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1  can ameliorate both the direct and indirect fibroproliferative actions of TGF-beta.
2 ich critically ill surgical patients develop fibroproliferative acute respiratory distress syndrome.
3                 Asbestos is a carcinogen and fibroproliferative agent in lung that may cause cell sig
4                      Fibrosis, microvascular fibroproliferative alterations, and autoantibody product
5 mbating chronic rejection by inhibiting both fibroproliferative and alloimmune responses.
6       Furthermore, the findings suggest that fibroproliferative and inflammatory lesions are independ
7 ung inflammation and the development of late fibroproliferative ARDS, or if it is predictive of a ben
8 ne 125 mg i.v. every 6 hrs was initiated for fibroproliferative ARDS.
9 ecular mechanisms governing inflammatory and fibroproliferative aspects of the disorder are not clear
10 played histological characteristics of bone, fibroproliferative cells, blood vessels, and adipose tis
11 poxic pulmonary hypertension includes marked fibroproliferative changes in the pulmonary artery (PA)
12 d 11 days after symptom onset, had pulmonary fibroproliferative changes.
13 lmonary lymphatics is a critical mediator of fibroproliferative changes.
14  0.001), but they also developed obstructive fibroproliferative coronary artery lesions much earlier
15                Keloid disease is a recurrent fibroproliferative cutaneous tumor of unknown pathogenes
16 of connective tissue growth factor (CTGF), a fibroproliferative cytokine, by transforming growth fact
17                               KD is a common fibroproliferative dermal lesion with an ill-defined tre
18                          Arthrofibrosis is a fibroproliferative disease characterised by excessive de
19                                         This fibroproliferative disease may be promoted by overproduc
20  fibrosis (IPF) is an insidious inflammatory fibroproliferative disease whose cause and course before
21 ls are known to be the key effector cells of fibroproliferative disease, but the specific matrix sign
22 ession at sites of lung injury in developing fibroproliferative disease.
23 pathic pulmonary fibrosis (IPF) is a lethal, fibroproliferative disease.
24                                      Chronic fibroproliferative diseases account for approximately 45
25 ic diseases are to discuss some of the major fibroproliferative diseases and to identify the common a
26                                              Fibroproliferative diseases are driven by dysregulated t
27                               Unfortunately, fibroproliferative diseases remain intractable to curren
28  are strongly implicated in the formation of fibroproliferative diseases such as proliferative vitreo
29                                              Fibroproliferative diseases, including the pulmonary fib
30 tants and are involved in other inflammation/fibroproliferative diseases, we hypothesized that the ex
31 a critical event in the genesis of pulmonary fibroproliferative diseases.
32 ted response has been implicated in multiple fibroproliferative diseases.
33 L-1 and has been associated with a number of fibroproliferative diseases.
34 s to the development and progression of this fibroproliferative disorder and identified TNF as a ther
35 ibrosis (IPF) is a progressive and incurable fibroproliferative disorder characterized by unrelenting
36   It is an increasingly common and disabling fibroproliferative disorder of the palmar fascia, which
37 ic pulmonary fibrosis (IPF) is a progressive fibroproliferative disorder refractory to current pharma
38 harmacological target for immunosuppression, fibroproliferative disorders, atherosclerosis, and strok
39 e receptor CXCR3 is functionally involved in fibroproliferative disorders, including liver fibrosis.
40 icellular protein that plays a major role in fibroproliferative disorders.
41 pathogenesis of pulmonary fibrosis and other fibroproliferative disorders.
42 ion of extracellular matrix observed in many fibroproliferative disorders.
43 ons is an effective therapeutic strategy for fibroproliferative disorders.
44  plays a central role in the pathogenesis of fibroproliferative disorders.
45 itors as potential therapy for patients with fibroproliferative disorders.
46 E prostanoid (EP) receptors in mediating the fibroproliferative effects of IL-1beta in ALI.
47 d serum tryptase were more likely to develop fibroproliferative end organ damage, and 3 of 9 died wit
48 sion subsets described previously, including fibroproliferative, inflammatory, and normal-like groups
49 mprovement were classified as normal-like or fibroproliferative intrinsic subsets.
50 ling that occurs during the development of a fibroproliferative lesion and could facilitate biologica
51 reased levels in cells derived from an early fibroproliferative lesion in a patient with fibrodysplas
52                     Keloid disease (KD) is a fibroproliferative lesion of unknown etiopathogenesis th
53 a knocked out (TNF-alphaRKO) fail to develop fibroproliferative lesions after asbestos exposure.
54                                        These fibroproliferative lesions lead to neointimal thickening
55 ed at 8 to 12 weeks and demonstrated intimal fibroproliferative lesions with a mild parenchymal monon
56 is associated with accumulation of fibrin in fibroproliferative lesions.
57 s in fibrin gels, an in vitro model of early fibroproliferative lesions.
58 signaling protected the mice from developing fibroproliferative lesions.
