ライフサイエンスコーパス: poststenotic

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1 guidewires; they include the measurement of poststenotic absolute coronary flow reserve, the relativ

2 oronary flow velocity and MPR ratios between poststenotic and angiographically normal vascular beds w

3 l perfusion reserve (MPR) were calculated in poststenotic and normal reference vascular beds.

4 el of cord compression in combination with a poststenotic decrease of (18)F-FDG uptake.

5 Poststenotic dilatation (PSD) occurs in a low-pressure r

6 Poststenotic dilatation of greater than 20% was present

7 ical thickness, parenchymal enhancement, and poststenotic dilatation were measured.

8 rdered flow of the midgraft stenosis yielded poststenotic dilatation.

9 Poststenotic Doppler average peak flow velocities (APV;

10 Poststenotic flow velocity increased from 6.6 +/- 6.1 to

11 ved from [15O]H2O PET with directly measured poststenotic intracoronary Doppler flow velocity data ac

12 nal blood flow (RBF) and GFR and accelerates poststenotic kidney (STK) tissue injury.

13 sized that miR-26a levels are reduced in the poststenotic kidney and that kidney repair achieved by a

14 factors and tubulointerstitial injury in the poststenotic kidney are poorly understood.

15 decreased tubular miR-26a expression in the poststenotic kidney may be responsible for tubular cell

16 stemic hypertension and tissue injury in the poststenotic kidney, restoring vessel patency alone is i

17 flow, perfusion, and GFR were reduced in the poststenotic kidney.

18 ith healthy control kidneys, swine and human poststenotic kidneys had 45.5+/-4.3% and 90.0+/-3.5% low

19 arly correlated (r = .60; P < .001), as were poststenotic PET MPR and Doppler CFR (r = .76; P < .0002

20 Midgraft stenosis exhibits poststenotic positive wall remodeling.

21 some of the reported variability from using poststenotic PSV to detect hemodynamically significant r

22 Poststenotic PSV was mildly dependent on end-organ vascu

23 ip between end-organ vascular resistance and poststenotic PSV.

24 Arterial rings obtained from the poststenotic region were more sensitive and responsive t

25 how high levels of phospho-Smad1/5 in ECs at poststenotic sites, where OSS occurs.

26 inhibited the increased EC uptake of BrdU at poststenotic sites.

27 d activity of von Willebrand factor (vWF) at poststenotic sites.

28 The poststenotic thrombus formation was critically dependent

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