Relevant bibliographies by topics / ApoE-/- mouse

Academic literature on the topic 'ApoE-/- mouse'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "ApoE-/- mouse":

1

Tai, Leon M., Katherine L. Youmans, Lisa Jungbauer, Chunjiang Yu, and Mary Jo LaDu. "Introducing HumanAPOEinto AβTransgenic Mouse Models." International Journal of Alzheimer's Disease 2011 (2011): 1–9. http://dx.doi.org/10.4061/2011/810981.

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Apolipoprotein E (apoE) and apoE/amyloid-β(Aβ) transgenic (Tg) mouse models are critical to understanding apoE-isoform effects on Alzheimer's disease risk. Compared to wild type,apoE−/−mice exhibit neuronal deficits, similar to apoE4-Tg compared to apoE3-Tg mice, providing a model for Aβ-independent apoE effects on neurodegeneration. To determine the effects of apoE on Aβ-induced neuropathology,apoE−/−mice were crossed with Aβ-Tg mice, resulting in a significant delay in plaque deposition. Surprisingly, crossing human-apoE-Tg mice withapoE−/−/Aβ-Tg mice further delayed plaque deposition, which eventually developed in apoE4/Aβ-Tg mice prior to apoE3/Aβ-Tg. One approach to address hAPOE-induced temporal delay in Aβpathology is an additional insult, like head injury. Another is crossing human-apoE-Tg mice with Aβ-Tg mice that have rapid-onset Aβpathology. For example, because 5xFAD mice develop plaques by 2 months, the prediction is that human-apoE/5xFAD-Tg mice develop plaques around 6 months and 12 months before other human-apoE/Aβ-Tg mice. Thus, tractable models for human-apoE/Aβ-Tg mice continue to evolve.
2

Vecchio, Filomena Lo, Paola Bisceglia, Bruno Pietro Imbimbo, Madia Lozupone, Raffaela Rita Latino, Emanuela Resta, Maurizio Leone, et al. "Are apolipoprotein E fragments a promising new therapeutic target for Alzheimer’s disease?" Therapeutic Advances in Chronic Disease 13 (January 2022): 204062232210816. http://dx.doi.org/10.1177/20406223221081605.

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Human apolipoprotein E (ApoE) is a 299-amino acid secreted glycoprotein that binds cholesterol and phospholipids. ApoE exists as three common isoforms (ApoE2, ApoE3, and ApoE4) and heterozygous carriers of the ε4 allele of the gene encoding ApoE ( APOE) have a fourfold greater risk of developing Alzheimer’s disease (AD). The enzymes thrombin, cathepsin D, α-chymotrypsin-like serine protease, and high-temperature requirement serine protease A1 are responsible for ApoE proteolytic processing resulting in bioactive C-terminal-truncated fragments that vary depending on ApoE isoforms, brain region, aging, and neural injury. The objectives of the present narrative review were to describe ApoE processing, discussing current hypotheses about the potential role of various ApoE fragments in AD pathophysiology, and reviewing the current development status of different anti-ApoE drugs. The exact mechanism by which APOE gene variants increase/decrease AD risk and the role of ApoE fragments in the deposition are not fully understood, but APOE is known to directly affect tau-mediated neurodegeneration. ApoE fragments co-localize with neurofibrillary tangles and amyloid β (Aβ) plaques, and may cause neurodegeneration. Among anti-ApoE approaches, a fascinating strategy may be to therapeutically overexpress ApoE2 in APOE ε4/ε4 carriers through vector administration or liposomal delivery systems. Another approach involves reducing ApoE4 expression by intracerebroventricular antisense oligonucleotides that significantly decreased Aβ pathology in transgenic mice. Differences in the proteolytic processing of distinct ApoE isoforms and the use of ApoE fragments as mimetic peptides in AD treatment are also under investigation. Treatment with peptides that mimic the structural and biological properties of native ApoE may reduce Aβ deposition, tau hyperphosphorylation, and glial activation in mouse models of Aβ pathology. Alternative strategies involve the use of ApoE4 structure correctors, passive immunization to target a certain form of ApoE, conversion of the ApoE4 aminoacid sequence into that of ApoE3 or ApoE2, and inhibition of the ApoE-Aβ interaction.
3

James, Niaya, Oyinkansola Shonde, Nahdia Jones, Verona E. Mulgrave, G. William Rebeck, and Joanne Allard. "Impact of APOE Genotype on Diet-induced Mitochondrial Adaptations in Mouse Skeletal Muscle." Innovation in Aging 5, Supplement_1 (December 1, 2021): 971. http://dx.doi.org/10.1093/geroni/igab046.3496.

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Abstract Apolipoprotein E (APOE), a component of lipoproteins that facilitates cholesterol transportation, has three variants in the human genome: APOE2, E3, and E4. Prior research found that carriers of APOE4 are more susceptible to developing Alzheimer's disease (AD) and other brain disorders than those who possess other APOE alleles, and that these carriers are also predisposed to mitochondrial impairment– an early characteristic of neuronal dysfunction. Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1ɑ) is a major biomarker for mitochondrial biogenesis and function and cytochrome c oxidase subunit IV (COX4) is the terminal enzyme of the mitochondrial respiratory chain. Decreased measures of these proteins indicate reduced mitochondrial function. Aside from genetic inheritance, lifestyle factors such as diet and exercise significantly impact one’s risk for mitochondrial dysfunction and AD. In these studies, we examined the impact of APOE variance on physiological adaptations induced by either exercise or a high-fat diet, with a focus on biomarkers of mitochondrial function. Western blots were used to measure COX4 and PGC-1ɑ levels in skeletal muscle tissue from female APOE3 and APOE4 knock-in transgenic mice. Based on performance on a motorized rotating rod and voluntary wheel-running, we deduced that female APOE4 mice exhibit reduced motor coordination and activity relative to APOE3 mice. APOE4 mice also had reduced COX4 levels that were increased by the high-fat diet. In contrast, COX4 levels in APOE3 mice were reduced in the high-fat diet group. Our data show that diet and APOE genotype interact to produce adaptations in mitochondrial proteins in skeletal muscle.
4

