ライフサイエンスコーパス: ICM

1 ICM altered neurite outgrowth, but only at concentration

2 ICM and TP transformations were simulated as a cometabol

3 ICM appears to be independently associated with a higher

4 ICM is now recognized as a primary specialty in Spain, S

5 ICM organoids show similarities to the in vivo system th

6 ICM patients had 27 appropriate ICD events, and NICM pat

7 ICM patients remain a clinical conundrum.

8 ICM pretreatment of aged rats with Box-A 24 h before E.

9 ICM pretreatment with Box-A also inhibited aging-induced

10 ICM was also independently related to lower risk of stro

11 ICM was independently associated with a lower risk of st

12 ICM was independently associated with an increased likel

13 ICMs isolated from more advanced blastocysts no longer r

14 Among these, only 2 (ICM) and 5 (NICM) miRNAs are normalized with LVAD.

15 During 46.7 patient-years, 6 (2.2%) ICM patients received an appropriate shock; 5 survived t

16 reater than or equal to 60 mL/min/1.73 m(2), ICM was not independently associated with AKI.

17 d systolic and diastolic function in 1 in 20 ICM and 1 in 5 NICM patients.

18 ial ablation could abolish all Epi-LAVA in 4 ICM and 2 ARVC patients, whereas all patients with NICM

19 ocardium after the CF-LVAD intervention (n=6 ICM, 5 non-ICM).

20 the isthmus could be identified in 56 (63%) ICM VTs and 12 (26%) NICM VTs ( P<0.01), whereas any cri

21 Among the 679 (ICM) and 570 (NICM) lncRNAs differentially expressed wit

22 Two (0.7%) ICM patients received an inappropriate shock.

23 A total of 74 ICM and 34 NICM were followed for 63 months (1-140) and

24 nate Epi-LAVA at least partially in 15 (83%) ICM, 2 (13%) NICM, and 11 (73%) ARVC patients, contribut

25 mus or exit) could be identified in 76 (85%) ICM VTs and 37 (79%) NICM VTs ( P=0.3).

26 Of 89 ICM VTs, the isthmus could be identified by endocardial

27 thways, however, much more severely affected ICM development (7-8 cells).

28 sion of FGFR2, it is FGFR1, expressed by all ICM cells, that is critical for establishment of a PrE i

29 Among ICM patients with AF detected, the median time to AF det

30 M both at ICE and TEE, 1 patient (2%) had an ICM at ICE and a negative TEE, and 53 patients (95%) had

31 n of Mek1/2 in ES cells helps to maintain an ICM-like epigenetic state, prolonged suppression results

32 ECG monitoring with an ICM was superior to conventional follow-up for detecting

33 ambulatory population when compared with an ICM.

34 .3 (4.4) hours/day) of simultaneous AFSW and ICM recordings in 24 patients.

35 We show that morula compaction and ICM formation depend on PC7 and the related proprotein c

36 with TCM compared with patients with DCM and ICM.

37 kappa B (NF-kappaB) in LUHMES cells, EMA and ICM induced caspase-3/7 activity.

38 ected from demethylation in the germline and ICM.

39 METHODS AND ICM and NICM patients who underwent LGE cardiac magnetic

40 Scintiscans of ICM-naive and ICM-administered patients were compared.

41 iate WCD therapy in newly diagnosed NICM and ICM patients according to cardiomyopathy etiology in an

42 success rates after VT ablation in NIDCM and ICM patients were similar, the long-term outcomes in NID

43 e show that proper development of the TE and ICM lineages is coordinated via combinatorial regulation

44 Proper development of the TE and ICM lineages is dependent upon establishment of specific

45 lastocyst and their allocation to the TE and ICM, suggesting that TE-ICM bias arises separately from

46 a major role in the specification of TE and ICM.

47 s capable of contributing to both the TE and ICM.

48 functionally contribute to establish TE- and ICM-specific transcriptional programs are poorly underst

49 .4+/-14.2 years, NICM 49.8+/-12.4 years, and ICM 57.5+/-8.0 years; P<0.001) and more frequently liste

50 A at the facing site, 48 (28%) applications (ICM: 20 of 71 [28%], NICM: 3 of 39 [8%], ARVC: 25 of 63

51 concentration to evaluate the delay between ICM administration and radioiodine therapy in patients w

52 sing cells was not significantly affected by ICM.

53 e nor NIS protein expression was affected by ICM.

