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Artículos de revistas sobre el tema "Mouse aorta"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 12 de febrero de 2022

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1

Zhu, Guanglang, Huiying Sun, Jiannan Wang, et al. "In Vivo Detection and Measurement of Aortic Aneurysm and Dissection in Mouse Models Using Microcomputed Tomography with Contrast Agent." Contrast Media & Molecular Imaging 2019 (March 6, 2019): 1–9. http://dx.doi.org/10.1155/2019/5940301.

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Objectives. The aim of this study was to evaluate the potential of microcomputed tomography (micro-CT) using the intravascular contrast agent ExiTron nano 12000 for aorta imaging and monitoring the dynamic changing process of the aorta in mouse models with aortic aneurysm and dissection. Materials and Methods. Experiments were performed on healthy mice and mice with aortic dissection. Mice that were developing aortic dissection and healthy mice underwent micro-CT imaging after injection of ExiTron nano 12000. Time-dependent signal enhancement (at 1, 2, 3, 6, and 12 hours after intravenous inje
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2

Guo, X., Y. Kono, R. Mattrey, and G. S. Kassab. "Morphometry and strain distribution of the C57BL/6 mouse aorta." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 5 (2002): H1829—H1837. http://dx.doi.org/10.1152/ajpheart.00224.2002.

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The goal of the present study was to obtain a systematic set of data along the length of the mouse aorta to study variations of morphometry (diameter, wall thickness, and curvature), strain, and stress of the mouse aorta. Five mice were imaged with a 13-MHz ultrasound probe to determine the in vivo diameter along the aorta. A cast was made of these aortas to validate the ultrasonic diameter measurements. The root mean squared and systematic errors for these measurements were 12.6% and 6.4% of the mean ultrasound diameter, respectively. The longitudinal variations of geometry, stress, and strai
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3

Silswal, Neerupma, Nikhil K. Parelkar, Michael J. Wacker, Mostafa Badr та Jon Andresen. "PPARα-Independent Arterial Smooth Muscle Relaxant Effects of PPARαAgonists". PPAR Research 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/302495.

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We sought to determine direct vascular effects of peroxisome proliferator-activated receptor alpha (PPARα) agonists using isolated mouse aortas and middle cerebral arteries (MCAs). The PPARαagonists GW7647, WY14643, and gemfibrozil acutely relaxed aortas held under isometric tension and dilated pressurized MCAs with the following order of potency: GW7647≫WY14643>gemfibrozil. Responses were endothelium-independent, and the use of PPARαdeficient mice demonstrated that responses were also PPARα-independent. Pretreating arteries with high extracellular K+attenuated PPARαagonist-mediated relaxat
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4

Hemmeryckx, Bianca, Marc F. Hoylaerts, Eveline Deloose, et al. "Age-associated pro-inflammatory adaptations of the mouse thoracic aorta." Thrombosis and Haemostasis 110, no. 10 (2013): 785–94. http://dx.doi.org/10.1160/th13-01-0022.

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SummaryArterial ageing may be associated with a reduction in vasodilation due to increased reactive oxygen species (ROS) production, whereas endothelial cell activation induces procoagulant changes. However, little is known on the effect of ageing on expression of anticoagulant endothelial markers such as endothelial protein C receptor (EPCR). To study age-associated alterations in smooth muscle cell (SMC) and endothelial cell (EC) structure and function, the aorta was isolated from 10-week-and 12– and 24-month-old C57BL/6J mice and analysed for its expression of genes involved in senescence,
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5

Agianniotis, A., A. Rachev, and N. Stergiopulos. "Active axial stress in mouse aorta." Journal of Biomechanics 45, no. 11 (2012): 1924–27. http://dx.doi.org/10.1016/j.jbiomech.2012.05.025.

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6

Cacicedo, José M., Marie-Soleil Gauthier, Nathan K. Lebrasseur, Ravi Jasuja, Neil B. Ruderman, and Yasuo Ido. "Acute exercise activates AMPK and eNOS in the mouse aorta." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 4 (2011): H1255—H1265. http://dx.doi.org/10.1152/ajpheart.01279.2010.

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Exercise can prevent endothelial cell (EC) dysfunction and atherosclerosis even in the absence of improvements in plasma lipids. However, the mechanisms responsible for these effects are incompletely understood. In this study we examined in mice whether an acute bout of exercise activates enzymes that could prevent EC dysfunction, such as AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS). We also examined whether exercise alters known regulators of these enzymes. C57BL/6 mice underwent a single bout of exhaustive treadmill exercise after which their aortas were a
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7

Lalli, M. Jane, Shunichi Shimizu, Roy L. Sutliff, Evangelia G. Kranias, and Richard J. Paul. "[Ca2+]ihomeostasis and cyclic nucleotide relaxation in aorta of phospholamban-deficient mice." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 3 (1999): H963—H970. http://dx.doi.org/10.1152/ajpheart.1999.277.3.h963.