Watson, Yassin, Brenae Nelson, Jamie Hernandez Kluesner, Caroline Tanzy, Shreya Ramesh, Zoey Patel, Kaci Hernandez Kluesner, Anita Singh, Vibha Murthy, and Cassie S. Mitchell. "Aggregate Trends of Apolipoprotein E on Cognition in Transgenic Alzheimer’s Disease Mice." Journal of Alzheimer's Disease 83, no. 1 (August 31, 2021): 435–50. http://dx.doi.org/10.3233/jad-210492.

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Background: Apolipoprotein E (APOE) genotypes typically increase risk of amyloid-β deposition and onset of clinical Alzheimer’s disease (AD). However, cognitive assessments in APOE transgenic AD mice have resulted in discord. Objective: Analysis of 31 peer-reviewed AD APOE mouse publications (n = 3,045 mice) uncovered aggregate trends between age, APOE genotype, gender, modulatory treatments, and cognition. Methods: T-tests with Bonferroni correction (significance = p < 0.002) compared age-normalized Morris water maze (MWM) escape latencies in wild type (WT), APOE2 knock-in (KI2), APOE3 knock-in (KI3), APOE4 knock-in (KI4), and APOE knock-out (KO) mice. Positive treatments (t+) to favorably modulate APOE to improve cognition, negative treatments (t–) to perturb etiology and diminish cognition, and untreated (t0) mice were compared. Machine learning with random forest modeling predicted MWM escape latency performance based on 12 features: mouse genotype (WT, KI2, KI3, KI4, KO), modulatory treatment (t+, t–, t0), mouse age, and mouse gender (male = g_m; female = g_f, mixed gender = g_mi). Results: KI3 mice performed significantly better in MWM, but KI4 and KO performed significantly worse than WT. KI2 performed similarly to WT. KI4 performed significantly worse compared to every other genotype. Positive treatments significantly improved cognition in WT, KI4, and KO compared to untreated. Interestingly, negative treatments in KI4 also significantly improved mean MWM escape latency. Random forest modeling resulted in the following feature importance for predicting superior MWM performance: [KI3, age, g_m, KI4, t0, t+, KO, WT, g_mi, t–, g_f, KI2] = [0.270, 0.094, 0.092, 0.088, 0.077, 0.074, 0.069, 0.061, 0.058, 0.054, 0.038, 0.023]. Conclusion: APOE3, age, and male gender was most important for predicting superior mouse cognitive performance.
5

Sheng, Huaxin, Daniel T. Laskowitz, Ellen Bennett, Donald E. Schmechel, Robert D. Bart, Ann M. Saunders, Robert D. Pearlstein, Allen D. Roses, and David S. Warner. "Apolipoprotein E Isoform-Specific Differences in Outcome from Focal Ischemia in Transgenic Mice." Journal of Cerebral Blood Flow & Metabolism 18, no. 4 (April 1998): 361–66. http://dx.doi.org/10.1097/00004647-199804000-00003.

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Apolipoprotein E (apoE), a 34-kD glycosylated lipid-binding protein, is expressed as three common isoforms in humans (E2, E3, or E4). Clinical evidence suggests that the apoE genotype (APOE) may be a risk factor for poor outcome after acute central nervous system injury. This was examined further in transgenic mice constructed with the human APOE3 or APOE4 gene under the control of human promoter and tissue expression elements. Presence of human apoE3 and apoE4 proteins in brains of human APOE homozygous transgenic mice was confirmed by Western blotting. APOE3 (n = 12) and APOE4 (n = 10) mice underwent 60 minutes of middle cerebral artery occlusion. After 24-hour recovery, infarct size was measured. Infarct volumes (mean ± standard deviation) were smaller in the APOE3 group (cortex: APOE3 = 18 ± 4 mm3; APOE4 = 30 ± 11 mm3, P = 0.04; subcortex: APOE3 = 12 ± 4 mm3; APOE4 = 18 ± 4 mm3, P = 0.003). Hemiparesis was less severe in APOE3 mice ( P = 0.02). These data indicate that human isoform-specific effects of apoE are relevant to acute pathomechanisms of focal ischemic brain damage when examined in the mouse. APOE transgenic mice may provide an appropriate model to examine the mechanistic basis for the differential effects of human apoE isoforms in acute central nervous system injury.
6

Zhao, Na, Olivia N. Attrebi, Yingxue Ren, Wenhui Qiao, Berkiye Sonustun, Yuka A. Martens, Axel D. Meneses, et al. "APOE4 exacerbates α-synuclein pathology and related toxicity independent of amyloid." Science Translational Medicine 12, no. 529 (February 5, 2020): eaay1809. http://dx.doi.org/10.1126/scitranslmed.aay1809.

