ライフサイエンスコーパス: CRS

1 CRS 3 also predicted sensitivity to first-line platinum

2 CRS accurately predicted HCC recurrence beyond MC in thi

3 CRS cases were categorized into four unique subgroups ba

4 CRS developed in 70% of patients, including 62.5% with g

5 CRS is a highly prevalent and heterogeneous condition.

6 CRS is associated with elevated circulating levels of se

7 CRS is the most common type of toxicity caused by CAR T

8 CRS was calculated by assigning 1 point each for initial

9 CRS was well validated in that all 3 factors remained in

10 CRS-207, live-attenuated Listeria monocytogenes-expressi

11 About 30,000 CRS regions are located near coding or long noncoding RN

12 recurrence risk beyond MC, ranging from 19% (CRS 0) to 67% (CRS 3) at 5 years.

13 patients, including 62.5% with grade 1 to 3 CRS (grade 1, 26%; grade 2, 32%; grade 3, 4.5%), 3.8% wi

14 A majority of cases of grade >/=4 CRS occurred during CAR T-cell dose finding.

15 ate-to-severe tricuspid regurgitation in 5/6 CRS type II patients.

16 beyond MC, ranging from 19% (CRS 0) to 67% (CRS 3) at 5 years.

17 A CRS symptom questionnaire was mailed to 23 700 primary c

18 Adult CRS patients (n = 560) who had undergone bilateral FESS

19 In WT mice after CRS and in unstressed mice with a BDNF loss-of-function

20 Morbidity after CRS remains significant, but standardized management fac

21 idity and mortality remain significant after CRS for PC.

22 riables to be associated with survival after CRS and HIPEC, but no definitive analysis has been made

23 ological variables on overall survival after CRS and HIPEC.

24 ognostic variables on overall survival after CRS and HIPEC.

25 alyses to characterize clinical efficacy and CRS severity associated with CTL019 therapy.

26 Heterologous prime/boost with Cy/GVAX and CRS-207 extended survival for patients with pancreatic c

27 tested prime/boost vaccination with GVAX and CRS-207 in pancreatic adenocarcinoma.

28 NS), leading to rapid resolution of GVHD and CRS.

29 rtant roles in homeostasis and immunity, and CRS significantly impairs these normal functions.

30 below 1 case per 10,000,000 population, and CRS incidence has been below 1 case per 5,000,000 births

31 Annual numbers of measles, rubella, and CRS cases, by importation status, outbreak size, and dis

32 elimination of endemic measles, rubella, and CRS had been sustained.

33 ld be reserved for neurologic toxicities and CRS not responsive to tocilizumab.

34 nding of airway remodelling processes in AR, CRS and asthma and presents mechanisms both shared and d

35 Four landrace carrots ("Becaria", "CRS", "Gonzalez" and "Rodriguez") and two marketable cul

36 Behaviorally, CRS significantly impeded spatial learning but enhanced

37 hology of patients with graft loss caused by CRS between 2006 and 2011 at our center.

38 ion of death-censored graft losses caused by CRS was 4.6% (7/152 patients).

39 entified seven cases of graft loss caused by CRS, six cases of CRS type II, and one case of CRS type

40 ent patterns of association with diseases by CRS phenotype may be due to CRSwNP sample size limitatio

41 Most genes increased by CRS were decreased after recovery but many remained alte

42 ese comorbidities cause CRS, are promoted by CRS, or share a systemic disease process with CRS.

43 not known whether these comorbidities cause CRS, are promoted by CRS, or share a systemic disease pr

44 Because respiratory-system compliance (CRS) is strongly related to the volume of aerated remain

45 study participants, 1,850 (24%) had current CRS symptoms, 1,765 (23%) had migraine headache, and 1,9

46 t, after prolonged (6 h per day for 21 days) CRS, mice show decreased hippocampal NF-alpha1 and FGF2

47 etion in patients who subsequently developed CRS.

48 8.5+/-4.1%) were allocated to receive either CRS (n=100) or (+)GRS (n=103).

49 uidelines for treating patients experiencing CRS and other adverse events following CAR T-cell therap

50 asthma improve after ESS, yet there are few CRS-specific factors associated with asthma QOL or contr

51 e response in patients with cystic fibrosis, CRS without nasal polyps, or CRS with nasal polyps.

