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13 results on '"Roy, R. Jack"'

1. Progressive Cardiac Metabolic Defects Accompany Diastolic and Severe Systolic Dysfunction in Spontaneously Hypertensive Rat Hearts

Author

Li, Jie, primary, Minczuk, Krzysztof, additional, Huang, Qiao, additional, Kemp, Brandon A., additional, Howell, Nancy L., additional, Chordia, Mahendra D., additional, Roy, R. Jack, additional, Patrie, James T., additional, Qureshi, Zoraiz, additional, Kramer, Christopher M., additional, Epstein, Frederick H., additional, Carey, Robert M., additional, Kundu, Bijoy K., additional, and Keller, Susanna R., additional

Published
2023
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4. Metformin Improves Cardiac Metabolism and Function, and Prevents Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats

Author

Li, Jie, primary, Minćzuk, Krzysztof, additional, Massey, James C., additional, Howell, Nancy L., additional, Roy, R. Jack, additional, Paul, Soumen, additional, Patrie, James T., additional, Kramer, Christopher M., additional, Epstein, Frederick H., additional, Carey, Robert M., additional, Taegtmeyer, Heinrich, additional, Keller, Susanna R., additional, and Kundu, Bijoy K., additional

Published
2020
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5. Metabolic Changes in Spontaneously Hypertensive Rat Hearts Precede Cardiac Dysfunction and Left Ventricular Hypertrophy

Author

Li, Jie, primary, Kemp, Brandon A., additional, Howell, Nancy L., additional, Massey, James, additional, Mińczuk, Krzysztof, additional, Huang, Qiao, additional, Chordia, Mahendra D., additional, Roy, R. Jack, additional, Patrie, James T., additional, Davogustto, Giovanni E., additional, Kramer, Christopher M., additional, Epstein, Frederick H., additional, Carey, Robert M., additional, Taegtmeyer, Heinrich, additional, Keller, Susanna R., additional, and Kundu, Bijoy K., additional

Published
2019
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8. Three-dimensional phase contrast angiography of the mouse aortic arch using spiral MRI

Author

Janiczek, Robert L., Blackman, Brett R., Roy, R. Jack, Meyer, Craig H., Acton, Scott T., and Epstein, Frederick H.

Subjects
Mice, Inbred C57BL, Mice, Imaging, Three-Dimensional, cardiovascular system, Animals, Humans, Magnetic Resonance Imaging, Cine, Aorta, Thoracic, Mice, Transgenic, Image Enhancement, Shear Strength, Article, Mathematics
Abstract

Atherosclerosis is a complex disease whose spatial distribution is hypothesized to be influenced by the local hemodynamic environment. The use of transgenic mice provides a mechanism to study the relationship between hemodynamic forces, most notably wall shear stress (WSS), and the molecular factors that influence the disease process. Phase contrast MRI using rectilinear trajectories has been used to measure boundary conditions for use in computational fluid dynamic models. However, the unique flow environment of the mouse precludes use of standard imaging techniques in complex, curved flow regions such as the aortic arch. In this article, two-dimensional and three-dimensional spiral cine phase contrast sequences are presented that enable measurement of velocity profiles in curved regions of the mouse vasculature. WSS is calculated directly from the spatial velocity gradient, enabling WSS calculation with a minimal set of assumptions. In contrast to the outer radius of the aortic arch, the inner radius has a lower time-averaged longitudinal WSS (7.06 ± 0.76 dyne/cm(2) vs. 18.86 ± 1.27 dyne/cm(2) ; P0.01) and higher oscillatory shear index (0.14 ± 0.01 vs. 0.08 ± 0.01; P0.01). This finding is in agreement with humans, where WSS is lower and more oscillatory along the inner radius, an atheroprone region, than the outer radius, an atheroprotective region.

Published
2011

9. Glucose Regulation of Load‐Induced mTOR Signaling and ER Stress in Mammalian Heart

Author

Sen, Shiraj, primary, Kundu, Bijoy K., additional, Wu, Henry Cheng‐Ju, additional, Hashmi, S. Shahrukh, additional, Guthrie, Patrick, additional, Locke, Landon W., additional, Roy, R. Jack, additional, Matherne, G. Paul, additional, Berr, Stuart S., additional, Terwelp, Matthew, additional, Scott, Brian, additional, Carranza, Sylvia, additional, Frazier, O. Howard, additional, Glover, David K., additional, Dillmann, Wolfgang H., additional, Gambello, Michael J., additional, Entman, Mark L., additional, and Taegtmeyer, Heinrich, additional

Published
2013
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12. Serial MRI Imaging Reveals Minimal Impact of Ketogenic Diet on Established Liver Tumor Growth.

Author

Byrne, Frances L., Hargett, Stefan R., Lahiri, Sujoy, Roy, R. Jack, Berr, Stuart S., Caldwell, Stephen H., and Hoehn, Kyle L.

Subjects
ANIMAL experimentation, GRAIN, KETOGENIC diet, LIVER tumors, MAGNETIC resonance imaging, MICE, NITROSOAMINES, TIME, TREATMENT effectiveness, DISEASE progression, DIAGNOSIS
Abstract

Rodent models of liver tumorigenesis have reproducibly shown that dietary sugar intake is a powerful driver of liver tumor initiation and growth. In contrast, dietary sugar restriction with ketogenic diets or calorie restriction generally prevents liver tumor formation. Ketogenic diet is viewed positively as a therapeutic adjuvant; however, most ketogenic diet studies described to date have been performed in prevention mode rather than treatment mode. Therefore, it remains unclear whether a ketogenic diet can be administered in late stages of disease to stall or reverse liver tumor growth. To model the clinically relevant treatment mode, we administered a ketogenic diet to mice after liver tumor initiation and monitored tumor growth by magnetic resonance imaging (MRI). Male C57BL/6 mice were injected with diethylnitrosamine (DEN) at 2 weeks of age and fed a chow diet until 39 weeks of age, when they underwent MRI imaging to detect liver tumors. Mice were then randomised into two groups and fed either a chow diet or switched to a ketogenic diet from 40–48 weeks of age. Serial MRIs were performed at 44 and 48 weeks of age. All mice had tumors at study completion and there were no differences in total tumor burden between diet groups. Although a ketogenic diet has marked protective effects against DEN-induced liver tumourigenesis in this mouse model, these data demonstrate that ketogenic diet cannot stop the progression of established liver tumors. [ABSTRACT FROM AUTHOR]

Published
2018
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