ライフサイエンスコーパス: ICH

1 ICH exhibits a concerted helical displacement upon activ

2 ICH induction in male mice caused profound HN loss in th

3 ICH occurred at a rate of 0.80% per year with warfarin r

4 ICH remained worse in blacks and better in Asians compar

5 ICH was found to be positively associated with having a

6 its corresponding trait, and data from 1,286 ICH cases and 1,261 matched controls to estimate the eff

7 08 incident MCE cases, 5,418 IS cases, 4,476 ICH cases, and 5,285 common controls, aged 30-79 years.

8 A total of 973 ICH patients were admitted in the study period.

9 In 855 patients with CT-confirmed acute ICH scanned within 48 h of symptom onset, we investigate

10 intensive BP lowering in patients with acute ICH is safe and effective in improving clinical outcomes

11 =3;efficacy outcome), in patients with acute ICH randomised to either intensive BP-lowering or standa

12 e studies including 4360 patients with acute ICH were pooled in meta-analysis.

13 Patients with acute ICH were retrospectively enrolled.

14 or preventing and treating established adult ICH, but collagen IV patients will require stratificatio

15 enyl butyric acid (PBA), which reduced adult ICH.

16 inished the beneficial effects of IL-4 after ICH.

17 entrations had better outcomes 90 days after ICH, confirming the role of TGF-beta1 in functional reco

18 ury and blood-brain barrier disruption after ICH can be assessed with multimodal MRI, and that periha

19 ciated with lower 30-day case fatality after ICH.

20 microglia/macrophages of STAT6 KO mice after ICH.

21 lume, functional outcome and mortality after ICH.

22 ssociated with lower 6-month mortality after ICH; this finding merits further study.

23 ranasal delivery of IL-4 nanoparticles after ICH hastened STAT6 activation and facilitated hematoma r

24 e) surgery improves functional outcome after ICH and to determine the optimal time window of the trea

25 prognostication of functional outcome after ICH.

26 g soluble AXL had poor 1-year outcomes after ICH onset, suggesting that therapeutically augmenting ef

27 atoma expansion or functional outcomes after ICH, regardless of haematoma location.

28 ation of functional long-term outcomes after ICH.

29 s, and our approach to prognostication after ICH.

30 oma resolution and functional recovery after ICH.

31 ereby facilitating functional recovery after ICH.

32 e risks and benefits of OAT resumption after ICH.

33 h3 in Col4a1(+/G498V) mice protected against ICH.

34 he concomitant generation of the alkyliodide ICH(2) SiMe(3) during the Mn-I exchange being essential

35 Both CPS and ICH varied by race/ethnicity.

36 Stroke incidence and ICH proportion are higher in China than in Western popul

37 for MCE and 1.22 (1.10-1.36) for both IS and ICH.

38 improved model fit for each of MCE, IS, and ICH, with small improvements in C-statistic and correct

39 erences in the change of the overall KAH and ICH scores were 0.92 points (95% confidence interval [CI

40 mes were the change from baseline in KAH and ICH scores.

41 arol maintenance dose, stroke recurrence and ICH in a Spanish cohort.

42 and eight patients had recurrent stroke and ICH events, respectively.

43 Virtual International Stroke Trials Archive-ICH trials dataset, Clot Lysis: Evaluating Accelerated R

44 encourage early management of OSA as well as ICH to optimize ophthalmic outcomes.

45 s a marker for oral anticoagulant-associated ICH (OAC-ICH), but the diagnostic specificity and progno

46 (RETRACE I + II; anticoagulation-associated ICH only) conducted at 22 participating centers, one Ger

47 s and outcomes of methamphetamine-associated ICH (Meth-ICH) versus Non-Meth-ICH.

48 ients with VKA-associated or NOAC-associated ICH and 1022 patients with non-OAC-ICH with heparin prop

49 udy (UKER-ICH; nonanticoagulation-associated ICH only), and 1 US-based prospective longitudinal singl

50 agulation- and nonanticoagulation-associated ICH), treated between January 2006 and December 2015.

51 re-hydrolytic state, both interfaces between ICHs and NBDs decreased exchange to similar extents rela

52 xhibited worse outcomes than WT mice in both ICH models and were less responsive to IL-4 treatment.

53 In both ICH models, STAT6 was activated in microglia/macrophages

54 Secondary analyses were stratified by ICH location and study cohort.

55 eatment-related cutoff values for cerebellar ICH.