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Phospholamban (PLB), a protein localized in the sarcoplasmic reticulum (SR), inhibits the SR Ca2+-ATPase; phosphorylation of PLB relieves this inhibition. We previously reported significant differences in contractility in aorta from mice in which the gene for PLB was ablated (PLB−). In this study, we measured intracellular Ca2+concentration ([Ca2+]i) with fura 2 in the intact mouse aorta to more directly test the hypothesis that these changes are ascribable to altered SR function in vivo. Ten micromoles per liter of the α-agonist phenylephrine (PE) increased [Ca2+]imonotonically to a steady st
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8

Amirbekian, Smbat, Robert C. Long, Michelle A. Consolini, et al. "In vivo assessment of blood flow patterns in abdominal aorta of mice with MRI: implications for AAA localization." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 4 (2009): H1290—H1295. http://dx.doi.org/10.1152/ajpheart.00889.2008.

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Abdominal aortic aneurysms (AAA) localize in the infrarenal aorta in humans, while they are found in the suprarenal aorta in mouse models. It has been shown previously that humans experience a reversal of flow during early diastole in the infrarenal aorta during each cardiac cycle. This flow reversal causes oscillatory wall shear stress (OWSS) to be present in the infrarenal aorta of humans. OWSS has been linked to a variety of proatherogenic and proinflammatory factors. The presence of reverse flow in the mouse aorta is unknown. In this study we investigated blood flow in mice, using phase-co
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9

Racho El-Akouri, R., G. Kurlberg, G. Dindelegan, J. Molne, A. Wallin, and M. Brannstrom. "Heterotopic uterine transplantation by vascular anastomosis in the mouse." Journal of Endocrinology 174, no. 2 (2002): 157–66. http://dx.doi.org/10.1677/joe.0.1740157.

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A method of heterotopic uterine transplantation was developed in the mouse as a model system for studies of uterine function and transplant immunology of the uterus. The model involved transplantation of the right uterine horn and the cervix by vascular anastomosis to a donor animal with the intact native uterus remaining in situ. F1-hybrids of inbred C57BL/6 x CBA/ca (B6 CBAF1) mice of 6-8 weeks of age (n=42) were used. The specific pelvic vascular anatomy of these mice was first examined by intra-aortal injection of a two-component silicon-rubber curing agent. The surgery of the donor animal
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10

Galkina, Elena, Alexandra Kadl, John Sanders, Danielle Varughese, Ian J. Sarembock, and Klaus Ley. "Lymphocyte recruitment into the aortic wall before and during development of atherosclerosis is partially L-selectin dependent." Journal of Experimental Medicine 203, no. 5 (2006): 1273–82. http://dx.doi.org/10.1084/jem.20052205.

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Atherosclerosis is an inflammatory disease of large arteries. Flow cytometry of aortic cell suspensions showed that B and T lymphocytes and some macrophages and dendritic cells are already present in the adventitia of normal/noninflamed mouse aortas. Adoptively transferred lymphocytes constitutively homed to the aorta and resided within the adventitia up to 7 d after transfer. Lymphocyte trafficking into normal/noninflamed or atherosclerosis-prone aortas was partially L-selectin dependent. Antigen-activated dendritic cells induced increased T lymphocyte proliferation within the aorta 72 h afte
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11

Ashton, Daryl, Paul Hieble, Bernard Gout, and Nambi Aiyar. "Vasodilatory Effect of Adrenomedullin in Mouse Aorta." Pharmacology 61, no. 2 (2000): 101–5. http://dx.doi.org/10.1159/000028388.

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12

Huang, Yi, Xiaomei Guo, and Ghassan S. Kassab. "Axial nonuniformity of geometric and mechanical properties of mouse aorta is increased during postnatal growth." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 2 (2006): H657—H664. http://dx.doi.org/10.1152/ajpheart.00803.2005.

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The hemodynamic conditions of aorta are relatively uniform prenatally and become more heterogeneous postnatally. Our objective was to quantify the heterogeneity of geometry and mechanical properties during growth and development. To accomplish this objective, we obtained a systematic set of data on the geometry and mechanical properties along the length of mouse aorta during postnatal development. C57BL/6 mice of ages 1–33 days were studied. The ascending aorta was cannulated in situ and preconditioned with several cyclic changes in pressure. We investigated the axial variations of geometry (d
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13

Zhou, Yingbi, Wessel P. Dirksen, Gopal J. Babu, and Muthu Periasamy. "Differential vasoconstrictions induced by angiotensin II: role of AT1 and AT2 receptors in isolated C57BL/6J mouse blood vessels." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 6 (2003): H2797—H2803. http://dx.doi.org/10.1152/ajpheart.00466.2003.