52 pikes within a burst was prolonged following CRS.

53 for CRS plus migraine, 1.88 (1.08, 3.25) for CRS plus fatigue, 1.95 (1.18, 3.21) for migraine plus fa

54 est were [OR (95% CI)] 1.49 (0.78, 2.85) for CRS plus migraine, 1.88 (1.08, 3.25) for CRS plus fatigu

55 ound that 11.9% of patients met criteria for CRS.

56 ach was used to estimate cost of illness for CRS from the 2011 Medical Expenditure Panel Survey datab

57 ct of specific therapeutic interventions for CRS.

58 We identified 1 study for DBS, 1 study for CRS and 4 studies for VNS.

59 mains the mainstay pharmacologic therapy for CRS, though indications for administration vary among ce

60 late these into more effective treatment for CRS.

61 behavior in both the naive and recovery from CRS conditions, but not in mice 24h subsequent to their

62 the content of beta-carotene extracted from "CRS" and Brasilia (29% and 75%) and decreased the conten

63 the content of beta-carotene extracted from "CRS" by 23% in "Rodriguez." In addition, steaming caused

64 Furthermore, CRS mice treated with LAC show resilience of the CRS-ind

65 Future CRS PROMs will need to incorporate clinical domains that

66 tablish classification rules for identifying CRS in school-aged children, using laboratory biomarkers

67 ere, we characterize the ILC2 compartment in CRS by investigating the correlations between ILC2s, Th2

68 However, the presence of DCs in CRS, especially in nasal polyps (NPs), has not been exte

69 es and could be associated with dysbiosis in CRS.

70 s, Th2 cells and Th2 cytokines expression in CRS patients.

71 the complex upper respiratory microbiome in CRS in comparison with healthy controls.

72 of ILC2s in coordinating the Th2 response in CRS remains to be elucidated.

73 this study was to characterize DC subsets in CRS.

74 g to higher disease control are warranted in CRS care.

75 is a great need for continued research into CRS that could facilitate the development of novel thera

76 hilst remodelling changes in AR are limited, CRS phenotypes demonstrate epithelial hyperplasia, incre

77 or additional study, given the dose-limiting CRS at higher doses and pharmacodynamic activity at lowe

78 The mean CRS-specific annual expenditure was $5955 (95% CI, $5087

79 isteria monocytogenes-expressing mesothelin (CRS-207, JNJ-64041757), and chimeric antigen receptor T-

80 ze of 5 mm or less (P < .001), high modified CRS (P = .009), male sex (P = .03), and no history of pr

81 ater than 30 ng/mL (P = .003), high modified CRS (P = .02), and extrahepatic disease (EHD) (P < .001)

82 d that a substantial fraction of human-mouse CRS regions (1) colocalize consistently with binding sit

83 ts with CRS without polyposis, and three non-CRS controls.

84 the EV portion of samples, compared with non-CRS samples.

85 novel EPOS control criteria, at least 40% of CRS patients are uncontrolled at 3-5 years after FESS.

86 About 19.5% of CRS patients were well controlled, with 36.8% of patient

87 aft recipient, who lost his graft because of CRS, we systematically investigated the frequency, the c

88 cations for screening guidelines and care of CRS patients.

89 Case Report: We present a case of CRS in a foetus of a non-diabetic mother and discuss the

90 S, six cases of CRS type II, and one case of CRS type I.

91 es of graft loss caused by CRS, six cases of CRS type II, and one case of CRS type I.

92 tissue-deforming processes characteristic of CRS.

93 to determine the direct health care costs of CRS from the perspective of the US government.

94 To study the degree of CRS control using novel EPOS control criteria at 3-5 yea

95 We propose that the diagnosis of CRS after renal transplantation should be based on the f

96 Early diagnosis of CRS is important for appropriate management.

97 ease within 5 years after a new diagnosis of CRS with nasal polyps (CRSwNP) and without nasal polyps

98 o doses of Cy/GVAX followed by four doses of CRS-207 (arm A) or six doses of Cy/GVAX (arm B) every 3

99 enhanced resilience, opposing the effects of CRS, as shown by an increased social interaction and red

100 Three days before the end of CRS, treatment with the putative, rapidly acting antidep

101 o which these changes last beyond the end of CRS.