54 Three-year monitoring by ICM in cryptogenic stroke patients demonstrated a signif

55 in patients with ischemic cardiomyopathies (ICM) and non-ICM (NICM) may differ in this regard.

56 cumented chronic and dilated cardiomyopathy (ICM, n = 61; NICM, n = 93) requiring durable support wit

57 pathy (DCM) and inflammatory cardiomyopathy (ICM).

58 omyopathy (NICM) or ischemic cardiomyopathy (ICM) against sudden cardiac death while awaiting re-eval

59 or (ICD) therapy in ischemic cardiomyopathy (ICM) and nonischemic cardiomyopathy (NICM) patients and

60 V) in patients with ischemic cardiomyopathy (ICM) and ventricular tachycardia (VT) is important for u

61 , its role in human ischemic cardiomyopathy (ICM) has never been analysed.

62 , but the impact of ischemic cardiomyopathy (ICM) has not been specifically investigated.

63 nt of patients with ischemic cardiomyopathy (ICM) have questioned both the added value of revasculari

64 the pathogenesis of ischemic cardiomyopathy (ICM) in animal models, substantial questions remain unan

65 ll (MSC) therapy in ischemic cardiomyopathy (ICM) is controversial.

66 myopathy (NICM) and ischemic cardiomyopathy (ICM), myocarditis patients were younger (myocarditis 43.

67 In patients with an ischemic cardiomyopathy (ICM), the combination of late potential (LP) abolition a

68 red with those with ischemic cardiomyopathy (ICM).

69 NIDCM compared with ischemic cardiomyopathy (ICM).

70 t failure caused by ischemic cardiomyopathy (ICM; n=16) or non-ICM (n=22) cardiomyopathy were isolate

71 tion heart failure (ischemic cardiomyopathy [ICM]).

72 ty-six patients (18 ischemic cardiomyopathy [ICM], 13 nonischemic dilated cardiomyopathy [NICM], 15 a

73 f scRNA-seq data from early and late 32-cell ICM cells.

74 We revealed that TE-deprived ICMs derived from 32-cell blastocysts are still able to

75 OG, GATA6, and the FGF/ERK pathway determine ICM cell fate.

76 We developed ICM organoids as a, to our knowledge, novel three-dimens

77 of appropriate therapies in newly diagnosed ICM was comparable to that observed in prior observation

78 d NICM and 271 patients with newly diagnosed ICM.

79 RNAs, but not miRNAs or mRNAs, distinguishes ICM from NICM.

80 point in the gene regulatory network driving ICM lineage specification.

81 at inhibition of RHO-ROCK signaling enhances ICM and suppresses TE characteristics through activation

82 ed pharmaceuticals and metabolites excluding ICM the elimination by ozonation, PAC, and UV at the sam

83 rganizations to create core competencies for ICM using consensus methodologies to establish common gr

84 ents (11%) had ICE and TEE both positive for ICM, 8 patients (15%) had a negative TEE but a positive

85 In group 3, 2 patients (3%) had ICM both at ICE and TEE, 1 patient (2%) had an ICM at IC

86 he role of CD56 in the pathogenesis of human ICM.

87 her show that starvation in pre-implantation ICM-derived mouse ESCs induces a reversible dormant stat

88 In ICM patients with primary prophylactic ICD, LGE border z

89 ival in NIDCM was 40.5% compared with 57% in ICM.

90 t impaired by durable CF-LVAD support and in ICM patients appears to be improved.

91 DNA-encoded genes in DCM versus no change in ICM.

92 sis to quantify free-iodide contamination in ICM.

93 Individual cytokines in ICM phenocopied the effects of ICM on NF-kappaB activati

94 l MIA models; or (3) individual cytokines in ICM.

95 d its relationship with systolic function in ICM.

96 us before (54+/-14%) CF-LVAD intervention in ICM patients, whereas sodium nitroprusside-evoked respon

97 is thought to be mediated by free iodide in ICM formulations, but this hypothesis has never been for

98 0 and 147 differentially expressed miRNAs in ICM and NICM, respectively, compared with nonfailing LV.

99 le (NCAM1)] is specifically overexpressed in ICM; it was the aim of the current study to further eluc

100 Appropriate ICD therapy can be predicted in ICM patients with primary prevention ICD by quantifying

101 Although free iodide was present in ICM formulations, in vitro uptake of iodide by NIS-expre

102 Pedagogic research in ICM could usefully focus on the interplay between educat

103 Glucose signaling has no role in ICM specification, and this process of developmental met

104 rk and its interaction with Erk signaling in ICM cells.