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Genetically altered mice are increasingly used as experimental models. However, ANG II responses in mouse blood vessels have not been well defined. Therefore, the aim of this study was to determine the role of ANG II in regulating major blood vessels in C57/BL6J mice with isometric force measurements. Our results showed that in mouse abdominal aorta ANG II induced a concentration-dependent contraction (EC50 4.6 nM) with a maximum contraction of 75.1 ± 4.9% at 100 nM compared with that of 60 mM K+. Similarly, femoral artery also exhibited a contractile response of 76.0 ± 3.4% to the maximum con
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14

Hipni, Rubiati. "PENGARUH EKSTRAK ETANOL BIJI JINTEN HITAM (Nigella Sativa) TERHADAP EKSPRESI ET-1 AORTA PADA MENCIT MODEL PREEKLAMPSIA." Medical Laboratory Technology Journal 2, no. 1 (2016): 37. http://dx.doi.org/10.31964/mltj.v2i1.37.

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<p style="text-align: justify;">Abstract: The objective of this research is to analyze the effects of ethanol extract of black cumin seeds (Nigella Sativa) to the expression of ET-1 Aorta given to the preeclampsia model mouse. The research design utilizes experimental and the kind of design used is posttest only control group design. Mice preeclampsia model. This research is divided into 6 groups, namely: Negative control, Positive control, Model + extract of black cumin seeds 500 mg/KgBB/day, 1000 mg/KgBB/day, 1500 mg/KgBB/day, and 2000 mg/KgBB/day. After conducting the surgery to the m
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15

Lantos, Ildikó, Valéria Endrész, Dezső Péter Virok, et al. "Chlamydia pneumoniaeInfection Exacerbates Atherosclerosis in ApoB100only/LDLR−/−Mouse Strain." BioMed Research International 2018 (2018): 1–12. http://dx.doi.org/10.1155/2018/8325915.

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Aims. Hyperlipidaemia model animals have been used to elucidate the role ofChlamydia pneumoniae (Cpn)infection in atherosclerosis. The aims of this study were to investigate the proatherogenic effect of multipleCpninfections in ApoB100only/LDLR−/−mice which based on lipid profile can be regarded as the most suitable mouse model of human hypercholesterolemia and to compare the lesion development to that in a major atherosclerosis model ApoE−/−mice.Methods and Results. Aorta samples of ApoB100only/LDLR−/−mice infected three times withCpnwere subjected to morphometric analyses. Morphometric evalu
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16

Davis, E. C. "Elastic lamina growth in the developing mouse aorta." Journal of Histochemistry & Cytochemistry 43, no. 11 (1995): 1115–23. http://dx.doi.org/10.1177/43.11.7560894.

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17

Qiao, Jian-Hua, Michael C. Fishbein, Linda L. Demer, and Aldons J. Lusis. "Genetic Determination of Cartilaginous Metaplasia in Mouse Aorta." Arteriosclerosis, Thrombosis, and Vascular Biology 15, no. 12 (1995): 2265–72. http://dx.doi.org/10.1161/01.atv.15.12.2265.

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18

Christy, Clare, Patrick W. F. Hadoke, Janice M. Paterson, John J. Mullins, Jonathan R. Seckl та Brian R. Walker. "11β-Hydroxysteroid Dehydrogenase Type 2 in Mouse Aorta". Hypertension 42, № 4 (2003): 580–87. http://dx.doi.org/10.1161/01.hyp.0000088855.06598.5b.

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19

Bény, Jean-Louis. "Characterization of Purine Receptors in Mouse Thoracic Aorta." Journal of Cardiovascular Pharmacology 44, no. 2 (2004): 171–77. http://dx.doi.org/10.1097/00005344-200408000-00005.

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20

Wagenseil, Jessica E. "A constrained mixture model for developing mouse aorta." Biomechanics and Modeling in Mechanobiology 10, no. 5 (2010): 671–87. http://dx.doi.org/10.1007/s10237-010-0265-z.

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21

Akimoto, Tetsu, and Marc R. Hammerman. "Fibroblast growth factor 2 promotes microvessel formation from mouse embryonic aorta." American Journal of Physiology-Cell Physiology 284, no. 2 (2003): C371—C377. http://dx.doi.org/10.1152/ajpcell.00193.2002.