102 ing the distinct phenotypes and endotypes of CRS affects prognosis and, most importantly, is necessar

103 logical changes during acute exacerbation of CRS may provide valuable clues to the pathogenesis and p

104 One form of CRS with polyps found worldwide is driven by the cytokin

105 The two main forms of CRS that have been long recognized, with and without nas

106 ponses, is a common feature of many forms of CRS.

107 rior studies have not examined the impact of CRS or endoscopic sinus surgery (ESS) upon asthma qualit

108 volve, and identification of the kinetics of CRS and predictive clinical and laboratory biomarkers of

109 Pathogenic mechanisms of CRS have recently become the focus of intense investigat

110 sought to examine the resident microbiota of CRS subtypes and determine whether bacterial diversity i

111 urden of disease estimates and monitoring of CRS control programs.

112 the presence of SCVs in sinonasal mucosa of CRS patients and whether the phenomenon of phenotype swi

113 INTERPRETATION: The number of CRS-R assessments has an impact on the clinical diagnosi

114 The odds of CRS was higher among patients who were white, younger, s

115 hree doses (two doses of Cy/GVAX plus one of CRS-207 or three of Cy/GVAX), OS was 9.7 versus 4.6 mont

116 l mucosa and medical intake as parameters of CRS control.

117 y, the LAC treatment during the last part of CRS enhanced resilience, opposing the effects of CRS, as

118 gression at the 50th and 75th percentiles of CRS-T scores, where higher percentiles reflect more adve

119 MP analysis may help identify phenotypes of CRS, and in distinguishing AERD from CRSwNP.

120 memory T cells as independent predictors of CRS.

121 o neoadjuvant chemotherapy in the setting of CRS and HIPEC for PMs.

122 The holy grail in the study of CRS is to identify specific drivers of mucosal inflammat

123 has identified novel phenotypic subgroups of CRS, but prognostic utility is unknown.

124 A subset of CRS patients develop nasal polyps (NPs), which are chara

125 Multiple subtypes of CRS have been described based on clinical and pathologic

126 In summary, the treatment of CRS is at an exciting crossroad.

127 ntly considered the mainstay of treatment of CRS, specifically glucocorticoids.

128 Phase II randomized clinical trials of CRS-207 as a boosting agent and in combination with immu

129 Our understanding of CRS continues to evolve, and identification of the kinet

130 Recent advancements in the understanding of CRS pathogenesis are highlighted in this review, with sp

131 n contrast, no relevant literature exists on CRS after kidney transplantation.

132 either on a conventional risk score (CRS) or CRS + GRS ((+)GRS).

133 ystic fibrosis, CRS without nasal polyps, or CRS with nasal polyps.

134 xperiment revealed expression of many of our CRS regions in human fetal brain, including 662 novel on

135 ta in a large cohort reveals that particular CRS phenotypes (asthma and purulence) are characterized

136 In particular, CRS can be divided into 2 major subgroups based on wheth

137 oducibility (kappa, 0.67) and predicted PFS (CRS 1 and 2 v 3: median, 12 v 18 months; adjusted hazard

138 Physiologically, CRS reduced long-term potentiation (LTP) of Schaffer col

139 s toward new treatment paradigms in polypoid CRS.

140 is Control Test provided the highest quality CRS-specific PROMs, whereas the EQ-5D provided the highe

141 is study included 666 patients that received CRS for PC between 2009 and 2014.

142 Recurrent CRS was defined as rhinosinusitis not controlled by appr

143 iratory allergies in patients with recurrent CRS (31% to 72%).

144 ficiencies in 13% of patients with recurrent CRS and 23% of patients with difficult-to-treat CRS.

145 topy was observed in patients with recurrent CRS.

146 ions between PCB-153 levels and ADHD-related CRS-T indices were assessed using multivariable quantile

147 tions using the Coma Recovery Scale-Revised (CRS-R) have an impact on diagnostic accuracy of patients

148 ergic rhinitis (AR), chronic rhinosinusitis (CRS) and asthma often co-exist.