105 MSC therapy with TESI in ICM patients improves 6MWD and MLHFQ score and reduces m

106 s in structures and processes of training in ICM across Europe, although there has been agreement on

107 der develops, which is fully incommensurate (ICM) in all three crystallographic directions.

108 Inspecting ICM organoids and mouse embryos, we describe a so far un

109 Intravenous ICM exposure was not predictive (OR: 0.91; 95% CI: 0.51,

110 ncluding the effects of eGFR and intravenous ICM exposure before imaging.

111 evaluate the association between intravenous ICM exposure and AKI in hospitalized pediatric patients

112 er imaging who underwent CT with intravenous ICM or abdominal US (control group) between January 2009

113 frequencies of AKI after CT with intravenous ICM to be similar to propensity score-matched ICM-unexpo

114 paired nonischemic (NICM; n=8) and ischemic (ICM; n=8) human failing LV samples collected before and

115 om nonfailing hearts and end-stage ischemic (ICM) or dilated (DCM) cardiomyopathic hearts.

116 osine (5-MeC) immunofluorescence in isolated ICMs, was minimally affected by inhibition of either pat

117 HMGB1 signaling with an intracisterna magna (ICM) injection of the competitive antagonist to HMGB1, B

118 site housing with Intensive Case Management (ICM) may be an appropriate and less-costly option for ho

119 Among mappable ICM VTs, critical circuit components can usually be iden

120 eimplantation, cells of the inner cell mass (ICM) adopt either an embryonic or an extraembryonic fate

121 he pluripotent cells of the inner cell mass (ICM) and epiblast of the peri-implantation mouse embryo,

122 Communication between the inner cell mass (ICM) and the trophoblast layer of the blastocyst is know

123 erential expression between inner cell mass (ICM) and trophectoderm (TE).

124 lastocyst consisting of the inner cell mass (ICM) and trophectoderm (TE).

125 ment, the generation of the inner cell mass (ICM) and trophoblast lineages comprises upregulation of

126 bryogenesis, cells from the inner cell mass (ICM) can be specified in epiblast (Epi) or primitive end

127 erm (TE) precursors and the inner cell mass (ICM) gives rise to the embryo.

128 trophectoderm (TE) from the inner cell mass (ICM) in the mouse blastocyst is determined by position-d

129 toderm (TE) and pluripotent inner cell mass (ICM) is one of the earliest events during mammalian embr

130 e able to contribute to the inner cell mass (ICM) just as diploid ESCs tagged with GFP.

131 the trophectoderm (TE) and inner cell mass (ICM) lineages in the mouse blastocyst correlates with ce

132 rom both human PSCs and the inner cell mass (ICM) of human blastocysts.

133 Cells of the inner cell mass (ICM) of the mouse blastocyst differentiate into the plur

134 t epiblast (EPI) within the inner cell mass (ICM) of the mouse blastocyst.

135 ineage specification in the inner cell mass (ICM) of the mouse blastocyst.

136 is first established in the inner cell mass (ICM) of the mouse blastocyst.

137 S) cells that resembles the inner cell mass (ICM) of the pre-implantation embryo.

138 n, the specification of the inner cell mass (ICM) to primitive endoderm (PE) and epiblast (EPI).

139 Within the inner cell mass (ICM), all cells relayed FGF/ERK signals with varying dur

140 ither trophectoderm (TE) or inner cell mass (ICM), followed by epiblast (EPI) or primitive endoderm (

141 mouse embryo generates the inner cell mass (ICM), which gives rise to the pluripotent epiblast and t

142 table human preimplantation inner cell mass (ICM)-like naive states with only WNT, MEK/ERK, and tanky

143 shares features with human inner cell mass (ICM).

144 toderm cells from an apolar inner cell mass (ICM).

145 rophectoderms [TEs] and one inner cell mass [ICM] analyzed per blastocyst; n = 390), we determine the

146 KI) compared with a propensity score-matched ICM-unexposed patient group.

147 CM to be similar to propensity score-matched ICM-unexposed patient groups; similar data in pediatric

148 by comparing with a propensity score-matched ICM-unexposed patient sample undergoing abdominal US.

