戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
1                                              SAE data were consistent with natalizumab's known safety
2                                              SAE was significantly associated with future CHD, stroke
3                                              SAE were defined as the occurrence of >=1 moderate, majo
4                                              SAE were more frequent in homograft conduit than other R
5                                              SAEs associated with hepatic decompensation were the mos
6                                              SAEs did not significantly affect QoL in emergency lapar
7                                              SAEs were also evident to drive recombination of intron-
8                                              SAEs were more common in patients with CKD 4/5, but all
9                                              SAEs were numerically more frequent in the rituximab gro
10 ed nuclear genes in both parental and rho(0) SAE cells in response to asbestos treatment.
11 l airway epithelial (SAE) cell model: rho(0) SAE cells lack the capacity to produce mitochondrial ROS
12 e effects of asbestos were minimal in rho(0) SAE cells.
13 d related to darapladib, was reported, and 1 SAE of severe diarrhea was reported in a placebo patient
14 recipients with prior HZ who developed >/= 1 SAE (0.95%) was not significantly different from that of
15      Sixteen patients (64%) experienced >/=1 SAE.
16 mary outcome measure was development of >/=1 SAE; secondary outcome measures were death, arteriothrom
17 mab was 1.06 [(0.84, 1.35); p=0.61] for >/=1 SAEs.
18 ght (80%) SOC participants had a total of 11 SAEs compared to 2 (20%) FMT participants with SAEs (bot
19                               A total of 143 SAEs occurred in 59 (10.6%) patients; only three events
20 anxiety and affective symptoms worsening (20 SAEs).
21 compensation were the most frequent, with 26 SAEs occurring in 19 patients (18%).
22           In the LASIK group, there were 287 SAEs (271 eyes of 226 patients; incidence of 0.4% or 1:2
23                                There were 29 SAEs considered to have some relationship with the injec
24                        However, only 2 of 36 SAEs were judged as definitely related to the convalesce
25  (23% of those entering the RCT) reported 39 SAEs.
26 baseline were associated with occurence of a SAE.
27  ciliated and basal cells, markedly abnormal SAE and alveolar macrophage transcriptomes, and elevated
28 re also able to produce S-adenosylethionine (SAE) from substrate ethionine.
29  years, the most frequent ocular serious AE (SAE) and AE were cataract (2.1%) and eye pain (14.6%), r
30 dverse events (AEs), and 1 had a serious AE (SAE).
31   Further, there were no ocular serious AEs (SAEs) and no cases of endophthalmitis.
32 e incidence of study eye ocular serious AEs (SAEs) and SAEs potentially related to systemic vascular
33                                 Serious AEs (SAEs) occurred infrequently.
34  day 42 postvaccination and for serious AEs (SAEs) through day 182 postvaccination.
35 nsolicited AEs for 29 days; and serious AEs (SAEs) throughout the study.
36 roups (90.9% versus 91.5%), but serious AEs (SAEs) were higher in the abatacept group (19.8 versus 6.
37                                 Serious AEs (SAEs) were recorded through 6 months postvaccination.
38 erse events (AEs) and number of serious AEs (SAEs) were similar across arms.
39 Es of special interest (AESIs), serious AEs (SAEs), and adverse drug reactions (ADRs) reported during
40 review of adverse events (AEs), serious AEs (SAEs), and new medical conditions for 6 months after FMT
41 rse events (AEs), and sometimes serious AEs (SAEs).
42  discontinuation or G/P-related serious AEs (SAEs).
43                      No related grade 3 AEs, SAEs, or grade 3 laboratory abnormalities occurred.
44 res were treatment-emergent AE (TEAE), AESI, SAE, and ADR occurrences.
45         Except in 1 patient with cancer, all SAEs resolved after appropriate treatment.
46 conduit than other RVOT substrates, although SAE type and severity differed between implant substrate
47                                     Although SAEs are likely to affect QoL, this has not been demonst
48  women were twice as likely to experience an SAE (OR for men, 0.50; P = .005).
49 up tended to be less likely to experience an SAE over the entire 25 months of the study.
50                                       AE and SAE occurred in 26% and 13% of cases, respectively, incl
51 is not associated with more side effects and SAE.
