ライフサイエンスコーパス: hemorrhage

1 ntrally and peripherally after intracerebral hemorrhage.

2 start anticoagulation after an intracerebral hemorrhage.

3 t failure, neurological deficit/seizure, and hemorrhage.

4 c (95% CI, 47.3-48.9) for acute intracranial hemorrhage.

5 outcomes in an animal model of intracerebral hemorrhage.

6 omised compensatory hemodynamic responses to hemorrhage.

7 in the treatment of noncompressible truncal hemorrhage.

8 enous retinal detachment along with vitreous hemorrhage.

9 surements and tested to minimize the risk of hemorrhage.

10 on-mediated brain injury after intracerebral hemorrhage.

11 ociated traction on the retina and sometimes hemorrhage.

12 Retinal and vitreous hemorrhage.

13 with traumatic brain injury or subarachnoid hemorrhage.

14 can identify infants with acute intracranial hemorrhage.

15 ied after an acute large-volume subarachnoid hemorrhage.

16 conferred survival benefit following severe hemorrhage.

17 ssociated with the outcomes of intracerebral hemorrhage.

18 ssist and closed-loop resuscitation in human hemorrhage.

19 e independently associated with intracranial hemorrhage.

20 attenuates brain injury after intracerebral hemorrhage.

21 ted skull fractures, or chronic intracranial hemorrhage.

22 ng still reduced prolonged bleeding time and hemorrhage.

23 nical complications, including intracerebral hemorrhage.

24 ociation with stable angina or intracerebral hemorrhage.

25 aminotransferase level elevation and rectal hemorrhage.

26 ssociated macrophages, vascular ectasia, and hemorrhage.

27 upper pulmonary lobe suggestive of alveolar hemorrhage.

28 e of intraretinal or subretinal fluid or new hemorrhage.

29 y of limb amputation, head injury, and torso hemorrhage.

30 yed cerebral ischemia following subarachnoid hemorrhage.

31 ET) are at high risk for both thrombosis and hemorrhage.

32 re their performances in discriminating DAVF hemorrhage.

33 th severe nonvariceal upper gastrointestinal hemorrhage.

34 hysicians to the possibility of intracranial hemorrhage.

35 and 3) factors associated with intracranial hemorrhage.

36 efficient in goal-directed resuscitation of hemorrhage.

37 were terminated immediately without causing hemorrhage.

38 0% for vessel discoloration, and 73%/96% for hemorrhages.

39 ng, vessel discoloration, and white-centered hemorrhages.

40 rs of nonfunctional blood vessels and severe hemorrhaging.

41 Symptomatic intracranial hemorrhage (1% vs 4%) and parenchymal hemorrhages type 1

42 ack patients aged 45 to 54 with subarachnoid hemorrhage (13.2/10000 to 10.3/10000 hospitalizations an

43 0.92 [95% CI, 0.65 to 1.28]) or extracranial hemorrhage (2.12 vs. 2.63 events per 100 person-years; H

44 we sought 1) the prevalence of intracranial hemorrhage; 2) survival and neurologic outcomes; and 3)

45 Response to hemorrhage (20% loss of blood volume), including plasma

46 nstrual age (4 eyes, 30.8%); and/or vitreous hemorrhage (3 eyes, 23.1%).

47 , thoracic pain (3%), upper gastrointestinal hemorrhage (3%), and vomiting (3%).

48 g) included choroidal effusion (1), vitreous hemorrhage (3), Descemet detachment (1), and persistent

49 tients (7.1%), and included 181 intracranial hemorrhage (42.5%), 100 brain deaths (23.5%), 85 stroke

50 ding, whereas those with 4-quadrant dot-blot hemorrhages (4Q DBH) had 3.84 higher HR of developing VH

51 tween patients with and without intracranial hemorrhage (68.3% vs 76.0%; p = 0.350).

52 lity was 79.6% in patients with intracranial hemorrhage, 68.2% in patients with stroke, and 50% in pa

53 cases showed restricted diffusion (43%) and hemorrhage (9%).

54 Retrospective analysis of all subarachnoid hemorrhage admissions.

55 Pulmonary hemorrhage after TTLB is common but rarely requires inte

56 g and 98 (32.6%) presented with intracranial hemorrhage; among the patients who could be assessed, th

57 A total of 46,735 intracerebral hemorrhage and 331,521 ischemic stroke cases.

58 ng boy with a history of idiopathic vitreous hemorrhage and a female infant with familial exudative v

59 usion of angiotensin II led to aortic medial hemorrhage and dissection.

