonary vascular remodeling in adult pulmonary hypertension (PH)...
June 9, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28626025/intranasal-administration-of-mesenchymoangioblast-derived-mesenchymal-stem-cells-abrogates-airway-fibrosis-and-airway-hyperresponsiveness-associated-with-chronic-allergic-airways-disease
#3
Simon G Royce, Siddharth Rele, Brad R S Broughton, Kilian Kelly, Chrishan S Samuel
Structural changes known as airway remodeling (AWR) characterize chronic/severe asthma and contribute to lung dysfunction. Thus, we assessed the in vivo efficacy of induced pluripotent stem cell and mesenchymoangioblast-derived mesenchymal stem cells (MCA-MSCs) on AWR in a murine model of chronic allergic airways disease (AAD)/asthma. Female Balb/c mice were subjected to a 9-wk model of ovalbumin (OVA)-induced chronic AAD and treated intravenously or intranasally with MCA-MSCs from weeks 9 to11. Changes in airway inflammation (AI), AWR, and airway hyperresponsiveness (AHR) were assessed...
June 16, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28625359/roles-of-arf6-in-cancer-cell-invasion-metastasis-and-proliferation
#4
REVIEW
Rui Li, Cheng Peng, Xianzhe Zhang, Yuewei Wu, Shida Pan, Yechen Xiao
ADP-ribosylation factor 6 (Arf6), a member of small GTPases ADP-ribosylation factor (Arf) family, expresses widely in mammalian cells and mainly regulates the functions of membrane traffic and actin remodeling. Current studies indicated that the activation and high expression of Arf6 protein may be significantly correlated with the invasion and metastasis of several tumors, such as breast cancer, pancreatic cancer, lung cancer, etc. Meanwhile, the ability of tumor invasion and metastasis can be suppressed when Arf6 activity is blocked by the inhibitors or small-interfering RNAs of Arf6...
June 15, 2017: Life Sciences
https://www.readbyqxmd.com/read/28622179/paucicellular-fibrointimal-proliferation-characterizes-pediatric-pulmonary-vein-stenosis-clinicopathologic-analysis-of-213-samples-from-97-patients
#5
Alexandra E Kovach, Philip M Magcalas, Christina Ireland, Kerry McEnany, Andre M Oliveira, Mark W Kieran, Christopher W Baird, Kathy Jenkins, Sara O Vargas
Pulmonary vein stenosis (PVS) is a luminal narrowing of extrapulmonary pulmonary veins. In pediatric patients, it arises following repair of congenital heart disease, particularly anomalous pulmonary venous return; in lung disease, especially prematurity; and rarely in isolation. The etiology is unknown and the course often fatal without lung transplantation. We hypothesized that systematic clinicopathologic review of pediatric PVS could provide further pathogenic insight. We included patients who underwent first resection of pulmonary venous tissue for symptomatic PVS at our pediatric referral center from 1995 to 2014...
June 15, 2017: American Journal of Surgical Pathology
https://www.readbyqxmd.com/read/28620066/mitochondrial-complex-iv-subunit-4-isoform-2-is-essential-for-acute-pulmonary-oxygen-sensing
#6
Natascha Sommer, Maik Huttemann, Oleg Pak, Susan Scheibe, Fenja Knöpp, Christopher Sinkler, Monika Malczyk, Mareike Gierhardt, Azadeh Esfandiary, Simone Kraut, Felix T Jonas, Christine Veith, Siddhesh Aras, Akylbek Sydykov, Nasim Alebrahimdehkordi, Klaudia Giehl, Matthias Hecker, Ralf P Brandes, Werner Seeger, Friedrich Grimminger, Hossein A Ghofrani, Ralph T Schermuly, Lawrence I Grossman, Norbert Weissmann
Rationale: Acute pulmonary oxygen sensing is essential to avoid life-threatening hypoxemia via hypoxic pulmonary vasoconstriction (HPV) which matches perfusion to ventilation. Hypoxia-induced mitochondrial superoxide release has been suggested as critical step in the signaling pathway underlying HPV. However, the identity of the primary oxygen sensor and mechanism of superoxide release in acute hypoxia, as well as its relevance for chronic pulmonary oxygen sensing remains unresolved. Objective: To investigate the role of the pulmonary specific isoform 2 of subunit 4 of mitochondrial complex IV (Cox4i2) and the subsequent mediators superoxide and hydrogen peroxide for pulmonary oxygen sensing and signaling...
