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1 ly involve the deep fascia and often lead to muscle necrosis.
2 types of DMD, including loss of mobility and muscle necrosis.
3 rial Ca(2+) overload, organelle rupture, and muscle necrosis.
4 chemia (CLI) involving the onset of ischemic muscle necrosis.
5 asciitis precedes and frequently accompanies muscle necrosis.
6 acrophages changes between the stage of peak muscle necrosis (4 weeks of age) and muscle regeneration
7 ic area) and severe (>5% mean necrotic area) muscle necrosis, an area under the receiver operating ch
8 o instability of the sarcolemma and skeletal muscle necrosis and atrophy.
9 ated macrophages to promote inflammation and muscle necrosis and in skeletal muscle fibers to limit r
10 netic disorders characterized by progressive muscle necrosis and premature death.
11 ologically, there was evidence of widespread muscle necrosis and regeneration, fiber splitting, and r
12 tendinous strain injury that help to prevent muscle necrosis and retain the function of necessary mus
13 arrying marker genes that are unable to halt muscle necrosis and the difficulty of stable transfer of
14 razolium staining to determine the amount of muscle necrosis and the location of muscle protection.
15  (MD) is a disease characterized by skeletal muscle necrosis and the progressive accumulation of fibr
16 ansition pore (MPTP) activation and skeletal muscle necrosis, and this same type of activity was obse
17  absence of dystrophin; calpastatin prevents muscle necrosis; and nitric oxide synthase prevents infl
18 th lines of Tg/mdx mice showed reductions in muscle necrosis at 4 weeks of age.
19  (calpain) activity in dystrophic muscle and muscle necrosis, but have not tested whether calpain act
20 ing myocarditis, myocardial and red skeletal muscle necrosis, correlate with the intensity of the inf
21  muscle regenerative capacity and preventing muscle necrosis could be an effective treatment for the
22 s, such as in escharotomy, which may lead to muscle necrosis endangering life and limb.
23                      Local anesthetics cause muscle necrosis, followed by regeneration, a process tha
24 tly was not due to differences in degrees of muscle necrosis, hemolysis, acute renal heme loading, or
25 ve membrane resealing in skeletal muscle and muscle necrosis; however, the function of dysferlin in t
26 in and the biochemical mechanisms leading to muscle necrosis in Becker muscular dystrophy are still u
27 m oxidative damage, and its absence leads to muscle necrosis in response to injury in Stra13-deficien
28 th anti-oxidant N-acetylcysteine ameliorates muscle necrosis in Stra13-/- mice.
29 py for DMD may hold promise for ameliorating muscle necrosis, inflammation, and fibrosis by inhibitin
30                                 Ameliorating muscle necrosis, inflammation, and fibrosis represents a
31                    Imatinib markedly reduced muscle necrosis, inflammation, and fibrosis, and signifi
32                                              Muscle necrosis, inflammation, fibrosis, and function we
33 as early onset, causes developmental delays, muscle necrosis, loss of ambulation, and death.
34 nicity was greater in patients who developed muscle necrosis (n = 15) than in those who did not (8.2%
35 istopathologic findings demonstrated limited muscle necrosis, reduced microvascular thrombosis, and e
36                                The resulting muscle necrosis (rhabdomyolysis) causes acute renal inju
37 ll muscular dystrophies are characterized by muscle necrosis that overtakes the regenerative capacity
38              The prominent onset of skeletal muscle necrosis was evident upon direct inspection of th
39 odels for muscular dystrophy, showed ongoing muscle necrosis with age, a hallmark of the human diseas
40  reviewed the records of 16 patients who had muscle necrosis without evidence of liver disease.