60 promotes neovascularization, and can induce hemorrhage and encourage tumor growth.

61 associated with the presence of intraplaque hemorrhage and heme degradation products, particularly b

62 ion, the associated significant risk of cyst hemorrhage and infection precluded this procedure.

63 APP/PS1;Clu(-/-) mice had significantly less hemorrhage and inflammation.

64 patients with PM nonaneurysmal subarachnoid hemorrhage and initial DSA negative for aneurysms, the y

65 Intracerebral hemorrhage and ischemic stroke admissions were identifie

66 ther palliative care use after intracerebral hemorrhage and ischemic stroke differs between hospitals

67 l salvage, and the extent of intramyocardial hemorrhage and microvascular obstruction varied dramatic

68 occlusion leading to increased intracranial hemorrhage and mortality.

69 o, 0.65; 95% CI, 0.50-0.84 for intracerebral hemorrhage and odds ratio, 0.62; 95% CI, 0.50-0.77 for i

70 one with cortical dysplasia, one with pineal hemorrhage and one with a brain tumor.

71 he ARMS2/HTRA1 locus with subretinal/sub-RPE hemorrhage and poorer visual acuity and of SNPs at the C

72 als had significantly reduced intraoperative hemorrhage and postoperative hematoma volumes compared t

73 hysical stressors (for example, hypotension, hemorrhage and presence of lipopolysaccharides).

74 e locally activated by hydrodynamic force in hemorrhage and rapidly deactivated downstream, providing

75 d warfarin, with lower rates of intracranial hemorrhage and reduced mortality.

76 a, cerebellum and brainstem, with or without hemorrhage and restricted diffusion.

77 the wide range of cardiac output produced by hemorrhage and resuscitation in large pigs, noninvasive

78 Experimental human hemorrhage and resuscitation.

79 , and cardiac function were monitored during hemorrhage and resuscitation.

80 n result in complications including vitreous hemorrhage and retinal detachment.

81 damage to blood vessels and, in rare cases, hemorrhage and shock.

82 lly, hospitalization rates for intracerebral hemorrhage and subarachnoid hemorrhage remained stable,

83 However, widespread hemorrhage and subsequent lethality does not occur until

84 y aneurysms represent a significant risk for hemorrhage and therefore must be addressed promptly once

85 stotripsy, in addition to areas of petechial hemorrhage and tissue disruption by means of cavitation-

86 of atherosclerotic plaques with intraplaque hemorrhage and ultimately holds promise for detection of

87 Subjects (n = 7) were subjected to hemorrhage and underwent a randomized fluid resuscitatio

88 To evaluate detection of hemorrhage and/or microaneurysm (H/Ma) using ultrawide f

89 12 of 15 eyes, associated with small retinal hemorrhages and intraretinal exudation.

90 rred with repeated episodes of conjunctival "hemorrhages" and chemosis with extended recovery periods

91 d loss requiring transfusion or intracranial hemorrhage) and thrombosis during ECMO support; (2) to i

92 had prior infarct, 8 had hypertensive brain hemorrhage, and 164 admissions for PSR were identified.

93 y of prematurity and severe intraventricular hemorrhage, and 8 years to achieve the rate from the bes

94 Geographic atrophy in the fellow eye, hemorrhage, and absence of sub-retinal pigment epitheliu

95 pelvic fracture, central line, intracranial hemorrhage, and blood transfusion).

96 Levels of BBB opening, hemorrhage, and cavitation signal were measured with MR

97 Ischemic stroke, intracranial hemorrhage, and death.

98 ely, these changes enhanced edema, prolonged hemorrhage, and impaired forelimb functional recovery.

99 ldren (aged >10-15 years) with larger tumor, hemorrhage, and lack of cyst.

100 risk, infarct size, salvage, intramyocardial hemorrhage, and microvascular obstruction should be stan

101 risk, infarct size, salvage, intramyocardial hemorrhage, and microvascular obstruction) is not well u

102 sured at nine time points spanning baseline, hemorrhage, and resuscitation.

103 fections can lead to vascular complications, hemorrhage, and shock due to the ability of DENV to infe

104 outcomes were ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage as defined by va

105 out vitreitis, retinal vasculitis, vitreous hemorrhage, and systemic amyloidosis.

106 At 2 years, rates of thrombosis, hemorrhage, and transformation were not significantly di

107 by neuronal injury, multiple brain petechial hemorrhages, and central nervous system inflammation, an

108 e risk for life-threatening/serious systemic hemorrhage, any rt-PA complication, in-hospital mortalit

109 Restricted diffusion and hemorrhage are rare.

110 infarction, major bleeding, or intracranial hemorrhage as an outcome.

