Мы используем Cookies Этот веб-сайт использует cookie-файлы, чтобы предлагать вам наиболее актуальную информацию. Просматривая этот веб-сайт, Вы принимаете cookie-файлы.
Golgi complex ultrastructure is disrupted in the ffr digestive tract.
2
These data indicate that ffr is required for both Golgi structure and vesicular trafficking, and ultimately lipid transport.
3
The zebrafish fat-free (ffr) mutation was identified in a physiological screen for genes that regulate lipid metabolism.
4
Through positional cloning, we have identified a causative mutation in a highly conserved and ubiquitously expressed gene within the ffr locus.
5
Enterocyte retention of an endosomal lipid marker in ffr larvae support the idea that altered vesicle trafficking contributes to the ffr mutant defect.
6
Although fat-free (ffr) mutant larvae were previously described to exhibit impaired lipid processes, we found they also had significantly reduced protease activity.
7
The position of the FFR with regard to broadcasting rights is acknowledged.
8
The predicted FFR for each stenosis was calculated with a novel formu-la.
9
Conclusions: There was no reduction in repeat revascularization or postoperative MI with FFR.
10
Methods: We analyzed a database of 269 patients undergoing FFR surgery.
11
Background: FFR is an indispensable tool to identify individual coronary stenoses causing ischemia.
12
It is anticipated that the FFR will make an announcement today.
13
BP of FFR was significantly higher than that of the controls.
14
Insulin sensitivity was significantly lower in FFR than in the controls.
15
Motorized FFR pullback during continuous intravenous adenosine infusion and OCT assessments was performed.
16
Forty-two percent of all FFR measurements were made in culprit lesions.