| LDR | | 00000nam u2200205 4500 |
| 001 | | 000000433361 |
| 005 | | 20200225140740 |
| 008 | | 200131s2019 ||||||||||||||||| ||eng d |
| 020 | |
▼a 9781687942470 |
| 035 | |
▼a (MiAaPQ)AAI22617842 |
| 040 | |
▼a MiAaPQ
▼c MiAaPQ
▼d 247004 |
| 082 | 0 |
▼a 612 |
| 100 | 1 |
▼a Meyers, Tatyana A. |
| 245 | 10 |
▼a Preclinical Models of Dystrophic Cardiomyopathy and Therapies for the Dystrophic Heart. |
| 260 | |
▼a [S.l.]:
▼b University of Minnesota.,
▼c 2019. |
| 260 | 1 |
▼a Ann Arbor:
▼b ProQuest Dissertations & Theses,
▼c 2019. |
| 300 | |
▼a 132 p. |
| 500 | |
▼a Source: Dissertations Abstracts International, Volume: 81-06, Section: B. |
| 500 | |
▼a Advisor: Townsend, DeWayne |
| 502 | 1 |
▼a Thesis (Ph.D.)--University of Minnesota, 2019. |
| 506 | |
▼a This item must not be sold to any third party vendors. |
| 520 | |
▼a Muscular dystrophies are a diverse group of genetic diseases characterized byprogressive muscle weakness and deterioration with wide variability in severity and affectedmuscle groups. Some of the more devastating muscular dystrophies result from the absenceof components of the dystrophin-glycoprotein complex (DGC). Disruption of the DGCcompromises sarcolemmal integrity in striated muscle, leading to increased myocyte injuryand death. These forms of muscular dystrophy often feature both skeletal muscle wastingand marked cardiomyopathy. The most common of these muscular dystrophies is Duchennemuscular dystrophy (DMD), caused by mutations in the dystrophin gene that result in theloss of this large membrane-stabilizing protein. DMD features a childhood onset and leads topremature death at ages ranging from the teens into the 30's, often from cardiorespiratoryfailure. DMD is an X-linked disorder, and is usually inherited from carrier mothers who alsoface a high risk of cardiomyopathy.Sarcoglycanopathies are a rarer group of autosomal recessive Limb Girdle musculardystrophies (LGMD) that arise from mutations in the sarcoglycan genes, sometimes leadingto an aggressive Duchenne-like disease course in patients of both sexes. Theheterotetrameric sarcoglycan complex is a key component of the DGC, and its loss inducessignificant myocyte pathology that can trigger childhood disease onset and premature death.Muscles and hearts devoid of the sarcolgycan complex display hallmark dystrophicpathology, including muscle wasting, loss of ambulation, and a high incidence of lethaldilated cardiomyopathy.The work presented here is driven by efforts to quantify the susceptibility ofdystrophic hearts to acute injury caused by increased cardiac workload, and to understandthe contribution of angiotensin signaling to dystrophic heart injury. It describes the followingkey findings: 1) angiotensin receptor blockers (ARBs) can markedly reduce acute injury indystrophin-null and sarcoglycan-null mouse hearts |
| 590 | |
▼a School code: 0130. |
| 650 | 4 |
▼a Physiology. |
| 690 | |
▼a 0719 |
| 710 | 20 |
▼a University of Minnesota.
▼b Integrative Biology and Physiology. |
| 773 | 0 |
▼t Dissertations Abstracts International
▼g 81-06B. |
| 773 | |
▼t Dissertation Abstract International |
| 790 | |
▼a 0130 |
| 791 | |
▼a Ph.D. |
| 792 | |
▼a 2019 |
| 793 | |
▼a English |
| 856 | 40 |
▼u http://www.riss.kr/pdu/ddodLink.do?id=T15493492
▼n KERIS
▼z 이 자료의 원문은 한국교육학술정보원에서 제공합니다. |
| 980 | |
▼a 202002
▼f 2020 |
| 990 | |
▼a ***1008102 |
| 991 | |
▼a E-BOOK |