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Zhao Q.-M.,Capital Medical University | Zhao X.,Capital Medical University | Feng T.-T.,Capital Medical University | Zhang M.-D.,Capital Medical University | And 5 more authors.
PLoS ONE | Year: 2013

Background: Detection of vulnerable plaques could be clinically significant in the prevention of cardiovascular events. We aimed to compare Fluorine-18 fluorodeoxyglucose (18F-FDG) uptake in vulnerable and stable plaques, and investigate the feasibility of predicting thrombosis events using Positron Emission Tomography/Computed Tomography (PET/CT) angiography. Methods: Atherosclerosis was induced in 23 male New Zealand white rabbits. The rabbits underwent pharmacological triggering to induce thrombosis. A pre-triggered PET/CTA scan and a post-triggered PET/CTA scan were respectively performed. 18F-FDG uptake by the aorta was expressed as maximal standardized uptake value (SUVmax) and mean SUV (SUVmean). SUVs were measured on serial 7.5 mm arterial segments. Results: Thrombosis was identified in 15 of 23 rabbits. The pre-triggered SUVmean and SUVmax were 0.768±0.111 and 0.804±0.120, respectively, in the arterial segments with stable plaque, and 1.097±0.189 and 1.229±0.290, respectively, in the arterial segments with vulnerable plaque (P<0.001, respectively). The post-triggered SUVmean and SUVmax were 0.849±0.167 and 0.906±0.191, respectively in the arterial segments without thrombosis, and 1.152±0.258 and 1.294±0.313, respectively in the arterial segments with thrombosis (P<0.001, respectively). The values of SUVmean in the pre-triggered arterial segments were used to plot a receiver operating characteristic curve (ROC) for predicting thrombosis events. Area under the curve (AUC) was 0.898. Maximal sensitivity and specificity (75.4% and 88.5%, respectively) were obtained when SUVmean was 0.882. Conclusions: Vulnerable and stable plaques can be distinguished by quantitative analysis of 18F-FDG uptake in the arterial segments in this rabbit model. PET/CT may be used for predicting thrombosis events and risk-stratification in patients with atherosclerotic disease. © 2013 Zhao et al.


Zhang M.-D.,Capital Medical University | Zhang M.-D.,Beijing Institute of Heart | Zhao X.-C.,Capital Medical University | Zhao X.-C.,Beijing Institute of Heart | And 9 more authors.
Cardiovascular Therapeutics | Year: 2015

Introduction: The relationship between the beneficial effects of pioglitazone in reducing clinical events and plaque inflammatory burden remains unknown. This study aimed to determine whether pioglitazone can reduce the number of plaque thrombosis incidences and whether decreasing plaque inflammation is the mechanism by which pioglitazone reduces plaque thromboses. Methods and Results: therosclerotic rabbits were divided into two groups: the atherosclerosis group (n = 13) and pioglitazone group (n = 10). The rabbits underwent pharmacological triggering to induce thrombosis. Serum inflammatory markers, FDG uptake, macrophage, and neovessel staining detected arterial inflammation. PET/CT scans were performed twice (baseline and posttreatment scans). Plaque area, macrophages, and neovessels were measured and the histologic sections were matched with the PET/CT scans. Serum MMP-9 and hsCRP were lower in the pioglitazone group compared to the atherosclerosis group. The SUVmean significantly decreased in the pioglitazone group (0.62 ± 0.21 vs. 0.55 ± 0.19, P = 0.008), but increased in the atherosclerosis group (0.61 ± 0.15 vs. 0.91 ± 0.20, P < 0.000). The incidence rate of plaque rupture, plaque area, macrophage density, and neovessel density was significantly lower in rabbits with pioglitazone than without (15% vs. 38%, P < 0.001; 18.00 ± 2.30 vs. 27.00 ± 1.60; P < 0.001; 8.80 ± 3.94 vs. 28.26 ± 2.49; P < 0.001; 16.50 ± 3.09 vs. 29.00 ± 2.11; P < 0.001, respectively). Moreover, plaque area and macrophage density were positively correlated with SUV values. Conclusions: Our study suggests that pioglitazone can reduce the number of plaque thrombosis incidences by decreasing plaque inflammation. 18F-FDG-PET/CT can detect plaque inflammation and assess the effects of antiatherosclerotic drugs. © 2015 John Wiley & Sons Ltd.


PubMed | Capital Medical University and General Hospital of Second Artillery of PLA
Type: Journal Article | Journal: Cardiovascular therapeutics | Year: 2015

The relationship between the beneficial effects of pioglitazone in reducing clinical events and plaque inflammatory burden remains unknown. This study aimed to determine whether pioglitazone can reduce the number of plaque thrombosis incidences and whether decreasing plaque inflammation is the mechanism by which pioglitazone reduces plaque thromboses.therosclerotic rabbits were divided into two groups: the atherosclerosis group (n = 13) and pioglitazone group (n = 10). The rabbits underwent pharmacological triggering to induce thrombosis. Serum inflammatory markers, FDG uptake, macrophage, and neovessel staining detected arterial inflammation. PET/CT scans were performed twice (baseline and posttreatment scans). Plaque area, macrophages, and neovessels were measured and the histologic sections were matched with the PET/CT scans. Serum MMP-9 and hsCRP were lower in the pioglitazone group compared to the atherosclerosis group. The SUVmean significantly decreased in the pioglitazone group (0.62 0.21 vs. 0.55 0.19, P = 0.008), but increased in the atherosclerosis group (0.61 0.15 vs. 0.91 0.20, P < 0.000). The incidence rate of plaque rupture, plaque area, macrophage density, and neovessel density was significantly lower in rabbits with pioglitazone than without (15% vs. 38%, P < 0.001; 18.00 2.30 vs. 27.00 1.60; P < 0.001; 8.80 3.94 vs. 28.26 2.49; P < 0.001; 16.50 3.09 vs. 29.00 2.11; P < 0.001, respectively). Moreover, plaque area and macrophage density were positively correlated with SUV values.Our study suggests that pioglitazone can reduce the number of plaque thrombosis incidences by decreasing plaque inflammation. (18)F-FDG-PET/CT can detect plaque inflammation and assess the effects of antiatherosclerotic drugs.


PubMed | General Hospital of Second Artillery of PLA
Type: Journal Article | Journal: International journal of molecular medicine | Year: 2012

The present study aimed to investigate the feasibility of isolating adipose-derived stem cells (ADSCs) by selecting cells that express the surface receptor CD105. Surface antigen expression of the unsorted cells was undertaken using FACS analysis. Primary adipose-derived cells were isolated. The second passage cells were incubated with anti-CD105 magnetic beads, and separated using a magnetic separator. Cell growth and colony formation was determined by counting and Giemsa staining, respectively. Cells also underwent histological immunohistochemical, and RT-PCR analyses to determine their chondrogenic, adipogenic and osteogenic potential. Increased cell proliferation and colony formation was observed in CD105-positive (CD105) as compared to the CD105-negative (CD105) cells (P<0.001). Following induction, the expression of type II collagen and the number of calcium deposits and lipid droplets in the CD105 ADCs were markedly higher than in the CD105 ADCs. Furthermore, increased alkaline phosphatase (AKP), leptin and PPAR2 mRNA expression was detected in the CD105 ADCs (P<0.01). Isolation of CD105 ADSCs by MACS was feasible. Thus, CD105 can be used as a relatively specific marker for the selection of ADSCs. Although the chondrogenic, adipogenic and osteogenic potential of these cells is suggestive of their potential for use in tissue engineering treatments, further in vivo studies are necessary.

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