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

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