149 ith intravenous iodinated contrast material (ICM) had a similar frequency of acute kidney injury (AKI

150 ith intravenous iodinated contrast material (ICM).

151 Here, mean ICM cell numbers decreased from 18-19 in controls to 11-

152 fect of the use of iodinated contrast media (ICM) administered intravenously.

153 e detection of six iodinated contrast media (ICM) and their phototransformation products (TPs) in sur

154 Iodinated contrast media (ICM) are commonly administered pharmaceutical agents.

155 ation of the iodinated X-ray contrast media (ICM) iopamidol, iopromide, iohexol, iomeprol, and diatri

156 In intensive care medicine (ICM), the differences in national training programs were

157 ference with iodinated oral contrast medium (ICM) in standard (sICM) and 25%-reduced (rICM) concentra

158 ions of the iodinated X-ray contrast medium (ICM) iomeprol were studied at the stream/groundwater int

159 kelvin), X-ray-emitting intracluster medium (ICM) is the dominant baryonic constituent of clusters of

160 rom normal retina into intercalary membrane (ICM) were noted: abrupt (73.33%) and gradual (26.67%).

161 ility; (2) an inflammatory cytokine mixture (ICM) comprised of five cytokines elevated in experimenta

162 molars, termed the inhibitory cascade model (ICM).

163 nitoring with an insertable cardiac monitor (ICM) is more effective than conventional follow-up (cont

164 cordings from an insertable cardiac monitor (ICM; Reveal LINQ).

165 he impact of implantable cardiac monitoring (ICM) in the prevention of stroke recurrence after a cryp

166 monitoring via insertable cardiac monitors (ICM).

167 astocysts produced in RN + PL contained more ICM cells and ATP than blastocysts cultured in our contr

168 rase (BHMT), which is expressed in the mouse ICM.

169 Mga mutant cells, and the survival of mutant ICM cells as well as ESCs is rescued in culture by the a

170 a negative TEE, and 53 patients (95%) had no ICM at ICE and TEE.

171 ter the CF-LVAD intervention (n=6 ICM, 5 non-ICM).

172 with ischemic cardiomyopathies (ICM) and non-ICM (NICM) may differ in this regard.

173 y ischemic cardiomyopathy (ICM; n=16) or non-ICM (n=22) cardiomyopathy were isolated from the left ve

174 ies from patients with ICM compared with non-ICM and donor controls, whereas responses to sodium nitr

175 impact on the outcomes of patients with non-ICMs (NICM) undergoing VT ablation.

176 tribute to a methyl pool required for normal ICM development and establishing initial embryonic DNA m

177 he clinical VT only was achieved in 18.3% of ICM and in 22.2% of NIDCM patients.

178 s achieved in 66.7% of NIDCM and in 77.4% of ICM patients.

179 ral anticoagulation prescription in 94.7% of ICM patients with AF detected at 6 months, 96.6% at 12 m

180 Finally, the ability of ICM to perturb iodide uptake in the thyroid may be used

181 intravenous or sublingual administration of ICM led to a reduction in radiotracer uptake by the thyr

182 udy provides evidence that biodegradation of ICM occurs at the field-scale also for predominantly den

183 diagnosis of DCM, and 91 had a diagnosis of ICM.

184 t to prospectively investigate the effect of ICM HF etiology on LVAD-associated improvement of cardia

185 er (NIS) were used to quantify the effect of ICM on iodide uptake.

186 and suggest a direct and selective effect of ICM on the thyroid.

187 The thyroid-selective effect of ICM was also observed in humans.

188 but did not completely mimic the effects of ICM on apoptosis.

189 cytokines in ICM phenocopied the effects of ICM on NF-kappaB activation and synaptic connectivity, b

190 tor Y-27632 exhibited elevated expression of ICM marker NANOG and reduced expression of CDX2 at the b

191 kM) clustering, and identified two groups of ICM cells: a group of cells from embryos with less than

192 meric dysfunction are molecular hallmarks of ICM in humans, our results provide strong evidence that

193 plays a pivotal role in the pathogenesis of ICM and may be a target for future immunotherapeutic str

194 sation (6.67%), and hill like projections of ICM into the vitreous cavity (26.67%).

195 Scintiscans of ICM-naive and ICM-administered patients were compared.

196 First, a photodegradation study of ICM in surface water using a sunlight lab-scale simulato

197 ion superior to OMT in improving survival of ICM patients.

