ライフサイエンスコーパス: Oil red O stain

1 y, as evidenced by hematoxylin and eosin and Oil Red O staining.

2 area in the aortic sinus was assessed using oil red O staining.

3 n inhibited lipid accumulation, as judged by Oil Red O staining.

4 us (high signal on T2W, r = 0.86) areas with Oil Red O staining.

5 ith dedifferentiation with loss of lipid and Oil Red O staining.

6 tion of bronchial alveolar lavage fluid with oil red O staining.

7 enic differentiation through quantitation by oil-red O staining.

8 sions at the aortic root were measured after oil-red O staining.

9 The presence of adipocytes was assessed by Oil-Red-O staining.

10 lly, adipogenesis was blocked as assessed by Oil Red O staining, adiponectin, and Glut1 and 4 express

11 Histological evaluation with oil red O staining also demonstrated graded TG accumulat

12 to 3T3-L1 preadipocytes completely prevented oil red O staining and blocked upregulation of aP2, pero

13 id-laden THP-1 macrophages was detected with oil red O staining and light microscopy.

14 Oil red O staining and quantitative mass spectroscopy re

15 ls were profoundly reduced, as determined by Oil Red O staining and transmission electron microscopy,

16 n by a specific short hairpin RNA attenuated Oil-Red-O staining and aP2 expression, suggesting that t

17 ld atherosclerosis (as ascertained by aortic Oil Red O staining) and a systemic increase in plasma AT

18 es was confirmed using immunohistochemistry, Oil Red O staining, and gene array expression analysis.

19 c steatosis, as indicated by histopathology, Oil Red O staining, and hepatic triglyceride levels.

20 hepatic triglycerides, the steatosis score, oil red-O staining, and lipid peroxidation.

21 pocyte markers FABP4 and PPARgamma mRNAs and Oil-red O-staining at the end of the differentiation sta

22 s were analyzed using Western blot analysis, Oil-Red-O staining, cyclic adenosine monophosphate radio

23 7BL/6 mice fed the Ath diet showed extensive oil red O-staining fatty streak aortic sinus lesions (20

24 Axl-/- mice had minimal Oil Red O+ staining, fewer microglia, and significantly

25 R2 ligand Pam(3)-Cys-Ala-Gly-OH (Pam) became Oil Red O-stained foam cells and showed increased choles

26 Positive oil red O staining for lipids and immunostaining for SRE

27 is in 3T3-L1 adipocytes was determined using Oil red O staining, gene-expression analysis, immunoblot

28 cumulation was documented morphologically by Oil Red O staining in cells exposed to palmitic acid, an

29 zone treatment, there was significantly more Oil Red O+ staining in the Axl-/- corpora callosa than i

30 tinocytes, which was paralleled by increased oil red O staining indicative of lipid accumulation, the

31 ora callosa of wildtype (WT) mice had robust Oil Red O+ staining indicative of ongoing phagocytosis.

32 tion of bronchial alveolar lavage fluid with oil red O staining is a useful diagnostic modality, espe

33 monstrated by accumulation of intracellular, Oil Red O-stained lipid droplets.

34 e intramural and pericapillary collection of Oil Red O-staining lipids in these hyperglyceridemic pat

35 ell adhesion molecule-1, lipid deposition by oil red O staining, lymphocyte infiltration (CD43-positi

36 ultures reduced adipogenesis, as assessed by oil red O staining (n=2).

37 rosclerotic lesion formation, as assessed by Oil Red O staining of en face aortas and aortic root cro

38 affin sections, thereby obviating cumbersome oil red O staining of frozen sections.

39 nto macrophage-rich atheromata identified by Oil Red O staining of lipid deposits.

40 icated by characteristic cell morphology and oil red O staining of lipid vacuoles.

41 ter 4 (GLUT4) and adiponectin expression and Oil Red O staining of neutral lipids.

42 cro-SPECT/CT, along with autoradiography and oil red O staining of tissues.

43 Oil red O staining of total aortas demonstrated reductio

44 hibit evidence of greater adipogenesis (+30% Oil Red O stain [ORO], +50% peroxisome proliferator-acti

45 sis-associated core isolates, as measured by oil red O staining (P= .02).

46 Lipid content in the aortic arch measured by oil red-O staining revealed a 1.5-fold increase in mice

47 Oil Red O staining showed many lipid droplets within the

48 um parameters, circadian locomotor activity, Oil Red O staining, transient transfection, luciferase r

49 Hematoxylin and eosin and Oil Red O staining were performed to determine steatosis

50 olished lipid lesion development, assayed by oil red O staining, whether the mice were fed a normal d

51 Comparison of oil red O staining with autoradiography demonstrated are