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1 polymorphic H13 allele in the development of obliterative airway disease (OAD) after murine heterotop
2                                  A model for obliterative airway disease (OAD) after tracheal allogra
3 tant role in the development of experimental obliterative airway disease (OAD) after transplantation.
4 er KCa3.1 contributes to the pathogenesis of obliterative airway disease (OAD) and whether knockout o
5 ty of this mAb to prevent the development of obliterative airway disease (OAD) in murine recipients o
6 d whether epithelial re-growth could prevent obliterative airway disease (OAD) in orthotopic tracheal
7 nsplanted allogeneic murine tracheas develop obliterative airway disease (OAD) leading to a lesion re
8 by the recipient CD4(+) T cells to show that obliterative airway disease (OAD) that developed in thes
9 formed in a murine model of anti-MHC-induced obliterative airway disease (OAD), a correlate of oblite
10 nd -2 was investigated in the development of obliterative airway disease (OAD), an experimental model
11 cally transplanted allograft airways develop obliterative airway disease (OAD), an immunologically me
12                      Using a murine model of obliterative airway disease (OAD), we recently demonstra
13 lly allogeneic mismatched recipients develop obliterative airway disease (OAD), which is a suitable m
14 examined the role airway epithelium plays in obliterative airway disease (OAD).
15 system in the pathogenesis of posttransplant obliterative airway disease (OAD).
16 experimental obliterative bronchiolitis [ie, obliterative airway disease (OAD)] in rat tracheal allog
17 brosis and obstruction of the small airways (obliterative airway disease [OAD]) mediated predominantl
18                    In untreated rats, marked obliterative airway disease developed over 60 days.
19 cts of rapamycin (RPM) on the development of obliterative airway disease in murine recipients of hete
20 osuppresive compounds to prevent and reverse obliterative airway disease in these animals.
21 e Janus kinase 1/3 inhibitor R507 to prevent obliterative airway disease was analyzed in preclinical
22  immunosuppressant that similarly diminished obliterative airway disease with systemic or inhaled adm
23 and Collagen-V leading to the development of obliterative airway lesions (OAD), correlate of chronic
24  of Vegfr1 and -2 blocking in development of obliterative airway lesions might be rewarding.
25                                         This obliterative airways disease (OAD) also develops in hete
26 irway tissue secondary to the development of obliterative airways disease.
27   Cardiac allograft vasculopathy (CAV) is an obliterative and diffuse form of vasculopathy and is the
28 , intima proliferation, and various forms of obliterative and plexiform-like lesions in pulmonary art
29 s the morphologic features of the acute vaso-obliterative and vasoproliferative stages of oxygen-indu
30  rejection is manifested in this BM group by obliterative arteriopathy and the epicardium and endocar
31                Two resected specimens showed obliterative arteriopathy indicative of chronic rejectio
32 is unique murine model of PAH-like plexiform/obliterative arteriopathy induced via a two-hit pathophy
33 on (PAH) that recapitulate the plexiform and obliterative arteriopathy seen in PAH patients and help
34 llograft inflammation and the development of obliterative arteriopathy.
35  immunological injury and the development of obliterative arteriopathy.
36  in an animal model of chronic rejection and obliterative arteriopathy.
37 resence of infectious organisms, transplant (obliterative) arteriopathy, neoplasia, relative proporti
38                                              Obliterative bronchiolitis (OB) after lung transplantati
39                                              Obliterative bronchiolitis (OB) after lung transplantati
40     CLAD has 2 histologic phenotypes, namely obliterative bronchiolitis (OB) and restrictive alveolar
41 id into the lung mediates the development of obliterative bronchiolitis (OB) in orthotopic WKY-to-F34
42                                              Obliterative bronchiolitis (OB) is a clinical syndrome m
43                                              Obliterative bronchiolitis (OB) is a devastating complic
44                                              Obliterative bronchiolitis (OB) is a dreaded and frequen
45                                              Obliterative bronchiolitis (OB) is the histopathological
46                                              Obliterative bronchiolitis (OB) is the most serious late
47                                              Obliterative bronchiolitis (OB) is the primary cause of
48                                              Obliterative bronchiolitis (OB) post-lung transplantatio
49    Chronic allograft rejection manifested as obliterative bronchiolitis (OB) remains the single great
50 Actuarial probability of remaining free from obliterative bronchiolitis (OB)* tended to be higher in
51                                              Obliterative bronchiolitis (OB), an important threat to
52  syndrome and its histopathologic correlate, obliterative bronchiolitis (OB), are a major source of m
53 unction (CLAD) and its obstructive form, the obliterative bronchiolitis (OB), are the main long-term
54 n bronchoalveolar lavage (BAL) had developed obliterative bronchiolitis (OB), but only 8 of the 38 su
55       Lung transplant survival is limited by obliterative bronchiolitis (OB), but the mechanisms of O
56 mmation, lymphocytic bronchiolitis (LB), and obliterative bronchiolitis (OB), causes substantial morb
57                                              Obliterative bronchiolitis (OB), chronic allograft rejec
58   Chronic lung allograft rejection, known as obliterative bronchiolitis (OB), is the leading cause of
59                                              Obliterative bronchiolitis (OB), or chronic allograft re
60 changed); both parameters correlated with an obliterative bronchiolitis (OB)-free state.
