ライフサイエンスコーパス: CRS

1 CRS arises from massive cytokine secretion and can be li

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

3 CRS is a highly prevalent and heterogeneous condition.

4 CRS is being increasingly recognized as a disease spectr

5 CRS is characterized by the rapid production of inflamma

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

7 CRS, occurring a median of 5 days (IQR: 2 to 7 days) aft

8 CRS-HIPEC improved overall survival (OS) in both crude a

9 CRS/HIPEC is an effective therapeutic strategy commonly

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

11 ent of 21 days), all occurred with grade >=2 CRS (31% patients with grade >=2 CRS), and 95% of events

12 h grade >=2 CRS (31% patients with grade >=2 CRS), and 95% of events occurred after an elevated tropo

13 ach occurred only in patients with grade >=2 CRS.

14 In the retrospective phase (2010 to 2014), CRS cases were retrieved from medical records, and in th

15 Subjects in control (n = 29), CRS without nasal polyps (CRSsNP, n = 86), and CRS with

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

17 tion of women with L-M scores >= 3, 4, or 6 (CRS(O) ) was 11.1%, 9.9%, and 5.7%, respectively, and 16

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

19 A total of 7476 CRS/HIPEC were analyzed.

20 A CRS endotype with a proinflammatory neutrophilic immune

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

22 ted methods that can pre-emptively prevent a CRS-like toxicity that would have otherwise occurred.

23 se tests and 3 commercial tests) that used a CRS.

24 In addition, CRS with fungal and non-fungal infections also demonstra

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

26 tory neurotoxicity typically occurring after CRS and characterized by impaired blood-brain barrier in

27 idity and mortality remain significant after CRS for PC.

28 ecificity, PLR, and NLR of NAA tests against CRS were 68% (95% CI, 41 to 87%), 98% (95% CI, 95 to 99%

29 47.3% of all CRS patients were uncontrolled based on evaluation of VA

30 T helper type 2 cell (Th2)-mediated allergic CRS mouse model, based on house dust mite (HDM) and Stap

31 e-associated cytokine changes differed among CRS subtypes and control tissues.

32 There was a graded relationship among CRS, elevated troponin, and CV events, and a shorter tim

33 In subgroup analysis, CRS with and without nasal polyps demonstrated a signifi

34 S without nasal polyps (CRSsNP, n = 86), and CRS with nasal polyps (eosinophilic NP: ENP, n = 81; non

35 omplications of medically refractory AKI and CRS and may restore normal electrolyte, acid-base, and f

36 ic workup, and medical management of AKI and CRS with an overview of indications, multidisciplinary t

37 In our asthma and CRS cohorts, miR-1 levels correlated inversely with its

38 quantified in nasal tissue from non-CRS and CRS subjects with nasal polyps.

39 treated with an optimized CTL019 dosing and CRS management strategy.

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

41 ol modifications in response to efficacy and CRS toxicity.

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

43 egative primary tumors, CEA <= 200 mug/L and CRS < 4.

44 gh incidence of reversible neurotoxicity and CRS.

45 luminate a novel approach to abrogate NI and CRS through GM-CSF neutralization, which may potentially

46 and plasma from control non-CRS patients and CRS patients.

47 erentiated into CRS without nasal polyps and CRS with nasal polyps (CRSwNP).

48 A cut-off value of the annual CRS/HIPEC caseload affecting the 90-day POM was calculat

49 his approach may eliminate the need for anti-CRS treatment and may improve the overall safety of CAR

50 d radiologic inflammation were classified as CRS(S+O) .

51 and 53 (6.4%) subjects had clinically based CRS (based on LM score >0).

52 ty-five (3.0%) subjects had clinically based CRS (based on LM score >=4), and 53 (6.4%) subjects had

53 evalence of 3.0% to 6.4% of clinically based CRS (depending on an LM cutoff point; ie, LM >= 4 or LM

54 symptoms according to EPOS; clinically based CRS also encompasses endoscopy and/or CT scanning.

55 ed seven (12.8%) had epidemiologically based CRS according to EPOS.

56 ing a combination of epidemiologically based CRS according to the European Position Paper on Rhinosin

57 Epidemiologically based CRS is based on nasal symptoms according to EPOS; clinic

58 study investigating the association between CRS and premorbid autoimmune diseases by using the Natio

59 onclusion, a significant association between CRS and premorbid autoimmune diseases has been identifie

60 The duration between CRS onset and tocilizumab administration was associated

61 Here we aimed to compare outcomes between CRS-HIPEC versus CRS alone (CRSa) among patients with PM

62 Both CRS without NP and CRSwNP displayed variable degrees of

63 he behavioral disorders which were caused by CRS.