52 ors examined the prognostic value of LAE and SAE for clinical CVD events among 6,235 Multi-Ethnic Stu
53  cells; this can be replicated using LAE and SAE immortalized basal cell lines derived from healthy n
54                                      LAE and SAE were derived from diastolic pulse contour analysis.
55  for decision making between splenectomy and SAE (AUC, 0.84).
56 nal requirements (2 vs 6 PRBC; P = 0.08) and SAEs lower (15% vs. 47%; P = 0.077) in the esophageal st
57 ilar in both groups, and unsolicited AEs and SAEs were all unrelated to the study vaccines.
58 ystemic reactions, adverse events (AEs), and SAEs were similar in both groups, and unsolicited AEs an
59    There was no correlation between dose and SAEs in any group.
60 e of study eye ocular serious AEs (SAEs) and SAEs potentially related to systemic vascular endothelia
61 ing B cells were isolated and yielded 6 anti-SAE clones, 2 each for SEA, SED, and SEE.
62 scribed in adult-onset dermatomyositis (anti-SAE autoantibodies) and juvenile dermatomyositis (anti-p
63 ew period, the clinical associations of anti-SAE and anti-p140 have been further described.
64 ps in which nearly all patients express anti-SAEs.
65 rtisol concentration (AP-SBE: p = 0.0017, AP-SAE: p = 0.0102).
66 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with
67           Twenty-nine AEs were classified as SAEs and mainly related to immune conditions.
68     No dose-related toxicity or attributable SAEs at the 1-year follow-up were observed.
69 ficients for correlation between model-based SAEs and American Community Survey direct estimates of n
70                              The model-based SAEs and direct survey estimates of COPD prevalence were
71 ficients for correlation between model-based SAEs and Missouri County-Level Study direct estimates fo
72 egression and poststratification model-based SAEs using single-year Behavioral Risk Factor Surveillan
73          Unweighted and weighted model-based SAEs were compared with direct estimates; unweighted mod
74                       Aggregated model-based SAEs were consistent with national prevalence estimates
75                                  Model-based SAEs were validated against national estimates directly
76  1 score, the mean difference in QoL between SAE and no-SAE patients was 0.140 in esophagectomy, 0.11
77              A novel method was developed by SAE-DLLME for chromium speciation in water and rice samp
78                              The most common SAE reported was either conjunctival erosion or dehiscen
79 ired supplemental oxygen was the most common SAE.
80                               In conclusion, SAEs after donation are rare but more often occurred in
81 t positive correlations between AP cortisol, SAE cortisol, K10 scores, and fat intake among female pa
82 ng ED patients with syncope who had a 30-day SAE, this blood test added little new information to the
83 2 (10.5% [95% CI, 9.0% to 12.1%]) had 30-day SAEs, 57 (3.9%) of which were identified after the index
84   An adjudicated composite outcome of 30-day SAEs, including death and cardiac (arrhythmic and nonarr
85 es assessed the combined effect of different SAEs.
86 sm of initiation of neuroinflammation during SAE, which ultimately leads to delirium and cognitive dy
87 g and driving acute neuroinflammation during SAE.
88 lasticity (LAE) and small artery elasticity (SAE) may predict cardiovascular disease (CVD) events bey
89  1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less
90           The most common treatment-emergent SAEs included dyspnea, pneumonia, febrile neutropenia, d
91 ociated with low rates of treatment-emergent SAEs, including immunologic reactions.
92      There were no 30-day treatment-emergent SAEs.
93            Sepsis-associated encephalopathy (SAE) is an acutely progressing brain dysfunction induced
94 e use of AAVE vs. Standard American English (SAE) is important for policy and scientific reasons.
95  against Staphylococcus aureus enterotoxins (SAEs).
96 AE2 subunit of human SUMO activation enzyme (SAE) underwent rapid nucleocytoplasmic shuttling and its
97           Surface-active artificial enzymes (SAEs) are designed and constructed by a general and nove
98 epithelia (LAE), and small airway epithelia (SAE) of nonsmokers and smokers were analyzed for express
99 g fluid metabolome, small airway epithelial (SAE) cell differential and transcriptome, alveolar macro
100 eted (rho(0)) human small airway epithelial (SAE) cell model: rho(0) SAE cells lack the capacity to p
101 ia of smoke-treated small airway epithelial (SAE) cells, respectively.