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The apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for late-onset Alzheimer’s disease mainly by driving amyloid-β pathology. Recently, APOE4 has also been found to be a genetic risk factor for Lewy body dementia (LBD), which includes dementia with Lewy bodies and Parkinson’s disease dementia. How APOE4 drives risk of LBD and whether it has a direct effect on α-synuclein pathology are not clear. Here, we generated a mouse model of synucleinopathy using an adeno-associated virus gene delivery of α-synuclein in human APOE-targeted replacement mice expressing APOE2, APOE3, or APOE4. We found that APOE4, but not APOE2 or APOE3, increased α-synuclein pathology, impaired behavioral performances, worsened neuronal and synaptic loss, and increased astrogliosis at 9 months of age. Transcriptomic profiling in APOE4-expressing α-synuclein mice highlighted altered lipid and energy metabolism and synapse-related pathways. We also observed an effect of APOE4 on α-synuclein pathology in human postmortem brains with LBD and minimal amyloid pathology. Our data demonstrate a pathogenic role of APOE4 in exacerbating α-synuclein pathology independent of amyloid, providing mechanistic insights into how APOE4 increases the risk of LBD.
7

Zhang, Xin, Long Wu, Russell H. Swerdlow, and Liqin Zhao. "Opposing Effects of ApoE2 and ApoE4 on Glycolytic Metabolism in Neuronal Aging Supports a Warburg Neuroprotective Cascade against Alzheimer’s Disease." Cells 12, no. 3 (January 25, 2023): 410. http://dx.doi.org/10.3390/cells12030410.

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Apolipoprotein E4 (ApoE4) is the most recognized genetic risk factor for late-onset Alzheimer’s disease (LOAD), whereas ApoE2 reduces the risk for LOAD. The underlying mechanisms are unclear but may include effects on brain energy metabolism. Here, we used neuro-2a (N2a) cells that stably express human ApoE isoforms (N2a-hApoE), differentiated N2a-hApoE neuronal cells, and humanized ApoE knock-in mouse models to investigate relationships among ApoE isoforms, glycolytic metabolism, and neuronal health and aging. ApoE2-expressing cells retained robust hexokinase (HK) expression and glycolytic activity, whereas these endpoints progressively declined with aging in ApoE4-expressing cells. These divergent ApoE2 and ApoE4 effects on glycolysis directly correlated with markers of cellular wellness. Moreover, ApoE4-expressing cells upregulated phosphofructokinase and pyruvate kinase with the apparent intent of compensating for the HK-dependent glycolysis reduction. The introduction of ApoE2 increased HK levels and glycolysis flux in ApoE4 cells. PI3K/Akt signaling was distinctively regulated by ApoE isoforms but was only partially responsible for the ApoE-mediated effects on HK. Collectively, our findings indicate that human ApoE isoforms differentially modulate neuronal glycolysis through HK regulation, with ApoE2 upregulating and ApoE4 downregulating, which markedly impacts neuronal health during aging. These findings lend compelling support to the emerging inverse-Warburg theory of AD and highlight a therapeutic opportunity for bolstering brain glycolytic resilience to prevent and treat AD.
8

Dafnis, Ioannis, Christina Raftopoulou, Christina Mountaki, Evgenia Megalou, Vassilis I. Zannis, and Angeliki Chroni. "ApoE isoforms and carboxyl-terminal-truncated apoE4 forms affect neuronal BACE1 levels and Aβ production independently of their cholesterol efflux capacity." Biochemical Journal 475, no. 10 (May 31, 2018): 1839–59. http://dx.doi.org/10.1042/bcj20180068.

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The β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) initiates the production of amyloid-β peptide (Aβ), which is central to the pathogenesis of Alzheimer's disease (AD). Changes in brain cholesterol homeostasis have been suggested to affect Aβ metabolism. Cholesterol homeostasis is maintained in the brain by apolipoprotein E (apoE). The apoE4 isoform constitutes the major risk factor for AD. Here, we investigated the effect of apoE forms on Aβ generation and on BACE1 levels. We also examined the potential involvement in these processes of cholesterol transporters ABCG1 and ABCG4 or the lipoprotein receptor SR-BI, which are implicated in cholesterol efflux to apoE. It was found that reconstituted lipoprotein-associated apoE isoforms promoted the increase of Aβ production and oligomerization and of BACE1 levels in human neuroblastoma SK-N-SH cells, with an apoE4 ≥ apoE3 > apoE2 potency rank order. Progressive carboxyl-terminal apoE4 deletions between residues 230–299 decreased the protein's ability to increase BACE1, while further truncations up to residue 166 prevented apoE4 from increasing BACE1 and Aβ levels in SK-N-SH and primary mouse neuronal cells. ABCG1, but not ABCG4 or SR-BI, moderately increased Aβ production and BACE1 levels in SK-N-SH cells. All apoE forms affected Aβ production/oligomerization and BACE1 levels in a pattern that did not follow that of their capacity to promote ABCG1, ABCG4 or SR-BI-mediated cholesterol efflux. Overall, our data indicate that apoE-containing lipoprotein particles can have a direct effect on BACE1 levels and Aβ secretion and possibly contribute to AD pathogenetic processes, independently of their capacity to promote cholesterol efflux.
9

Demby, Tamar, G. William Rebeck, Christopher Albanese, Olga C. Rodriguez, Yichien Lee, and Jeanne Mandelblatt. "3367 A Mouse Model of APOE Genotype in Chemotherapy Related Cognitive Impairment." Journal of Clinical and Translational Science 3, s1 (March 2019): 1. http://dx.doi.org/10.1017/cts.2019.6.