64 PFC prevented behavioral deficits induced by CRS, and VGF knockdown in vmPFC increased susceptibility

65 member-led organizational structure (called "CRS Focus Groups") that provided new opportunities for m

66 ery and heated intraperitoneal chemotherapy (CRS & HIPEC) is the current standard of care in selected

67 When complete CRS is possible, CRS-HIPEC may be considered a valuable

68 h PMs from GC who were treated with complete CRS with curative intent (no residual nodules > 2.5 mm)

69 There were 42 confirmed CRS cases in the retrospective phase and 53 confirmed CR

70 in the retrospective phase and 53 confirmed CRS cases in the prospective phase.

71 entinel sites reporting laboratory-confirmed CRS cases in all 9 provinces of South Africa.

72 Baseline data on laboratory-confirmed CRS will enable planning and monitoring of RCV implement

73 ed to describe the epidemiology of confirmed CRS in South Africa prior to introduction of RCVs in the

74 Compared with CRSa, CRS-HIPEC improved OS and recurrence-free survival, with

75 osinusitis (CRS) with nasal polyps (CRSwNP), CRS without nasal polyps, and controls without CRS.

76 etion in patients who subsequently developed CRS.

77 These age-related patterns in each CRS were confirmed by statistically adjusting atopy stat

78 r day 2 and day 3 doses to be held for early CRS.

79 can rapidly terminate (<3 h) a pre-existing CRS-like toxicity and two unrelated methods that can pre

80 nusitisCoach (mSC), a mobile application for CRS patients.

81 e platforms to screen novel therapeutics for CRS.

82 S) and the administration of tocilizumab for CRS.

83 In France, CRS/HIPEC is a safe procedure with an acceptable 90-day

84 Amongst patients suffering from CRS with nasal polyps, a statistically significant reduc

85 onin, and CV events, and a shorter time from CRS onset to tocilizumab was associated with a lower rat

86 MMP28, and CTSK was observed in tissue from CRS subjects with nasal polyps compared to control tissu

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

88 Upon IPTW analysis, in CRS-HIPEC and CRSa groups, median OS was 18.8 versus 12.

89 neutrophils and eosinophils was analyzed in CRS without NP and CRSwNP by measuring cell and activati

90 ng a contribution of vascular dysfunction in CRS pathophysiology.

91 vascular pathways and top genes involved in CRS.

92 o a suggested model of precision medicine in CRS.

93 xpression of S100A9 and MMPs are observed in CRS nasal tissue and S100A9 stimulated MMP3 responses to

94 ols, and increased MMP3 and MMP7 observed in CRS subjects with nasal polyps compared to CRS subjects

95 abundances and biologic processes present in CRS and its endotypes compared with in healthy patients.

96 ecise and personalized medical treatments in CRS.

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

98 eria, and objective radiologic inflammation (CRS(O) ) was based on the Lund-Mackay (L-M) score using

99 ed to identify and characterize inflammatory CRS endotypes, as well as to determine whether age was a

100 age is associated with specific inflammatory CRS endotypes or immune signatures.

101 I], euro 64,016 to euro 76,661) for interval CRS compared with euro 85,791 (95% CrI, euro 78,766 to e

102 rI, euro 78,766 to euro 93,935) for interval CRS plus HIPEC.

103 hold in the Netherlands, indicating interval CRS and HIPEC is cost effective for this patient populat

104 The mean QALY in the interval CRS group was 2.12 (95% CrI, 1.66 to 2.64 QALYs) and 2.6

105 95% CrI, 2.11 to 3.28 QALYs) in the interval CRS plus HIPEC group.

106 iveness of the addition of HIPEC to interval CRS in patients with ovarian cancer.

107 sts of treating these patients with interval CRS and HIPEC in countries with comparable health care s

108 s of the trial data, treatment with interval CRS and HIPEC in patients with stage III ovarian cancer

109 e and the USA and can be differentiated into CRS without nasal polyps and CRS with nasal polyps (CRSw

110 logic processes provide further insight into CRS pathogenesis and its endotypes.

