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1 uring S. aureus pneumonia, inducing necrotic pulmonary injury.
2 edical disorders such as cardiac failure and pulmonary injury.
3 cruitment of leukocytes, and immune-mediated pulmonary injury.
4 ypoxia-reoxygenation-induced exacerbation of pulmonary injury.
5 atment was started 5-7 d after initiation of pulmonary injury.
6 role in regulating inflammatory responses to pulmonary injury.
7 ering miR-146 inhibitor to females increased pulmonary injury.
8 ptase (TERT) deficiency in a murine model of pulmonary injury.
9       The dose-limiting toxicity was diffuse pulmonary injury.
10 ions, preserving systemic oxygenation during pulmonary injury.
11  provides potent protection against ischemic pulmonary injury.
12 e clinical relevance of elevated histones in pulmonary injury.
13 mph duct ligation (LDL) before T/HS prevents pulmonary injury.
14 +) T cells in vivo abolishes the type 2-like pulmonary injury.
15 e aggregation, activation, and microvascular pulmonary injury.
16 ed to otherwise healthy animals resulting in pulmonary injury.
17 ctions, was tested for the ability to reduce pulmonary injury.
18 nto the plasma and by indices of gastric and pulmonary injury.
19  concomitant with attenuation of hepatic and pulmonary injury.
20 ng a selective and alternative target during pulmonary injury.
21 immunologic, infectious, ischemic, and toxic pulmonary injuries.
22  as a baseline model for incorporating other pulmonary injuries.
23 e first 8 patients had fatal regimen-related pulmonary injury, a complication not found among 11 subs
24      The evolution of BPD from a disorder of pulmonary injury affecting moderately preterm infants, t
25  of the role of proinflammatory cytokines in pulmonary injury after ARF, the anti-inflammatory cytoki
26                                       Lethal pulmonary injury after bleomycin treatment was higher in
27 contributes to the attenuation of HPV and to pulmonary injury after challenge with endotoxin.
28 accelerating parasite clearance and reducing pulmonary injury after infection with a lung-migrating h
29 in impaired bacterial clearance and worsened pulmonary injury and death.
30 C and bacterial clearance, resulting in less pulmonary injury and decreased death.
31 in mice using the bleomycin-induced model of pulmonary injury and fibrosis.
32  were treated with bleomycin or vehicle, and pulmonary injury and fibrotic responses were compared.
33  has not been investigated in the context of pulmonary injury and immune responses related to the ons
34                    In contrast, all of these pulmonary injury and inflammatory parameters were increa
35 quelae that contributes to radiation-induced pulmonary injury and IPF.
36  in reduction (P</=.05) of organism-mediated pulmonary injury and of pulmonary infiltrates detected b
37             We examined the role of CXCR3 in pulmonary injury and repair in vivo.
38 plays a central role in free radical-induced pulmonary injury and repair.
39 conclusion, radiation- and bleomycin-induced pulmonary injury and respiratory death are ameliorated b
40 close correlation between the development of pulmonary injury and TNF-alpha levels in this model of s
41 events correlate with evidence of histologic pulmonary injury and underscore the role of adhesion mol
42  imaging manifestations of vaping-associated pulmonary injury, and the possibility of this condition
43 alveolar lavage fluid after asbestos-induced pulmonary injury, and this response is markedly enhanced
44    Host mediated damage is also a culprit in pulmonary injury as both innate and adaptive immune cell
45 ith metastatic breast cancer, mice developed pulmonary injury as early as 1 day posttransplant.
46                                              Pulmonary injury, as defined by an increase in bronchoal
47 y be a contributing factor to the upsurge in pulmonary injuries associated with using e-cigarette/vap
48 ective against permeability edema and remote pulmonary injury but not protective against histologic m
49      Arterial air emboli arising from severe pulmonary injury can cause ischaemic complications-espec
50            In murine intra-abdominal sepsis, pulmonary injury cannot be considered the etiology of de
51        Neurogenic vasoplegia exacerbates the pulmonary injury caused by brain death and primes the lu
52                                   Repetitive pulmonary injury causes fibrosis and inflammation that u
53 ve in a rat model of sepsis-induced indirect pulmonary injury (cecal ligation and puncture).