149 lammation, including chronic rhinosinusitis (CRS) and cystic fibrosis.

150 ways associated with chronic rhinosinusitis (CRS) are not fully understood.

151 ion in patients with chronic rhinosinusitis (CRS) are not known.

152 ngly recognized that chronic rhinosinusitis (CRS) comprises a spectrum of different diseases with dis

153 criteria to evaluate chronic rhinosinusitis (CRS) control, taking into consideration the severity of

154 Chronic rhinosinusitis (CRS) has a broad range of comorbidities.

155 Chronic rhinosinusitis (CRS) has been known as a disease with strong infectious

156 Chronic rhinosinusitis (CRS) has been linked to the gram-positive bacteria Staph

157 l classifications of chronic rhinosinusitis (CRS) have weak prognostic utility regarding treatment ou

158 dy the prevalence of chronic rhinosinusitis (CRS) in a general-population sample.

159 ons in patients with chronic rhinosinusitis (CRS) in hopes of elucidating mechanisms of disease and b

160 Chronic rhinosinusitis (CRS) is a prevalent multifactorial disease process in wh

161 Chronic rhinosinusitis (CRS) is a troublesome, chronic inflammatory disease that

162 Chronic rhinosinusitis (CRS) is an inflammatory disease of the upper airways tha

163 Chronic rhinosinusitis (CRS) is an inflammatory disease that affects 2% to 16% o

164 Chronic rhinosinusitis (CRS) is an inflammatory process in the nasal cavity and

165 Patients with chronic rhinosinusitis (CRS) often have comorbid asthma.

166 g cause or causes of chronic rhinosinusitis (CRS) over the past 20 or more years have expanded from a

167 ichment was noted in chronic rhinosinusitis (CRS) patients; however, the role of ILC2s in coordinatin

168 ng function, asthma, chronic rhinosinusitis (CRS), and atopy with age using a large European sample.

169 s, including asthma, chronic rhinosinusitis (CRS), and eosinophilic esophagitis.

170 Ps) of patients with chronic rhinosinusitis (CRS), as well as in bronchoalveolar lavage fluid, after

171 ied respondents with chronic rhinosinusitis (CRS), migraine headache, and fatigue symptoms.

172 ng the management of chronic rhinosinusitis (CRS), PROMs will play an essential role in informing and

173 ies in patients with chronic rhinosinusitis (CRS).

174 ects with asthma and chronic rhinosinusitis (CRS).

175 ic rhinitis (AR) and chronic rhinosinusitis (CRS).

176 s, a three-tier chemotherapy response score (CRS) system was developed and applied to an independent

177 D based either on a conventional risk score (CRS) or CRS + GRS ((+)GRS).

178 ere used to generate a candidate risk score (CRS).

179 sly reported recurrence clinical risk score (CRS).

180 Severe CRS was characterized by hemodynamic instability, capill

181 ial activation, were increased during severe CRS and also before lymphodepletion in patients who subs

182 ntation of and identify biomarkers of severe CRS in 133 adult patients who received CD19 CAR T cells.

183 infusion for patients at high risk of severe CRS.

184 nt from the reference diagnosis based on six CRS-R assessments.

185 ciations were no longer significant for some CRS subgroups.

186 s evaluated by composite reference standard (CRS).

187 n (DBS) and cortical responsive stimulation (CRS) are newer neurostimulation therapies with recently

188 y demonstrates how chronic restraint stress (CRS) modulates gene expression in response to a novel st

189 er day for 7 days) chronic restraint stress (CRS), do not display depressive-like behavior.

190 with a history of chronic-restraint stress (CRS).

191 o prolonged 21-day chronic restraint stress (CRS).

192 fter administering chronic restraint stress (CRS; 6 hours/day for >/=21 consecutive days) to adult ma

193 Structured (CRS overlapping) enhancer RNAs and extended 3' ends have

194 -to-rescue rate after cytoreductive surgery (CRS) for peritoneal carcinomatosis (PC) in a tertiary ce

195 Cytoreductive surgery (CRS) with hyperthermic intraperitoneal chemotherapy (HIP

196 Scientific interest in cardiorenal syndrome (CRS) affecting the native kidneys is increasing.

197 Backgound: Caudal regression syndrome (CRS) is an uncommon disorder in which there is abnormal

198 with severity of cytokine release syndrome (CRS) and preinfusion tumor burden in pediatric ALL.

