scholarly journals In-Vitro Investigation of Flow Profiles in Arteries Using the Photoplethysmograph

Author(s):  
Kristjan Pilt ◽  
James M. May ◽  
Panayiotis A. Kyriacou
2008 ◽  
Vol 35 (S 01) ◽  
Author(s):  
H Leske ◽  
A Baiker ◽  
C Schichor ◽  
J.C Tonn ◽  
R Goldbrunner ◽  
...  

2010 ◽  
Vol 51 (8) ◽  
pp. 4151 ◽  
Author(s):  
Henri Sueke ◽  
Stephen B. Kaye ◽  
Timothy Neal ◽  
Amanda Hall ◽  
Stephen Tuft ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gautier Follain ◽  
Naël Osmani ◽  
Valentin Gensbittel ◽  
Nandini Asokan ◽  
Annabel Larnicol ◽  
...  

AbstractTumor progression and metastatic dissemination are driven by cell-intrinsic and biomechanical cues that favor the growth of life-threatening secondary tumors. We recently identified pro-metastatic vascular regions with blood flow profiles that are permissive for the arrest of circulating tumor cells. We have further established that such flow profiles also control endothelial remodeling, which favors extravasation of arrested CTCs. Yet, how shear forces control endothelial remodeling is unknown. In the present work, we aimed at dissecting the cellular and molecular mechanisms driving blood flow-dependent endothelial remodeling. Transcriptomic analysis of endothelial cells revealed that blood flow enhanced VEGFR signaling, among others. Using a combination of in vitro microfluidics and intravital imaging in zebrafish embryos, we now demonstrate that the early flow-driven endothelial response can be prevented upon specific inhibition of VEGFR tyrosine kinase and subsequent signaling. Inhibitory targeting of VEGFRs reduced endothelial remodeling and subsequent metastatic extravasation. These results confirm the importance of VEGFR-dependent endothelial remodeling as a driving force of CTC extravasation and metastatic dissemination. Furthermore, the present work suggests that therapies targeting endothelial remodeling might be a relevant clinical strategy in order to impede metastatic progression.


2020 ◽  
Vol 21 (12) ◽  
pp. 2718-2728
Author(s):  
Elsayed M. Abdel Bary ◽  
Ammar N. Harmal ◽  
Mona E. Ibrahim ◽  
Moustafa A. Gouda

2020 ◽  
Vol 1571 ◽  
pp. 012010
Author(s):  
V P Veiko ◽  
Yu Yu Karlagina ◽  
E E Egorova ◽  
E A Zernitskaya ◽  
D S Kuznetsova ◽  
...  

1988 ◽  
Vol 67 (3) ◽  
pp. 577-581 ◽  
Author(s):  
Y. Jima ◽  
T. Koulourides

This in vitro investigation studied the remineralization of experimental caries lesions in bovine enamel by use of three methods: (1) surface microhardness, (2) microradiography, and (3) abrasion biopsy for mineral density and fluoride content. The lesions were produced by a two-day exposure to 0.01 mol/L lactic acidlsodium hydroxide buffer partially saturated with 3.0 mmol/L Ca, 1.8 mmol/L P, in 1% CMC, at pH 4.0 and 37°C. The lesions were exposed to a remineralizing solution containing 3.0 mmol/L Ca, 1.8 mmol/L P, and 3 ppm F in 1% CMC at pH 7.0 and 37°C for two, six, and ten days, with solution changes every two days. The data derived from the three methods are presented in sequence from the baseline and at days two, six, and ten of the remineralizing treatment. Microhardness measurements showed hardness recoveries of 35.9, 78.9, and 87.5%, respectively. Microradiography suggested complete recovery with the ten-day remineralization. Abrasion biopsy of successive 10-μm layers to a depth of 100 μm indicated 15.2, 39.8, and 68.8% mineral density recoveries, with fluoride content of the surface layer increasing from a baseline of 300 ppm to 4600, 9000, and 9800 ppm F for the 2, 6, 10 days of remineralization, respectively. Subsequent acid-etching of thin sections from the ten-day-remineralized specimens showed that the fluoride-enriched remineralized area was more resistant to acid dissolution than was the underlying nonnal enamel.


2002 ◽  
Vol 23 (3) ◽  
pp. 555-566 ◽  
Author(s):  
P J Dunmore-Buyze ◽  
M Moreau ◽  
A Fenster ◽  
D W Holdsworth

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