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1 polymorphic H13 allele in the development of obliterative airway disease (OAD) after murine heterotop
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
12 lly allogeneic mismatched recipients develop obliterative airway disease (OAD), which is a suitable m
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
18 cts of rapamycin (RPM) on the development of obliterative airway disease in murine recipients of hete
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
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
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
34 resence of infectious organisms, transplant (obliterative) arteriopathy, neoplasia, relative proporti
36 id into the lung mediates the development of obliterative bronchiolitis (OB) in orthotopic WKY-to-F34
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
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
50 mmation, lymphocytic bronchiolitis (LB), and obliterative bronchiolitis (OB), causes substantial morb
52 Chronic lung allograft rejection, known as obliterative bronchiolitis (OB), is the leading cause of
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
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
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
82 ication of lung transplantation, may promote obliterative bronchiolitis leading to graft failure in l
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
87 assified as stable (DL-S, n = 11), or having obliterative bronchiolitis syndrome (DL-OBS, n = 4).
90 isorders include constrictive bronchiolitis (obliterative bronchiolitis, bronchiolitis obliterans), a
91 nifestations of chronic rejection, including obliterative bronchiolitis, interstitial fibrosis, and o
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
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
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
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,
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
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
138 ed and sexual function is no longer desired, obliterative procedures, which are better tolerated, may
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
143 PVR-TIPS may be considered for patients with obliterative PVT who are otherwise appropriate candidate
148 Wnt-betaC and Wnt-PCP pathways contribute to obliterative vascular disease in both the systemic and p
150 first genetically modified mouse model with obliterative vascular remodeling and pathophysiology rec
153 onset of chronic rejection characterized by obliterative vasculopathy and the rejection of secondary
155 temic sclerosis involves a proliferative and obliterative vasculopathy resulting from endothelial cel
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