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1 tic lesions, without anchoring to a specific fibrotic lesion.
2 g MI coupled with a reduced infarct size and fibrotic lesion.
3  for PGE2 deficiency in the evolution of the fibrotic lesion.
4 se have pronounced lumican expression in the fibrotic lesions.
5 advanced disease, there is less Slit2 in the fibrotic lesions.
6  plaque morphology and was the highest among fibrotic lesions.
7 mine reduced matrix expression and mitigated fibrotic lesions.
8 of the cellular origin of the characteristic fibrotic lesions.
9  molecules into fibrils, a main component of fibrotic lesions.
10 gical by activating apoptosis selectively in fibrotic lesions.
11 f epithelial hyperplasia in association with fibrotic lesions.
12 -alpha actin and are associated with various fibrotic lesions.
13  there are high levels of CTGF expression in fibrotic lesions.
14 ize of the fibroblast population in existing fibrotic lesions.
15 e fibroblast population size within existing fibrotic lesions.
16 the time period necessary for development of fibrotic lesions.
17            Growing evidence suggests that in fibrotic lesions, a subset of blood monocytes enters the
18 nary epithelial cells at sites of developing fibrotic lesions after 14 and 30 days of inhalation.
19 n a mouse genetic model dramatically reduces fibrotic lesions after obstructive injury, underscoring
20 o prevents this regeneration, leading to pre-fibrotic lesions and deficient oxygen exchange.
21 heterogeneity of cell types proliferating in fibrotic lesions and exclude pericytes and two epithelia
22 tolerated, reduced the severity of pulmonary fibrotic lesions and extracellular matrix remodeling, an
23        Rapamycin also exacerbated cystic and fibrotic lesions and impaired kidney function in these m
24                The SUV(max) and SUV(mean) of fibrotic lesions and LC were measured and CT-density-cor
25 s of isoniazid in individuals with pulmonary fibrotic lesions and LTBI (n = 27830) found a reduction
26                                     However, fibrotic lesions and lymphocytic infiltration were obser
27  of CKD, depletion of FBN1 ameliorated renal fibrotic lesions and mitigated vascular rarefaction.
28  mice developed periductular onion-skin type fibrotic lesions and pronounced ductular reaction starti
29 sion proteins exhibit increased retention in fibrotic lesions and reduced systemic toxicity.
30  first time sustained Egr-1 up-regulation in fibrotic lesions and suggests that Egr-1 has a role in t
31                                  Hepatocyte, fibrotic lesion, and bile duct (cancer) were classified
32 hrombin are upregulated in wound healing and fibrotic lesions, and inhibition of these proteases atte
33 GF gene therapy markedly ameliorated hepatic fibrotic lesions, as demonstrated by reduced alpha-smoot
34 thway in the development of inflammation and fibrotic lesions associated with BOOP and ARDS.
35 ced BOOP, but still develop inflammation and fibrotic lesions associated with reovirus 1/L-induced AR
36 l, do not develop pulmonary inflammation and fibrotic lesions associated with reovirus 1/L-induced BO
37 lent deposition of interstitial collagen and fibrotic lesions at days 7 and 14 after administration.
38 ytes have been implicated as contributors to fibrotic lesions because of the transdifferentiation pot
39 idney disease and correlated positively with fibrotic lesion but negatively with kidney function.
40 liorated glomerulosclerosis and interstitial fibrotic lesions, but did not affect serum phosphorus an
41 he fibroconnective tissues of these advanced fibrotic lesions consistently revealed dense staining fo
42 Myc, and that lung fibroblasts isolated from fibrotic lesions constitutively express growth-promoting
43 f connective tissue growth factor present in fibrotic lesions contributes to the phenotype of sclerod
44 -fmk, inhibited apoptosis, inflammation, and fibrotic lesion development in reovirus 1/L-induced BOOP
45 especially IFN-gamma, may play a key role in fibrotic lesion development.
46 before reovirus 1/L infection also inhibited fibrotic lesion development.
47 BAL fluid, and myofibroblasts present in the fibrotic lesions expressed FOXF1 by in situ hybridizatio
48                        In healing wounds and fibrotic lesions, fibroblasts and monocyte-derived fibro
49 this process with regard to wound repair and fibrotic lesion formation that is likely applicable to o
50 y events during both normal wound repair and fibrotic lesion formation.