56 ment in patients with spontaneous cerebellar ICH are lacking, and the risk of bias in published serie

57 nts (40% female) with spontaneous cerebellar ICH.

58 Among 578 patients with cerebellar ICH, propensity score-matched groups included 152 patien

59 Among patients with cerebellar ICH, surgical hematoma evacuation, compared with conserv

60 ment guidelines for patients with cerebellar ICH.

61 ts may represent a general mechanism of deep ICH.

62 studied a genetic model of spontaneous deep ICH using Col4a1(+/G498V) and Col4a1(+/G1064D) mouse lin

63 ain tissues from patients with sporadic deep ICH.

64 ain tissues from patients with sporadic deep ICH.

65 However, deep ICHs are rare in some aggressive small vessel diseases t

66 Quality by design (ICH-Topic Q8) requires a prospective summary of the desi

67 P < .0001) artificial intelligence-detected ICH examinations with reprioritization.

68 O in either the CNS or periphery exacerbated ICH outcomes.

69 ar Study/2002-2018) of patients with a first ICH with follow-up to 10 years, we determined the long-t

70 ranial haemorrhage (ICH) and classifies five ICH subtypes from unenhanced head computed-tomography sc

71 neurogenesis and improve function following ICH injury.

72 he specific responses of microglia following ICH with the aim of identifying pathways that may aid in

73 The developed method was validated following ICH recommendations.

74 ags abnormal noncontrast CT examinations for ICH was implemented in a busy academic neuroradiology pr

75 shing that helical mobility is important for ICH catalytic efficiency.

76 n could represent a translational target for ICH.

77 rant studies on HN as therapeutic target for ICH.SIGNIFICANCE STATEMENT Astrocytes are critical for m

78 igation as a clinically feasible therapy for ICH.

79 ctoferrin to present a potential therapy for ICH.

80 t limits bleeding and rescues the brain from ICH.

81 ole of TGF-beta1 in functional recovery from ICH.

82 or transient ischaemic attack) or a further ICH following study entry.

83 e were non-significant trends towards future ICH with statins.

84 ents with primary intracerebral haemorrhage (ICH) are at increased long-term risks of recurrent strok

85 aneous cerebellar intracerebral haemorrhage (ICH) differ.

86 rease the risk of intracerebral haemorrhage (ICH) in patients with a previous stroke remains uncertai

87 progression after intracerebral haemorrhage (ICH) induced by collagenase in mice using a preclinical

88 Intracerebral haemorrhage (ICH) is a life-threatening emergency, the incidence of w

89 he acute phase of intracerebral haemorrhage (ICH) is beneficial.

90 disease including intracerebral haemorrhage (ICH), and common collagen IV variants are a risk factor

91 s (non-traumatic) intracerebral haemorrhage (ICH).

92 ife (HRQoL) after intracerebral haemorrhage (ICH).

93 stroke recurrence, intracranial haemorrhage (ICH) and acenocoumarol maintenance dose in a Spanish pop

94 that detects acute intracranial haemorrhage (ICH) and classifies five ICH subtypes from unenhanced he

95 y lifestyle and ideal cardiovascular health (ICH) scores of 1,216 children 9 to 13 years old was perf

96 tress (CPS) and ideal cardiovascular health (ICH), as defined by the American Heart Association's 202

97 omains (NBDs) contact intracellular helices (ICHs).

98 ic stroke (IS) and intracerebral hemorrhage (ICH) account for an equal number of deaths in China, des

99 Intracerebral hemorrhage (ICH) accounts for a disproportionate amount of stroke-re

100 ognostic factor in intracerebral hemorrhage (ICH) and is associated with permanent shunt dependency i

101 torial spontaneous intracerebral hemorrhage (ICH) and whether it is modified by key baseline characte

102 ot sign to predict intracerebral hemorrhage (ICH) expansion with standardized multiphase computed tom

103 ts with cerebellar intracerebral hemorrhage (ICH) has not been established.

104 ic stroke (IS) and intracerebral hemorrhage (ICH) in a cohort of Chinese adults.

105 Intracerebral hemorrhage (ICH) is a devastating form of stroke affecting millions

106 Spontaneous deep intracerebral hemorrhage (ICH) is a devastating subtype of stroke without specific

107 Intracerebral hemorrhage (ICH) is an especially feared complication in patients wi

108 le sclerosis (MS), intracerebral hemorrhage (ICH), and neuromyelitis optica (NMO).