198 ndicate contrast medium preference, taste of ICM (with a five-point scale), and adverse effects.

199 in vitro culture, confirming totipotency of ICM cells at this stage.

200 ects with >50% false-positive AF episodes on ICM were excluded.

201 stroke were randomized to control (n=220) or ICM (n=221) and followed for </=36 months.

202 dy of 5,307 consecutive patients with DCM or ICM, no history of sustained ventricular arrhythmias, wh

203 structure reappears, along with second-order ICM Bragg peaks, which polarized neutron data demonstrat

204 All other ICM did not show significant reactivity, regardless of t

205 tolerated VT was performed in 111 patients (ICM 71, NICM 40).

206 Of 445 patients (ICM 228, NICM 217) undergoing VT ablation, detailed entr

207 ds to the death of proliferating pluripotent ICM cells in vivo and in vitro, and the death of embryon

208 l of 171 of 200 study participants preferred ICM to BCM, with no taste differences between sICM and r

209 table acquisition of a human preimplantation ICM-like ground state via modulation of WNT signaling, a

210 states without passing through the previous ICM state, in contrast to what is observed in vivo.

211 Patients receiving ICM were also found to have significantly higher rates o

212 ardiac monitoring and 123 patients receiving ICM.

213 Gene expression profiling of 534 single ICM cells identified distinct downstream targets associa

214 ousing (using rent supplements) and off-site ICM services.

215 METHODS AND About 157 patients with stable ICM and no substantial impairment of kidney function rec

216 ocardial injury even in patients with stable ICM.

217 ound that after this first restriction step, ICM cells still retain fate flexibility, manifested by a

218 cation to the TE and ICM, suggesting that TE-ICM bias arises separately from embryonic-abembryonic bi

219 We demonstrated that ICM reduce thyroid uptake of iodide independently of fre

220 The ICM detected 82 episodes of AF >=1 hour while the AFSW w

221 The ICM therefore provides a developmental framework for exp

222 nt to those two post-treatments, such as the ICM diatrizoate, can be substantially removed only by hi

223 In both the ICM and NIDCM subgroups, procedure failure and incomplet

224 thod that enable us to evaluate directly the ICM heating rate from the dissipation of turbulence.

225 t embryonic stem (ES) cells derived from the ICM generate and shed microvesicles (MVs), a major class

226 y clusters, radiative energy losses from the ICM occur on timescales much shorter than the age of the

227 Cystic spaces in the ICM (46.67%), schisis-like spitting of the ICM (30%), an

228 spitting of the ICM (30%), and breaks in the ICM (6.67%) were seen as well.

229 reduced to a level equivalent to that in the ICM and is non-random, with gain of methylation at speci

230 ises upregulation of Nanog expression in the ICM and its silencing in the trophoblast.

231 Cumulative AF detection rates in the ICM arm increased progressively during this period (3.7%

232 e pluripotent state we found to exist in the ICM at E3.25-HNC is the in vivo counterpart of a new, ve

233 ound massive underlying heterogeneity in the ICM cells at E3.25-HNC with over 3,800 genes with transc

234 brillation (PAF) detection was higher in the ICM cohort compared to the conventional cardiac monitori

235 had been detected in 8.9% of patients in the ICM group (19 patients) versus 1.4% of patients in the c

236 ad been detected in 12.4% of patients in the ICM group (29 patients) versus 2.0% of patients in the c

237 ove the prediction of aneuploidy risk in the ICM in over 86% of clinical cases enrolled.

238 tion in the TE lineage and repression in the ICM lineage.

239 ects on cell numbers and 5-MeC levels in the ICM were completely rescued by methionine (immediate SAM

240 al number of four inner-cell contacts in the ICM, which activates Oct4 in the preimplantation embryo.

241 chanisms of fate decisions that occur in the ICM.

242 were recorded in real time at 300Hz into the ICM+ monitoring software (Cambridge University Enterpris

243 e ICM (46.67%), schisis-like spitting of the ICM (30%), and breaks in the ICM (6.67%) were seen as we

244 zation to enable proper specification of the ICM and TE lineages.

245 ool, and that the lineage composition of the ICM is conserved regardless of its size.

246 epresentation, along with a splitting of the ICM peaks along the h direction which indicates that the

247 Below15 K the k component of the ICM structure reappears, along with second-order ICM Bra

248 Although the size of the ICM was unaffected in Fgf4 null mutant embryos, it entir

249 associated with the high variability of the ICM wastewater discharge into the investigated stream.