51           In particular, stiffened matrix in fibrotic lesions has been shown to promote pathogenic my
52 y in human IBD-fibrosis strictures and mouse fibrotic lesions, highlighting their physiological relev
53  by KRT8(+) alveolar epithelial cells lining fibrotic lesions in a mouse model of interstitial lung d
54 at PPAR-gamma agonists also ameliorate renal fibrotic lesions in both diabetic nephropathy and nondia
55 the development of reovirus 1/L-induced BOOP fibrotic lesions in CBA/J mice and suggests that T(H)1-d
56                                           In fibrotic lesions in human and mouse lungs, we found exte
57 h type 2 cytokines (IL-4 and IL-13), whereas fibrotic lesions in IL-5(-/-) animals were accompanied b
58 llin was prominently expressed in subretinal fibrotic lesions in mice.
59 gene expression profile, and ability to form fibrotic lesions in model organisms.
60                                              Fibrotic lesions in models were represented with combina
61 ation of ICG-001 also effectively attenuated fibrotic lesions in obstructive nephropathy.
62 blation of tPA attenuated renal interstitial fibrotic lesions in obstructive nephropathy.
63 le role for CTGF in promoting development of fibrotic lesions in phenytoin-induced gingival overgrowt
64 , were consistently localized to the edge of fibrotic lesions in PSC explants.
65 ncreased activation of fibrotic pathways and fibrotic lesions in the heart.
66       Histopathological examination revealed fibrotic lesions in the hearts of the older D166V mice.
67        AFSC were observed to localize within fibrotic lesions in the lung, showing preferential targe
68 mitochondrial defects, reduced occurrence of fibrotic lesions in the myocardium, prevention of cardia
69 IPF hallmarks, including the ability to form fibrotic lesions in zebrafish embryos and mouse lungs, a
70 overexpressed by fibroblasts present in skin fibrotic lesions, including scleroderma.
71 niformly across the kidney parenchyma, renal fibrotic lesions initiate at certain focal sites in whic
72  elimination of fibroblasts actively forming fibrotic lesions is an effective therapeutic strategy fo
73 tabolism of collagen, the major component of fibrotic lesions, is, in part, regulated by integrins.
74                                In wounds and fibrotic lesions, mast cells degranulate to release tryp
75 ontribute to the progression of inflammatory-fibrotic lesions of atherosclerosis.
76 ronchitis, to subepithelial and intraluminal fibrotic lesions of bronchiolitis obliterans by day 28.
77                                     Advanced fibrotic lesions of eosinophilic granuloma, containing m
78 non-invasive imaging of active cathepsins in fibrotic lesions of patients with IPF.
79   Parenchymal and bronchial inflammatory and fibrotic lesions other than acute cellular rejection (AC
80 TGF)-beta1 in the tumor microenvironment and fibrotic lesions plays a critical role in tumor progress
81          Prematurely dying animals had focal fibrotic lesions predominantly present in the left ventr
82 -) mice showed a patchy expression of FAP in fibrotic lesions, preferentially in the transition zone
83 velopment of epithelial cell hyperplasia and fibrotic lesions, respectively.
84                        In healing wounds and fibrotic lesions, some of the monocytes differentiate in
85                                           In fibrotic lesions, spatially restricted generation of bio
86                                Hyperplastic, fibrotic lesions subsequently developed in the same regi
87 fic features of the myofibroblast in diverse fibrotic lesions, such as systemic sclerosis; kidney, li
88  cytokine pathway, exhibited more pronounced fibrotic lesions than did wild-type animals.
89 ocalization within subepithelial tissues and fibrotic lesions that was dependent on Ybt biosynthesis
90 and the subsequent conduction slowing in the fibrotic lesions was a necessary but not sufficient cond
91   Importantly, the number of WT1(+) cells in fibrotic lesions was correlated with severity of lung di
92 al effect on neighboring myocytes within the fibrotic lesions was the sufficient condition necessary
93                                              Fibrotic lesions were observed in 19 of 49 survivors (39
94                                              Fibrotic lesions were observed in 33 of 171 patients (19
95                                              Fibrotic lesions were sub-RPE in 46.1%, mixed in 29.8%,
96 ed throughout the lung, but inflammation and fibrotic lesions were usually confined to focal areas.
97 ected mice both inhibited the development of fibrotic lesions when administered early in the time-cou
98 e time-course and promoted the resolution of fibrotic lesions when corticosteroid administration was
99 ndant in human IBD-fibrosis tissue and mouse fibrotic lesions, where they co-localize with AIEC.
100  numbers of GFP(+) cells to appear in active fibrotic lesions, while only a few GFP(+) cells could be
101 nti-TGF-beta Ab selectively inhibits chronic fibrotic lesions without affecting autoantibody producti
102 circuits formed throughout the noncontiguous fibrotic lesions, without anchoring to a specific fibrot
103 ssue growth factor by fibroblasts present in fibrotic lesions would be expected to contribute directl

 
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