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To delineate the roles that oxygen and fibroblast growth factors (FGFs) play in the process of angiogenesis from the embryonic aorta, we cultured mouse embryonic aorta explants (thoracic level to lateral vessels supplying the mesonephros and metanephros) in a three-dimensional type I collagen gel matrix. During 8 days of culture under 5% O2, but not room air, the addition of FGF2 to explants stimulated the formation of Gs-IB4-positive, CD31-positive, and Flk-1-positive microvessels in a concentration-dependent manner. FGF2-stimulated microvessel formation was inhibited by sequestration of FGF2
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22

Akimoto, Tetsu, Helen Liapis, and Marc R. Hammerman. "Microvessel formation from mouse embryonic aortic explants is oxygen and VEGF dependent." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 2 (2002): R487—R495. http://dx.doi.org/10.1152/ajpregu.00699.2001.

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To delineate the roles of O2 and vascular endothelial growth factor (VEGF) in the process of angiogenesis from the embryonic aorta, we cultured mouse embryonic aorta explants (thoracic level to lateral vessels supplying the mesonephros and metanephros) in a three-dimensional type I collagen gel matrix. During 8 days of culture under 5% O2, but not room air, the addition of VEGF to explants stimulated the formation of CD31-positive, Flk-1-positive, Gs-IB4-positive structures in a concentration-dependent manner. Electron microscopy showed the structures to be capillary-like. VEGF-induced capilla
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23

Wagenseil, Jessica E., Nandan L. Nerurkar, Russell H. Knutsen, Ruth J. Okamoto, Dean Y. Li, and Robert P. Mecham. "Effects of elastin haploinsufficiency on the mechanical behavior of mouse arteries." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 3 (2005): H1209—H1217. http://dx.doi.org/10.1152/ajpheart.00046.2005.

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Supravalvular aortic stenosis (SVAS) is associated with decreased elastin and altered arterial mechanics. Mice with a single deletion in the elastin gene (ELN+/−) are models for SVAS. Previous studies have shown that elastin haploinsufficiency in these mice causes hypertension, decreased arterial compliance, and changes in arterial wall structure. Despite these differences, ELN+/− mice have a normal life span, suggesting that the arteries remodel and adapt to the decreased amount of elastin. To test this hypothesis, we performed in vitro mechanical tests on abdominal aorta, ascending aorta, an
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24

Ansari, Habib R., Ahmed Nadeem, M. A. Hassan Talukder, Shilpa Sakhalkar, and S. Jamal Mustafa. "Evidence for the involvement of nitric oxide in A2B receptor-mediated vasorelaxation of mouse aorta." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (2007): H719—H725. http://dx.doi.org/10.1152/ajpheart.00593.2006.

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We have investigated the role of adenosine and its analogs on vasorelaxation of mouse aorta in intact endothelium with rank order of potency as follows: 5′- N-ethylcarboxamidoadenosine (NECA) > 2-chloroadenosine > adenosine ≫ CGS-21680, which is consistent with the profile of A2B-adenosine receptor (A2BAR). In endothelium-intact tissues, acetylcholine produced relaxation ranging from 65 to 80% in phenylephrine (PE, 10−7 M)-precontracted mouse aorta, whereas no relaxation was observed in endothelium-denuded tissues. The A2BAR antagonist alloxazine (10−5 M) shifted concentration-response c
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25

Kriska, Tamas, Cody Cepura, Devora Magier, Lawan Siangjong, Kathryn M. Gauthier, and William B. Campbell. "Mice lacking macrophage 12/15-lipoxygenase are resistant to experimental hypertension." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 11 (2012): H2428—H2438. http://dx.doi.org/10.1152/ajpheart.01120.2011.

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In mouse arteries, Alox15 [leukocyte-type 12/15-lipoxygenase (LO)] is assumed to regulate vascular function by metabolizing arachidonic acid (AA) to dilator eicosanoids that mediate the endothelium-dependent relaxations to AA and acetylcholine (ACh). We used Alox15−/− mice, made by targeted disruption of the Alox15 gene, to characterize its role in the regulation of blood pressure and vascular tone. Systolic blood pressures did not differ between wild-type (WT) and Alox15−/− mice between 8–12 wk of age, but Alox15−/− mice exhibited resistance toward both NG-nitro-l-arginine-methyl ester (l-NAM
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26

Guo, Xiaomei, Yoram Lanir, and Ghassan S. Kassab. "Effect of osmolarity on the zero-stress state and mechanical properties of aorta." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 4 (2007): H2328—H2334. http://dx.doi.org/10.1152/ajpheart.00402.2007.

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Some pathological conditions may affect osmolarity, which can impact cell, tissue, and organ volume. The hypothesis of this study is that changes in osmolarity affect the zero-stress state and mechanical properties of the aorta. To test this hypothesis, a segment of mouse abdominal aorta was cannulated in vivo and mechanically distended by perfusion of physiological salt (NaCl) solutions with graded osmolarities from 145 to 562 mosM. The mechanical (circumferential stress, strain, and elastic modulus) and morphological (wall thickness and wall area) parameters in the loaded state were determin
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27

Nayeem, Mohammed A., Samuel M. Poloyac, John R. Falck, et al. "Role of CYP epoxygenases in A2AAR-mediated relaxation using A2AAR-null and wild-type mice." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 5 (2008): H2068—H2078. http://dx.doi.org/10.1152/ajpheart.01333.2007.