109 levels and risk of intracerebral hemorrhage (ICH), but it remains unclear whether this association is

110 y occurs following intracerebral hemorrhage (ICH), but the mechanisms underlying this phenomenon rema

111 a risk factor for intracerebral hemorrhage (ICH).

112 eneficial in acute intracerebral hemorrhage (ICH).

113 ications following intracerebral hemorrhage (ICH).

114 sms after onset of intracerebral hemorrhage (ICH).

115 antation following intracerebral hemorrhage (ICH).

116 ts presenting with intracerebral hemorrhage (ICH).

117 identification and intracranial hemorrhage (ICH) detection.

118 d as microbleed and intracranial hemorrhage (ICH) rates.

119 of ischemic stroke, intracranial hemorrhage (ICH), hospitalization for gastrointestinal (GI) bleeding

120 ulant effects after intracranial hemorrhage (ICH).

121 ma clearance after intracerebral hemorrhage [ICH]), and (3) reduced proinflammatory responses.

122 nt catalysis modulates isocyanide hydratase (ICH) conformational dynamics throughout its catalytic cy

123 ombined impact of intracranial hypertension (ICH) and obstructive sleep apnea (OSA) on optic nerve fu

124 of recurrent ICH events than non-lobar ICH; ICH location did not influence risk of subsequent ischae

125 In ICH survivors, lobar ICH location was associated with a

126 potential causal role of LDL cholesterol in ICH.

127 teractions between CPS and race/ethnicity in ICH models were not significant.

128 ssociated with a non-significant increase in ICH (RR 1.36, 95% CI 0.96 to 1.91; n=103 525), but signi

129 on of a thioimidate covalent intermediate in ICH microcrystals during catalysis.

130 Intraventricular administration of MSCs in ICH rat model showed improved behavior and alleviated br

131 ve been implicated in playing vital roles in ICH outcomes.

132 Of 4,677 included ICH patients, 1,017 (21.7%) were affected by ECL (German

133 High (>/=14) NIHSS score, larger ICH and proxy responders were associated with low scores

134 of Health Stroke Scale (NIHSS) score, larger ICH, presence of intraventricular extension and use of p

135 stroke, dementia and lower QALYs after lobar ICH highlight the need for more effective prevention for

136 ean/SD age 75.5/13.1), 109 (42.7%) had lobar ICH, 144 (56.5%) non-lobar ICH and 2 (0.8%) had uncertai

137 ted with admission haematoma volume in lobar ICH (beta, 0.25; SE, 0.12; p=0.03), but there was no rel

138 ed with admission haematoma volumes in lobar ICH.

139 were also lower after lobar versus non-lobar ICH (2.9 vs 3.8 for non-lobar, p=0.04).

140 nt-years); and 39 in patients with non-lobar ICH (AER 2.97 per 100 patient-years).

141 ICH were higher after lobar versus non-lobar ICH (lobar=4.0%, 2.7-7.2 vs 1.1%, 0.3-2.8; p=0.02).

142 a was also higher for lobar versus non-lobar ICH (n/% lobar=20/36.4% vs 16/20.8%, p=0.047), and there

143 and 9 in patients presenting with non-lobar ICH (n=580, AER 0.69 per 100 patient-years).

144 (42.7%) had lobar ICH, 144 (56.5%) non-lobar ICH and 2 (0.8%) had uncertain location.

145 Compared with non-lobar ICH, the substantially higher 10-year risks of recurrent

146 risk of recurrent ICH events than non-lobar ICH; ICH location did not influence risk of subsequent i

147 In ICH survivors, lobar ICH location was associated with a higher risk of recurr

148 ultivariable Cox regression found that lobar ICH was associated with ICH recurrence (HR 8.96, 95% CI

149 years); 29 in patients presenting with lobar ICH (AER 3.12 per 100 patient-years); and 39 in patients

150 years); 35 in patients presenting with lobar ICH (n=447, AER 3.77 per 100 patient-years); and 9 in pa

151 essure, stroke), and observed that all major ICHs on enoxaparin occurred in the setting of a PANWARDS

152 this study was to determine whether the max-ICH (maximally treated ICH) Score provides improved and

153 tive poor outcome attribution), that the max-ICH Score provided a clinical net benefit compared with

154 unctional outcome prognostication by the max-ICH Score provided good and superior discrimination in p

155 The max-ICH Score provides valid and improved prognostication of

156 tudy compared the prognostication of the max-ICH Score versus the ICH Score regarding diagnostic accu

157 Mean ICH scores varied by race/ethnicity ( P<0.01) and were s

158 There was no difference in mean ICH-volume between the two groups (standard mean differe

159 We measured ICH and PHO volume on CT; PHO was measured by oedema ext

160 anticoagulation, 60.5% vs 63.8%; and median ICH volume, 20.5 cm3 vs 18.8 cm3).