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OBJECTIVES/SPECIFIC AIMS: Chemotherapy-related cognitive impairment (CRCI) affects 15-35% of breast cancer survivors and constitutes a significant challenge for survivor quality of life. Among older breast cancer survivors who received chemotherapy treatment, carriers of at least one ɛ4 allele of the APOE gene, which encodes apolipoprotein E, are at higher risk for developing CRCI than non-carriers. APOE4 is well characterized as the strongest genetic risk factor for Alzheimer’s disease, but how it contributes to CRCI is not yet understood, and no animal models of APOE genotype and CRCI have yet been established. To better understand how APOE4 acts as a risk factor for CRCI, we used APOE targeted replacement (TR) mice to develop a model of its effects on cognition following treatment with doxorubicin, a chemotherapy drug commonly used in breast cancer treatment. METHODS/STUDY POPULATION: Twelve-to-thirteen month old APOE3 and APOE4 targeted replacement mice expressing human APOE3 or human APOE4 under control of the endogenous murine promoter were treated with 10 mg/kg doxorubicin or equivolume saline given via two IP injections spaced one week apart. One week post-treatment, mice were tested using Open Field and Elevated Zero apparatuses to assess baseline locomotive activity and anxiety and exploratory behaviors. Five weeks post-treatment, mice were assessed using the Barnes Maze over four days of training trials and one 72 hour memory probe. RESULTS/ANTICIPATED RESULTS: We found no differences in Open Field and Elevated Zero behavior, indicating limited influence of doxorubicin treatment on locomotive and anxiety behaviors in both genotypes. During Barnes Maze training, APOE4 mice treated with doxorubicin showed increased latency compared to untreated APOE4 mice as well as treated and untreated APOE3 mice, indicating deficiencies in spatial learning. In APOE3 mice, no differences in performance were seen between doxorubicin-treated and untreated mice (n = 15-16/group, p <.0001). DISCUSSION/SIGNIFICANCE OF IMPACT: These results indicate that APOE4 targeted replacement mice have specific cognitive vulnerabilities to doxorubicin treatment that can be reliably detected using the Barnes Maze assessment. Future directions include experiments to determine how other chemotherapy drugs or drug combinations impact cognition of APOE4 mice. Ultimately this model may be used to assess preventive measures or therapies for CRCI in the vulnerable APOE4 carrier population with the ability to validate cognitive impacts of these interventions.
10

Staurenghi, Erica, Valerio Leoni, Marco Lo Iacono, Barbara Sottero, Gabriella Testa, Serena Giannelli, Gabriella Leonarduzzi, and Paola Gamba. "ApoE3 vs. ApoE4 Astrocytes: A Detailed Analysis Provides New Insights into Differences in Cholesterol Homeostasis." Antioxidants 11, no. 11 (November 1, 2022): 2168. http://dx.doi.org/10.3390/antiox11112168.

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The strongest genetic risk factor for sporadic Alzheimer’s disease (AD) is the presence of the ε4 allele of the apolipoprotein E (ApoE) gene, the major apolipoprotein involved in brain cholesterol homeostasis. Being astrocytes the main producers of cholesterol and ApoE in the brain, we investigated the impact of the ApoE genotype on astrocyte cholesterol homeostasis. Two mouse astrocytic cell lines expressing the human ApoE3 or ApoE4 isoform were employed. Gas chromatography–mass spectrometry (GC-MS) analysis pointed out that the levels of total cholesterol, cholesterol precursors, and various oxysterols are altered in ApoE4 astrocytes. Moreover, the gene expression analysis of more than 40 lipid-related genes by qRT-PCR showed that certain genes are up-regulated (e.g., CYP27A1) and others down-regulated (e.g., PPARγ, LXRα) in ApoE4, compared to ApoE3 astrocytes. Beyond confirming the significant reduction in the levels of PPARγ, a key transcription factor involved in the maintenance of lipid homeostasis, Western blotting showed that both intracellular and secreted ApoE levels are altered in ApoE4 astrocytes, as well as the levels of receptors and transporters involved in lipid uptake/efflux (ABCA1, LDLR, LRP1, and ApoER2). Data showed that the ApoE genotype clearly affects astrocytic cholesterol homeostasis; however, further investigation is needed to clarify the mechanisms underlying these differences and the consequences on neighboring cells. Indeed, drug development aimed at restoring cholesterol homeostasis could be a potential strategy to counteract AD.
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Dissertations / Theses on the topic "ApoE-/- mouse":

1

Reverté, Soler Ingrid. "Neurobehavioural effects associated with postnatal exposure to decabromodiphenyl ether in apoe2, apoe3 and apoe4 transgenic mice." Doctoral thesis, Universitat Rovira i Virgili, 2012. http://hdl.handle.net/10803/76782.

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El Decabromodifenil èter (BDE-209) és un retardant de la flama àmpliament utilitzat i font de preocupació a causa de la toxicitat mostrada per altres Difenil Èters Polibromats (PBDEs). La presència de PBDEs en la llet materna fa preocupant la seva exposició durant el desenvolupament. Pensem que l’exposició primerenca a BDE-209 pot produir efectes a llarg termini i interactuar amb factors genètics, com el genotip de l’ApolipoproteinaE. Ratolins portadors de les diferents isoformeshumanes de l’ApoE foren tractats amb una dosi oral aguda de 0, 10 o 30 mg / kg de BDE-209 en el dia postnatal 10 i van ser avaluats per neurocomportament durant el desenvolupament, a l'edat adulta i la vellesa. L’exposició a BDE-209 indueix un retard en el desenvolupament físic i neuromotor i en la compactació de la mielina en els ratolins ApoE2, disminueix els nivells de tiroxina lliure en les femelles adultes i disminueix l'activitat en ratolins ApoE4. Els efectes més consistents durant tota la vida s'observen en ratolins ApoE3 i consisteixen en problemes d'aprenentatge als 4 mesos, i problemes d'aprenentatge i memòria i un augment de l'ansietat als 12 mesos.
Decabromodiphenyl Ether (BDE-209) is a flame retardant widely used and source of concern because ofthe toxicity showed by other Polibrominateddiphenyl ethers (PBDEs). The presenceof PBDEs in human’s breast milkmakes worrying its exposure during development. We hypothesised that an early exposure to BDE-209 can induce long-term impairments and interact with genetic factors, such as ApolipoproteinE genotype. Mice carrying the different Human ApoE isoforms treated with an acute oral dose of 0, 10 or 30 mg/kg of BDE-209 on postnatal day 10 were assessed for neurobehaviourduring development, in young adulthood and old age. BDE-209 exposure inducesadelay in physic and neuromotordevelopment and in myelin compaction in ApoE2 mice, decreases the levels of free thyroxin in adult femalesand decreases activity in ApoE4 mice. The most consistent effects across the lifespan are observed in ApoE3 mice and consist of impaired learning at 4 months, and impaired learning and memory and increased anxiety at 12 months.
2

