Results 111 to 120 of about 551,312 (317)

Preservation of aortic valve in type A aortic dissection complicated by aortic regurgitation

open access: yesThe Journal of Thoracic and Cardiovascular Surgery, 1991
Two hundred fifty-two patients underwent operation for type A aortic dissection at Stanford University Medical Center from 1963 to 1987 and Duke University Medical Center from 1975 to 1988. Sixty-seven percent had an acute type A dissection and 33% had a chronic type A dissection.
J I, Fann   +8 more
openaire   +2 more sources

Endogenous Engineering Reprograms Extracellular Vesicles for Enhanced Therapeutic Function

open access: yesAdvanced Science, EarlyView.
This review explains how Extracellular vesicles‐producing cells can be endogenously engineered to load therapeutic proteins and nucleic acids. We summarize physiological and genetic strategies that harness native sorting pathways for selective cargo loading.
Jinghui Wang   +10 more
wiley   +1 more source

Structure-function relationships in the aortic valve [PDF]

open access: yes, 2012
PhDGlobally, heart valve dysfunction constitutes a large portion of the cardiovascular disease load, causing high rates of mortality in European and industrialized countries.
Anssari-Benam, Afshin
core  

Inhibition of tumor necrosis factor α–stimulated monocyte adhesion to human aortic endothelial cells by AMP-activated protein kinase [PDF]

open access: yes, 2008
<b>Objective</b>— Proatherosclerotic adhesion of leukocytes to the endothelium is attenuated by NO. As AMP-activated protein kinase (AMPK) regulates endothelial NO synthesis, we investigated the modulation of adhesion to cultured human aortic
Kohlhaas, C.F., Salt, I.P., Ewart, M-A.
core   +1 more source

Endoluminal rescue of false lumen graft deployment in TEVAR for type B aortic dissection: a case report and literature review

open access: yesFrontiers in Cardiovascular Medicine
BackgroundThoracic endovascular aortic repair (TEVAR) has increasingly become the preferred surgical intervention for Stanford type B aortic dissection (TBAD).
Hong Jiang Zhu, Feng Yan, Peng Peng Zhao
doaj   +1 more source

Noninvasive Focal Gene Delivery into the Cerebellum of Non‐Human Primates using Focused Ultrasound

open access: yesAdvanced Science, EarlyView.
Focal and non‐invasive viral vector delivery in non‐human primates remains a major challenge in translational neuroscience. Low‐intensity focused ultrasound was used to transiently open the blood–brain barrier and enable targeted gene delivery to the cerebellum.
Noelia Esteban‐García   +11 more
wiley   +1 more source

Injectable Hydrogel with Rapid Coagulation, Low Swelling, and High Burst Pressure Tolerance Properties for Long‐Term Management of Bleeding Wound

open access: yesAdvanced Science, EarlyView.
An injectable PACmC hydrogel with “rigid island‐flexible chain” architecture is developed, featuring low swelling (49.2% within 7 d), strong wet adhesion (46.5 kPa), and high burst pressure (701 mm Hg), which can achieve rapid hemostasis and long‐term sealing in rabbit and porcine models of hepatic and splenic hemorrhage.
Yang Ouyang   +12 more
wiley   +1 more source

P503: Historical prospective study of the link between JAK2-V617F and thoracic aortic aneurysm

open access: yesGenetics in Medicine Open, 2023
Deqiong Ma   +7 more
doaj   +1 more source

Integrated Single‐Cell and Spatial Analysis Reveals a Metabolic‐Immune Axis Driving Aortic Dissection

open access: yesAdvanced Science, EarlyView.
Single‐cell and spatial profiling of 110 human thoracic aortic samples reveals a stromal–immune circuit driving aortic dissection. An elastin‐rich fibroblast subset is depleted with age and markedly reduced in disease, weakening aortic wall integrity.
Jing Tao   +25 more
wiley   +1 more source

CK2α Deficiency Drives Myocardial Fibrosis via Desmin‐Induced Mitochondrial Dysfunction

open access: yesAdvanced Science, EarlyView.
CK2α preserves mitochondrial homeostasis by phosphorylating Desmin to recruit Cryab, ensuring proper filament assembly. CK2α deficiency disrupts this interaction, causing mitochondrial dysfunction, metabolic shifts, bioenergetic failure, and oxidative stress—ultimately establishing a pro‐fibrotic environment that drives cardiac fibrosis.
Canjie Ma   +12 more
wiley   +1 more source

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