161 emographics, Meth-ICH is similar to Non-Meth ICH in hospital course and outcome.

162 e identified as Meth-ICH and 350 as Non-Meth ICH.

163 Meth-ICH and Non-Meth-ICH were defined by history of abuse an

164 Meth-ICH was more common in Hispanics (14.6%) and Whites (10.

165 patients, 61 (9.0%) were identified as Meth-ICH and 350 as Non-Meth ICH.

166 Despite difference in demographics, Meth-ICH is similar to Non-Meth ICH in hospital course and ou

167 omes of methamphetamine-associated ICH (Meth-ICH) versus Non-Meth-ICH.

168 Non-Meth-ICH was more likely to have history of hypertension (72.

169 Meth-ICH and Non-Meth-ICH were defined by history of abuse and urine drug scre

170 ne-associated ICH (Meth-ICH) versus Non-Meth-ICH.

171 Patients with Meth-ICH were more often younger (51.2 vs. 62.2 years, p < 0.

172 glucose, with higher levels indicating more ICH and less cardiovascular risk (score range, 0-7).

173 -rank p=0.645; VKA-ICH: 27/1406 (1.9%), NOAC-ICH 1/130 (0.8%), non-OAC-ICH 14/880 (1.6%); p=0.577).

174 ding IHC among non-OAC-ICH, VKA-ICH and NOAC-ICH in this observational cohort analysis.

175 patients with non-OAC-ICH, VKA-ICH and NOAC-ICH, mortality and functional outcome at 3 months betwee

176 ence rates among patients with VKA-ICH, NOAC-ICH and non-OAC-ICH (log-rank p=0.645; VKA-ICH: 27/1406

177 haematoma expansion were comparable in NOAC-ICH versus VKA-ICH (OR: 0.76; 95% CI 0.49 to 1.19, p=0.2

178 d-fluid level is not useful in excluding OAC-ICH.

179 The specificity of blood-fluid level for OAC-ICH was 99.4%; the sensitivity was 4.2%.

180 r for oral anticoagulant-associated ICH (OAC-ICH), but the diagnostic specificity and prognostic valu

181 patients with VKA-ICH, NOAC-ICH and non-OAC-ICH (log-rank p=0.645; VKA-ICH: 27/1406 (1.9%), NOAC-ICH

182 /1406 (1.9%), NOAC-ICH 1/130 (0.8%), non-OAC-ICH 14/880 (1.6%); p=0.577).

183 ssociated ICH and 1022 patients with non-OAC-ICH with heparin prophylaxis between 2006 and 2015.

184 pears to be safe regarding IHC among non-OAC-ICH, VKA-ICH and NOAC-ICH in this observational cohort a

185 ng hospital stay among patients with non-OAC-ICH, VKA-ICH and NOAC-ICH, mortality and functional outc

186 d alert clinicians to the possibility of OAC-ICH, but absence of a blood-fluid level is not useful in

187 data (IPD) meta-analysis of 4 observational ICH studies incorporating 6580 patients treated at 64 ho

188 ons with a primary or secondary diagnosis of ICH were further identified.

189 ith brain metastases also had a diagnosis of ICH, which was significantly associated with longer leng

190 4,145 (2.85%) had a concurrent diagnosis of ICH.

191 reversal (pr)VEP (2013-2014) and history of ICH based on direct measurement, papilledema, or classic

192 re also uncertainties about the influence of ICH location on risks of recurrent stroke, disability, d

193 ong-term anticoagulation, the interaction of ICH with neurodegenerative diseases, and our approach to

194 asculopathies accounting for the majority of ICH, there are a broad range of potential causes, and ef

195 ive function in a mouse collagenase model of ICH.

196 Finally, in mouse models of ICH, spleen shrinkage could be related to innervations f

197 d- and collagenase-injection mouse models of ICH, through modulation of microglia/macrophage function

198 3 activity, is involved in the occurrence of ICH in Col4a1 mutant mice, by raising the intravascular

199 defect may be required for the occurrence of ICH.

