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1 essed them for the presence of ricin and for histological damage.
2 incided with reduced lung, liver, and kidney histological damage.
3 egulation of proinflammatory genes, and less histological damage.
4 rrelates with the loss of renal function and histological damage.
5 generation and progression to patchy chronic histological damage.
6 ntly improves neurological score and reduces histological damage.
7 often noted in adult cartilage lacking overt histological damage.
8 their magnitude correlated with severity of histological damage.
10 usion, in the treated hearts, there was less histological damage and less apoptosis of cardiac muscle
13 he key mediators in the subsequent cycles of histological damage and repair, and clinical relapse and
16 ductions in clinical colitis scores, colonic histological damage, and colonic inflammation compared w
18 B-269970 resulted in lower clinical disease, histological damage, and proinflammatory cytokine levels
19 d loss, weight loss, colon shortening, colon histological damage, and splenomegaly than did wild-type
20 neurobehavioral deficits, E/I imbalance, and histological damage are all ameliorated by treatment wit
22 stem cells are of great interest to recover histological damage caused by neuro-degenerative disease
26 scores for clinical disease activity and for histological damage in the joints were both significantl
27 vere and/or sustained, can result in chronic histological damage of which interstitial fibrosis and t
29 eficit scores, overall performance category, histological damage scores (viable neuron counts in CA1
31 sacrifice of experimental animals to assess histological damage, thus counteracting the principles o
32 r) or B2F1 Stm(r) developed hematuria and/or histological damage to glomeruli or thrombocytopenia, co
33 m sulfate (DSS)-induced clinical disease and histological damage to the colonic mucosa were significa
35 Logistic regression analysis revealed that histological damage was (P = 0.0017) independently assoc
36 linical chemistry results normalized, and no histological damage was apparent 3 weeks after autograft
37 pients no progressive clinically significant histological damage was apparent in follow-up protocol b
39 a single 6-min bilateral carotid occlusion, histological damage was evident in the CA1 region of hip
43 fluid secretion, mannitol permeability, and histological damage were measured in ileal loops in vivo
45 fibrosis, inflammatory gene expression, and histological damage were not significantly different fro
46 in the IC group and had moderately increased histological damage when compared to the Na-NP group.
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