199 life-threatening cytokine release syndrome (CRS) in healthy volunteers, which had not been predicted

200 Cytokine release syndrome (CRS) is a potentially life-threatening toxicity that has

201 Cytokine release syndrome (CRS) severity was the only factor after CAR-T-cell infus

202 Cytokine release syndrome (CRS), a systemic inflammatory response caused by cytokin

203 notable toxicity, cytokine release syndrome (CRS), posing a unique challenge for toxicity management.

204 n associated with cytokine release syndrome (CRS).

205 f GVHD-associated cytokine release syndrome (CRS-hyperpyrexia, high levels of proinflammatory cytokin

206 Congenital rubella syndrome (CRS) case identification is challenging in older childre

207 s, rubella, and congenital rubella syndrome (CRS) from the Western hemisphere, the Pan American Healt

208 sing the Conners' Rating Scale for Teachers (CRS-T).

209 Thus, during short-term CRS, hippocampal NF-alpha1 expression is upregulated and

210 lower LDL-C levels (92.3+/-32.9 mg/dL) than CRS participants (P=0.02) but not participants with low

211 cases have a different pathophysiology than CRS and requires different management.

212 rdensome condition, and suggests either that CRS promotes onset of other diseases or is an indicator

213 The CRS system is reproducible and shows prognostic signific

214 The CRS, an ongoing birth cohort study, enrolled 1,246 parti

215 Among the CRS subtypes examined, only 2 conditions (presence of pu

216 Biodiversity was similar between the CRS and control groups.

217 C did not reduce, but slightly enhanced, the CRS-increased length and number of intersections of pyra

218 istently low lung function trajectory in the CRS (Tucson Children's Respiratory Study).

219 d more often in the (+)GRS group than in the CRS group (39% versus 22%, P<0.01).

220 enus level, Prevotella spp. decreased in the CRS group, while Staphylococcus spp. increased from both

221 he Concordance probability estimation of the CRS was 0.73 in the derivation cohort and 0.71 in the va

222 Validation of the CRS was performed in the validation cohort.

223 mice treated with LAC show resilience of the CRS-induced structural remodeling of medial amygdala (Me

224 the (+)GRS group had a lower LDL-C than the CRS group (96.5+/-32.7 versus 105.9+/-33.3 mg/dL; P=0.04

225 established to train pathologists to use the CRS system.

226 ey were assessed at least six times with the CRS-R within a 10-day period.

227 ons, but not in mice 24h subsequent to their CRS exposure.

228 The three-tier CRS system applied to omental samples from the validatio

229 er HD preculture, and this may contribute to CRS in humans because of the close association of Fcgamm

230 stress impairing LTP and spatial learning to CRS modifying physical properties of spiking in place ce

231 agement for 4 months, and difficult-to-treat CRS was defined as noncontrollable rhinosinusitis despit

232 and 23% of patients with difficult-to-treat CRS.

233 rrent landscape of CD19 CAR clinical trials, CRS pathophysiology and management, and remaining challe

234 iated with higher prevalence of uncontrolled CRS, whereas allergy, asthma and smoking status did not

235 to mitigate morbidity in patients undergoing CRS/HIPEC.

236 rioperative morbidity in patients undergoing CRS/HIPEC.

237 tration and morbidity in patients undergoing CRS/HIPEC.

238 uncover the pathogenic mechanisms underlying CRS.

239 orting long-term efficacy (>5 years) of VNS, CRS and DBS in patients with refractory focal/partial ep

240 ypothesized that driving pressure (DeltaP=VT/CRS), in which VT is intrinsically normalized to functio

241 When CRS subgroups were modeled separately, these association

242 hest quality validated PROMs for adults with CRS were (1) the 22-item Sinonasal Outcome Test (19 poin

243 een instruments were specific to adults with CRS, and one was a generic quality-of-life instrument (E

244 quality of PROMs being used for adults with CRS.