111 e colony-stimulating factor (GMCSF) is a key CRS-promoting protein.

112 ib for R/R CLL were well tolerated, with low CRS severity, and led to high rates of MRD-negative resp

113 current ibrutinib were associated with lower CRS severity and lower serum concentrations of CRS-assoc

114 HDF) cohort had a 90% CR rate and manageable CRS.

115 uency at which subjects transition from mild CRS to severe CRS.

116 th CRSwNP, 30 patients with AERD, and 64 non-CRS controls.

117 in nasal tissues and plasma from control non-CRS patients and CRS patients.

118 ases was quantified in nasal tissue from non-CRS and CRS subjects with nasal polyps.

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

120 ity to better understand real-life burden of CRS.

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

122 S severity and lower serum concentrations of CRS-associated cytokines, despite equivalent in vivo CAR

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

124 The traditional description of CRS in terms of two phenotypes based on the presence or

125 macrophages contribute to the development of CRS and neurotoxicity after CAR-T cell therapy.

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

127 sociated with frequent acute exacerbation of CRS (AECRS).

128 C cohort represents a heterogeneous group of CRS patients with a diverse pattern of major symptoms.

129 The impact of CRS on sleep quality and daily life activities was signi

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

131 Incidence of CRS is higher in countries with no rubella-containing va

132 ably and accurately predict the induction of CRS by immune therapeutics.

133 inical cardiovascular (CV) manifestations of CRS include tachycardia, hypotension, troponin elevation

134 y account for the clinical manifestations of CRS.

135 ance in research on the immune mechanisms of CRS has revealed various new endotypes that hold promise

136 te lymphoblastic leukemia xenograft model of CRS and neuroinflammation (NI), GM-CSF neutralization re

137 Our mouse model of CRS displayed an allergic response to HDM + SEB administ

138 In a rabbit model of CRS, TEMPS was maintained in rabbit sinuses and effectiv

139 The median age of mothers of CRS cases was 21 years in the retrospective phase (range

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

141 surgery were associated with higher odds of CRS(S+O) .

142 Men had higher odds of CRS(S+O) compared to women.

143 he latest research on the pathophysiology of CRS with a focus on potential novel biomarkers and treat

144 We aimed to calculate the prevalence of CRS using a combination of epidemiologically based CRS a

145 ignificant reduction in NI and prevention of CRS.

146 abolishes macrophage-dependent secretion of CRS biomarkers, including monocyte chemoattractant prote

147 ticosteroids in subjects with early signs of CRS is without negative impact on the antitumor potency

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

149 The threshold of CRS/HIPEC number per center per year above which the 90-

150 s to improve efficacy and reduce toxicity of CRS treatment.

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

152 ist tocilizumab is approved for treatment of CRS, there is no approved treatment of neurotoxicity ass

153 ogress has been made in the understanding of CRS pathophysiology: from the epithelium and epithelial-

154 to reduce mortality related to either AKI or CRS, apart from supportive care and volume status manage

155 Notably, no neurological toxicity or CRS (greater than grade 1) occurred in any of the 25 pat

156 s toward new treatment paradigms in polypoid CRS.

157 y understood compared with those of polypoid CRS.

158 When complete CRS is possible, CRS-HIPEC may be considered a valuable therapy for stric

159 ore, alternative strategies that can prevent CRS and neurotoxicity associated with CAR T-cell treatme

160 o We conclude that it is possible to prevent CRS by using "all-in-one" GMCSF-knockout CAR T-cells.

161 ored a therapeutic route aimed at preventing CRS rather than limiting its consequences.

162 putational pipeline-MPRAflow-for quantifying CRS activity from different MPRA designs.

163 sion cohort, 3 of 6 patients with refractory CRS concurrent with culture-positive sepsis died, and 3

164 to 2017) clinicians at study sites reported CRS cases monthly.

165 r neuron-specific knockout of Pdcd4 reverses CRS-induced depression-like behaviors.

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

167 in both healthy and chronic rhinosinusitis (CRS) cohorts.

168 Chronic rhinosinusitis (CRS) epidemiology has been largely studied using symptom

169 Chronic rhinosinusitis (CRS) has a complex and multifactorial pathogenesis with

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

171 Chronic rhinosinusitis (CRS) is a chronic inflammatory disease associated with a

172 Chronic rhinosinusitis (CRS) is a common condition associated with inflammation

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

174 Evidence shows that chronic rhinosinusitis (CRS) is associated with prior presence of autoimmune dis

175 Chronic rhinosinusitis (CRS) is complicated by frequent acute exacerbations lead

176 e pathophysiology of chronic rhinosinusitis (CRS) is continuously evolving.