54 rtment exhibited increased survival and less pulmonary injury compared with the appropriate wild-type
55 at neutrophil extracellular traps exacerbate pulmonary injury during influenza pneumonia.
56 ic effects of extracellular histones in that pulmonary injury during influenza was exacerbated.
57 ICAM-1 after the induction of AP ameliorates pulmonary injury, even in the face of severe pancreatic
58 esolution of established neutrophil-mediated pulmonary injury evoked by intratracheal instillation or
59 pical signaling as a driver of host-mediated pulmonary injury following influenza infection.
60  several clinical disorders including direct pulmonary injury from pneumonia and aspiration as well a
61 pneumonia and aspiration as well as indirect pulmonary injury from trauma, sepsis, and other disorder
62      We have examined CD8(+) T cell-mediated pulmonary injury in a transgenic model in which adoptive
63 o be significant mediators of pancreatic and pulmonary injury in pancreatitis, and both the onset and
64 mphocytes (CTLs) produce lethal, progressive pulmonary injury in recipient mice expressing the viral
65     We have used the silica-induced model of pulmonary injury in the rat to study the pattern of coll
66 Ventilation of cadaver lungs with AG induces pulmonary injury in this model.
67 toxin challenge preserved HPV and attenuated pulmonary injury in wild-type mice but did not prevent t
68  acute absence of kidney function results in pulmonary injury independent of renal ischemia and highl
69                                              Pulmonary injury induced by isolated alpha-hemolysin or
70 on of oncogenic K-Ras in mouse lung elevated pulmonary injury, inflammation and tumorigenesis, but re
71 ocus on emphysema, based on the concept that pulmonary injury involves stages of initiation (by expos
72                         We hypothesized that pulmonary injury is associated with hepatic ischemia-rep
73 ting diseases such as human asthma, in which pulmonary injury is associated with the activity of IL-5
74            We also proposed that this remote pulmonary injury is attenuated through inactivation of c
75                      We conclude that remote pulmonary injury is significantly decreased by concomita
76                      We conclude that remote pulmonary injury is significantly influenced by the exte
77 es are complicated by the presence of severe pulmonary injury, massive blood loss, significant fluid
78 IAV, virus clearance, and the development of pulmonary injury, neutrophils can serve as APCs to anti-
79 CD4 T cells only, CD8 T cells only, or both, pulmonary injury occurs via different paths, depending o
80 .40; p = .02) and among subjects with direct pulmonary injury (OR, 1.75; 95% CI, 1.04-2.95; p = .04).
81 betes (ORadj 0.58, 95% CI 0.36-0.92), direct pulmonary injury (ORadj 3.78, 95% CI 2.45-5.81), hematol
82 eutic targets, since pancreatitis-associated pulmonary injury results in significant morbidity and is
83  bone marrow also confers protection against pulmonary injury, revealing that PPT-A gene expression i
84                       In different models of pulmonary injury, SOD3 is reduced; however, it is unclea
85 rugs do not directly inhibit immune-mediated pulmonary injury that is a significant component of dise
86 ld-type newborn mice resulted in significant pulmonary injury that was prevented by deletion of TLR4
87 ssing NY1DD mice with Rag1(-/-) mice reduced pulmonary injury that was restored by adoptive transfer
88 important chemotherapy and radiation-induced pulmonary injuries, the pathologic mechanisms, where kno
89  4-5 day course of the development of lethal pulmonary injury, the effector CTLs, while necessary for
90 domestic swine before and after induction of pulmonary injury, the ventilators for mild and moderate
91 f p38 mitogen activated kinase decreases the pulmonary injury through attenuated production of TNF-al
92                                              Pulmonary injury was assessed at 24 hrs by histology and
93                   Each of these variables of pulmonary injury was lessened in animals receiving CNI-1
94                               Pancreatic and pulmonary injury was quantitated by histology, measureme
95 ose-dependent manner, and the pancreatic and pulmonary injuries were much severer in HTG mice than no
96  pathways related to airway inflammation and pulmonary injury were enriched (FDR<0.05) among these pr
97 iratory distress syndrome (ARDS) is a severe pulmonary injury, which is associated with both ischemic
98 ntifying at-risk individuals with persistent pulmonary injury who may require intensive follow-up car