111 , intracerebral hemorrhage, and subarachnoid hemorrhage as defined by validated diagnosis code algori

112 A) display enhanced angiogenic sprouting and hemorrhage as well as enlarged jugular lymph sacs and ly

113 ant use was associated with a higher rate of hemorrhage at baseline (66.8% vs. 56.4%; adjusted OR, 1.

114 The FCT, SHRM thickness, and hemorrhage at baseline were all significant predictors o

115 For patients with subarachnoid hemorrhage, autoregulation reactivity index was the only

116 For patients with subarachnoid hemorrhage, autoregulation reactivity index was the only

117 ll patients with a diagnosis of subarachnoid hemorrhage between 2009 and 2014.

118 f 57 eyes (1.8%) showed a transient vitreous hemorrhage, biopsy yield was 100% for genetic analysis,

119 A major neonatal condition, GM hemorrhage can lead to cerebral palsy, hydrocephalus, an

120 ific hazard, 2.12 [1.14-3.96]; p = 0.02) and hemorrhage (cause-specific hazard, 3.17 [1.41-7.13]; p =

121 ificant differences were found in postpartum hemorrhage, cesarean section, and elevated creatinine ki

122 ertension, hemorrhagic retinopathy, vitreous hemorrhage, combined traction and rhegmatogenous retinal

123 sion (SAAP) combines thoracic aortic balloon hemorrhage control with intra-aortic oxygenated perfusio

124 aling fully corrected the BBB disruption and hemorrhage defects of Gpr124-CKO mice, with rescue of th

125 rticipants (4.08%) had retinal or subretinal hemorrhage detected on 1- or 2-year photographs; these h

126 ens, radiographic presentation, or pulmonary hemorrhage did not alter predictive values.

127 The rate of symptomatic intracranial hemorrhage did not differ significantly between the two

128 of sodium nitrite after severe subarachnoid hemorrhage differentially influences quantitative electr

129 lation who are also at risk of intracerebral hemorrhage due to cerebral amyloid angiopathy, the resul

130 angiogenesis and selective vulnerability to hemorrhage during development.

131 lla GPVI-depleted mice showed increased lung hemorrhage during infection, but not to the extent obser

132 necessary for host defense and prevention of hemorrhage during sepsis, but the role of platelet GPVI

133 rtality at 90 days, symptomatic intracranial hemorrhage, emboli to new territory, and vasospasm were

134 The remaining 2 eyes had vitreous hemorrhage; endoscopic vitrectomy was done in them to de

135 nce allows in vivo monitoring of intraplaque hemorrhage, establishing a preclinical technology to ass

136 Ischemic stroke, intracranial hemorrhage, extracranial bleeding, and myocardial infarc

137 sted odds ratio for symptomatic intracranial hemorrhage for those on NOACs was 0.92 (95% confidence i

138 patients with severe upper gastrointestinal hemorrhage from ulcers or other lesions, Doppler probe g

139 R >/= 0.7 or the presence of a notch or disc hemorrhage) from fundus photographs taken with a nonmydr

140 brain injury, defined as an intraventricular hemorrhage grade of 3 or greater or cystic periventricul

141 al morbidity, defined as an intraventricular hemorrhage grade of 3 or greater, cystic periventricular

142 ncluding primary and secondary intracerebral hemorrhage, hemorrhagic transformation of ischemic injur

143 ith respect to the reduction of intracranial hemorrhage (HR, 0.38; 95% CI, 0.26-0.56).

144 tion appeared to be higher for intracerebral hemorrhage (HR, 1.9; 95% CI, 1.5-2.4) and subarachnoid h

145 associated with a >13-fold increased risk of hemorrhage (HR, 13.26; 95% CI, 3.33-52.85; P < .0001).

146 (HR, 1.9; 95% CI, 1.5-2.4) and subarachnoid hemorrhage (HR, 2.4; 95% CI, 1.7-3.5) than for ischemic

147 curred in 4 cases (15%), including pulmonary hemorrhage, hypotension requiring vasoactive support, co

148 negative prognostic factor in intracerebral hemorrhage (ICH) and is associated with permanent shunt

149 ssure (BP) reduction for acute intracerebral hemorrhage (ICH) are inconsistent.

