Secondary Hypertrophic
Mostrando 13-24 de 30 artigos, teses e dissertações.
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13. Diagnosis of cytomegalovirus infection in pediatric Menetrier's disease by in situ hybridization.
A previously healthy 7-year-old boy presented with a protein-losing enteropathy secondary to a hypertrophic gastropathy. The diagnosis of cytomegalovirus (CMV) infection was established by detection of CMV inclusion bodies in gastric biopsy samples and by hybridization with a CMV probe. This report further strengthens the association between CMV and pediatri
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14. Enzymic analysis of endomyocardial biopsy specimens from patients with cardiomyopathies.
Myocardial biopsies have been obtained from patients with hypertrophic or congestive cardiomyopathies. Marker enzymes for the principal subcellular organelles of the myocardium were estimated using highly sensitive assay procedures. The results were compared with those obtained in tissue from patients with valvular heart disease with good or poor left ventri
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15. Cell kinetics of growth cartilage in spondylo-metaphyseal chondrodysplasia (smc) mice.
The gene for spondylo-metaphyseal chondrodysplasia (smc) in the mouse disrupts the formation of growth plate cartilage. No cartilage columns are found in the head of the tibia and secondary centres of ossification appear very late. The number of cells labelled with tritiated thymidine is sharply reduced at 16, 18 and 21 days of age but hypertrophic cell heig
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16. Conditional inactivation of Has2 reveals a crucial role for hyaluronan in skeletal growth, patterning, chondrocyte maturation and joint formation in the developing limb
The glycosaminoglycan hyaluronan (HA) is a structural component of extracellular matrices and also interacts with cell surface receptors to directly influence cell behavior. To explore functions of HA in limb skeletal development, we conditionally inactivated the gene for HA synthase 2, Has2, in limb bud mesoderm using mice that harbor a floxed allele of
Company of Biologists.
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17. The development of articular cartilage: I. The spatial and temporal patterns of collagen types.
Articular cartilage is both morphologically and biochemically heterogeneous. Its susceptibility to degenerative diseases such as arthritis and its limited repair capacity have made cartilage the focus of intense study; surprisingly, little is known of its development. Using a panel of specific antibodies, we have documented the temporal and spatial patterns
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18. A Functional and Structural Study of Troponin C Mutations Related to Hypertrophic Cardiomyopathy*
Recently four new hypertrophic cardiomyopathy mutations in cardiac troponin C (cTnC) (A8V, C84Y, E134D, and D145E) were reported, and their effects on the Ca2+ sensitivity of force development were evaluated (Landstrom, A. P., Parvatiyar, M. S., Pinto, J. R., Marquardt, M. L., Bos, J. M., Tester, D. J., Ommen, S. R., Potter, J. D., and Ackerman, M. J. (2008)
American Society for Biochemistry and Molecular Biology.
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19. Constitutive activation of MEK1 in chondrocytes causes Stat1-independent achondroplasia-like dwarfism and rescues the Fgfr3-deficient mouse phenotype
We generated transgenic mice that express a constitutively active mutant of MEK1 in chondrocytes. These mice showed a dwarf phenotype similar to achondroplasia, the most common human dwarfism, caused by activating mutations in FGFR3. These mice displayed incomplete hypertrophy of chondrocytes in the growth plates and a general delay in endochondral ossificat
Cold Spring Harbor Laboratory Press.
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20. Nongenetically transmitted disproportionate ventricular septal thickening associated with left ventricular outflow obstruction.
Clinical, haemodynamic, and morphological features are described in 2 patients with disproportionate ventricular septal thickening, left ventricular outflow obstruction with systolic anterior motion of the anterior mitral leaflet, and either acquired or congenital heart disease. The disproportionate septal thickening in these patients appeared to be secondar
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21. Impaired endochondral ossification and angiogenesis in mice deficient in membrane-type matrix metalloproteinase I
Membrane-type matrix metalloproteinase I (MT1-MMP)-deficient mice were found to have severe defects in skeletal development and angiogenesis. The craniofacial, axial, and appendicular skeletons were severely affected, leading to a short and domed skull, marked deceleration of postnatal growth, and death by 3 wk of age. Shortening of bones is a consequence of
The National Academy of Sciences.
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22. Ras-dependent pathways induce obstructive hypertrophy in echo-selected transgenic mice
To overcome the genetic and interindividual variability frequently noted in complex phenotypes, we used echocardiographic selection to develop a substrain of myosin light chain (MLC)–Ras (RAS) transgenic mice with an enhanced ventricular hypertrophic phenotype. These echo-selected mice were then compared with wild-type (WT) animals and a pressure overload
The National Academy of Sciences of the USA.
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23. Hemodynamic versus adrenergic control of cat right ventricular hypertrophy.
The purpose of this study was to determine whether cardiac hypertrophy in response to hemodynamic overloading is a primary result of the increased load or is instead a secondary result of such other factors as concurrent sympathetic activation. To make this distinction, four experiments were done; the major experimental result, cardiac hypertrophy, was asses
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24. Temporal and mutation-specific alterations in Ca2+ homeostasis differentially determine the progression of cTnT-related cardiomyopathies in murine models
Naturally occurring mutations in cardiac troponin T (cTnT) result in a clinical subset of familial hypertrophic cardiomyopathy. To determine the mechanistic links between thin-filament mutations and cardiovascular phenotypes, we have generated and characterized several transgenic mouse models carrying cTnT mutations. We address two central questions regardin
American Physiological Society.