ライフサイエンスコーパス: muscle inflammation

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1 py of lipopolysaccharide-induced cremasteric muscle inflammation.

2 markedly reduced the severity of HRS-induced muscle inflammation.

3 at higher risk for cancer, lung disease, or muscle inflammation.

4 ed Ccr2(-/-) but not Ccl2(-/-) mice restored muscle inflammation.

5 en associated with subacute onset and marked muscle inflammation.

6 cells, anti-T. cruzi antibody response, and muscle inflammation.

7 ise, in a distribution that may mimic active muscle inflammation.

8 of AnxA2 in dysferlin deficient mice reduced muscle inflammation, adipogenic replacement of myofibers

9 cludes facilitating myofiber repair, chronic muscle inflammation and adipogenic replacement of dysfer

10 nd patient lacking dysferlin exhibit chronic muscle inflammation and adipogenic replacement of the my

11 ss of NOS from dystrophic muscle exacerbates muscle inflammation and fiber damage by inflammatory cel

12 AMPD1 deficiency is acquired prior to overt muscle inflammation and is responsible, at least in part

13 We tested whether muscle-derived NO affects muscle inflammation and membrane lysis that occur in mod

14 nloading followed by reloading, which causes muscle inflammation and membrane lysis.

15 d the activity of NF-kappaB, a key player in muscle inflammation and myogenesis.

16 rly visceral adipose tissue, can also induce muscle inflammation and negatively regulate myocyte meta

17 udied the mechanisms by which CCL2 regulates muscle inflammation and regeneration.

18 l injections of imatinib at the peak of limb muscle inflammation and the onset of diaphragm fibrosis.

19 Myositis is characterised by muscle inflammation and weakness.

20 Muscle inflammation assessed by MRI, myometry, and blood

21 tective effect was associated with decreased muscle inflammation, but no changes in adipose tissue in

22 Many patients show muscle inflammation, but the molecular mechanisms that i

23 Heart and Skeletal Muscle Inflammation (HSMI), recently associated with a n

24 urden at the site of infection, and improved muscle inflammation in a dose-dependent manner, without

25 sults demonstrate the importance of skeletal muscle inflammation in aging-mediated insulin resistance

26 er dendritic cells (DCs) are constituents of muscle inflammation in juvenile dermatomyositis (DM).

27 idea that plasmacytoid DCs are mediators of muscle inflammation in juvenile DM.

28 entral to the initiation and perpetuation of muscle inflammation in juvenile DM.

29 in induced robust, statistically significant muscle inflammation in multiple congenic strains of C57B

30 immunocompetent mice, however, of prominent muscle inflammation in the absence of infectious virus s

31 Bladder smooth muscle inflammation-induced cell death is accompanied by

32 g contractions and by quantifying markers of muscle inflammation, injury, oxidative damage and regene

33 nt and delay disease progression by reducing muscle inflammation/injury and improving force/myogenesi

34 Muscle inflammation is often associated with its expansi

35 Muscle inflammation is often present in dysferlin defici

36 Although muscle inflammation is widely recognized in dysferlinopa

37 n enhances insulin action by reducing local (muscle) inflammation, leading to improved insulin signal

38 Conversely, muscle inflammation markedly amplified mechanical curren

39 stidyl-tRNA synthetase (HRS) triggers florid muscle inflammation (relative to appropriate control pro

40 uman cytokine profiling and murine models of muscle inflammation suggest that tRNA synthetases themse

41 ve immune responses that culminate in severe muscle inflammation that is the hallmark of idiopathic i

42 Modified muscle use can result in muscle inflammation that is triggered by unidentified ev

43 n of the complement system is a component of muscle inflammation that results from changes in muscle

44 Muscle inflammation was assessed by immunohistochemistry

45 ed that the ability of murine HisRS to drive muscle inflammation was not dependent on B cell receptor

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