102 y disease (COPD), a small airway epithelial (SAE) disorder that is a risk factor for non-small cell l
103                 The small airway epithelium (SAE), the first site of smoking-induced lung pathology,
104 mpounds, a Sharpless asymmetric epoxidation (SAE) route yielded in a direct fashion the required comp
105                   Such small area estimates (SAEs) often lack rigorous external validation.
106 y flexible to generate small-area estimates (SAEs) to meet data needs at different geographic levels.
107 tes by using a novel, small area estimation (SAE) method.
108 is of the SAM analog S-adenosyl-l-ethionine (SAE) and show SAE is a mechanistically-equivalent SAM-al
109 t was the only ocular serious adverse event (SAE) that occurred.
110                   One serious adverse event (SAE) that resulted in death was potentially related to t
111 3.5%) experienced >=1 serious adverse event (SAE), with infection the most common (4.1%).
112 of individuals with a serious adverse event (SAE); of these, 33 (87%) reported more SAEs in ClinicalT
113 a risk of procedural serious adverse events (SAE) and exposure to ionizing radiation.
114 ne were followed for serious adverse events (SAE) for 28 days after vaccination.
115 of treatment-related serious adverse events (SAE) than patients randomized to standard BP control (<1
116  incidence of AE and serious adverse events (SAE) was calculated.
117           IS-related serious adverse events (SAE) were reported in 47% of patients, with 4 presenting
118 s, rates of systemic serious adverse events (SAEs) after anti-VEGF treatment have been low.
119 ividuals at risk for serious adverse events (SAEs) after exposure to ivermectin, using thresholds of
120  density can develop serious adverse events (SAEs) after ivermectin treatment.
121 ncidence of systemic serious adverse events (SAEs) among patients with neovascular age-related macula
122 cluded the number of serious adverse events (SAEs) and quantification of viral RNA in blood.
123                     Surgical adverse events (SAEs) are associated with poor outcome.
124 onversion rates, and serious adverse events (SAEs) during treatment.
125  vaccine causes rare serious adverse events (SAEs) following immunization.
126 the risk of systemic serious adverse events (SAEs) in patients receiving anti-VEGF for DME compared w
127  disease and vaccine serious adverse events (SAEs) may be imprecise.
128         Overall, 123 serious adverse events (SAEs) occurred in 49 patients (47%).
129                      Serious adverse events (SAEs) occurred with similar frequency in treated versus
130             No ocular severe adverse events (SAEs) or SAEs considered related to darapladib were repo
131 and 210, adverse and serious adverse events (SAEs) to Study Day 210.
132 mptomatic dengue and serious adverse events (SAEs) up to Month 36 in both parts.
133 ps, the incidence of serious adverse events (SAEs) was 10.1% and 9.1%, respectively, and the rate of
134                       Severe adverse events (SAEs) were also distributed equally over both treatment
135                   No serious adverse events (SAEs) were attributable to study drug, as determined by
136  rate, and number of Serious Adverse Events (SAEs) were compared.
137    The frequencies of severe adverse events (SAEs) were higher in the bevacizumab arm (n = 63) compar
138                      Serious adverse events (SAEs) were more common in CTP class B/C versus CTP class
139                      Serious adverse events (SAEs) were more common in the renal dysfunction groups t
140                      Serious adverse events (SAEs) were reported in 2 rituximab-treated patients (pne
141  were predefined and serious adverse events (SAEs) were reported to ethics committees and a central s
142  FDA definitions for serious adverse events (SAEs) were used, and all events were reviewed by an inde
143        There were 15 serious adverse events (SAEs) with a non-significantly higher percentage occurri
144 ients with 1 or more serious adverse events (SAEs) within 90 days (multiplicity-adjusted thresholds f
145 ited/unsolicited and serious adverse events (SAEs), biochemical/hematological parameters, cell-mediat
146 d treatment-emergent serious adverse events (SAEs), five of whom had immune-related SAEs, including t
147 The incidence of all serious adverse events (SAEs), including mortality rate (0.3%), in the first 4 h
148 rse events (AEs) and serious adverse events (SAEs), including one patient death.
149 ed the incidences of serious adverse events (SAEs), medically important infections (MIIs), and death.