200 and sensory deficits in the chronic phase of ICH, we noted significant cognitive impairment, which wa

201 ed in field settings for triage (presence of ICH), especially where low radiation dose is desired.

202 ng-term anticoagulation had a higher risk of ICH (OR 1.49; CI 1.15-1.91).

203 elevant biomarker for evaluating the risk of ICH before tPA administration.

204 nt factors associated with increased risk of ICH were enrollment in Asia or Latin America, older age,

205 DL levels were associated with lower risk of ICH, providing support for a potential causal role of LD

206 ng-term anticoagulation had a higher risk of ICH.

207 vated LDL is associated with reduced risk of ICH.

208 0.65-0.98; p = 0.03) and 41% lower risks of ICH (OR = 0.59; 95% CI = 0.42-0.82; p = 0.002), respecti

209 -13), and concerns about the excess risks of ICH associated with lowering LDL-C(14,15) may have preve

210 cognitive impairment in the chronic stage of ICH recovery.

211 Modern treatment of ICH focuses on rapid stabilization, often requiring urge

212 ntrols to estimate the effect of each PRS on ICH risk.

213 addresses the evidence of statin therapy on ICH and other clinical outcomes in patients with previou

214 ients with previous ischaemic stroke (IS) or ICH.

215 associations of fibrinogen with MCE, IS, or ICH were identified.

216 3), but there was no relationship with other ICH outcomes when stratified by haematoma location or st

217 he risk ratios (RR) for the primary outcome (ICH) and secondary outcomes (IS, any stroke, mortality a

218 HP CNV or rs200999 with functional outcome, ICH volume or PHO volume.

219 tivation/degranulation, IVIG attenuated post-ICH mast cell activation.

220 ependency for aresorptive hydrocephalus post-ICH.

221 in a substantial proportion of patients post-ICH.

222 and ipsilateral hemispheres up to 5 wk post-ICH.

223 The exposure was APT preceding ICH diagnosis.

224 There was no difference in prespecified ICH rates.

225 or no treatment) in patients with a previous ICH or IS.

226 In patients with previous ICH, statins had no significant impact on the pooled RR

227 Of 255 cases with primary ICH (mean/SD age 75.5/13.1), 109 (42.7%) had lobar ICH,

228 e included patients with neuroimaging-proven ICH, available DNA and 6-month follow-up in an observati

229 ICH with history of OSA; group 3, recurrent ICH absent history of OSA; and group 4, recurrent ICH wi

230 bsent history of OSA; and group 4, recurrent ICH with history of OSA.

231 There were 45 recurrent ICH events (absolute event rate (AER) 1.88 per 100 patie

232 ficant impact on the pooled RR for recurrent ICH (1.04, 95% CI 0.86 to 1.25; n=23 695); however, stat

233 s associated with a higher risk of recurrent ICH events than non-lobar ICH; ICH location did not infl

234 Annual rates of recurrent ICH were higher after lobar versus non-lobar ICH (lobar=

235 History of OSA, in addition to recurrent ICH, is associated with greatest risk of optic neuropath

236 nged P100 latency with resolved vs recurrent ICH and OSA.

237 ly150) that modulate helical mobility reduce ICH catalytic turnover and alter its pre-steady-state ki

238 ce with the established disease also reduced ICH.

239 In exploratory analyses, 3K3A-APC reduced ICH rates compared to placebo from 86.5% to 67.4% in the

240 ighlights the clinical relevance of reducing ICH by using apixaban rather than warfarin and avoiding

241 d methods are completely validated regarding ICH guidelines.

242 in patients with factor Xa inhibitor-related ICH are needed.

243 cacy of PCCs for factor Xa inhibitor-related ICH in a large, multicenter cohort of patients.

244 PCCs after apixaban- and rivaroxaban-related ICH provided a high rate of excellent or good hemostasis

245 tients with apixaban- or rivaroxaban-related ICH who received PCCs between January 1, 2015, and March

246 ere divided into 4 groups: group 1, resolved ICH absent history of OSA; group 2, resolved ICH with hi

247 ICH absent history of OSA; group 2, resolved ICH with history of OSA; group 3, recurrent ICH absent h

248 SCORE-IT (Spot Sign Score in Restricting ICH Growth) is a preplanned prospective observational st

249 Small ICH volume (OR: volume <4.4 mL: 0.18 (0.04-0.78); p=0.02

250 of adults with imaging confirmed spontaneous ICH.

