Characterizing the binding mechanism of fixed sites on the isolated tectorial membrane of the mouse

Thesis (M.Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 1998.Includes bibliographical references (leaves 38-39).by Rosanne Rouf.M.Eng

Signal Transmission in the Auditory System

Contains table of contents for Section 3 and reports on four research projects.National Institutes of Health Grant R01 DC00194National Institutes of Health Grant P01 DC00119National Science Foundation Grant IBN 96-04642W.M. Keck Foundation Career Development ProfessorshipNational Institutes of Health Grant R01 DC00238Thomas and Gerd Perkins Award ProfessorshipAlfred P Sloan Foundation Instrumentation GrantJohn F. and Virginia B. Taplin Award in Health Sciences and TechnologyNational Institutes of Health/National Institute of Deafness and Other Communication DisordersNational Institutes of Health/National Institute of Deafness and Other Communication Disorders Grant PO1 DC0011

Signal Transmission in the Auditory System

Contains table of contents for Section 3, an introduction and reports on five research projects.National Institutes of Health Grant R01-DC-00194National Institutes of Health Grant P01-DC-00119Charles S. Draper Laboratory Contract DL-H-496015National Institutes of Health Grant R01 DC00238National Institutes of Health Grant R01-DC02258National Institutes of Health Grant T32-DC00038National Institutes of Health Grant RO1 DC00235National Institutes of Health Grant P01-DC00361National Institutes of Health Contract N01-DC-6-210

Signal Transmission in the Auditory System

Contains table of contents for Section 3, an introduction and reports on seven research projects.National Institutes of Health Grant P01-DC-00119National Institutes of Health Grant R01-DC-00194National Institutes of Health Grant R01 DC00238National Institutes of Health Grant R01-DC02258National Institutes of Health Grant T32-DC00038National Institutes of Health Grant P01-DC00361National Institutes of Health Grant 2RO1 DC00235National Institutes of Health Contract N01-DC2240

Four-Chamber Intracardiac Thrombi Complicating Wild-Type TTR Amyloidosis

Cardiac amyloidosis is a rare disease, and its prevalence varies depending on the type of amyloid protein involved. Several case reports make reference to the increased risk of thrombosis and thromboembolic events in cardiac amyloidosis. We report a case of rapidly evolving, multichamber thrombi in a patient who was ultimately diagnosed with wild-type TTR cardiac amyloidosis

Anomalous Origin of the Right Coronary Artery Causing Myocardial Ischemia: A Case for a Multimodality Imaging Approach

A 46-year-old man was admitted with non-ST elevation myocardial infarction and newly diagnosed acutely decompensated heart failure. Echocardiogram demonstrated left ventricular ejection fraction of 30% with basal inferior and inferolateral akinesis. Coronary angiography showed mild diffuse coronary artery disease and an anomalous right coronary artery arising from the left coronary cusp. Further imaging was consistent with ischemia in the right coronary distribution. Etiology of ischemia was thought to be the anomalous right coronary artery, and surgical unroofing of the right coronary ostium was performed. Here, we report a multimodality imaging approach, including cardiac magnetic resonance, cardiac computed tomographic angiography, and single-photon emission computed tomography, to support the diagnosis and management of a patient with anomalous right coronary artery arising from the left coronary cusp

Multi-Scale Biomechanical Remodeling in Aging and Genetic Mutant Murine Mitral Valve Leaflets: Insights into Marfan Syndrome

<div><p>Mitral valve degeneration is a key component of the pathophysiology of Marfan syndrome. The biomechanical consequences of aging and genetic mutation in mitral valves are poorly understood because of limited tools to study this in mouse models. Our aim was to determine the global biomechanical and local cell-matrix deformation relationships in the aging and Marfan related <em>Fbn1</em> mutated murine mitral valve. To conduct this investigation, a novel stretching apparatus and gripping method was implemented to directly quantify both global tissue biomechanics and local cellular deformation and matrix fiber realignment in murine mitral valves. Excised mitral valve leaflets from wild-type and <em>Fbn1</em> mutant mice from 2 weeks to 10 months in age were tested in circumferential orientation under continuous laser optical imaging. Mouse mitral valves stiffen with age, correlating with increases in collagen fraction and matrix fiber alignment. <em>Fbn1</em> mutation resulted in significantly more compliant valves (modulus 1.34±0.12 vs. 2.51±0.31 MPa, respectively, P<.01) at 4 months, corresponding with an increase in proportion of GAGs and decrease in elastin fraction. Local cellular deformation and fiber alignment change linearly with global tissue stretch, and these slopes become more extreme with aging. In comparison, <em>Fbn1</em> mutated valves have decoupled cellular deformation and fiber alignment with tissue stretch. Taken together, quantitative understanding of multi-scale murine planar tissue biomechanics is essential for establishing consequences of aging and genetic mutations. Decoupling of local cell-matrix deformation kinematics with global tissue stretch may be an important mechanism of normal and pathological biomechanical remodeling in valves.</p> </div