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1 ase levels and induced neutrophilic skeletal muscle inflammation.
2 py of lipopolysaccharide-induced cremasteric muscle inflammation.
3 markedly reduced the severity of HRS-induced muscle inflammation.
4  at higher risk for cancer, lung disease, or muscle inflammation.
5 ed Ccr2(-/-) but not Ccl2(-/-) mice restored muscle inflammation.
6 en associated with subacute onset and marked muscle inflammation.
7  cells, anti-T. cruzi antibody response, and muscle inflammation.
8 ise, in a distribution that may mimic active muscle inflammation.
9 lt in persistent expression without inducing muscle inflammation.
10 of AnxA2 in dysferlin deficient mice reduced muscle inflammation, adipogenic replacement of myofibers
11 cludes facilitating myofiber repair, chronic muscle inflammation and adipogenic replacement of dysfer
12 nd patient lacking dysferlin exhibit chronic muscle inflammation and adipogenic replacement of the my
13 Risk factors for TMD include localized joint/muscle inflammation and estrogen status.
14 ss of NOS from dystrophic muscle exacerbates muscle inflammation and fiber damage by inflammatory cel
15  AMPD1 deficiency is acquired prior to overt muscle inflammation and is responsible, at least in part
16  We tested whether muscle-derived NO affects muscle inflammation and membrane lysis that occur in mod
17 nloading followed by reloading, which causes muscle inflammation and membrane lysis.
18 d the activity of NF-kappaB, a key player in muscle inflammation and myogenesis.
19 rly visceral adipose tissue, can also induce muscle inflammation and negatively regulate myocyte meta
20 udied the mechanisms by which CCL2 regulates muscle inflammation and regeneration.
21 l injections of imatinib at the peak of limb muscle inflammation and the onset of diaphragm fibrosis.
22                 Myositis is characterised by muscle inflammation and weakness.
23 estoration in affected dogs but also induces muscle inflammation, and Cas9-specific humoral and cytot
24                                              Muscle inflammation assessed by MRI, myometry, and blood
25 tective effect was associated with decreased muscle inflammation, but no changes in adipose tissue in
26                           Many patients show muscle inflammation, but the molecular mechanisms that i
27                           Heart and Skeletal Muscle Inflammation (HSMI), recently associated with a n
28 st score correlates with the early stages of muscle inflammation identified by histological analysis
29 urden at the site of infection, and improved muscle inflammation in a dose-dependent manner, without
30 sults demonstrate the importance of skeletal muscle inflammation in aging-mediated insulin resistance
31 er dendritic cells (DCs) are constituents of muscle inflammation in juvenile dermatomyositis (DM).
32  idea that plasmacytoid DCs are mediators of muscle inflammation in juvenile DM.
33 entral to the initiation and perpetuation of muscle inflammation in juvenile DM.
34 in induced robust, statistically significant muscle inflammation in multiple congenic strains of C57B
35  immunocompetent mice, however, of prominent muscle inflammation in the absence of infectious virus s
36                               Bladder smooth muscle inflammation-induced cell death is accompanied by
37 g contractions and by quantifying markers of muscle inflammation, injury, oxidative damage and regene
38 nt and delay disease progression by reducing muscle inflammation/injury and improving force/myogenesi
39                                              Muscle inflammation is often associated with its expansi
40                                              Muscle inflammation is often present in dysferlin defici
41                                     Although muscle inflammation is widely recognized in dysferlinopa
42 n enhances insulin action by reducing local (muscle) inflammation, leading to improved insulin signal
43                                  Conversely, muscle inflammation markedly amplified mechanical curren
44 stidyl-tRNA synthetase (HRS) triggers florid muscle inflammation (relative to appropriate control pro
45 uman cytokine profiling and murine models of muscle inflammation suggest that tRNA synthetases themse
46 ve immune responses that culminate in severe muscle inflammation that is the hallmark of idiopathic i
47            Modified muscle use can result in muscle inflammation that is triggered by unidentified ev
48 n of the complement system is a component of muscle inflammation that results from changes in muscle
49 , contributes to neonatal nociception during muscle inflammation through a novel neuroimmune loop inv
50 L-6, monocyte chemoattractant protein-1) and muscle inflammation Tlr4/Myd88 pathway (Toll-like recept
51                                              Muscle inflammation was assessed by immunohistochemistry
52 ed that the ability of murine HisRS to drive muscle inflammation was not dependent on B cell receptor