Results 101 to 110 of about 23,483 (241)

Abnormal wave reflections and left ventricular hypertrophy late after coarctation of the aorta repair [PDF]

open access: yes, 2017
Patients with repaired coarctation of the aorta are thought to have increased afterload due to abnormalities in vessel structure and function. We have developed a novel cardiovascular magnetic resonance protocol that allows assessment of central ...
Khushnood, Abbas   +7 more
core   +2 more sources

Calpain‐2‐Mediated Endothelial Focal Adhesion Disruption in Thoracic Aortic Dissection

open access: yesAdvanced Science, EarlyView.
The elevated expression of Capn2 in endothelial cells activates focal adhesion signaling by cleaving Talin1 and assembling Itgav, which compromises the integrity of the endothelial barrier and induces vascular inflammation. Inhibition of calpain through both pharmacological and transgenic approaches has effectively suppressed the onset and progression ...
Xiaomei Teng   +10 more
wiley   +1 more source

Misrepair mechanism in the development of atherosclerotic plaques [PDF]

open access: yesarXiv, 2015
Atherosclerosis is a disease characterized by the development of atherosclerotic plaques (APs) in arterial endothelium. The APs in part of an arterial wall are inhomogeneous on size and on distribution. In order to understand this in-homogeneity, the pathology of APs is analyzed by Misrepair mechanism, a mechanism proposed in our Misrepair-accumulation
arxiv  

Machine Learning Framework to Identify Individuals at Risk of Rapid Progression of Coronary Atherosclerosis: From the PARADIGM Registry. [PDF]

open access: yes, 2020
Background Rapid coronary plaque progression (RPP) is associated with incident cardiovascular events. To date, no method exists for the identification of individuals at risk of RPP at a single point in time.
Al'Aref, Subhi J   +35 more
core  

Abnormal development of placenta in HtrA1-deficient mice [PDF]

open access: yes, 2015
Abnormal levels of High temperature requirement A1 (HtrA1) protein have been repeatedly observed in sera and placentas of preeclampsia patients. To understand the functions of HtrA1 in placentation and in the etiology of preeclampsia, we established ...
Hasan, Md. Zobaer   +4 more
core   +1 more source

CCDC80 Protects against Aortic Dissection and Rupture by Maintaining the Contractile Smooth Muscle Cell Phenotype

open access: yesAdvanced Science, EarlyView.
Aortic dissection (AD) is accompanied by a decrease in CCDC80 in vascular smooth muscle cells (VSMCs). CCDC80 can interact with JAK2, and VSMC‐specific CCDC80 deficiency accelerates the progression of AD by activating the JAK2/STAT3 pathway involved in regulating the phenotype switching and function of VSMCs.
Qingqing Xiao   +18 more
wiley   +1 more source

Relating normal human cardiac development to the anatomical findings in the congenitally malformed heart

open access: yesClinical Anatomy, Volume 38, Issue 3, Page 296-313, April 2025.
Abstract A proper appreciation of cardiac development can now provide the necessary background to understand the anatomical findings in the congenitally malformed heart. We recently presented an account of human cardiac development based on reconstructions of histological datasets from human embryos aged between 3.5 and 8 weeks subsequent to conception.
Jill P. J. M. Hikspoors   +5 more
wiley   +1 more source

Laminins Regulate Placentation and Pre-eclampsia: Focus on Trophoblasts and Endothelial Cells

open access: yesFrontiers in Cell and Developmental Biology, 2020
Pre-eclampsia is a systemic vascular disease characterized by new-onset hypertension and/or proteinuria at ≥20 weeks of gestation and leads to high rates of maternal and perinatal morbidity and mortality.
Min Liu   +3 more
doaj   +1 more source

Transendocardial injection of expanded autologous CD34+ cells after myocardial infarction: Design of the EXCELLENT trial

open access: yesESC Heart Failure, Volume 12, Issue 2, Page 1455-1463, April 2025.
Abstract Aims The extent of irreversible cardiomyocyte necrosis after acute myocardial infarction (AMI) is a major determinant of residual left ventricular (LV) function and clinical outcome. Cell therapy based on CD34+ cells has emerged as an option to help repair the myocardium and to improve outcomes.
Jerome Roncalli   +17 more
wiley   +1 more source

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