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1 ncorporated lipid droplets that stained with oil red O.
2 and whole descending aorta were stained with Oil Red O.
3 ipids using histological slices stained with Oil-Red-O.
4 ogic staining with hematoxylin and eosin and oil red O and also by quantitative triglyceride measurem
5          Intramyocardial lipid staining with oil red O and gene expression analysis was performed on
6                                              Oil red O and neutral lipid staining indicated that HCV
7 , as demonstrated by decreased staining with oil red O and reduced peroxisome proliferator-activated
8                               Costaining for oil red O and the SMC-specific marker SM alpha-actin of
9 luding increased epidermal lipid staining by Oil Red O and TLR3-dependent increases in lamellar bodie
10 r lipid content and macrophage content after oil-red O and immunostaining, respectively.
11 the aortic sinus plaques were measured after oil-red O and Mac-1 antibody staining, respectively, and
12 tain), collagen (Masson's trichrome), lipid (oil red O), and leukocytes (anti-CD45).
13 TSP4 knock-in mice, lesions size measured by Oil Red O did not change, but the lesions accumulated mo
14 trast to conventional drusen the lipid stain Oil Red O failed to stain RPD.
15 killed at 6 months; aortas were stained with oil red O for planimetry and with antibodies against con
16  that CARS microscopy is more sensitive than Oil Red O histology for the detection of microvesicular
17 nt sections (rho = 0.32, P < 0.001) and with oil red O histomorphometry (rho = 0.35, P = 0.001).
18 therosclerosis was determined by en face and Oil red O imaging.
19 cols (hemotoxylin and eosin, Van Giessen and Oil Red O) is demonstrated in a study of human liver tis
20            Frozen sections were stained with oil red O or Sudan black or were analyzed by HSPM.
21                     Cells were recovered for Oil Red O (ORO) staining as well as immunocytochemistry
22                                              Oil Red O (ORO) staining showed abnormal lipid accumulat
23 ere analyzed by means of immunofluorescence, oil red O (ORO) staining, and triglyceride quantitation.
24 or without the lipase inhibitors resulted in oil red O-positive areas, resembling intrapancreatic fat
25                    We characterized cerebral Oil Red O-positive lipid-laden cells (LLC) of aging mice
26                              The presence of oil red O-positive, neutral lipid droplets in tissue bio
27 ion of the aortic lesional area stained with oil red O revealed that CKD-bMPOKO mice had significantl
28 hibit evidence of greater adipogenesis (+30% Oil Red O stain [ORO], +50% peroxisome proliferator-acti
29                          Variable amounts of Oil Red O-stainable lipid material were demonstrated bot
30 R2 ligand Pam(3)-Cys-Ala-Gly-OH (Pam) became Oil Red O-stained foam cells and showed increased choles
31 monstrated by accumulation of intracellular, Oil Red O-stained lipid droplets.
32 ultures reduced adipogenesis, as assessed by oil red O staining (n=2).
33 sis-associated core isolates, as measured by oil red O staining (P= .02).
34                 Histological evaluation with oil red O staining also demonstrated graded TG accumulat
35 to 3T3-L1 preadipocytes completely prevented oil red O staining and blocked upregulation of aP2, pero
36 ight microscopy, some extended with modified oil red O staining and energy-dispersive radiographic sp
37 id-laden THP-1 macrophages was detected with oil red O staining and light microscopy.
38  qualitatively and semi-quantitatively using Oil Red O staining and light microscopy.
39                                              Oil red O staining and quantitative mass spectroscopy re
40 ls were profoundly reduced, as determined by Oil Red O staining and transmission electron microscopy,
41                                     Positive oil red O staining for lipids and immunostaining for SRE
42 (-/-) mice exhibited significantly decreased oil red O staining in both aortic roots and aortas compa
43 cumulation was documented morphologically by Oil Red O staining in cells exposed to palmitic acid, an
44 tinocytes, which was paralleled by increased oil red O staining indicative of lipid accumulation, the
45 tion of bronchial alveolar lavage fluid with oil red O staining is a useful diagnostic modality, espe
46 rosclerotic lesion formation, as assessed by Oil Red O staining of en face aortas and aortic root cro
47 affin sections, thereby obviating cumbersome oil red O staining of frozen sections.