Martinic, Goran (Gary), of Western Sydney Hawkesbury University, of Science Technology and Environment College, and School of Environment and Agriculture. "Cyclodextrins as potential human anti-atherosclerotic agents." THESIS_CSTE_EAG_Martinic_G.xml, 2001. http://handle.uws.edu.au:8081/1959.7/129.

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Cyclodextrins (CDs) are naturally occurring cyclic oligosaccharides. Since it is believed that OxC blocks the removal of normal cholesterol from cells in the artery wall, it is possible that selective removal of OxC in the vessel wall in-vivo may prevent or reverse atherosclerosis.As a prelude to major studies, this research project was designed to answer two critical questions; 1/. What is the best route for delivery of CD. 2/. How do animals (apoE-/- mice) tolerate it. Pilot studies were established and results noted. These studies have provided valuable information in the apoE-/- mouse for subsequent studies to prevent or reverse atherosclerosis in this animal model.
Master of Science (Hons)
3

Haskett, Darren. "Progressive Alterations in Microstructural Organization and Biomechanical Response in the ApoE Mouse Model of Aneurysm and the Underlying Changes in Biochemistry." Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/581126.

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Abdominal Aortic Aneurysm (AAA) is a complex disease that leads to a localized dilation of the infrarenal aorta that develops over years. Longitudinal information in humans has been difficult to obtain for this disease, therefore mouse models have become increasingly used to study the development of AAAs. The objective of this study was to determine any changes that occur in the biomechanical response and fiber microstructure in the apolipoprotein E difficient (ApoE-/-) angiotensin II (AngII) infused mouse model of aneurysm during disease progression, as well as determine some of the underlying changes in biochemistry, and demonstrate a novel method of reducing any pathogenic protease activity. Using a Microbiaxial Opto-Mechanical Device (MOD), ex vivo studies included adult aortas of ApoE-/- AngII infused mice excised and tested for mechanical response simultaneously imaged using two-photon microscopy to assess the microstructure at multiple time points. In vitro and ex vivo studies have shown changes in protease concentrations with the use of FRET based proteolytic beacons able to provide a non-destructive method to quantify protease activity measured against mechanical and microstructural changes. In vitro studies have demonstrated protease activity can be reduced using a molecule providing a positive feedback mechanism for protease inhibition and possibly provide a reduction in aneurysm progression.
4

Harris, Julian David. "Development of recombinant adeno-associated virus and second generation adenovirus vectors for the gene transfer of human apolipoprotein E (ApoE) in the APOE deficient mouse." Thesis, Royal Holloway, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420867.

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5

Armour, Danielle Louise. "Role of 11β-hydroxysteroid dehydrogenase type 2 in protection against inflammation during atherogenesis : studies in the Apoe-/- /11β-HSD2-/- double knockout mouse." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4431.

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It is well established that atherosclerosis, an inflammatory response to chronic injury in the blood vessel wall, plays a leading role in the development and progression of cardiovascular disease. Mineralocorticoid receptor (MR) over-activation has been implicated in atherosclerosis. In mineralocorticoid-target tissues, 11β- Hydroxysteroid dehydrogenase type 2 (11β-HSD2) inactivates glucocorticoids, conferring aldosterone specificity upon the normally unselective MR. Recent evidence suggests that 11β-HSD2 may also afford protection of MR in the cells of the vasculature, providing possible mechanisms by which MR activation may directly promote atherosclerosis. Consistent with this, Apoe-/-/11β-HSD2-/- double knockout (DKO) mice show accelerated atheroma development. The present thesis tested the hypothesis that inactivation of 11β-HSD2, allowing inappropriate activation of MR in cells of the vasculature, accelerates atherogenesis through promotion of a pro-inflammatory environment with increased endothelial cell expression of adhesion molecules and subsequent macrophage infiltration into plaques. DKO mice received either the MR antagonist eplerenone (200mg/kg/day) or vehicle in normal chow diet from 2 months of age for 12 weeks. Eplerenone significantly decreased atherosclerotic burden in brachiocephalic arteries of DKO mice, an effect that was accompanied by alterations in the cellular composition of plaques such that a more stable collagen- and smooth muscle cell- rich plaque was formed. Eplerenone treatment was also associated with a reduction in vascular inflammation as demonstrated by a significant reduction in macrophage infiltration into DKO plaques. The accelerated atherogenesis in DKO mice was clearly evident by 3 months of age, a time point at which Apoe-/- mice were completely lesion free. By 6 months, some Apoe-/- mice had developed lesions whilst all DKO mice at this age showed much larger plaques. Compared to Apoe-/- mice, the cellular composition of DKO plaques was altered favouring vulnerability and inflammation, with increased macrophage and lipid content and decreased collagen content. To investigate the possible underlying mechanisms responsible for increased inflammatory cell content, the expression of vascular cell adhesion molecule 1 (VCAM-1) was compared in DKO and Apoe-/- brachiocephalic arteries. VCAM-1 immunostaining was significantly greater on the endothelial cells of DKO arteries at 3 months compared to age-matched Apoe-/- mice. At 6 months, DKO and Apoe-/- mice had similar expression of VCAM-1. Finally, mouse aortic endothelial cells (MAECs) were used to investigate the mechanism of adhesion molecule up-regulation in the absence of 11β-HSD2. Both aldosterone and TNF-α, included as a positive control, dramatically increased VCAM-1 expression in MAECs. Spironolactone pre-treatment blocked the effect of aldosterone, suggesting an MR-mediated mechanism. Corticosterone alone had no effect on VCAM-1 expression. However, inhibition of 11β-HSD2 by pre-treatment with glycyrrhetinic acid allowed corticosterone to induce a significant increase in the number of VCAM-1-stained MAECs, demonstrating functional expression of 11β- HSD2 in MAECs. Consistent with 11β-HSD2 involvement, VCAM-1 up-regulation by corticosterone in the presence of glycyrrhetinic acid was reversed by blockade of MR with spironolactone. In conclusion, loss of 11β-HSD2 activity leading to inappropriate activation of MR in atherosclerotic mice promotes plaque vulnerability and increases vascular infiltration of macrophages which accelerates plaque growth, possibly through enhanced MR- mediated endothelial cell expression of VCAM-1.
6

