Cardiovascular Diseases
Courtesy of Byung-Heon Lee
Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University
Daegu, Korea
Imaging of atherosclerosis with AP-1 peptide conjugated with HGC-Cy7.5
AP-1-HGC-Cy7.5, a synthetic atherosclerotic plaque-specific peptide (AP-1) conjugated with hydophobically modified glycol chitosan (HGC) nanoparticles containing CY7.5 near-infrared fluorescent dye, was administered intravenously via the tail vein into lipoprotein receptor deficient (LDLr-/-) mice fed with a high-cholesterol diet and control mice fed a normal chow diet. The mice were imaged 6 hours after administration.
Top: Fluorescence intensity map of an LDLr-/- mouse after administration with AP-1-HGC-Cy7.5.
Bottom: Fluorescence intensity map of a control mouse after administration with AP-1-HGC-Cy7.5.
Application Note
The ART Optix small animal imaging system applied to cardiovascular research (PDF: 215 Kb)
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Online Presentation
KIST/PU Phage Display Selection of Tissue-Specific Homing Peptides and their Theragnostic Applications
Byung-Heon Lee / September 2007.
Courtesy of Byung-Heon Lee
Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University
Daegu, Korea
Imaging of AP-1 homing to atherosclerotic plaques in LDLr-/- mice
Images on the left: AP-1, an atherosclerotic plaque-specific peptide, was assembled with HGC-CY7.5 nanoparticles and intravenously administered into LDL receptor-deficient (LDL-/-) mice. The mice were imaged 1 hour (top) and 6 hours (bottom) after administration.
Images on the right: As a control, HGC-CY7.5 nanoparticles were intravenously administered into LDL-/- mice. The mice were imaged 1 hour (top) and 6 hours (bottom) after administration.
Online Presentation
KIST/PU Phage Display Selection of Tissue-Specific Homing Peptides and their Theragnostic Applications
Byung-Heon Lee / September 2007.
ART Advanced Research Technologies Inc.
Visualization of atherosclerotic plaques in the aorta using anti-ICAM-Cy5.5
ApoE KO mice, which develop atherosclerotic plaques that historically resemble those found in humans, were fed a high fat diet to accelerate atherogenesis and plaque formation. As a control, C57B1/6 wild-type mice were fed a regular diet for the same period of time. Anti-ICAM labeled with Cy5.5 (50 mg) was injected via the tail vein of both groups and the mice were then imaged at various time points.
From the left: Fluorescence intensity images of C57B1/6 control and ApoE KO mice 24h/48h after injection. Comparison between control and positive cases demonstrates the targeting capability of ICAM, while longitudinal studies indicate an increase of ICAM over time in the same mouse.
ART Advanced Research Technologies Inc.
Visualization of atherosclerotic plaques in the aorta using anti-ICAM-Cy5.5
ApoE KO mice, which develop atherosclerotic plaques that historically resemble those found in humans, were fed a high fat diet to accelerate atherogenesis and plaque formation. As a control, C57B1/6 wild-type mice were fed a regular diet for the same period of time. Anti-ICAM labeled with Cy5.5 (50 mg) was injected via the tail vein of both groups and the mice were then imaged at various time points.
Image: Concentration volume slices of ApoE KO mouse 24h/48h after injection.
ART Advanced Research Technologies Inc.
Visualization of atherosclerotic plaques in the aorta using anti-VCAM-Cy5.5
ApoE KO mice, which develop atherosclerotic plaques that historically resemble those found in humans, were fed a high fat diet to accelerate atherogenesis and plaque formation. As a control, C57B1/6 wild-type mice were fed a regular diet for the same period of time. Anti-VCAM labeled with Cy5.5 (50 mg) was injected via the tail vein of both groups and the mice were then imaged at various time points.
From the left: Fluorescence intensity images of C57B1/6 control and ApoE KO mice 24h/48h after injection. Comparison between control and positive cases demonstrates the targeting capability of VCAM, while longitudinal studies indicate an increase of VCAM over time in the same mouse.
Courtesy of Abedelnasser Abulrob
National Research Council of Canada, Institute for Biological Sciences
Ottawa, Canada
Dynamic analysis of the blood-brain barrier disruption in experimental stroke
A group of mice were subjected to occlusion of the left middle cerebral artery (MCAO) for one hour using an intraluminal filament. At the end of the ischemic injury induction, 100 nmol of a Cy5.5 near-infrared fluorescent probe was injected via the tail vein. Imaging was done at various time points.
Top: Fluorescence intensity prior to MCAO/reperfusion injury.
Bottom: Fluorescence intensity after 24 hours of MCAO/reperfusion injury. The average fluorescence intensity signal over the group of injured mice was 6 times higher in the ischemic left hemisphere compared to the contra-lateral hemisphere. Comparatively, the baseline average fluorescence intensities for left and right hemispheres before ischemia were similar.