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We hypothesized that A2A adenosine receptor (A2AAR) activation causes vasorelaxation through cytochrome P-450 (CYP) epoxygenases and endothelium-derived hyperpolarizing factors, whereas lack of A2AAR activation promotes vasoconstriction through Cyp4a in the mouse aorta. Adenosine 5′- N-ethylcarboxamide (NECA; 10−6 M), an adenosine analog, caused relaxation in wild-type A2AAR (A2AAR+/+; +33.99 ± 4.70%, P < 0.05) versus contraction in A2AAR knockout (A2AAR−/−; −27.52 ± 4.11%) mouse aortae. An A2AAR-specific antagonist (SCH-58261; 1μM) changed the NECA (10−6 M) relaxation response to contracti
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28

Le, Victoria P., Jeffrey K. Cheng, Jungsil Kim, et al. "Mechanical factors direct mouse aortic remodelling during early maturation." Journal of The Royal Society Interface 12, no. 104 (2015): 20141350. http://dx.doi.org/10.1098/rsif.2014.1350.

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Numerous diseases have been linked to genetic mutations that lead to reduced amounts or disorganization of arterial elastic fibres. Previous work has shown that mice with reduced amounts of elastin ( Eln+/− ) are able to live a normal lifespan through cardiovascular adaptations, including changes in haemodynamic stresses, arterial geometry and arterial wall mechanics. It is not known if the timeline and presence of these adaptations are consistent in other mouse models of elastic fibre disease, such as those caused by the absence of fibulin-5 expression ( Fbln5−/− ). Adult Fbln5−/− mice have d
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29

Ropinski, Timo, Sven Hermann, Rainer Reich, Michael Schafers, and Klaus Hinrichs. "Multimodal Vessel Visualization of Mouse Aorta PET/CT Scans." IEEE Transactions on Visualization and Computer Graphics 15, no. 6 (2009): 1515–22. http://dx.doi.org/10.1109/tvcg.2009.169.

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Rudic, R. Daniel, Peter McNamara, Dermot Reilly, et al. "Bioinformatic Analysis of Circadian Gene Oscillation in Mouse Aorta." Circulation 112, no. 17 (2005): 2716–24. http://dx.doi.org/10.1161/circulationaha.105.568626.

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31

Wang, Shiying, Sunil Unnikrishnan, Elizabeth B. Herbst, Alexander L. Klibanov, Frank William Mauldin, and John A. Hossack. "Ultrasound Molecular Imaging of Inflammation in Mouse Abdominal Aorta." Investigative Radiology 52, no. 9 (2017): 499–506. http://dx.doi.org/10.1097/rli.0000000000000373.

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Agianniotis, Aristotelis, and Nikos Stergiopulos. "Wall properties of the apolipoprotein E-deficient mouse aorta." Atherosclerosis 223, no. 2 (2012): 314–20. http://dx.doi.org/10.1016/j.atherosclerosis.2012.06.014.

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Stadelmann, Vincent A., Gabrielle Boyd, Martin Guillot, Jean-Guy Bienvenu, Charles Glaus, and Aurore Varela. "Automatic Quantification of Atherosclerosis in Contrast-Enhanced MicroCT Scans of Mouse Aortas Ex Vivo." International Journal of Biomedical Imaging 2021 (September 20, 2021): 1–9. http://dx.doi.org/10.1155/2021/4998786.

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Objective. While microCT evaluation of atherosclerotic lesions in mice has been formally validated, existing image processing methods remain undisclosed. We aimed to develop and validate a reproducible image processing workflow based on phosphotungstic acid-enhanced microCT scans for the volumetric quantification of atherosclerotic lesions in entire mouse aortas. Approach and Results. 42 WT and 42 apolipoprotein E knockout mouse aortas were scanned. The walls, lumen, and plaque objects were segmented using dual-threshold algorithms. Aortic and plaque volumes were computed by voxel counting and
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34

Takaoka, Naohisa, Lee Ann Campbell, Amy Lee, Michael E. Rosenfeld, and Cho-Chou Kuo. "Chlamydia pneumoniae Infection Increases Adherence of Mouse Macrophages to Mouse Endothelial Cells In Vitro and to Aortas Ex Vivo." Infection and Immunity 76, no. 2 (2007): 510–14. http://dx.doi.org/10.1128/iai.01267-07.