250 entation appears, and the k component of the ICM wave vector disappears.

251 Since the ICM exists only transiently in vivo, it remains unclear

252 iptional profile stabilizes earlier than the ICM and prior to blastocyst formation.

253 ion of how this energy is transferred to the ICM remains open.

254 e show that molar complexity conforms to the ICM, following a linear, morphogenetic gradient along th

255 euploidy detection in TE biopsies toward the ICM's chromosomal constitution.

256 ive activities of FGFR1 and FGFR2 within the ICM coordinate establishment of two distinct lineages.

257 itive endoderm (PE) specification within the ICM.

258 equired for lineage establishment within the ICM.

259 g and speed of lineage commitment within the ICM.

260 pensity score-matched sample (925 exposed to ICM [mean age +/- standard deviation, 8 years +/- 6; 484

261 /- 6; 484 female patients]; 925 unexposed to ICM [mean age, 7 years +/- 6; 484 female patients]).

262 quence, the positive-predictive value toward ICM configuration was significantly lower for segmental

263 All data were captured at 300 Hz using ICM+ (Cambridge Enterprise, Cambridge, United Kingdom) b

264 nd optimal cerebral perfusion pressure using ICM+ software (Cambridge Enterprise, University of Cambr

265 Data were collected and pre-processed using ICM+ software.

266 ation (myocarditis 11% versus NICM 2% versus ICM 4%; P<0.001), biventricular mechanical circulatory s

267 port (myocarditis 19% versus NICM 2%, versus ICM 2%; P<0.001), and extracoroporeal membrane oxygenati

268 s 1A (myocarditis 44% versus NICM 21% versus ICM 21%; P<0.001), with significantly higher need for me

269 tion (myocarditis 5% versus NICM 0.4% versus ICM 1%; P<0.001).

270 [95% confidence interval, 1.63-3.79] versus ICM and hazard ratio, 2.12 [95% confidence interval, 1.4

271 tion, as TE derives from outer cells whereas ICM from inner cells.

272 me of transcriptional stabilization, whereas ICM cells still retain the ability to regenerate TE up t

273 ns that also reduced cell viability, whereas ICM reduced synapse number independent of changes in cel

274 y-seven patients, 63 with NIDCM and 164 with ICM, presenting with sustained VT were ablated with radi

275 iarrhea with BCM, but none had diarrhea with ICM.

276 mbryos, and associate these differences with ICM/TE differences.

277 Canadian cities, scattered site housing with ICM services compared with usual access to existing hous

278 receiving continuous cardiac monitoring with ICM during the last 3 years.

279 Median CV in patients with ICM and controls was 0.41 m/s and 0.65 m/s, respectively

280 ntly and similarly improved in patients with ICM and NICM.

281 ntation therapeutic options in patients with ICM and NICM.

282 nted (P<0.05) in arteries from patients with ICM compared with non-ICM and donor controls, whereas re

283 eriod of 41.4 +/- 29.0 months, patients with ICM had better survival when receiving CRT with a defibr

284 We enrolled 6 patients with ICM undergoing VT ablation and 5 with structurally norma

285 Patients with ICM who received MSCs via transendocardial stem cell inj

286 In patients with ICM, CV in areas with no visible fibrosis was 0.81 m/s (

287 coronary BMC administration in patients with ICM, suggesting that the beneficial effects of BMC appli

288 urthermore, when compared with patients with ICM, the presence of T cells and macrophages was signifi

289 ced myocyte size compared with patients with ICM.

290 resonance imaging (LGE-CMR) in patients with ICM.

291 to impaired cell retention in patients with ICM.

292 tracoronary BMC application in patients with ICM.

293 th LGE-CMR fibrosis density in patients with ICM.

294 questions in the management of patients with ICM.

295 P<0.01) were both higher among patients with ICM.

296 6 months, we found that 5% of subjects with ICM and 21% of subjects with NICM achieved left ventricu

297 udden cardiac death in 8.0% among those with ICM but in only 0.4% of those with DCM.

298 ibrillator therapy, as opposed to those with ICM.

299 idated on data collected in 24 patients with ICMs and a history of paroxysmal AF who simultaneously w

300 to the receptor(s) responding to FGF4 within ICM cells, we combined single-cell-resolution quantitati