177 for diseases such as chronic rhinosinusitis (CRS) is particularly challenging because of the small na

178 The prevalence of chronic rhinosinusitis (CRS) measured in epidemiologic studies is 5% to 12%.

179 cytokine profiles in chronic rhinosinusitis (CRS) need to be investigated for precision medicine.

180 Chronic rhinosinusitis (CRS) occurs in >10% of the adult population in Europe an

181 effects of aging on chronic rhinosinusitis (CRS) pathophysiology have not been well defined but migh

182 Chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) is a chronic inflammator

183 subjects with AERD, chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP), CRS without nasal polyp

184 Chronic rhinosinusitis (CRS) with nasal polyps is a common chronic condition.

185 Chronic rhinosinusitis (CRS) without nasal polyps (CRSsNP) is a common disease t

186 eature of asthma and chronic rhinosinusitis (CRS), and the endothelium plays a key role in eosinophil

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

188 ted in patients with chronic rhinosinusitis (CRS).

189 n (CEA) >200 mug/L, and clinical risk score (CRS) >=4.

190 r risk score (BRS) with clinical risk score (CRS) enabled pre and postoperative assignment of patient

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

192 Severe CRS was characterized by hemodynamic instability, capill

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

194 sive myeloma, following treatment for severe CRS and encephalopathy.

195 Toxicity was low, with no severe CRS.

196 onse without causing neurotoxicity or severe CRS, representing a safe and potent anti-CD19 CAR T cell

197 subjects transition from mild CRS to severe CRS.

198 Moderate-to-severe CRS is managed with the IL-6 receptor antagonist tociliz

199 Patients with severe CRS may develop capillary leak syndrome and disseminated

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

201 omparison to a composite reference standard (CRS) for anti-C. pneumoniae antibody status of human ser

202 e standard or a combined reference standard (CRS) for TBM.

203 Symptom status (CRS(S) ) was based on guideline criteria, and objective

204 Chronic restraint stress (CRS) up-regulated Pdcd4 expression in hippocampus via de

205 se vmPFC following chronic restraint stress (CRS), and were increased by ketamine in mouse vmPFC.

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

207 he NOD-scid IL2rg(null) (NSG) mouse to study CRS in vivo.

208 to-rescue (FTR) after cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPE

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

210 y (HIPEC) to interval cytoreductive surgery (CRS) improved recurrence-free and overall survival in pa

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

212 Cytoreductive surgery (CRS) yields promising results, but the impact of hyperth

213 idney injury (AKI) and cardiorenal syndrome (CRS) are increasingly prevalent in hospitalized patients

214 oxicities such as cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity s

215 can cause severe cytokine-release syndrome (CRS) and neurotoxicity, impeding their therapeutic appli

216 xicity, including cytokine-release syndrome (CRS) and neurotoxicity, limits broader application.

217 These include cytokine release syndrome (CRS) and neurotoxicity.

218 toxicity such as cytokine release syndrome (CRS) and neurotoxicity.

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

220 ence and grade of cytokine release syndrome (CRS) and the administration of tocilizumab for CRS.

221 I and 1 grade II cytokine-release syndrome (CRS) cases at the highest dose in the absence of graft-v

222 cidence of severe cytokine release syndrome (CRS) in a subject treated with a CAR T-cell product comp

223 Cytokine release syndrome (CRS) is a life-threatening treatment-related toxicity th

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

225 been plagued by a cytokine release syndrome (CRS) that can harm or even kill the cancer patient.

226 ficacy and reduce cytokine release syndrome (CRS), we conducted a pilot study to evaluate the safety

227 rotoxicity and/or cytokine release syndrome (CRS), which were associated with greater CAR T-cell pers

228 life-threatening cytokine release syndrome (CRS).

229 events, including cytokine release syndrome (CRS).

230 neurotoxicity and cytokine release syndrome (CRS).

231 n associated with cytokine release syndrome (CRS).

