ライフサイエンスコーパス: capillarization

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1 atriuretic peptide expression, and sustained capillarization.

2 escence, and whether this effect was lost in capillarization.

3 an important determinant of skeletal muscle capillarization.

4 ed to overall measures of peripheral villous capillarization.

5 phosphorylation of Akt and increased muscle capillarization.

6 t role in the maintenance of skeletal muscle capillarization across the life span.

7 The NO-dependent pathway is impaired in capillarization and activation of this pathway downstrea

8 phosphoprotein 1(-/-) mice leads to immature capillarization and blunted arteriolarization.

9 combinant Emc10 enhanced infarct border-zone capillarization and exerted a sustained beneficial effec

10 le vascular beds, promoting liver sinusoidal capillarization and portal hypertension, ischemic heart

11 ut mice were protected from arsenite-induced capillarization and protein nitration.

12 oximity to liver sinusoidal endothelial cell capillarization and stellate cell activation demonstrate

13 hat a Nox2-based oxidase is required for SEC capillarization and that it may play a central role in v

14 nvestigate if AMPK regulates skeletal muscle capillarization and the angiogenic responses to exercise

15 Wheel running (28 days) increased capillarization and this response was AMPK independent.

16 cise training program for the measurement of capillarization and VEGF mRNA.

17 proliferation, metabolic zonation, sinusoid capillarization, and hepatic stellate cell activation we

18 correlations between VEGF protein and muscle capillarization are consistent with VEGF being an import

19 ion of both angiogenesis and pathogenic LSEC capillarization, as well as demonstrating a role for S1P

20 (4) AMPK regulates basal VEGF expression and capillarization, but is not necessary for exercise-induc

21 Capillarization, characterized by loss of differentiatio

22 cells (SECs), including SEC defenestration, capillarization, increased junctional PECAM-1 expression

23 Capillarization, lack of liver sinusoidal endothelial ce

24 toration, portal inflammation and sinusoidal capillarization may not regress after viral eradication.

25 We hypothesize that capillarization of sinusoidal endothelial cells (SEC) is

26 After MI, however, capillarization of the infarct border zone was impaired

27 that affect liver function such as sinusoid capillarization or loss of metabolic zonation are common

28 Capillarization precedes hepatic fibrosis.

29 nd can be interpreted as a component of the "capillarization" process of the hepatic sinusoid.

30 ural demonstration of SEC defenestration and capillarization, quantitative immunofluorescence analysi

31 60-2770 accelerated the complete reversal of capillarization (restored differentiation of LSECs) with

32 e processes of sinusoidal defenestration and capillarization that characterize liver fibrosis.

33 onal changes in SEC signaling for sinusoidal capillarization that may be initial events in pathogenic

34 signaling for angiogenesis or liver sinusoid capillarization, the mechanism for initiating these effe

35 increased sinusoidal endothelial cell (SEC) capillarization, vascularization of the peribiliary vasc

36 Capillarization was characterized by ectopic basement me

37 Resting capillarization was lower in AMPK DN compared to WT.

38 etraining, at a time point long after muscle capillarization was observed to be similar to pre-traini

39 Conversely, no changes in sinusoidal capillarization were observed after treatment, as assess

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