59 kines are produced during the development of fibroproliferative lung disease.
60 ) is a prevalent, progressive, and incurable fibroproliferative lung disease.
61                    Despite the importance of fibroproliferative lung disorders, no safe and effective
62 re upregulated prior to the development of a fibroproliferative lung lesion, and thus may play a cent
63 s sarcoma-associated herpesvirus (KSHV) in a fibroproliferative malignancy of macaques that has simil
64 roperitoneal fibromatosis (RF) is a vascular fibroproliferative neoplasm which has many morphological
65 insic gene expression subsets (inflammatory, fibroproliferative, normal-like, and limited) are observ
66 ration, cartilage erosion, bone erosion, and fibroproliferative pannus) or frozen, cryosectioned, and
67                                          The fibroproliferative phase of acute respiratory distress s
68 CXC chemokines have an important role in the fibroproliferative phase of ARDS via the regulation of a
69 int to a newly described role for HGF in the fibroproliferative phase of RA-associated synovitis.
70  suppresses TGF-beta1-induced myofibroblast (fibroproliferative) phenotypic genes, for example, alpha
71  they are not necessary for the formation of fibroproliferative plaques.
72 chiolitis obliterans syndrome is caused by a fibroproliferative process in lung allografts resulting
73 echanistic research has focused on the local fibroproliferative process in the lung.
74 (IH) formation that induces inflammatory and fibroproliferative processes and ultimately restenosis.
75           EGFR activation is associated with fibroproliferative processes in human lung disease and a
76 rombin may be important for inflammatory and fibroproliferative processes in wound healing.
77 ute radiation toxicity and in sustaining the fibroproliferative processes that lead to chronic radiat
78 Angiogenesis and vascular remodeling support fibroproliferative processes; however, no study has addr
79   Concordantly, abrogation of QKI attenuated fibroproliferative properties of VSMCs, while potently i
80 pathic pulmonary fibrosis (IPF) is a chronic fibroproliferative pulmonary disorder for which there ar
81                                          The fibroproliferative reaction to acute lung injury may lim
82                                              Fibroproliferative remodeling in smooth muscle-rich holl
83 mation results from chronic inflammation and fibroproliferative remodeling in the vascular wall.
84 g by ameliorating cell death and stimulating fibroproliferative repair.
85                    One of these involves the fibroproliferative response after acute lung injury, whi
86    Mice deficient in PTEN showed a prolonged fibroproliferative response after tissue injury, and imm
87 U/kg), Stat1-/- mice exhibited a more severe fibroproliferative response and significantly elevated t
88 TGF-alpha is associated with a marker of the fibroproliferative response in sustained ARDS.
89                                The excessive fibroproliferative response leading to luminal narrowing
90 atent TGF-beta1, resulting in promotion of a fibroproliferative response over an inflammatory respons
91 tion and that they likely play a role in the fibroproliferative response seen in human acute lung inj
92 ress syndrome (ARDS) frequently results in a fibroproliferative response that precludes effective alv
93                                          The fibroproliferative response to acute lung injury (ALI) r
94                Such mechanisms may drive the fibroproliferative response to ALI.
95 ch Hh-responsive cells accumulate during the fibroproliferative response to chronic cholestatic liver
96 RNA and protein expression and the degree of fibroproliferative response to inhaled asbestos fibers a
97  no soluble TNF-alpha display an accentuated fibroproliferative response to low shear stress (P:<0.05
98                                 Although the fibroproliferative response to lung injury occurs with a
99  and smooth muscle cells, and it reduces the fibroproliferative response to vascular injury.
100 overexpression on liver angiogenesis and the fibroproliferative response using a Tet-inducible bitran
101 cates medial calcification, the inflammatory-fibroproliferative response, and inflammation-mediated e
102                           Matriptase-induced fibroproliferative responses and the receptor involved w
103 ies to reduce lung levels of MMP-8 may limit fibroproliferative responses to injury in the human lung
104 n in QKI activity can ameliorate pathogenic, fibroproliferative responses to vascular injury.
105        Thus, we explored the role of CD69 in fibroproliferative responses using a mouse model of peri
106      TLR3-mediated cytokine, type 1 IFN, and fibroproliferative responses were examined in TLR3 wild-
107 ulted in defective cytokine, type I IFN, and fibroproliferative responses.
108                                              Fibroproliferative scars are an important clinical probl
109  fibrosis are likely to benefit those with a fibroproliferative signature.
110 ve connections between the inflammatory- and fibroproliferative-specific genes.
111 n the inflammatory subset do not move to the fibroproliferative subset, and vice versa.
112 fective therapeutic agents for SSc and other fibroproliferative vasculopathies in which EndoMT plays
113 EndoMT may play a role in the development of fibroproliferative vasculopathies.
114 olved in the pathogenesis of the progressive fibroproliferative vasculopathy which is a hallmark of s

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