150 at 3 months were all serious adverse events (SAEs), SAEs related to implant placement or removal, SAE
151 ify risk factors for serious adverse events (SAEs), thereby limiting their influence on sedation prac
152 rily vaccine-related serious adverse events (SAEs)--up to 3 months after administration of a single d
153 OC using FMT-related serious adverse events (SAEs).
154 bleeding and without serious adverse events (SAEs).
155 subjects (29.0%) had serious adverse events (SAEs).
156 nts did not have any serious adverse events (SAEs).
157 d treatment-emergent serious adverse events (SAEs).
158        There were 39 serious adverse events (SAEs); SAEs believed to be directly related to IUC use (
159 2-months for safety (serious adverse events [SAE]), and efficacy endpoints: ejection fraction, Minnes
160 irty-nine episodes of serious-adverse-events(SAEs) were reported among 30(43%) patients, including fi
161 gram (CARSEP) V Self-assessment Examination (SAE) from 1997 to 2002 were scored and analyzed, includi
162                                  We examined SAE gene expression in 178 individuals, including health
163                 Four outcomes were examined: SAEs, significant interventions performed in response to
164 e exercise (SBE), and saliva after exercise (SAE) cortisol concentration (AP-SBE: p = 0.0017, AP-SAE:
165 re subjects in the placebo group experienced SAEs (P = .02).
166  (9.2%) in the ranibizumab group experienced SAEs.
167 lated in adenocarcinoma versus smoke-exposed SAE.
168 t outcomes, resulting in significantly fewer SAEs and interventions than ketamine combined with propo
169 , BM donors maintained an increased risk for SAEs (0.99% for BM vs 0.31% for PBSC; OR, 3.20; P < .001
170          BM donors had an increased risk for SAEs (2.38% for BM vs 0.56% for PBSC; odds ratio [OR], 4
171 ients) and a mean 2.2+/-1.2% higher risk for SAEs (range, 0.5%-15.8% more harm in individual patients
172       OAE, whose potency did not differ from SAE, protected ROS-exposed Caco2 cells against oxidative
173 ared with nonsmokers, and whether changes in SAE DNA methylation were linked to the transcriptional o
174 re found to associate with its expression in SAE.
175 r any CVD per standard-deviation increase in SAE was 0.71 (95% confidence interval: 0.61, 0.83; P < 0
176 04 unique genes differentially methylated in SAE DNA of smokers compared with nonsmokers, with 67% of
177 se in nuclear DNA oxidative damage and MN in SAE cells.
178 aB and proinflammatory signaling pathways in SAE cells.
179 was no statistically significant increase in SAEs in the pooled groups receiving ibuprofen alone vs w
180 ected individuals at risk of post-ivermectin SAEs in West and Central Africa from 1995 to 2025.
181 ageal stents have greater efficacy with less SAEs than balloon tamponade in the control of EVB in tre
182 ck population to generate census-block-level SAEs of COPD prevalence which could be conveniently aggr
183 as identified the mechanism used to localize SAE to the nucleus.
184 omatic participants free of overt CVD, lower SAE added prognostic information for CVD, CHD, stroke, a
185 uria was significantly associated with lower SAE: relative difference = -6% (95% CI: -10, -1).
186 n C were incrementally associated with lower SAE: third quintile relative difference = -5% (95% confi
187 lTrials.gov, 11 publications did not mention SAEs, 5 reported them as zero or not occurring, and 21 r
188 p-nitrophenolate catalyzed by esterase-mimic SAE.
189                                 Twelve-month SAE incidence was 28.2% with allo-hMSCs versus 63.5% wit
190 ent lower response rates and experience more SAEs.
191 vent (SAE); of these, 33 (87%) reported more SAEs in ClinicalTrials.gov.
192                                         Most SAEs were single, disease-related events occurring durin
193 of SAEs was very low, and the nature of most SAEs was manageable, demonstrating a low-risk safety pro
194                                           No SAEs occurred in the study eye.
195                                           No SAEs were reported.
196                                  Notably, no SAEs related to icatibant occurred in patients with card
197                                There were no SAEs clearly related to methylprednisolone administratio
198                                There were no SAEs related to FMT.
199 ary artery occlusion), whereas there were no SAEs reported in placebo-treated patients.
200 he mean difference in QoL between SAE and no-SAE patients was 0.140 in esophagectomy, 0.110 in the Cr
201                   The incidence of nonocular SAEs was 8.8% in the IAI group and 9.8% in the laser gro
202 phthalmitis, and the incidences of nonocular SAEs were low.
