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1 Components of e-cigarette aerosol have known pulmonary toxicity.
2 0), which was related to greater cardiac and pulmonary toxicity.
3 thereby, improve its efficacy and reduce its pulmonary toxicity.
4 outcomes, including severe hypoglycaemia and pulmonary toxicity.
5  major susceptibility gene for ozone-induced pulmonary toxicity.
6 4% of patients; there were three deaths from pulmonary toxicity.
7 ematurely due to a high rate of grade 4 to 5 pulmonary toxicity.
8 ter experimental infarction without apparent pulmonary toxicity.
9                     There was one late fatal pulmonary toxicity.
10 monary toxicity, and one patient had grade 2 pulmonary toxicity.
11 ctively), and mean lung dose correlated with pulmonary toxicity.
12 an be associated with clinically significant pulmonary toxicity.
13  = 4 acute esophagitis and/or grade > or = 3 pulmonary toxicity.
14 quiring steroids (64%), but no deaths due to pulmonary toxicity.
15 either sensitive nor specific for diagnosing pulmonary toxicity.
16  but were discontinued due to a high rate of pulmonary toxicity.
17 ll-tolerated with no evidence of significant pulmonary toxicity.
18 t be explained by misdiagnosis of persisting pulmonary toxicity.
19 ionship between micro- or nanoparticles with pulmonary toxicity.
20  in grade 4 esophageal and grade 3 or higher pulmonary toxicities.
21 othyroidism (6%), hyperthyroidism (0.9%-2%), pulmonary toxicity (1%-17%), peripheral neuropathy (0.3%
22 epatic venoocclusive disease (VOD) (5%), and pulmonary toxicity (4%).
23 ry, we postulated that it might also mediate pulmonary toxicity after IL-2 administration.
24 e neurodegeneration exacerbates ototoxicity, pulmonary toxicity and autophagy-based cellular defects.
25 er elucidate the molecular mechanism causing pulmonary toxicity and determine a dose-response curve.
26 x 10(12) vp, one patient experienced grade 4 pulmonary toxicity, and one patient died 25 days after h
27      Five patients (13.9%) had grades 3 to 5 pulmonary toxicity, and one patient had grade 2 pulmonar
28         Risk factors predictive of bleomycin pulmonary toxicity are proposed.
29 egies to lower graft failure and hepatic and pulmonary toxicity are urgently needed.
30    However, because of the high incidence of pulmonary toxicity associated with this schedule of pacl
31        In patients who do not die from acute pulmonary toxicity, both OS and PFS seem equal, despite
32                                    Bleomycin pulmonary toxicity (BPT) has been well described in Hodg
33  The role of TNFalpha in the exacerbation of pulmonary toxicity caused by LPS injection and in the ev
34 d to endocrine and reproductive dysfunction, pulmonary toxicity, cerebrovascular injury, neurologic a
35  thoracic radiotherapy had treatment-related pulmonary toxicity compared with one (1%) of those witho
36                      Prolonged cytopenia and pulmonary toxicity each occurred in three of eight patie
37 olid tumors, we observed two cases of severe pulmonary toxicity following intravenous infusion of thi
38                     There was no evidence of pulmonary toxicity from the therapy, with no differences
39                                     Although pulmonary toxicity from these drugs has occasionally bee
40                                              Pulmonary toxicity has recently been recognized as a pot
41 nt cases, 43 patients with sirolimus-induced pulmonary toxicity have now been reported.
42 h-dose BEAM alone, and included grade 3 or 4 pulmonary toxicity in 10 patients.
43 nefits of screening for long-term cardiac or pulmonary toxicity in asymptomatic cancer survivors who
44 l neuropathy, hematological dysfunction, and pulmonary toxicity in cancer patients.
45             No mortality was attributable to pulmonary toxicity in either group.
46                             Hyperoxia causes pulmonary toxicity in part by injuring alveolar epitheli
47       We aimed to assess disease control and pulmonary toxicity in patients who previously received r
48 atients because of a concerning incidence of pulmonary toxicity in the first 24 patients.