Martinic, Gary. "Cyclodextrins as potential human anti-atherosclerotic agents." Thesis, View thesis View thesis, 2001. http://handle.uws.edu.au:8081/1959.7/129.

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Cyclodextrins (CDs) are naturally occurring cyclic oligosaccharides. Since it is believed that OxC blocks the removal of normal cholesterol from cells in the artery wall, it is possible that selective removal of OxC in the vessel wall in-vivo may prevent or reverse atherosclerosis.As a prelude to major studies, this research project was designed to answer two critical questions; 1/. What is the best route for delivery of CD. 2/. How do animals (apoE-/- mice) tolerate it. Pilot studies were established and results noted. These studies have provided valuable information in the apoE-/- mouse for subsequent studies to prevent or reverse atherosclerosis in this animal model.
7

Ampem, Prince Tuffour. "The Transient Receptor Potential Canonical 3 (TRPC3) Channel: Novel Role in Endothelial Cell Apoptosis and its Impact on Atherosclerosis." University of Toledo Health Science Campus / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=mco1493230041479167.

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Nakouzi, Ghunwa Akram. "Genetic and Phenotypic Response of Neural Tube Defect Mouse Mutants to Folic Acid." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1246538783.

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Hoffman, Jared D. "THE PREBIOTIC INULIN BENEFICIALLY MODULATES THE GUT-BRAIN AXIS BY ENHANCING METABOLISM IN AN APOE4 MOUSE MODEL." UKnowledge, 2018. https://uknowledge.uky.edu/pharmacol_etds/24.

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Alzheimer’s disease (AD) is the most common form of dementia and a growing disease burden that has seen pharmacological interventions primarily fail. Instead, it has been suggested that preventative measures such as a healthy diet may be the best way in preventing AD. Prebiotics are one such potential measure and are fermented into metabolites by the gut microbiota and acting as gut-brain axis components, beneficially impact the brain. However, the impact of prebiotics in AD prevention is unknown. Here we show that the prebiotic inulin increased multiple gut-brain axis components such as scyllo-inositol and short chain fatty acids in the gut, periphery, and in the case of scyllo-inositol, the brain. We found in E3FAD and E4FAD mice fed either a prebiotic or control diet for 4-months, that the consumption of the prebiotic inulin can beneficially alter the gut microbiota, modulate metabolic function, and dramatically increase scyllo-inositol in the brain. This suggests that the consumption of prebiotics can beneficially impact the brain by enhancing metabolism, helping to decrease AD risk factors.
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Schröck, Evelin, P. Zschieschang, Peter O’Brien, Anne Helmrich, T. Hardt, A. Matthaei, and Karen Stout-Weider. "Spectral karyotyping of human, mouse, rat and ape chromosomes – applications for genetic diagnostics and research." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-137653.

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Spectral karyotyping (SKY) is a widely used methodology to identify genetic aberrations. Multicolor fluorescence in situ hybridization using chromosome painting probes in individual colors for all metaphase chromosomes at once is combined with a unique spectral measurement and analysis system to automatically classify normal and aberrant chromosomes. Based on countless studies and investigations in many laboratories worldwide, numerous new chromosome translocations and other aberrations have been identified in clinical and tumor cytogenetics. Thus, gene identification studies have been facilitated resulting in the dissection of tumor development and progression. For example, different translocation partners of the TEL/ETV6 transcription factor that is specially required for hematopoiesis within the bone marrow were identified. Also, the correct classification of complex karyotypes of solid tumors supports the prognostication of cancer patients. Important accomplishments for patients with genetic diseases, leukemias and lymphomas, mesenchymal tumors and solid cancers are summarized and exemplified. Furthermore, studies of disease mechanisms such as centromeric DNA breakage, DNA double strand break repair, telomere shortening and radiation-induced neoplastic transformation have been accompanied by SKY analyses. Besides the hybridization of human chromosomes, mouse karyotyping has also contributed to the comprehensive characterization of mouse models of human disease and for gene therapy studies
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Books on the topic "ApoE-/- mouse":

1

Sandler, Corey. Official Sega Genesis and Game Gear strategies, 3RD Edition. New York: Bantam Books, 1992.