61 isk factor for the subsequent development of obliterative bronchiolitis (OB).
62 ognized small-airway histological process of obliterative bronchiolitis (OB).
63 ut survival is limited by the development of obliterative bronchiolitis (OB).
64 ion, epithelial damage, and eventual luminal obliterative bronchiolitis (OB).
65 afts develop chronic rejection manifested as obliterative bronchiolitis (OB).
66 ajor histological features of posttransplant obliterative bronchiolitis (OB).
67 iogenesis during development of experimental obliterative bronchiolitis [ie, obliterative airway dise
68 ection, manifested as small airway fibrosis (obliterative bronchiolitis [OB]), is the main obstacle t
69                                              Obliterative bronchiolitis after lung transplantation is
70             The etiology and pathogenesis of obliterative bronchiolitis after lung transplantation re
71 ulate T-cell responses in the development of obliterative bronchiolitis after lung transplantation.
72 geneic immune response in the development of obliterative bronchiolitis after lung transplantation.
73 e critical role of T cells in development of obliterative bronchiolitis among human lung allograft re
74 s treated with CMVIG had lower incidences of obliterative bronchiolitis and death from obliterative b
75 of obliterative bronchiolitis and death from obliterative bronchiolitis and longer survival compared
76         Nine patients with histologic active obliterative bronchiolitis and progressively worsening a
77                    In this study, we induced obliterative bronchiolitis and studied the contribution
78 cessive amount of NO promotes posttransplant obliterative bronchiolitis by destroying airway epitheli
79 tes to the development of lung rejection and obliterative bronchiolitis by mediating effector T lymph
80 (angiographic); and incidence and death from obliterative bronchiolitis defined by pathological crite
81 logical lesions similar to those typical for obliterative bronchiolitis developed in vivo after recon
82 ith cyclosporine, in preventing and treating obliterative bronchiolitis in heart-lung and lung allogr
83 hymal cells, which is a lesion comparable to obliterative bronchiolitis in human lung transplant reci
84 n with histologic features characteristic of obliterative bronchiolitis in human lung transplant reci
85 ubtypes all contribute to the development of obliterative bronchiolitis in the heterotopic mouse trac
86                                              Obliterative bronchiolitis is a frequent, morbid, and us
87                                              Obliterative bronchiolitis is the major cause of long-te
88 ication of lung transplantation, may promote obliterative bronchiolitis leading to graft failure in l
89                              The 14 analyzed obliterative bronchiolitis lesions showed variations in
90  tissue level, and protein signatures for 14 obliterative bronchiolitis lesions were established.
91 essive, fibrotic occlusion of small airways, obliterative bronchiolitis lesions, which ultimately lea
92         Efforts to reduce the development of obliterative bronchiolitis may require the antagonism of
93 ose of this study was to investigate whether obliterative bronchiolitis might occur after xenogenic p
94 o develop a murine chimera model that mimics obliterative bronchiolitis of lung allograft recipients
95                                              Obliterative bronchiolitis remains a major long-term com
96 assified as stable (DL-S, n = 11), or having obliterative bronchiolitis syndrome (DL-OBS, n = 4).
97  because of chronic rejection in the form of obliterative bronchiolitis syndrome (OBS).
98                         Mechanistic study of obliterative bronchiolitis would be aided by development
99  many obstructive airway diseases, including obliterative bronchiolitis, asthma, Swyer-James syndrome
100 isorders include constrictive bronchiolitis (obliterative bronchiolitis, bronchiolitis obliterans), a
101                                           In obliterative bronchiolitis, expiratory CT scan may be th
102 nifestations of chronic rejection, including obliterative bronchiolitis, interstitial fibrosis, and o
103          Chronic inflammation, a hallmark of obliterative bronchiolitis, is known to induce lymphangi
104 ET-1 expression did not vary with rejection, obliterative bronchiolitis, or infection.
105 These data show that in this murine model of obliterative bronchiolitis, these chemokines are differe
106 tatins during postoperative Year 1 developed obliterative bronchiolitis, whereas the cumulative incid
107 y of HO-1 accelerates the development of the obliterative bronchiolitis-like lesion.
108 tology to study the airway injury related to obliterative bronchiolitis.
109 ave value in the prevention and treatment of obliterative bronchiolitis.
110 gainst the mesenchymal cell proliferation of obliterative bronchiolitis.
111 afts develop chronic rejection manifested as obliterative bronchiolitis.
112  baseline) and/or the presence of histologic obliterative bronchiolitis.
113 e (OAD) leading to a lesion resembling human obliterative bronchiolitis.
114 etely effective therapy for the treatment of obliterative bronchiolitis.
115 erative airway disease (OAD), a correlate of obliterative bronchiolitis.
116 to the small human airway grafts, and caused obliterative bronchiolitis.
117 rlying another chronic inflammatory disease, obliterative bronchiolitis.
118 tion-associated chronic complications, e.g., obliterative bronchiolitis.