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ABSTRACT Interactions between monocytes/macrophages and endothelial cells play an important role in the pathogenesis of atherosclerosis, and the adherence of monocytes to the arterial endothelium is one of the early events in atherogenesis. In the present study, peritoneal macrophages harvested from green fluorescent protein (GFP) transgenic mice were used to analyze how Chlamydia pneumoniae infection affects the adherence of GFP-macrophages to mouse endothelial cells in vitro and to the aorta from normolipidemic and hyperlipidemic mice ex vivo. In vitro studies showed that C. pneumoniae-infec
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35

Taguchi, Kumiko, Haruka Narimatsu, Takayuki Matsumoto, and Tsuneo Kobayashi. "ERK-containing microparticles from a diabetic mouse induce endothelial dysfunction." Journal of Endocrinology 241, no. 3 (2019): 221–33. http://dx.doi.org/10.1530/joe-18-0616.

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Endothelial dysfunction is a hallmark of diabetic vascular complications. Microparticles (MPs) are small vesicles shed from the surface of blood and vascular cells that act as stimuli and during apoptosis. Circulating MPs of diabetic rats have been shown to induce endothelial dysfunction. However, the underlying mechanisms require further study. In this study, we investigated how MPs from diabetic mice affect endothelial function. MPs were collected from streptozotocin-induced diabetic mice and Institute of Cancer Research (ICR) mice as controls. The levels of MPs were assessed and characteriz
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36

Matsuda, Naoyuki, Hiroki Teramae, Seiji Yamamoto, Ken-ichi Takano, Yasuo Takano, and Yuichi Hattori. "Increased death receptor pathway of apoptotic signaling in septic mouse aorta: effect of systemic delivery of FADD siRNA." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 1 (2010): H92—H101. http://dx.doi.org/10.1152/ajpheart.00069.2009.

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Recent evidence suggests that apoptotic cell death plays an important role in the pathophysiology of sepsis. Because there is extensive apoptosis of vascular endothelial cells in sepsis, we examined whether the death receptor pathway of apoptotic signaling is altered in thoracic aortas from mice with polymicrobial sepsis, as produced by cecal ligation and puncture (CLP). In septic aorta, total and surface expression levels of the two death receptors tumor necrosis factor receptor 1 and Fas were highly upregulated. Furthermore, marked increases in the mRNA and protein levels of Fas-associated d
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37

Sanan, David A., Zuleika Ladha, and Dale L. Newland. "High Throughput Quantitative Analysis of Atherosclerosis tn Mice." Microscopy and Microanalysis 6, S2 (2000): 554–55. http://dx.doi.org/10.1017/s1431927600035261.

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For the past 7 years we have been measuring atherosclerosis in murine models of the human disease, constantly honing our methods for quantitating the atherosclerotic response of mice that have been genetically, dietarily or pharmaceutically manipulated to help understand and control the disease process.With the advent of genetically modified mouse models, investigators now have more robust atherosclerotic responses to quantitate. The surface area of lesions along the entire length of the aorta is a key parameter used to evaluate these responses. We routinely perform quantitative morphometry of
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Zhou, Mei, Yuan Chen, Qian Quyang, Shang-Xi Liu, and Zhan-Jun Pang. "Reduction of the Oxidative Injury to the Rabbits with Established Atherosclerosis by Protein Bound Polysaccharide from Coriolus Vesicolor." American Journal of Chinese Medicine 28, no. 02 (2000): 239–49. http://dx.doi.org/10.1142/s0192415x00000283.

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Recent evidence has emerged that macrophage glutathione (GSH) content and selenium dependent glutathione peroxidase (SeGSHPx) activity are inversely related to cell-mediated oxidation of LDL, and intervention means to enhance the macrophage GSH-SeGSHPx status may contribute to attenuation of the atherosclerotic process. Our previous works showed that protein bound polysaccharide (PSK) injected intraperitoneally could enhance SeGSHPx activity and mRNA content of mouse macrophages. The aim of the present study is to demonstrate whether PSK can reduce the oxidative injury to the established ather
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39

Chu, Alice, Eric T. Ordonez, and Marc K. Hellerstein. "Measurement of mouse vascular smooth muscle and atheroma cell proliferation by 2H2O incorporation into DNA." American Journal of Physiology-Cell Physiology 291, no. 5 (2006): C1014—C1021. http://dx.doi.org/10.1152/ajpcell.00191.2006.