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Sandler, Corey. Official Sega Genesis and Game Gear strategies, 2ND Edition. Toronto: Bantam Books, 1991.

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Official Sega Genesis and Game Gear Strategies, '94 Edition. New York, NY: Random House, Electronic Publishing, 1993.

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Book chapters on the topic "ApoE-/- mouse":

1

Beer, Michael, Sandra Doepping, Markus Hildner, Gabriele Weber, Rolf Grabner, Desheng Hu, Sarajo Kumar Mohanta, Prasad Srikakulapu, Falk Weih, and Andreas J. R. Habenicht. "Laser-Capture Microdissection of Hyperlipidemic/ApoE−/− Mouse Aorta Atherosclerosis." In Methods in Molecular Biology, 417–28. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-163-5_35.

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de Beer, F. C., M. C. de Beer, and J. D. Sipe. "Identification of apo-SAA isoforms in man and mouse." In Amyloid and Amyloidosis 1990, 890–93. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3284-8_217.

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Sipe, J. D., M. C. De Beer, and F. C. De Beer. "Strain Specific Variation in Expression of Novel Mouse apo-SAA Isoforms." In Amyloid and Amyloidosis 1990, 115–18. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3284-8_29.

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Alikhani, Nyosha, Rulan Novosyadlyy, Rosalyn Ferguson, Shoshana Yakar, and Derek LeRoith. "ApoE-Deficient Mouse Model Exhibits Significantly Enhanced Mammary Tumor Growth and Pulmonary Metastases." In BASIC/TRANSLATIONAL - Lipids, Lipoproteins & Cardiovascular Disease, P1–597—P1–597. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p13.p1-597.

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Conference papers on the topic "ApoE-/- mouse":

1

Vengrenyuk, Yuliya, Theodore J. Kaplan, Luis Cardoso, Gwendalyn J. Randolph, and Sheldon Weinbaum. "Biomechanical Modeling of Atherosclerotic Lesions in ApoE Deficient Mice." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206571.

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Cardiovascular disease remains the principal killer in the western world despite major advances in treatment of its patients [1]. It is generally accepted that sudden rupture of vulnerable plaque followed by thrombus formation underlies most cases of myocardial infarction and is responsible for more than a half of 500,000 coronary heart disease deaths every year. Although histopathological analysis of postmortem specimens have provided important data on histological features of ruptured human plaques, there is an urgent need for good representative animal models of plaque rupture. Over the last decade and a half, genetically engineered mice have been widely used to study the pathogenesis and potential treatment of atherosclerotic lesions, as well as genetic, hormonal and environmental influences on development of atherosclerosis. Though many of the features of plaque development and progression that occur in human plaques are similarly observed in murine plaques, these mouse models have long been regarded as poor models to study plaque rupture because the aortic sinus lesions seldom show any signs of fibrous cap disruption. Several recent studies reported potentially unstable atherosclerotic lesions in older apoE-deficient mice in another anatomic site, the proximal part of the brachiocephalic artery (BCA) [2, 3]. The unusual stability of aortic lesions compared to the BCA lesions in ApoE knockout mice is an unexplained paradox in developing a mouse model of plaque rupture. In this paper, we use histology based finite element analysis to evaluate peak circumferential stresses in aortic and BCA lesions from high fat fed ApoE KO mice.
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Campbell, Ian C., Daiana Weiss, John N. Oshinski, and W. Robert Taylor. "Histological Determination of Murine Plaque Mechanics and Implications for Plaque Rupture." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19295.

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Among the most common models in atherosclerosis research is the atherosclerosis-prone mouse. Genetically manipulated mouse strains such as the ApoE−/− mouse will reliably form plaques under certain conditions, and these lesions have been noted to exhibit morphological and biochemical similarities with human atherosclerotic plaques. Unlike plaques in humans, however, murine plaques are not observed to rupture and form occlusive thrombi [1]. As atherosclerosis and its complications are the leading cause of death in the modern world, a comprehensive understanding of the mechanisms of plaque disruption is essential to develop diagnostic and interventional techniques. Although the mouse model is frequently employed to study plaque formation, its validity for studying plaque disruption events such as rupture or erosion has been questioned.
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Trachet, Bram, Marjolijn Renard, Gianluca De Santis, Steven Staelens, Julie De Backer, Luca Antiga, Bart Loeys, and Patrick Segers. "A Quantitative Comparison Between Baseline Hemodynamics and End-Stage Aneurysm Formation in ApoE −/− Mice." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53452.

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The pathogenesis of abdominal aortic aneurysm (AAA) formation still remains debated. Hemodynamics have been suggested to play a (modulating) role, but no follow-up studies have been performed due to (a.o.) a lack of human data before disease initiation. We therefore used an established mouse model of AAA [1] to study whether AAA develops at locations experiencing disturbed flow. We set up a framework to obtain mouse-specific Computational Fluid Dynamics (CFD) simulations of the mouse abdominal aorta, combining: (i) an in vivo assessed geometric model [2] and (ii) in vivo measured boundary conditions. A distance map was generated to link baseline and end-stage aortic morphologies after AAA development, and the relationship between baseline hemodynamics and end-stage dilatation was quantified.
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Haskett, Darren, Urs Utzinger, Mohamad Azhar, and Jonathan Vande Geest. "Progressive Alterations in Biomechanical Response of a Mouse Model of Aneurysm." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80321.

