scholarly journals A Rac/Cdc42 exchange factor complex promotes formation of lateral filopodia and blood vessel lumen morphogenesis

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Sabu Abraham ◽  
Margherita Scarcia ◽  
Richard D. Bagshaw ◽  
Kathryn McMahon ◽  
Gary Grant ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Exchange Factor ◽  
Vessel Lumen

scholarly journals Cellular and molecular mechanisms underlying blood vessel lumen formation

BioEssays ◽  
2013 ◽  
Vol 36 (3) ◽  
pp. 251-259 ◽  
Author(s):  
Marta S. Charpentier ◽  
Frank L. Conlon
Keyword(s):  
Blood Vessel ◽  
Molecular Mechanisms ◽  
Lumen Formation ◽  
Vessel Lumen

Development and Biomechanical Characterization of a Novel Bilayer Vascular Graft

2010 ◽  
Author(s):  
Krishna Madhavan ◽  
Walter Bonani ◽  
Craig Lanning ◽  
Wei Tan
Keyword(s):  
Blood Vessel ◽  
Vascular Graft ◽  
Bypass Surgery ◽  
Small Diameter ◽  
Native Artery ◽  
Vessel Lumen ◽  
Unmet Demand ◽  
Tissue Engineered Blood Vessels ◽  
Synthetic Grafts

Vascular grafts are currently used to treat cardiovascular diseases such as arthrosclerosis by bypass surgery and as vascular access in hemodialysis [1]. There are a number of types of grafts including autologous vessels (such saphenous vein), synthetic grafts (such as expanded polytetrafluoroethylene) and tissue engineered blood vessels. Currently synthetic grafts are most commonly used as blood vessel replacements and there are a number of problems associated with them. One main impediment is that these grafts are not suitable for small-diameter (less than 6mm) vessel replacement [1, 2], due to high occlusion rates. The major concern over the other alternatives such as autologous vessels and tissue engineered products is their availability. Thus, new approaches to constructing biomimetic small-diameter blood vessel equivalents, that are immediately available, may address the unmet demand in this area. Therefore, we have designed a novel bilayer vascular construct which is made up of a nanofibrous intimal-equivalent as thromboresistant vessel lumen and a mimetic extracellular matrix (ECM) as medial-equivalent for smooth muscle cells (SMC) from native artery to invade and remodel the ECM.

Closed contour edge detection of blood vessel lumen and outer wall boundaries in black-blood MR images

1999 ◽  
Vol 17 (2) ◽  
pp. 257-266 ◽  
Author(s):  
Chun Yuan ◽  
Eugene Lin ◽  
Jacob Millard ◽  
Jenq–Neng Hwang
Keyword(s):  
Blood Vessel ◽  
Edge Detection ◽  
Outer Wall ◽  
Black Blood ◽  
Closed Contour ◽  
Mr Images ◽  
Vessel Lumen

Atypical complement receptor C5aR2 transports C5a to initiate neutrophil adhesion and inflammation

2019 ◽  
Vol 4 (35) ◽  
pp. eaav5951 ◽  
Author(s):  
Yoshishige Miyabe ◽  
Chie Miyabe ◽  
Vinidhra Mani ◽  
Thorsten R. Mempel ◽  
Andrew D. Luster
Keyword(s):  
Endothelial Cells ◽  
Blood Vessel ◽  
Chemokine Receptor ◽  
Murine Model ◽  
Neutrophil Adhesion ◽  
Complement Receptor ◽  
C5a Receptor ◽  
Vessel Lumen ◽  
Chemokine Ligands ◽  
Complement C5a

Chemoattractant-induced arrest of circulating leukocytes and their subsequent diapedesis is a fundamental component of inflammation. However, how tissue-derived chemoattractants are transported into the blood vessel lumen to induce leukocyte entry into tissue is not well understood. Here, intravital microscopy in live mice has shown that the “atypical” complement C5a receptor 2 (C5aR2) and the atypical chemokine receptor 1 (ACKR1) expressed on endothelial cells were required for the transport of C5a and CXCR2 chemokine ligands, respectively, into the vessel lumen in a murine model of immune complex–induced arthritis. Transported C5a was required to initiate C5aR1-mediated neutrophil arrest, whereas transported chemokines were required to initiate CXCR2-dependent neutrophil transdendothelial migration. These findings provide new insights into how atypical chemoattractant receptors collaborate with “classical” signaling chemoattractant receptors to control distinct steps in the recruitment of neutrophils into tissue sites of inflammation.

scholarly journals Zebrafish Models of Cerebrovascular Disease

2014 ◽  
Vol 34 (4) ◽  
pp. 571-577 ◽  
Author(s):  
Brian P Walcott ◽  
Randall T Peterson
Keyword(s):  
Blood Vessel ◽  
Cerebrovascular Disease ◽  
Large Scale ◽  
Hemorrhagic Stroke ◽  
Brain Parenchyma ◽  
Cerebral Vasculature ◽  
Vessel Lumen ◽  
Vessel Structure ◽  
Genetic And Environmental Factors ◽  
Genetically Manipulated