232 Congenital rubella syndrome (CRS) includes disorders associated with intrauterine rub

233 and Development's Creditor Reporting System (CRS) aid activities database to generate estimates of RM

234 The CRS group consisted of 30,611 patients, and the comparis

235 The CRS group included adult patients newly diagnosed with C

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

237 If the CRS is a functional regulatory element, it will lead to

238 ations of MMP3 and MMP7 were elevated in the CRS groups compared to controls.

239 ritoneal cancer index remained higher in the CRS-HIPEC group (6 v 2; P = .003).

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

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

242 Outcomes included scores on the CRS disease severity visual analog scale (VAS), 22-item

243 ent's medication burden and address only the CRS symptoms.

244 s could potentially avoid a life-threatening CRS while enhancing CAR T cell tumoricidal activity.

245 changes in immunologic profiles according to CRS subtypes.

246 n CRS subjects with nasal polyps compared to CRS subjects without polyps.

247 to elucidate potential mechanisms leading to CRS in humans, we have established a type 2/T helper typ

248 Although insults related to CRS toxicity might be transient and reversible in most i

249 opment and associated with not responding to CRS & HIPEC.

250 firm the high disease burden in uncontrolled CRS patients, clearly impacting quality of life.

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

252 f targeted therapies in severe, uncontrolled CRS.

253 to mitigate morbidity in patients undergoing CRS/HIPEC.

254 Of these patients, 180 underwent CRS-HIPEC and 97 CRSa.

255 ed summary estimates than studies which used CRS.

256 ents that benefit RMNCH was determined using CRS purpose codes for all donors except Gavi, the Vaccin

257 to compare outcomes between CRS-HIPEC versus CRS alone (CRSa) among patients with PMs from GC.

258 b was administered to 56 patients (41%) with CRS, at a median of 27 h (IQR: 16 to 48 h) after onset.

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

260 pathways and top biomarkers associated with CRS may facilitate the development of new targeted deliv

261 gression to evaluate factors associated with CRS(S+O) .

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

263 Combining BRS with CRS will allow better management of cardiac patients at

264 included adult patients newly diagnosed with CRS between 2001 and 2013.

265 ety-eight percent of mothers of infants with CRS were young women 14-30 years old, indicating a poten

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

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

268 significantly overexpressed in patients with CRS compared to controls, suggesting a contribution of v

269 re particularly significant in patients with CRS compared to controls.

270 eling pathways were present in patients with CRS compared with in healthy patients.

271 ntify a high-risk phenotype of patients with CRS for preventive interventions to reduce exacerbation

272 retrospective cohort study of patients with CRS from January 1, 2014, to May 31, 2016.

273 Specifically, patients with CRS had a higher significant association with ankylosing

274 Patients with CRS had a higher significant association with premorbid

275 Aged patients with CRS have a unique inflammatory signature that correspond

276 il-driven inflammation in aged patients with CRS might be less likely to respond to corticosteroids a

277 agement of CV complications in patients with CRS require awareness and multidisciplinary collaboratio

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

279 Of the 3109 patients with CRS who were identified, 600 (19.3%) were classified as

280 out nasal polyps (CRSsNP), and patients with CRS with nasal polyps (CRSwNP) before surgery.

281 btained from healthy patients, patients with CRS without nasal polyps (CRSsNP), and patients with CRS

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

283 oteome of healthy patients and patients with CRS.

284 issue biopsies of controls and patients with CRS.

285 nonasal tissue eosinophilia in patients with CRS.

286 mediators were measured in 147 patients with CRS.

287 le in complement activation in patients with CRS.

288 ng individualized care for all patients with CRS.

289 tial in asthmatic patients and patients with CRS.

290 ined from control patients and patients with CRS.

291 The respective proportion with CRS(S+O) was 1.7%, 1.6%, and 0.45% among women and 8.8%,

292 A cohort of patients with CPM treated with CRS & HIPEC was recruited and divided according to progn

293 All patients treated with CRS/HIPEC between 2009 and 2018 in France were identifie

294 proving patient selection for treatment with CRS & HIPEC and in future research into novel and person

295 o identify those suitable for treatment with CRS & HIPEC and to identify targets for existing repurpo

296 ts with CPM not responding to treatment with CRS & HIPEC, to identify those suitable for treatment wi

297 S without nasal polyps, and controls without CRS.

298 omparison group included individuals without CRS, with 1:4 frequency matching for gender, age, and in

299 th nasal polyps (n = 7) and patients without CRS (n = 5).

300 es of non-durable clinical responses without CRS or neurotoxicity.