203    Using genome-wide methylation analysis of SAE DNA of nonsmokers and smokers, the data identified 2
204    We aimed to study the molecular events of SAE to capture its onset and progression into the centra
205 Importantly, we observed a high frequency of SAE in triple therapy, especially in patients with liver
206                             The incidence of SAE during TPVR in the C3PO-QI registry is high, but mor
207                                Photolysis of SAE bound to HydG forms an ethyl radical trapped in the
208 d intermediate cells, reduced proportions of SAE ciliated and basal cells, markedly abnormal SAE and
209 metabolome profile, increased proportions of SAE secretory and intermediate cells, reduced proportion
210 .90; P = 0.12 for difference), regardless of SAE subgroup or whether the SAE was identified after the
211                         The relative risk of SAE was 1.44 (97.5% CI, 0.79 to 2.64; P = .18).
212  lower in the bevacizumab arm (60% vs 75% of SAEs).
213 story of HZ (0.66%), and the distribution of SAEs in the 2 groups was comparable.
214            Significantly negative effects of SAEs on QoL were demonstrated in a range of procedures.
215                             The frequency of SAEs was 5% to 48%.
216                     The overall frequency of SAEs was very low, and the nature of most SAEs was manag
217 be a surrogate for the severity of impact of SAEs on patients.
218                        The overall impact of SAEs on QoL scores was determined by combining results f
219 evaluate the economic and societal impact of SAEs thereby defining the threshold for safe practice.
220 de alone resulted in the lowest incidence of SAEs (17 [0.4%]) and significant interventions (37 [0.9%
221                      The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3%
222 5% CI, 2.3-8.7) had the highest incidence of SAEs.
223 e promise to help elucidate the mechanism of SAEs.
224 ce of 0.4% or 1:228 eyes), and the number of SAEs in PRK group was 65 (65 eyes of 39 patients; incide
225 68% versus 55%; P = 0.30), but the number of SAEs per patient was higher in the treated group (2.7 ve
226 rring, and 21 reported a different number of SAEs.
227      A time-to-event analysis of patterns of SAEs indicated that subjects in the periodontal therapy
228  allowed adjustment for strong predictors of SAEs.
229                          The overall rate of SAEs (0.12 per patient-year) did not increase with long-
230                        The increased rate of SAEs requires further assessment.
231  with long-term use of ranibizumab; rates of SAEs potentially related to treatment were consistent wi
232 nchocerciasis in 2025 while being at risk of SAEs, justifying continued efforts in research and devel
233              At present, the mechanism(s) of SAEs is(are) poorly understood but our advances in under
234                   Individual patient data on SAEs, assigned drug and dosing regimen, and baseline pro
235                                          One SAE of myocardial infarction, not considered related to
236                                   Twenty-one SAEs and 2 deaths were reported, all assessed by investi
237    There were no differences in mortality or SAEs between the intervention group (n=536) and the sham
238    No ocular severe adverse events (SAEs) or SAEs considered related to darapladib were reported.
239                                      Overall SAE rates were 23.09 (control) and 20.80 (IAI); overall
240 multilevel regression and poststratification SAEs from 2011 Behavioral Risk Factor Surveillance Syste
241  the same catalytic site to form the product SAE.
242 to SAEs and determine whether they recognize SAEs through their complementarity-determining regions (
243  338 patients (3.6%) had a treatment-related SAE during a median follow-up of 3.3 years.
244 risk for MACE or death and treatment-related SAE to allow for individualized BP treatment goals based
245 overdoses accounted for 25 of the 29 related SAEs.
246 ents (SAEs), five of whom had immune-related SAEs, including two with adrenal insufficiency, two with
247 there were 25 reported incidences of related SAEs, including mortality (n = 4), transfusion-associate
248                           No product-related SAEs were observed.
249 isk factors associated with sedation-related SAEs.
250                           No vaccine-related SAEs occurred during the 3 months of follow-up of 4004 s
251  compared to placebo, and no vaccine-related SAEs or deaths.