49 ression-free survival, overall survival, and pulmonary toxicity in the intention-to-treat population.
50 arone can be safely used, with an acceptable pulmonary toxicity, in patients with heart failure.
51                         Groupings paralleled pulmonary toxicity markers, though they were better subs
52 g-term toxicities, including cardiomyopathy, pulmonary toxicity, myelodysplastic syndromes (MDS), and
53              Other long-term effects include pulmonary toxicity, nephrotoxicity, neurotoxicity, decre
54                                              Pulmonary toxicity occurred in 10% of patients.
55                          Late grade > or = 3 pulmonary toxicity occurred in 17%.
56 aclitaxel dose of 175 mg/m(2), dose-limiting pulmonary toxicity occurred in only one patient at flavo
57 o 135 mg/m(2), dose-limiting neutropenia and pulmonary toxicity occurred when flavopiridol was escala
58                                          The pulmonary toxicity of cationic lipid is dose-dependent.
59                                              Pulmonary toxicity of CTL infusion was seen in 3 patient
60 sis was to identify the clinical spectrum of pulmonary toxicity of cyclophosphamide.
61 tion of TNF-alpha inhibitors in treating the pulmonary toxicity of IL-2 immunotherapy.
62  terms of their potential for explaining the pulmonary toxicity of monocrotaline.
63 as seen, though children with DS had greater pulmonary toxicity (P <.01) during induction and mucosit
64 anisms by which pertussis toxin (PTX) exerts pulmonary toxicity remain unknown, but may involve its a
65  For patients with germ cell cancer, various pulmonary toxicity risk factors have been hypothesized f
66 d after treatment with BEP to disclose valid pulmonary toxicity risk factors.
67 nce on the incidence of long-term cardiac or pulmonary toxicity secondary to chemotherapy, radiothera
68  syndrome (IPS), we propose the term delayed pulmonary toxicity syndrome (DPTS) to better describe th
69      Previously, we have described a delayed pulmonary toxicity syndrome (DPTS) which characterizes t
70 at has stronger anticancer activity and less pulmonary toxicity than bleomycin (BLM).
71 re life-threatening or fatal neutropenia and pulmonary toxicity than the sequential MOPP-ABVD arm, wh
72 t three cases of suspected sirolimus-induced pulmonary toxicity that occurred in three renal transpla
73              ABVD chemotherapy induced acute pulmonary toxicity that required bleomycin dose modifica
74       For patients who received steroids for pulmonary toxicity, there was a subsequent improvement i
75       We report the first documented case of pulmonary toxicity to mycophenolate mofetil in this arti
76 eived thoracic radiotherapy had any recorded pulmonary toxicity versus 29 (40%) of 73 patients with n
77 quency of grade 3 or worse treatment-related pulmonary toxicities was similar (one patient in each gr
78                                              Pulmonary toxicity was assessed in mice exposed by oroph
79                   In this study, CNT-induced pulmonary toxicity was investigated by exposing BALB/c m
80        The diagnosis of sirolimus-associated pulmonary toxicity was made after an exhaustive work-up
81                               Grade > or = 3 pulmonary toxicity was not seen in any of these 24 patie
82             A trend toward increased odds of pulmonary toxicity was noted (OR 2.0, 95% CI 0.9 to 5.3)
83 ere adverse events, including esophageal and pulmonary toxicity, was similar on both arms.
84                      Side effects other than pulmonary toxicity were common, and included skin rash (
85  radiation or chemotherapies associated with pulmonary toxicity were not associated with increased ri
86                         Disease response and pulmonary toxicity were prospectively assessed by Immune
87 rsistent, non-resolvable dermal, ocular, and pulmonary toxicities, which led to early termination of
88                   There was no difference in pulmonary toxicity, with grade >=3 AEs in 20.6% and 19.3