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1 degenerative muscle disease of aging humans, sporadic inclusion body myositis.
2 osis, frontotemporal lobar degeneration, and sporadic inclusion body myositis.
3 cts, mtDNA alterations may be accelerated in sporadic inclusion body myositis.
4 the current concepts of the pathogenesis of sporadic inclusion-body myositis.
5 hy of the muscle fibers that are specific to sporadic inclusion-body myositis.
6 so provide new avenues toward the therapy of sporadic inclusion-body myositis.
7 bute only slightly to muscle fiber damage in sporadic inclusion-body myositis.
8 l and important clues to the pathogenesis of sporadic inclusion-body myositis.
9 ments in individual cells from patients with sporadic inclusion body myositis, a late-onset inflammat
11 transthyretin Val122Ile allele who has both sporadic inclusion body myositis and cardiac amyloidosis
12 malities in scattered muscle fibers occur in sporadic inclusion body myositis and clinically similar
13 oportion of mtDNA deletions in patients with sporadic inclusion body myositis and control subjects, m
16 le for T-cell activation in polymyositis and sporadic inclusion-body myositis and the cause of vacuol
17 agged-red fibers are common in patients with sporadic inclusion body myositis, and multiple [correcti
18 and consequences of genes that predispose to sporadic inclusion-body myositis, and of human muscle fi
21 80 to 90% of the vacuolated muscle fibers of sporadic inclusion body myositis contained well-defined,
22 ory cells that characterize polymyositis and sporadic inclusion-body myositis from the non-specific,
24 e immunostained muscle biopsy specimens from sporadic inclusion body myositis, hereditary inclusion b
26 ibody against a 43 kDa muscle autoantigen in sporadic inclusion body myositis (IBM) and demonstrated
36 heir consequences, and correlate findings in sporadic inclusion-body myositis muscle biopsies with in
37 nced by the recent identification within the sporadic inclusion-body myositis muscle fibers of severa
38 ry component may only slightly contribute to sporadic inclusion-body myositis muscle-fiber damage.
43 lated tau, are the characteristic feature of sporadic inclusion body myositis (s-IBM) muscle biopsies
44 n immunodeficiency virus infection (HIV-PM), sporadic inclusion body myositis (s-IBM), dermatomyositi
47 lated to seeking the pathogenic mechanism of sporadic inclusion-body myositis (s-IBM) and hereditary
51 ultiprotein-aggregates are characteristic of sporadic inclusion-body myositis (s-IBM) muscle fibers.
58 uding the TAR DNA binding protein TDP-43, in sporadic inclusion body myositis (sIBM) sarcoplasm are i
60 allmarks of the skeletal muscle pathology in sporadic inclusion body myositis (sIBM), have remained e
65 rder associated with aging and is related to sporadic inclusion body myositis, the most common acquir
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