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Vascular smooth muscle cell (VSMC) and leukocyte proliferation are central features of atherosclerosis. Using 2H2O to label the deoxyribose moiety of newly synthesized DNA in VSMC and atheroma cells from mouse aorta, we developed a method to measure DNA replication and, hence, cell division. Cell turnover/proliferation in aortae from normal and apolipoprotein E (ApoE)-knockout ( ApoE−/−) mice was measured. Mice were injected with 2H2O to achieve 2% body water enrichments and then maintained on 4% 2H2O in drinking water for weeks to months. DNA from the intimal-medial layer of the aorta was ext
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40

Guo, Xiaomei, and Ghassan S. Kassab. "Variation of mechanical properties along the length of the aorta in C57bl/6 mice." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 6 (2003): H2614—H2622. http://dx.doi.org/10.1152/ajpheart.00567.2003.

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The objective of the present study is to obtain a systematic set of data on the mechanical properties along the entire length of the mouse aorta. The ascending aorta of seven mice was cannulated near the aortic valve, and the aorta was preconditioned with several cyclic changes in pressure. The perfusion pressure was then increased in 30-mmHg increments from 0 to 150 mmHg. Cab-O-Sil, colloidal silica, was mixed into the perfusate to prevent flow through the microvessels and hence attain zero-flow distensions. Our results show that the residual circumferential strain leads to a uniformity of tr
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41

Kiugel, Max, Sanna Hellberg, Meeri Käkelä, et al. "Evaluation of [68Ga]Ga-DOTA-TCTP-1 for the Detection of Metalloproteinase 2/9 Expression in Mouse Atherosclerotic Plaques." Molecules 23, no. 12 (2018): 3168. http://dx.doi.org/10.3390/molecules23123168.

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Background: The expression of matrix metalloproteinases 2/9 (MMP-2/9) has been implicated in arterial remodeling and inflammation in atherosclerosis. We evaluated a gallium-68 labeled peptide for the detection of MMP-2/9 in atherosclerotic mouse aorta. Methods: We studied sixteen low-density lipoprotein receptor deficient mice (LDLR-/-ApoB100/100) kept on a Western-type diet. Distribution of intravenously-injected MMP-2/9-targeting peptide, [68Ga]Ga-DOTA-TCTP-1, was studied by combined positron emission tomography (PET) and contrast-enhanced computed tomography (CT). At 60 min post-injection,
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42

Chen, Zheying, Alan Daugherty, and Mary Sheppard. "2464 Sexual dimorphism in a mouse model of syndromic thoracic aortic aneurysm." Journal of Clinical and Translational Science 2, S1 (2018): 27. http://dx.doi.org/10.1017/cts.2018.121.

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OBJECTIVES/SPECIFIC AIMS: Pre-clinical and clinical observations have noted that increased aortic dilation is associated with male sex. Using an experimental model of severe, syndromic thoracic aortic aneurysms, we quantify aortic dilation and elastin stability in male Versus female mice. METHODS/STUDY POPULATION: Ascending aortas from male and female FBN1mgR/mgR mice and their wild type littermates were assessed every 4 weeks from 6 to 18 weeks of age by ultrasound. Measurements were taken luminal edge to luminal edge in diastole. At termination, aortas were harvested for RT-PCR analysis of e
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43

Villablanca, Amparo C., Kristine A. Lewis, Doris Tham, and John C. Rutledge. "Differential regulation of gene expression by ovariectomy in mouse aorta." Physiological Genomics 12, no. 3 (2003): 175–85. http://dx.doi.org/10.1152/physiolgenomics.00040.2002.

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The purpose of this study was to investigate the effects of ovarian hormones on gene expression in the vascular wall. Our approach employed an RT-PCR-based cloning strategy of DNA differential display analysis and verification/confirmation of differential expression by semi-quantitative PCR and real-time PCR. mRNA analysis of normal aortas from intact and ovariectomized female C57BL/6J mice, showed altered expression of 20 genes with significant (>70%) sequence homology to known genes. Eight were selected for further study based on the genes’ known function and potential relevance to vascul
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44

Kim, Seung Kyum, Joshua J. Avila, and Michael P. Massett. "Strain survey and genetic analysis of vasoreactivity in mouse aorta." Physiological Genomics 48, no. 11 (2016): 861–73. http://dx.doi.org/10.1152/physiolgenomics.00054.2016.

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Understanding the genetic influence on vascular reactivity is important for identifying genes underlying impaired vascular function. The purpose of this study was to characterize the genetic contribution to intrinsic vascular function and to identify loci associated with phenotypic variation in vascular reactivity in mice. Concentration response curves to phenylephrine (PE), potassium chloride (KCl), acetylcholine (ACh), and sodium nitroprusside (SNP) were generated in aortic rings from male mice (12 wk old) from 27 inbred mouse strains. Significant strain-dependent differences were found for
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45

Fanchaouy, M., R. Bychkov, J. J. Meister, and J. L. Beny. "Stretch-elicited calcium responses in the intact mouse thoracic aorta." Cell Calcium 41, no. 1 (2007): 41–50. http://dx.doi.org/10.1016/j.ceca.2006.04.030.