245 The risk of other diseases associated with CRS adds to the burden of an already highly burdensome c

246 diseases were most strongly associated with CRS cases who reported smell loss and facial pain and/or

247 o evaluate potential factors associated with CRS subgroups.

248 direct medical expenditures associated with CRS.

249 essure and had the weakest associations with CRS cases who did not report these symptoms.

250 We enrolled children with CRS born between 1998 and 2003 and compared their immune

251 red with children without CRS, children with CRS had more RUBV-specific IgG (P < .001), a stronger C

252 We enrolled 32 children with CRS, 31 mothers, and 62 children without CRS.

253 centration lower (P = .001) in children with CRS, compared with their mothers.

254 Among patients with CRS 0, no other factors were significantly associated wi

255 Fifty-six patients with CRS and 26 control subjects were studied.

256 Nasal tissue was obtained from patients with CRS and control subjects.

257 Sinus swabs from patients with CRS and healthy subjects collected during endoscopic sin

258 ion of the sinus microbiota in patients with CRS and its clinical subtypes has yet to be performed.

259 thelial barrier dysfunction in patients with CRS and other mucosal diseases.

260 urce of OSM-producing cells in patients with CRS and severe asthma.

261 tissue (UT) from controls and patients with CRS as well as in NP.

262 nnate TH2-promoting factors in patients with CRS based on recent experimental data.

263 Samples from patients with CRS had greater bacterial abundance and lower diversity,

264 nized that a large minority of patients with CRS have a steroid-resistant phenotype, identification o

265 These results suggest that patients with CRS have altered nasal microbiota and decreased diversit

266 itutional prospective study of patients with CRS in whom initial medical therapy failed who then self

267 of epithelial dysregulation in patients with CRS is overproduction of eosinophil-promoting C-C chemok

268 Patients with CRS often present with uncontrolled asthma, and ESS impr

269 Analysis of samples from patients with CRS showed that OSM mRNA and protein levels were highly

270 mmunity have been described in patients with CRS that predispose to increased sinus mucosal bacterial

271 ial biofilm is present in most patients with CRS undergoing surgical intervention, and its presence i

272 g that increased OSM levels in patients with CRS was locally stimulated and produced.

273 iciency, and IgM deficiency in patients with CRS was performed by using logit transformation of the p

274 OMs validated for use in adult patients with CRS were identified.

275 In 27 patients with CRS who were followed postoperatively, those with better

276 amples were obtained from five patients with CRS with polyposis, three patients with CRS without poly

277 control subjects (n = 15) and patients with CRS without NP (CRSsNP) (n = 16) and CRSwNP (n = 17), mR

278 with CRS with polyposis, three patients with CRS without polyposis, and three non-CRS controls.

279 tential therapeutic benefit in patients with CRS, although the extent to which this is realized in pa

280 y (8% to 34%) was increased in patients with CRS, as was the prevalence of respiratory allergies in p

281 Patients with CRS, both with and without polyps, and comorbid asthma c

282 discovering autoantibodies in patients with CRS, we sought to investigate the nature, extent, and lo

283 ublished after 1990 describing patients with CRS, which was defined as symptomatic rhinosinusitis for

284 le in complement activation in patients with CRS.

285 m for complement activation in patients with CRS.

286 ontinued medical management in patients with CRS.

287 oncept of community ecology in patients with CRS.

288 ncy is a frequent condition in patients with CRS.

289 mation in control subjects and patients with CRS.

290 biota and their secreted EV in patients with CRS.

291 mucociliary clearance in most patients with CRS.

292 in patients with AERD than in patients with CRS.

293 activation in nasal tissue of patients with CRS.

294 RS, or share a systemic disease process with CRS.

295 d in the immunopathogenesis of subjects with CRS and nasal polyps experiencing exacerbation.

296 ting from colorectal cancer are treated with CRS and HIPEC.

297 es for children with versus children without CRS gave 100% specificity with >65% sensitivity.

298 Compared with children without CRS, children with CRS had more RUBV-specific IgG (P < .

299 d a group of similarly aged children without CRS.

300 ith CRS, 31 mothers, and 62 children without CRS.