June 15, 2017: Circulation Research
https://www.readbyqxmd.com/read/28613935/obstructive-sleep-apnea-and-subclinical-interstitial-lung-disease-in-mesa
#7
John S Kim, Anna J Podolanczuk, Priya Borker, Steven M Kawut, Ganesh Raghu, Joel D Kaufman, Karen D Hinckley Stukovsky, Eric A Hoffman, R Graham Barr, Daniel J Gottlieb, Susan S Redline, David J Lederer
RATIONALE: Obstructive sleep apnea (OSA) has been postulated to contribute to idiopathic pulmonary fibrosis by promoting alveolar epithelial injury via tractional forces and intermittent hypoxia. OBJECTIVE: To determine whether OSA is associated with subclinical interstitial lung disease (ILD) and with biomarkers of alveolar epithelial injury and remodeling. METHODS: We performed cross-sectional analyses of 1,690 community-dwelling adults who underwent 15-channel in-home polysomnography and thoracic computed tomography (CT) imaging in the Multi-Ethnic Study of Atherosclerosis...
June 14, 2017: Annals of the American Thoracic Society
https://www.readbyqxmd.com/read/28611184/regulation-of-the-ubiquitylation-and-deubiquitylation-of-creb-binding-protein-modulates-histone-acetylation-and-lung-inflammation
#8
Jianxin Wei, Su Dong, Rachel K Bowser, Andrew Khoo, Lina Zhang, Anastasia M Jacko, Yutong Zhao, Jing Zhao
Cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB)-binding protein (CBP) is a histone acetyltransferase that plays a pivotal role in the control of histone modification and the expression of cytokine-encoding genes in inflammatory diseases, including sepsis and lung injury. We found that the E3 ubiquitin ligase subunit FBXL19 targeted CBP for site-specific ubiquitylation and proteasomal degradation. The ubiquitylation-dependent degradation of CBP reduced the extent of lipopolysaccharide (LPS)-dependent histone acetylation and cytokine release in mouse lung epithelial cells and in a mouse model of sepsis...
June 13, 2017: Science Signaling
https://www.readbyqxmd.com/read/28604766/the-deubiquitinating-enzymes-usp4-and-usp17-target-hyaluronan-synthase-2-and-differentially-affect-its-function
#9
M Mehić, V K de Sa, S Hebestreit, C-H Heldin, P Heldin
The levels of hyaluronan, a ubiquitous glycosaminoglycan prominent in the extracellular matrix, is balanced through the actions of hyaluronan-synthesizing enzymes (HAS1, 2 and 3) and degrading hyaluronidases (Hyal 1, 2, 3 and PH20). Hyaluronan accumulates in rapidly remodeling tissues, such as breast cancer, due to deregulated expression of the HAS2 gene and/or alterations of HAS2 activity. The activity of HAS2 is regulated by post-translational modifications, including ubiquitination. In order to identify deubiquitinating enzymes (DUBs) that are involved in de-ubiquitination of HAS2, a complementary (cDNA) library of 69 Flag-HA-tagged human DUBs cloned into retroviral vectors was screened in human embryonic kidney (HEK) 293T cells for their ability to de-ubiquitinate myc-tagged HAS2...
June 12, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28598585/epithelioid-hemangioendotheliomas-of-the-liver-and-lung-in-children-and-adolescents
#10
REVIEW
Simone Hettmer, Geoffroy Andrieux, Jochen Hochrein, Philipp Kurz, Jochen Rössler, Silke Lassmann, Martin Werner, Nikolas von Bubnoff, Christoph Peters, Ewa Koscielniak, Monika Sparber-Sauer, Charlotte Niemeyer, Thomas Mentzel, Hauke Busch, Melanie Boerries
Epithelioid hemangioendothelioma (EHE) is a rare, vascular sarcoma. Visceral forms arise in the liver/ lungs. We review the clinical and molecular phenotype of pediatric visceral EHE based on the case of a 9-year-old male child with EHE of the liver/lungs. His tumor expressed the EHE-specific fusion oncogene WWTR1-CAMTA1. Molecular characterization revealed a low somatic mutation rate and activated interferon signaling, angiogenesis regulation, and blood vessel remodeling. After polychemotherapy and resection of lung tumors, residual disease remained stable on oral lenalidomide...