Application Note
Time-Resolved Fluorescence Imaging of Blood-Brain Barrier Disruption in Living Mice (PDF: 496 Kb)
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Paper
Dynamic analysis of the blood-brain barrier disruption in experimental stroke using time-domain in vivo fluorescence imaging
Abedelnasser Abulrob, Eric Brunette, Jacqueline Slinn, Ewa Baumann, and Danica Stanimirovic. Molecular Imaging, Volume 7, Number 6 / November-December 2008: pp. 248-262.
Courtesy of Abedelnasser Abulrob
National Research Council of Canada, Institute for Biological Sciences
Ottawa, Canada
3D representation of the blood-brain barrier disruption in experimental stroke
A group of mice were subjected to occlusion of the left middle cerebral artery (MCAO) for one hour using an intraluminal filament. At the end of the ischemic injury induction, 100 nmol of a Cy5.5 near-infrared fluorescent probe was injected via the tail vein. Imaging was done at various time points.
Image: Reconstructed concentration volumetric planes showing X-axis (coronal), Y-axis (sagittal), and Z-axis (axial) planes superimposed on the 3D image of the head profile. The higher Cy5.5-protein concentration in the damaged left hemisphere compared to the uninjured section was confirmed by histologic analysis. This study demonstrates the ability of the Optix system to visualize brain damage through the skull.
Application Note
Time-Resolved Fluorescence Imaging of Blood-Brain Barrier Disruption in Living Mice (PDF: 496 Kb)
Log in to download ART application notes.
Paper
Dynamic analysis of the blood-brain barrier disruption in experimental stroke using time-domain in vivo fluorescence imaging
Abedelnasser Abulrob, Eric Brunette, Jacqueline Slinn, Ewa Baumann, and Danica Stanimirovic. Molecular Imaging, Volume 7, Number 6 / November-December 2008: pp. 248-262.
Courtesy of Abedelnasser Abulrob
National Research Council of Canada, Institute for Biological Sciences
Ottawa, Canada
Longitudinal imaging of the blood-brain barrier disruption
Images represent longitudinal imaging of the blood-brain barrier disruption before and after 20 minutes of left middle cerebral artery occlusion (MCAO) followed by reperfusion for up to 14 days. Mice were injected with 100 nmol Cy5.5 15 minutes prior to each imaging session.
Top row: Concentration volume planes prior to MCAO/reperfusion injury and 1 day after MCAO/reperfusion injury.
Bottom row: Concentration volume planes 7 and 14 days after MCAO/reperfusion injury.
Application Note
Time-Resolved Fluorescence Imaging of Blood-Brain Barrier Disruption in Living Mice (PDF: 496 Kb)
Log in to download ART application notes.
Paper
Dynamic analysis of the blood-brain barrier disruption in experimental stroke using time-domain in vivo fluorescence imaging
Abedelnasser Abulrob, Eric Brunette, Jacqueline Slinn, Ewa Baumann, and Danica Stanimirovic. Molecular Imaging, Volume 7, Number 6 / November-December 2008: pp. 248-262.
Courtesy of Abedelnasser Abulrob
National Research Council of Canada, Institute for Biological Sciences
Ottawa, Canada
Fluorescence lifetime imaging of renal ischemia reperfusion injury
Prior to undergoing ischemia-reperfusion injury of the left kidney, a group of mice are imaged to obtain a baseline scan. The animals were then subjected to occlusion of the left renal vascular pedicle for 1 hour using a vascular clamp. After the clamp was removed, the animals were reperfused for 6 hours and intravenously injected with 10 nmol of Cy5.5 via the tail vein. Images were acquired 15 minutes after injection.
Top: Fluorescence lifetime image from baseline scan prior to ischemia-reperfusion injury. Fluorescence average weighted lifetime values for both kidneys are equivalent.
Bottom: Average weighted lifetime values for the right healthy kidney after ischemia-reperfusion injury is significantly different than the values for the left ischemic kidney and normal kidneys. Results demonstrate that the fluorescence signal in the right healthy kidney was mainly caused by the Cy5.5 probe, while endogenous fluorescence accounted for the signal in the left ischemic kidney and normal kidneys.
Application Note
Fluorescence Lifetime Imaging of Renal Ischemia Reperfusion Injury (PDF: 516 Kb)
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Paper
In vivo time-domain optical imaging of renal ischemia-reperfusion injury: discrimination based on fluorescence lifetime
Abedelnasser Abulrob, Eric Brunette, Jacqueline Slinn, Ewa Baumann, and Danica Stanimirovic. Molecular Imaging, Volume 6, Number 5 / September-October 2007: pp. 304-314.
“The time-domain mode of acquisition, based on time-correlated single-photon counting, enables more accurate recovery of probe concentration. Moreover, fluorescence lifetime-based imaging can discriminate exogenous near-infrared probes from autofluorescence based on their photophysical decay constants, even when their fluorescence intensities are comparable.”
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