48 nto macrophage-rich atheromata identified by Oil Red O staining of lipid deposits.
49 icated by characteristic cell morphology and oil red O staining of lipid vacuoles.
50 ter 4 (GLUT4) and adiponectin expression and Oil Red O staining of neutral lipids.
51  more atherosclerosis as assessed by en face Oil Red O staining of the aorta (4.7+/-2.9% versus 1.9+/
52 cro-SPECT/CT, along with autoradiography and oil red O staining of tissues.
53                                              Oil red O staining of total aortas demonstrated reductio
54                                              Oil Red O staining showed many lipid droplets within the
55 romenes were comprehensively evaluated using Oil Red O staining technique, LDH activity measurement,
56                    Hematoxylin and eosin and Oil Red O staining were performed to determine steatosis
57                                Comparison of oil red O staining with autoradiography demonstrated are
58 ld atherosclerosis (as ascertained by aortic Oil Red O staining) and a systemic increase in plasma AT
59 lly, adipogenesis was blocked as assessed by Oil Red O staining, adiponectin, and Glut1 and 4 express
60 es was confirmed using immunohistochemistry, Oil Red O staining, and gene array expression analysis.
61 c steatosis, as indicated by histopathology, Oil Red O staining, and hepatic triglyceride levels.
62 is in 3T3-L1 adipocytes was determined using Oil red O staining, gene-expression analysis, immunoblot
63 AD3), and vascular phenotype was assessed by Oil Red O staining, histology, and immunofluorescence in
64 ell adhesion molecule-1, lipid deposition by oil red O staining, lymphocyte infiltration (CD43-positi
65 ation were analyzed using alizarin red S and oil red O staining, respectively.
66 metry-based lipidomics, targeted lipidomics, Oil Red O staining, Seahorse analysis, quantitative PCR,
67 um parameters, circadian locomotor activity, Oil Red O staining, transient transfection, luciferase r
68 olished lipid lesion development, assayed by oil red O staining, whether the mice were fed a normal d
69 ith dedifferentiation with loss of lipid and Oil Red O staining.
70 tion of bronchial alveolar lavage fluid with oil red O staining.
71 y, as evidenced by hematoxylin and eosin and Oil Red O staining.
72  area in the aortic sinus was assessed using oil red O staining.
73 n inhibited lipid accumulation, as judged by Oil Red O staining.
74 us (high signal on T2W, r = 0.86) areas with Oil Red O staining.
75 diet and vascular lesions were quantified by Oil Red-O staining of the serial sectioned aortic root a
76 Lipid content in the aortic arch measured by oil red-O staining revealed a 1.5-fold increase in mice
77  hepatic triglycerides, the steatosis score, oil red-O staining, and lipid peroxidation.
78          Biopsies evaluated immune response, Oil Red-O staining, ceramide, and triacylglycerol levels
79 enic differentiation through quantitation by oil-red O staining.
80 sions at the aortic root were measured after oil-red O staining.
81 n by a specific short hairpin RNA attenuated Oil-Red-O staining and aP2 expression, suggesting that t
82 s were analyzed using Western blot analysis, Oil-Red-O staining, cyclic adenosine monophosphate radio
83   The presence of adipocytes was assessed by Oil-Red-O staining.
84 zone treatment, there was significantly more Oil Red O+ staining in the Axl-/- corpora callosa than i
85 ora callosa of wildtype (WT) mice had robust Oil Red O+ staining indicative of ongoing phagocytosis.
86                      Axl-/- mice had minimal Oil Red O+ staining, fewer microglia, and significantly
87 7BL/6 mice fed the Ath diet showed extensive oil red O-staining fatty streak aortic sinus lesions (20
88 e intramural and pericapillary collection of Oil Red O-staining lipids in these hyperglyceridemic pat
89 pocyte markers FABP4 and PPARgamma mRNAs and Oil-red O-staining at the end of the differentiation sta
90                       Fish were stained with oil red O to assess hepatic lipid accumulation, and we a
91 on and histochemical staining (Alizarin Red, Oil Red O, Toluidine Blue).
92   Additionally, frozen sections stained with Oil Red O were analyzed to assess lipid accumulation in