251 participant data of consecutive spontaneous ICH patients (n = 4,677) from 2 retrospective German-wid

252 ical treatment of supratentorial spontaneous ICH aimed at clot removal.

253 ical treatment of supratentorial spontaneous ICH may be beneficial, in particular with minimally inva

254 n IV variants are a risk factor for sporadic ICH.

255 Clinical Relevance of Microbleeds in Stroke) ICH study were included (mean age 73.3 years; 57.4% male

256 d contralateral hemispheres, suggesting that ICH also induces functional alterations in distal brain

257 phagocytes to engulf red blood cells in the ICH brain and in primary cultures.

258 ctivated motions permit water entry into the ICH active site for intermediate hydrolysis.

259 In the outward-facing state, the ICH-NBD1 interface showed decreased exchange, while the

260 gnostication of the max-ICH Score versus the ICH Score regarding diagnostic accuracy (discrimination

261 terface showed decreased exchange, while the ICH-NBD2 interface showed less of an effect.

262 ded a clinical net benefit compared with the ICH Score (14.1 vs 2.1 net predicted poor outcomes per 1

263 on in patients without ECL compared with the ICH Score (area under the receiver operating curve [AURO

264 his evaluation system is set up according to ICH/GCP, World Medical Association Declaration of Helsin

265 of novel medical and surgical approaches to ICH treatment that are being tested in clinical trials.

266 use as a method of delivering MSCs to treat ICH.

267 Additionally, treated ICH rats showed significantly reduced expression of IL-1

268 rmine whether the max-ICH (maximally treated ICH) Score provides improved and clinically useful progn

269 outcome was also comparable between the two ICH groups.

270 German prospective single-center study (UKER-ICH; nonanticoagulation-associated ICH only), and 1 US-b

271 We applied a validated ICH prediction risk score PANWARDS (platelets, albumin,

272 C-ICH and non-OAC-ICH (log-rank p=0.645; VKA-ICH: 27/1406 (1.9%), NOAC-ICH 1/130 (0.8%), non-OAC-ICH

273 be safe regarding IHC among non-OAC-ICH, VKA-ICH and NOAC-ICH in this observational cohort analysis.

274 al stay among patients with non-OAC-ICH, VKA-ICH and NOAC-ICH, mortality and functional outcome at 3

275 nsion were comparable in NOAC-ICH versus VKA-ICH (OR: 0.76; 95% CI 0.49 to 1.19, p=0.236).

276 rude incidence rates among patients with VKA-ICH, NOAC-ICH and non-OAC-ICH (log-rank p=0.645; VKA-ICH

277 We demonstrated that while ICH induced mast cell activation/degranulation, IVIG att

278 ion found that lobar ICH was associated with ICH recurrence (HR 8.96, 95% CI 3.36 to 23.87, p<0.0001)

279 5; p = 0.002) were inversely associated with ICH risk, no significant associations were found for HDL

280 ionwide and identify factors associated with ICH.

281 ere used to identify factors associated with ICH.

282 was used to identify factors associated with ICH.

283 ble Cox regression found no association with ICH location (HR 1.13, 95% CI 0.66 to 1.92, p = 0.659).

284 and equally strong inverse associations with ICH, which were confirmed by genetic analyses and LDL-C-

285 oembolism (VTE) prophylaxis in patients with ICH appears to be safe regarding IHC among non-OAC-ICH,

286 Patients with ICH between January 2011 and December 2017 were studied.

287 -day case fatality with 32,295 patients with ICH from 214 other hospitals in England and Wales using

288 Patients with ICH were more likely to have a longer length of stay (me

289 We discuss management of patients with ICH who continue to require long-term anticoagulation, t

290 al outcome at 3 months between patients with ICH with and without IHC.

291 large heterogeneous cohort of patients with ICH, prior APT was not associated with haematoma expansi

292 Among 1420 patients with ICH, there were 782 (55.1%) lobar and 596 (42.0%) deep h

293 t includes a limited number of patients with ICH.

294 gly associated with outcome in patients with ICH.

295 occurred in 1.7% (42/2416) of patients with ICH.

296 l to lymphocyte ratio (NLR) in patients with ICH.

297 nwarranted care limitations in patients with ICH.

298 ata suggest an association of ER stress with ICH due to a COL4A2 mutation.

299 ith stroke recurrence and four variants with ICH (p < 0.05).

300 cteristics between patients with and without ICH were assessed by chi-square, Mann-Whitney U, and ANO