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46

Zingales, Veronica, Sebastiano Alfio Torrisi, Gian Marco Leggio, Claudio Bucolo, Filippo Drago, and Salvatore Salomone. "Pharmacological and Genetic Evidence of Dopamine Receptor 3-Mediated Vasoconstriction in Isolated Mouse Aorta." Biomolecules 11, no. 3 (2021): 418. http://dx.doi.org/10.3390/biom11030418.

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Dopamine receptors (DRs) are generally considered as mediators of vasomotor functions. However, when used in pharmacological studies, dopamine and/or DR agonists may not discriminate among different DR subtypes and may even stimulate alpha1 and beta-adrenoceptors. Here, we tested the hypothesis that D2R and/or D3R may specifically induce vasoconstriction in isolated mouse aorta. Aorta, isolated from wild-type (WT) and D3R−/− mice, was mounted in a wire myograph and challenged with cumulative concentrations of phenylephrine (PE), acetylcholine (ACh), and the D3R agonist 7-hydrxy-N,N-dipropyl-2-
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47

Capettini, L. S. A., S. F. Cortes, M. A. Gomes, et al. "Neuronal nitric oxide synthase-derived hydrogen peroxide is a major endothelium-dependent relaxing factor." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 6 (2008): H2503—H2511. http://dx.doi.org/10.1152/ajpheart.00731.2008.

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Endothelium-dependent vasorelaxation in large vessels is mainly attributed to Nω-nitro-l-arginine methyl ester (l-NAME)-sensitive endothelial nitric oxide (NO) synthase (eNOS)-derived NO production. Endothelium-derived hyperpolarizing factor (EDHF) is the component of endothelium-dependent relaxations that resists full blockade of NO synthases (NOS) and cyclooxygenases. H2O2 has been proposed as an EDHF in resistance vessels. In this work we propose that in mice aorta neuronal (n)NOS-derived H2O2 accounts for a large proportion of endothelium-dependent ACh-induced relaxation. In mice aorta rin
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48

Ng, Hooi H., Gunes S. Yildiz, Jacqueline M. Ku, Alyson A. Miller, Owen L. Woodman, and Joanne L. Hart. "Chronic NaHS treatment decreases oxidative stress and improves endothelial function in diabetic mice." Diabetes and Vascular Disease Research 14, no. 3 (2017): 246–53. http://dx.doi.org/10.1177/1479164117692766.

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Hydrogen sulphide (H2S) is endogenously produced in vascular tissue and has anti-oxidant and vasoprotective properties. This study investigates whether chronic treatment using the fast H2S donor NaHS could elicit a vasoprotective effect in diabetes. Diabetes was induced in male C57BL6/J mice with streptozotocin (60 mg/kg daily, ip for 2 weeks) and confirmed by elevated blood glucose and glycated haemoglobin levels. Diabetic mice were then treated with NaHS (100 µmol/kg/day) for 4 weeks, and aortae collected for functional and biochemical analyses. In the diabetic group, both endothelium-depend
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Farra, Yasmeen M., Jacqueline Matz, Bhama Ramkhelawon, Jessica M. Oakes, and Chiara Bellini. "Structural and functional remodeling of the female Apoe−/− mouse aorta due to chronic cigarette smoke exposure." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 6 (2021): H2270—H2282. http://dx.doi.org/10.1152/ajpheart.00893.2020.

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We studied the effects of chronic cigarette smoking on the structure and function of the aorta in a mouse model of nose-only aerosol inhalation. Our data indicated that exposure to cigarette smoke impairs vascular function by reducing the ability of the aorta to store elastic energy and by decreasing aortic distensibility. Combined with a more vulnerable atherosclerotic phenotype, these findings reveal the biomechanical mechanisms that support the development of cardiovascular disease due to cigarette smoking.
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50

Choi, Jae-Hoon, Yoonkyung Do, Cheolho Cheong, et al. "Identification of antigen-presenting dendritic cells in mouse aorta and cardiac valves." Journal of Experimental Medicine 206, no. 3 (2009): 497–505. http://dx.doi.org/10.1084/jem.20082129.

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Presumptive dendritic cells (DCs) bearing the CD11c integrin and other markers have previously been identified in normal mouse and human aorta. We used CD11c promoter–enhanced yellow fluorescent protein (EYFP) transgenic mice to visualize aortic DCs and study their antigen-presenting capacity. Stellate EYFP+ cells were readily identified in the aorta and could be double labeled with antibodies to CD11c and antigen-presenting major histocompatability complex (MHC) II products. The DCs proved to be particularly abundant in the cardiac valves and aortic sinus. In all aortic locations, the CD11c+
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