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Abdominal aortic aneurysm (AAA) is a complex disease that leads to a localized dilation of the infrarenal aorta, the rupture of which is associated with significant morbidity and mortality, however the underlying mechanisms by which such changes remains an important unanswered question in the literature. Animal models of AAA can be used to study how changes in the microstructural and biomechanical behavior of aortic tissues develop as disease progresses in these animals. We chose here to investigate changes in mechanical characteristics with time in the established Apolipoprotein E deficient (ApoE−/−) angiotensin II (AngII) infused mouse model of AAA.
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Wang, Ying, John A. Johnson, Abigail Fulp, Michael A. Sutton, and Susan M. Lessner. "Adhesive Strength of Atherosclerotic Plaques Depends on Collagen Content." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80433.

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Atherosclerotic plaque rupture is a major cause of myocardial infarction, coronary thrombosis and stroke. In a previous study, we proposed a new plaque rupture mechanism, plaque separation at the shoulder, and developed a novel quantitative mechanical test to measure the adhesive strength between the atherosclerotic plaque and the underlying vascular wall in mouse models using the local energy release rate, G, as a quantifiable metric for direct comparison of plaque separation strengths (1). We have now investigated structure-function relationships between the local energy release rate and local plaque composition. We hypothesize that adhesive strength varies with plaque composition in mice of different genotypes, and that it correlates with collagen deposition and macrophage content in lesions. Mice which are genetically deficient in matrix metalloproteinase 12 (MMP12), have previously been shown to demonstrate altered lesion composition (2). Therefore, we used apoE knockout (KO) and apoE MMP-12 double knockout (DKO) mice for our experiments and expected to see a difference in local energy release rates between strains.
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Trachet, Bram, Marjolijn Renard, Joris Bols, Steven Staelens, Bart Loeys, and Patrick Segers. "Hemodynamics in Ascending and Abdominal Aorta Aneurysm Formation in the ApoE−/− Angiotensin II Mouse Model." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80243.

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Aortic aneurysm is a pathological dilatation of the aorta that can be life-threatening when it ruptures. Aneurysms occur throughout the entire aorta but there is a predisposition for the ascending and the abdominal aorta, an observation that cannot be fully explained by the current knowledge of the disease pathophysiology. ApoE −/− mice infused with angiotensin II have recently been reported to develop not only abdominal [1], but also ascending aortic aneurysms [2]. These animals thus provide the perfect model to compare aneurysm progression in both aortic locations and to investigate whether disturbed hemodynamics play a role in the initial phase of aneurysm growth. In this study, both imaging and computational biomechanics techniques were used to elucidate the flow field at the location of the aneurysm prior to onset of the disease.
7

Demby, Tamar C., Yichien Lee, Olga Rodriguez, Christopher Albanese, Jeanne Mandelblatt, and G. William Rebeck. "Abstract 667: A mouse model of APOE to define effects of doxorubicin on cognition." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-667.

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Demby, Tamar C., Yichien Lee, Olga Rodriguez, Christopher Albanese, Jeanne Mandelblatt, and G. William Rebeck. "Abstract 667: A mouse model of APOE to define effects of doxorubicin on cognition." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-667.

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Mahmoud, Ahmed M., Bunyen Teng, S. Jamal Mustafa, and Osama M. Mukdadi. "High-Frequency Ultrasound Tissue Classification of Atherosclerotic Plaques in an APOE-KO Mouse Model Using Spectral Analysis." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-13061.

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Small animal models have been widely used in cardiovascular research when studying the development and treatment of different diseases. This kind of research has promoted the development of noninvasive techniques to assess cardiac tissue and blood vessels of small animals. Recently, we have developed a high-frequency ultrasound imaging system for small animals, in particular, mouse and rat models. In this work, we aim to elucidate the usefulness of using spectral analysis of the received radiofrequency (RF) ultrasound signals to extract quantitative parameters to assess mechanical properties of cardiac and vascular tissues. A custom system that employs high-frequency single-element ultrasound transducers (30–120 MHz) is used for scanning. Various signal and image processing techniques are applied on the received ultrasound signals to reconstruct high resolution B-mode and spectral images. In vitro imaging of isolated heart and vessels of APOE-KO “knock-out” mouse model with atherosclerosis was performed. Power spectral densities (PSD) of RF signals were evaluated within various regions of interests (ROI) including degassed water, normal cardiac tissue, and cardiac tissue with atheroma. Various parameters were extracted from the power spectrum such as the maximum power (Pmax), the frequency at maximum power (Fpeak), and the variance of power spectrum (Pvar). Results of the preliminary spectral analysis indicated larger values for the Pmax, Fpeak, and Pvar parameters for ROI contains atheroma than other regions. For example using the envelop data, the normalized maximum power (Pmax) value for cardiac tissue with atheroma was 0.0 ± 0.789 (dB), whereas for normal tissues it was about −13.71± 0.267 (dB). These results suggest the use spectral images as a quantitative method when assessing mouse hearts and blood vessels noninvasively.
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Zhu, Hui, Jessica Shih, David S. Long, John R. Hagaman, Nobuyo Maeda, and Morton H. Friedman. "Different Strains of Mice Exhibit Different Aortic Arch Geometry and Plaque Distribution: A Fluid Dynamic Effect." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175844.

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In earlier work, we observed different patterns of disease distribution in the aortic arches of apolipoprotien E (apoE)-deficient C57BL/6 (B6) and 129/SvEv (129) mouse strains [1]. In the relatively young mice (6 mo old), fatty plaques are seen mainly in the aortic root area, extending into the right innominate artery (RIA), with very little plaque in the more distal aortic arch in the B6 strain. However, in the 129 strain, plaques are found more in the inner curvature of the aortic arch but less in the sinus area than in B6 strain (Fig. 1).

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