June 9, 2017: Pediatric Blood & Cancer
https://www.readbyqxmd.com/read/28597783/reverse-cardiac-remodelling-after-lung-transplantation-in-eisenmenger-syndrome
#11
Nejc Pavsic, Barbara Salobir, Katja Prokselj
No abstract text is available yet for this article.
April 2017: Acta Cardiologica
https://www.readbyqxmd.com/read/28597778/genomic-stability-of-pulmonary-artery-endothelial-colony-forming-cells-in-culture
#12
Kylie M Drake, Chiara Federici, Heng T Duong, Suzy A Comhair, Serpil C Erzurum, Kewal Asosingh, Micheala A Aldred
Pulmonary vascular remodeling, including proliferation and migration of pulmonary artery endothelial cells (PAEC), is a pathologic hallmark of pulmonary arterial hypertension (PAH). Multiple studies have shown evidence of increased levels of DNA damage and lineage-specific genetic changes in PAH lung vascular cells, suggesting increased genomic instability. Highly proliferative endothelial colony-forming cell (ECFC) clones can be isolated from PAEC. Here we utilized ECFC to track chromosomal copy number of 20 PAH and eight control clones across serial passages using genome-wide microarrays...
April 2017: Pulmonary Circulation
https://www.readbyqxmd.com/read/28597764/microct-analysis-of-vascular-morphometry-a-comparison-of-right-lung-lobes-in-the-sugen-hypoxic-rat-model-of-pulmonary-arterial-hypertension
#13
Erin M Faight, Kostas Verdelis, Lee Zourelias, Rong Chong, Raymond L Benza, Kelly J Shields
Pulmonary arterial hypertension (PAH) is a rare disease characterized by significant vascular remodeling within the lung. Clinical computed tomography (CT) scans are routinely used to aid in PAH diagnosis. Animal models, including the Sugen-hypoxic rat model (SU/hyp), of PAH closely mimic human PAH development. We have previously used micro-computed tomography (microCT) to find extensive right lung vascular remodeling in the SU/hyp. We hypothesized that the individual right lung lobes may not contribute equally to overall lung vascular remodeling...
April 2017: Pulmonary Circulation
https://www.readbyqxmd.com/read/28596292/the-pde4-inhibitor-chf-6001-and-lamas-inhibit-bronchoconstriction-induced-remodelling-in-lung-slices
#14
Loes Em Kistemaker, Tjitske A Oenema, Hoeke A Baarsma, I Sophie T Bos, Martina Schmidt, Fabrizio Facchinetti, Maurizio Civelli, Gino Villetti, Reinoud Gosens
Background Combination therapy of PDE4 inhibitors and anticholinergics induces bronchoprotection in COPD. Mechanical forces that arise during bronchoconstriction may contribute to airway remodelling. Therefore, we investigated the impact of PDE4 inhibitors and anticholinergics on bronchoconstriction-induced remodelling. Because of the different mechanism of action of PDE4 inhibitors and anticholinergics, we hypothesized functional interactions of these two drug classes. Methods Guinea pig precision cut lung slices were pre-incubated with the PDE4-inhibitors CHF-6001 or roflumilast and/or the anticholinergics tiotropium or glycopyorrolate, followed by stimulation with methacholine (10 μM) or TGF -β1 (2 ng/mL) for 48 hours...
June 8, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28596268/application-of-euclidean-distance-mapping-for-assessment-of-basement-membrane-thickness-distribution-in-asthma
#15
Leila B Mostaco-Guidolin, Soheil M Hajimohammadi, Dragos Mihai Vasilescu, Tillie-Louise Hackett
Abnormal thickening of the airway basement membrane is one of the hallmarks of airway remodeling in asthma. Current protocols for measuring the basement membrane involve the use of stained tissue sections and measurements of the basement membrane thickness at certain intervals, followed by the calculation of the geometric mean thickness for each airway. This report describes an automated, unbiased approach which uses colour segmentation to identify structures of interest on stained sections and euclidean distance mapping to measure the thickness distribution of airway structures...
June 8, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28590142/intra-amniotic-soluble-endoglin-impairs-lung-development-in-neonatal-rats
#16
Santhosh T Somashekar, Ibrahim Sammour, Jian Huang, Juan Dominguez-Bendala, Ricardo Pastori, Silvia Alvarez-Cubela, Eneida Torres, Shu Wu, Karen C Young
Soluble endoglin (sENG) is increased in the amniotic fluid of mothers with pre-eclampsia and chorioamnionitis. Preterm infants born to mothers with these disorders have an increased risk of aberrant lung development. Whether this increased risk is secondary to elevated sENG levels is unclear. The objective of this study was to determine whether intrauterine exposure to an adenovirus over-expressing sENG impairs neonatal lung angiogenesis by modulating lung eNOS signaling. Pregnant Sprague-Dawley rats were randomly assigned to receive ultrasound guided intra-amniotic injections of adenovirus over-expressing sENG (Ad-sENG) or control adenovirus (Ad-control) on embryonic day 17 (E17)...