252                           No vaccine-related SAEs were reported.
253 national health surveys to generate reliable SAEs for population health outcomes at all administrativ
254 AEs related to implant placement or removal, SAEs related to stimulation, neurological deterioration,
255                           Of the 36 reported SAEs, there were 25 reported incidences of related SAEs,
256            Among the 84 trials that reported SAEs in ClinicalTrials.gov, 11 publications did not ment
257         The proportion of subjects reporting SAEs occurring within 42 days postvaccination (ZV, 0.6%;
258 nths were all serious adverse events (SAEs), SAEs related to implant placement or removal, SAEs relat
259 There were 39 serious adverse events (SAEs); SAEs believed to be directly related to IUC use (n = 7)
260                                 Thirty-seven SAE-specific, IgG- or IgA-expressing B cells were isolat
261 ueous extracts of onions (OAE) and shallots (SAE) were evaluated for their antioxidant and cytoprotec
262 analog S-adenosyl-l-ethionine (SAE) and show SAE is a mechanistically-equivalent SAM-alternative for
263 red to females (p = 0.0559), and significant SAE cortisol concentration differences were also recorde
264  A, SED, and SEE were used to isolate single SAE-specific B cells from the nasal polyps of 3 patients
265 tion rate (GFR), and albuminuria with small (SAE) and large (LAE) arterial elasticity and aortic dist
266 gG1, and those of high affinity for specific SAEs, assayed by means of ELISA and surface plasmon reso
267                        The lowest (stiffest) SAE quartile had a hazard ratio of 2.28 (95% confidence
268 g postoperative QoL in patients who suffered SAEs were identified.
269                        These results suggest SAEs as a common driver in recombination of intron-lacki
270            The rates of all primary systemic SAE outcomes were similar after treatment with anti-VEGF
271 kens, in which speakers use AAVE rather than SAE speech features.
272                                 We show that SAE occupies the active site in a manner similar to SAMe
273                    Our findings suggest that SAEs are responsible for recombination and elevated dive
274                                          The SAE method used age, race, gender, smoking, and poverty
275 eline systolic BP, and diastolic BP, and the SAE model had 8 variables including treatment interactio
276                       The MACE/death and the SAE model had C statistics of 0.72 and 0.70, respectivel
277 l stimuli in a rapid manner, we assessed the SAE of smokers for genome-wide DNA methylation changes c
278 iliated cells; 3) ACE2 is upregulated in the SAE by smoking, significantly in men; 4) levels of miR-1
279       Because the expression of genes in the SAE cell line was prerequisite for their identification,
280 ould play a role in ACE2 upregulation in the SAE of smokers; and 5) ACE2 is expressed in airway epith
281  with lower expression in the SAE; 2) in the SAE, ACE2 is expressed in basal, intermediate, club, muc
282 rachea and LAE, with lower expression in the SAE; 2) in the SAE, ACE2 is expressed in basal, intermed
283 alters the DNA methylation patterning of the SAE and that, for some genes, these changes are associat
284              The applied KF component of the SAE was more difficult than the factual MCQ component (0
285 plied (9 KF cases) knowledge portions of the SAE, and the effect of examination preparation, examinat
286 ), regardless of SAE subgroup or whether the SAE was identified after the index ED visit.
287                                        These SAEs can simultaneously stabilize Pickering emulsions an
288                                     Thirteen SAEs were reported in relation to collection of IS, or 0
289 the percentages of death or life-threatening SAEs were lower in the bevacizumab arm (60% vs 75% of SA
290  to AEs was 3.5% and discontinuations due to SAEs was 1.3%, while in patients treated with SC adalimu
291 e aimed to understand antibodies reactive to SAEs and determine whether they recognize SAEs through t
292                      Four patients underwent SAE after unsuccessful observation.
293 ormation about risk of YF disease vs vaccine SAEs.
294 ived unsuccessful nonsurgical treatment with SAE.
295 Es compared to 2 (20%) FMT participants with SAEs (both FMT unrelated; P = 0.02).
296 e correctly reclassified 3% of patients with SAEs at the expense of incorrectly reclassifying 2% of p
297              The proportion of patients with SAEs in groups receiving IBU was 15%, and in the PCM-alo
298 ere significantly higher among patients with SAEs than those without them (median, 626.5 ng/L vs. 81
299 o define the risk of, and associations with, SAE and high-dose radiation exposure using large-scale r
300 rrectly reclassifying 2% of patients without SAEs.

 
Page Top