Perturbations in cerebral blood flow and abnormalities in blood vessel structure are the hallmarks of cerebrovascular disease. While there are many genetic and environmental factors that affect these entities through a heterogeneous group of disease processes, the ultimate final pathologic insult in humans is defined as a stroke, or damage to brain parenchyma. In the case of ischemic stroke, blood fails to reach its target destination whereas in hemorrhagic stroke, extravasation of blood occurs outside of the blood vessel lumen, resulting in direct damage to brain parenchyma. As these acute events can be neurologically devastating, if not fatal, development of novel therapeutics are urgently needed. The zebrafish ( Danio rerio) is an attractive model for the study of cerebrovascular disease because of its morphological and physiological similarity to human cerebral vasculature, its ability to be genetically manipulated, and its fecundity allowing for large-scale, phenotype-based screens.

scholarly journals Computer modeling of different shaped patches in classical carotid endarterectomy

2021 ◽  
Vol 23 (4) ◽  
pp. 132-142
Author(s):  
V. G. Loginova ◽  
Yu. N. Zakharov ◽  
A. N. Kazantsev ◽  
Yu. I. Shokin ◽  
E. V. Evtushenko ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Carotid Endarterectomy ◽  
Computer Modeling ◽  
Patient Flow ◽  
Carotid Bifurcation ◽  
Patch Selection ◽  
Vessel Lumen ◽  
Long Term Follow Up ◽  
Using Data ◽  
Ultrasonic Doppler Velocimetry

Objective: to construct geometric models of carotid bifurcation and build a computer modeling for carotid endarterectomy (CEA) operations with patches of various configurations.Materials and methods. The method uses reconstructed models of a healthy blood vessel obtained from a preoperative computed tomography (CT) study of the affected blood vessel of a particular patient. Flow in the vessel is simulated by computational fluid dynamics using data from the patient's ultrasonic Doppler velocimetry and CT angiography. Risk factors are assessed by hemodynamic indices at the vessel wall associated with Wall Shear Stress (WSS).Results. We used the proposed method to study the hemodynamic results of 10 virtual CEA operations with patches of various shapes on a reconstructed healthy artery of a particular patient. The reason for patch implantation was to ensure that the vessel lumen is not narrowed as a result of the surgery, since closing the incision without a patch can reduce the vessel lumen circumference by 4–5 mm, which adversely affects blood flow. On the other hand, too wide a patch creates aneurysmorphic deformation of the internal carotid artery (ICA) mouth, which is not optimal due to formation of a large recirculation zone. In this case, it was found that the implanted patch width of about 3 mm provides an optimal hemodynamic outcome. Deviations from this median value, both upward and downward, impair hemodynamics. The absence of a patch gives the worst of the results considered.Conclusion: The proposed computer modeling technique is able to provide a personalized patch selection for classical CEA with low risk of restenosis in the long-term follow-up.

scholarly journals Angiogenesis in mammary Paget disease: histopathological analyses of blood vessel density and angiogenic factors

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Yuri Akishima-Fukasawa ◽  
Naoko Honma ◽  
Hideaki Ogata ◽  
Yoshikiyo Akasaka ◽  
Tetuo Mikami
Keyword(s):  
Blood Flow ◽  
Blood Vessel ◽  
Vessel Density ◽  
Lumen Area ◽  
Immunohistochemical Expression ◽  
Clinical Imaging ◽  
Paget Disease ◽  
Vessel Lumen ◽  
And Control ◽  
Expression Score

Abstract Background We examined the vascularity of mammary Paget disease histologically to confirm the increased blood flow observed previously by clinical imaging. The relationships among blood vessel density (BVD), histopathological parameters of blood flow in the nipple, and the expression of angiogenic factors such as basic fibroblast growth factor (bFGF) and vascular endothelial growth factor A (VEGFA) were examined. Methods We calculated the average CD34-positive BVD and podoplanin (D2–40)-positive lymphatic vessel density (LVD) and the proportion of proliferating of endothelial cells in 14 Paget disease, 3 dermatitis biopsy, and 14 age-matched control cases. As a parameter related to blood flow in the nipple, the total CD34-positive blood vessel lumen area relative to the entire nipple area was measured in each Paget disease and control case using an automated image analysis system. Immunohistochemical expression of bFGF and VEGFA in Paget cells was also examined. Results The average BVD and LVD were significantly higher in the Paget disease cases than in the dermatitis (p = 0.003) and control (p < 0.001) cases. The proportion of proliferating endothelial cells was also increased in the Paget disease cases. The ratio of the CD34-positive blood vessel lumen area to nipple area was also significantly higher in the Paget disease than control cases (p = 0.003). The average BVD was correlated with the average LVD (r = 0.734, p < 0.001) and ratio of the blood vessel lumen area to nipple area (r = 0.692, p < 0.001). Immunohistochemical expression of bFGF was strong in all Paget disease cases, with a significantly higher expression score in the Paget disease than dermatitis (p = 0.003) and control (p < 0.001) cases. The bFGF, but not VEGFA, expression score, was strongly correlated with the average BVD (r = 0.818, p < 0.001) and ratio of the blood vessel lumen area to nipple area (r = 0.503, p = 0.006). Conclusion These results provide direct histopathological evidence of a marked increase in nipple blood flow in Paget disease detected by clinical imaging. bFGF is considered to play a pivotal role in angiogenesis in mammary Paget disease.

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