June 7, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28586065/valsartan-attenuates-pulmonary-hypertension-via-suppression-of-mitogen-activated-protein-kinase-signaling-and-matrix-metalloproteinase-expression-in-rodents
#17
Yuyan Lu, Haipeng Guo, Yuxi Sun, Xin Pan, Jia Dong, Di Gao, Wei Chen, Yawei Xu, Dachun Xu
It has previously been demonstrated that the renin-angiotensin system is involved in the pathogenesis and development of pulmonary hypertension (PH). However, the efficacy of angiotensin II type I (AT1) receptor blockers in the treatment of PH is variable. The present study examined the effects of the AT1 receptor blocker valsartan on monocrotaline (MCT)‑induced PH in rats and chronic hypoxia‑induced PH in mice. The results demonstrated that valsartan markedly attenuated development of PH in rats and mice, as indicated by reduced right ventricular systolic pressure, diminished lung vascular remodeling and decreased right ventricular hypertrophy, compared with vehicle treated animals...
June 6, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28579250/dna-methylation-of-extracellular-matrix-remodeling-genes-in-children-exposed-to-arsenic
#18
Tania Gonzalez-Cortes, Rogelio Recio-Vega, Robert Clark Lantz, Binh T Chau
Several novel mechanistic findings regarding to arsenic's pathogenesis has been reported and some of them suggest that the etiology of some arsenic induced diseases are due in part to heritable changes to the genome via epigenetic processes such as DNA methylation, histone maintenance, and mRNA expression. Recently, we reported that arsenic exposure during in utero and early life was associated with impairment in the lung function and abnormal receptor for advanced glycation endproducts (RAGE), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) sputum levels...
June 1, 2017: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/28577568/pirfenidone-inhibits-myofibroblast-differentiation-and-lung-fibrosis-development-during-insufficient-mitophagy
#19
Yusuke Kurita, Jun Araya, Shunsuke Minagawa, Hiromichi Hara, Akihiro Ichikawa, Nayuta Saito, Tsukasa Kadota, Kazuya Tsubouchi, Nahoko Sato, Masahiro Yoshida, Kenji Kobayashi, Saburo Ito, Yu Fujita, Hirofumi Utsumi, Haruhiko Yanagisawa, Mitsuo Hashimoto, Hiroshi Wakui, Yutaka Yoshii, Takeo Ishikawa, Takanori Numata, Yumi Kaneko, Hisatoshi Asano, Makoto Yamashita, Makoto Odaka, Toshiaki Morikawa, Katsutoshi Nakayama, Kazuyoshi Kuwano
BACKGROUND: Pirfenidone (PFD) is an anti-fibrotic agent used to treat idiopathic pulmonary fibrosis (IPF), but its precise mechanism of action remains elusive. Accumulation of profibrotic myofibroblasts is a crucial process for fibrotic remodeling in IPF. Recent findings show participation of autophagy/mitophagy, part of the lysosomal degradation machinery, in IPF pathogenesis. Mitophagy has been implicated in myofibroblast differentiation through regulating mitochondrial reactive oxygen species (ROS)-mediated platelet-derived growth factor receptor (PDGFR) activation...
June 2, 2017: Respiratory Research
https://www.readbyqxmd.com/read/28577052/-analysis-of-therapy-relevant-receptors-in-bone-marrow-carcinosis-comparison-of-pathological-and-clinical-parameters
#20
G Massenkeil, C Gropp, H Kreipe, K Hussein
BACKGROUND: Bone marrow carcinosis is a sign of advanced tumor stage with nonspecific clinical and hematological symptoms. Diagnosis is based on bone marrow biopsy and histopathology, but biopsies are not part of the standard work-up in oncological diseases and data on the correlation between clinical presentation and pathological findings are sparse. MATERIAL AND METHODS: In a retrospective single-center study, data from 20 tumor patients with bone marrow carcinosis were analyzed...
June 2, 2017: Der Pathologe
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