119 s isolated from the airways of patients with obliterative bronchiolitis.
120 ine heterotopic tracheal allograft model for obliterative bronchiolitis.
121 mplicated in late graft failure secondary to obliterative bronchiolitis.
122 s in the mouse heterotopic tracheal model of obliterative bronchiolitis.
123 tic cells (DC) is thought to be important in obliterative bronchiolitis/bronchiolitis obliterans synd
124  characterized by the pathologic findings of obliterative bronchiolitis: neutrophil influx and extrac
125 -treated kidneys had more extensive arterial obliterative changes and glomerulosclerosis after 24 wee
126                              Elafin reverses obliterative changes in pulmonary arteries via elastase
127                        Biliary atresia is an obliterative cholangiopathy of infancy that is fatal if
128 an unusually accelerated and diffuse form of obliterative coronary arteriosclerosis, determines long-
129 is obliterans (BO), a common and devastating obliterative disorder of small airways following lung tr
130 t the cause is probably multifactorial, with obliterative extrahepatic cholangiopathy as the common e
131  could cause biliary atresia, an idiopathic, obliterative infantile disease of bile ducts that is the
132 ture of key pathological lesions (plexiform, obliterative, intima+media hypertrophy, and adventitia)
133                           Based on the fibro-obliterative lesion found during bronchiolitis obliteran
134 uman patients, induce formation of plexiform/obliterative lesions and defined the molecular mechanism
135 esions occur as solitary lesions, concentric-obliterative lesions appear to be only associated with,
136  vascular remodeling caused by plexiform and obliterative lesions, media hypertrophy, inflammatory ce
137 n compared with intima+media hypertrophy and obliterative lesions.
138  in an attempt to treat established vascular-obliterative lung disease.
139             Forty-four patients with chronic obliterative main PVT were identified during our institu
140 trate that plexiform (n = 14) and concentric-obliterative (n = 6) lesions occur distal to branch poin
141 bliterans syndrome (BOS), a process of fibro-obliterative occlusion of the small airways in the trans
142 of a Sugen-hypoxia rat model of severe angio-obliterative PAH, concordant with profiles observed in P
143 hophysiology of ROP involves an initial vaso-obliterative phase followed by vaso-proliferative phase
144 TRAIL does not play a major role in the vaso-obliterative phase of oxygen-induced retinopathy.
145         Tumorous swelling, eosinophilia, and obliterative phlebitis are other frequently observed fea
146  by tumefactive lesions, storiform fibrosis, obliterative phlebitis, and accumulation of IgG4-express
147 of IgG4(+) plasma cells, storiform fibrosis, obliterative phlebitis, and mild to moderate eosinophili
148 f IgG4(+) plasma cells, tumefactive lesions, obliterative phlebitis, and mild to moderate eosinophili
149  tissue infiltration, storiform fibrosis and obliterative phlebitis, reflecting a dysregulated immune
150 acytic infiltration, storiform fibrosis, and obliterative phlebitis.
151 sitive plasma cells, storiform fibrosis, and obliterative phlebitis.
152 sociated with germinal centers, fibrosis and obliterative phlebitis.
153 pancreatic ducts and ductules, combined with obliterative phlebitis.
154                                     Chronic, obliterative portal vein (PV) thrombosis (PVT) represent
155 ed and sexual function is no longer desired, obliterative procedures, which are better tolerated, may
156               Biliary atresia, a progressive obliterative process involving the bile ducts, has its o
157   Graft arterial disease (GAD) is a vascular obliterative process mediated via the Th1 cytokine inter
158 mune system activation with autoimmunity; an obliterative, proliferative small vessel vasculopathy; a
159 apies for the treatment of asthma or chronic obliterative pulmonary disease.
160  vascular remodeling in a rat model of angio-obliterative pulmonary hypertension.
161 PVR-TIPS may be considered for patients with obliterative PVT who are otherwise appropriate candidate
162  after lung transplantation is bronchiolitis obliterative syndrome (BOS).
163 be categorised broadly by reconstructive and obliterative techniques.
164 d inflammation are mechanistically linked to obliterative tissue fibrosis.
165 ial amount of smooth muscle cells within the obliterative tissue was of donor origin.
166 ertension (PAH), endothelial dysfunction and obliterative vascular disease are associated with DNA da
167 ertension (PAH), endothelial dysfunction and obliterative vascular disease are associated with DNA da
168 Wnt-betaC and Wnt-PCP pathways contribute to obliterative vascular disease in both the systemic and p
169 tics observed in patients with PAH and other obliterative vascular diseases.
170  first genetically modified mouse model with obliterative vascular remodeling and pathophysiology rec
171 ts indicate that LG3 is a novel regulator of obliterative vascular remodeling during rejection.
172                   However, the mechanisms of obliterative vascular remodeling remain elusive; hence,
173  onset of chronic rejection characterized by obliterative vasculopathy and the rejection of secondary
174 e connective tissue disease characterized by obliterative vasculopathy and tissue fibrosis.
175 temic sclerosis involves a proliferative and obliterative vasculopathy resulting from endothelial cel
176 rying degrees of skin and organ fibrosis and obliterative vasculopathy.

 
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