150 ormance of APT MRI in detecting intracranial hemorrhage (ICH) at hyperacute, acute and subacute stage

151 on is a therapeutic dilemma in intracerebral hemorrhage (ICH) care, particularly for lobar hemorrhage

152 ) spot sign is associated with intracerebral hemorrhage (ICH) expansion and may mark those patients m

153 using the spot sign to predict intracerebral hemorrhage (ICH) expansion with standardized multiphase

154 Intracerebral hemorrhage (ICH) is a devastating disease without effect

155 Intracerebral hemorrhage (ICH) is a devastating form of stroke that re

156 Spontaneous intracranial hemorrhage (ICH) is also a frequent occurrence in these

157 Intracerebral hemorrhage (ICH) is one of the most devastating and disa

158 Concern about intracerebral hemorrhage (ICH) is the primary reason for withholding t

159 Intracranial hemorrhage (ICH) was the most common site of bleeding re

160 crease the risk for spontaneous intracranial hemorrhage (ICH), an effect that is in theory linked to

161 events (SSEE), major bleeding, intracranial hemorrhage (ICH), and all-cause death.

162 ulators of tissue damage after intracerebral hemorrhage (ICH), but how this function is regulated is

163 Following intracerebral hemorrhage (ICH), the activation of mast cell contribute

164 requency and characteristics of intracranial hemorrhage (ICH), the factors associated with the risk o

165 urine brain after experimental intracerebral hemorrhage (ICH), we found robust phenotypic changes in

166 usion changes in patients with intracerebral hemorrhage (ICH).

167 oor outcome following an acute intracerebral hemorrhage (ICH).

168 Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-II) randomized clinical trial.

169 , lacunar ischemic strokes, and intracranial hemorrhages), immunodeficiency and bone marrow failure.

170 ng occurred in 70.2%, including intracranial hemorrhage in 16%, and was independently associated with

171 ar hypertension in 44 eyes (11.3%), vitreous hemorrhage in 31 eyes (7.9%), and transient hypotony in

172 (3 of 48 eyes), and choroidal detachment or hemorrhage in 8.3% (4 of 48 eyes).

173 ascular permeability and suppressed alveolar hemorrhage in an orthotopic transplant model for up to 3

174 crovascular obstruction, and intramyocardial hemorrhage in both acute setting and later follow-up exa

175 promising therapy for reducing perioperative hemorrhage in elective surgeries.

176 al model that can predict acute intracranial hemorrhage in infants at increased risk of abusive head

177 te and timely identification of intracranial hemorrhage in infants without a history of trauma in who

178 nd dense-granule secretion, show no signs of hemorrhage in models of skin or lung inflammation.

179 resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and g

180 esent a stronger risk factor associated with hemorrhage in patients with lateral sinus DAVFs than doe

181 ND & AIMS: For 4 decades, stigmata of recent hemorrhage in patients with nonvariceal lesions have bee

182 , renal function, and the reflex response to hemorrhage in sheep with normotension (control) or with

183 histopathology of necrotizing vasculitis and hemorrhage in the brain.

184 orrelated with BW and GA, although including hemorrhage in the grading algorithm only minimally impro

185 Unadjusted rates of symptomatic intracranial hemorrhage in the NOAC, warfarin, and none groups were 4

186 reventive therapy for reducing perioperative hemorrhage in the rodent model of surgical brain injury

187 multivariable model to identify intracranial hemorrhage in well-appearing infants using the Ziplex Sy

188 0.68-0.98]) were associated with intraplaque hemorrhage in women but not in men.

189 and vitreous inflammation, sectoral retinal hemorrhages in areas of ischemia, and predilection for v

190 Hemorrhage increased heart rate and plasma renin activit

191 fect of NAC in a mouse model of intracranial hemorrhage induced by in situ collagenase type VII injec

192 SAAP can effect ROSC from hemorrhage-induced electrocardiographic asystole in larg

193 Survival rates remain low after hemorrhage-induced traumatic cardiac arrest (TCA).

194 val over REBOA in this large animal model of hemorrhage-induced traumatic cardiac arrest with NCTH.

195 ge, neutrophils infiltrate the intracerebral hemorrhage-injured brain.

196 ify tissue-specific molecular targets for GM hemorrhage intervention.

197 Hemorrhage into the brain of term newborns often results

198 re calculated with and without incorporating hemorrhage into the standardized grading protocol.

199 ne, ischemic stroke, aneurysmal subarachnoid hemorrhage, intracerebral hematoma, and trauma.

200 the clinical characteristics of intraocular hemorrhages (IOHs) in infants in the Telemedicine Approa

201 Purpose To investigate intraplaque hemorrhage (IPH) development and change over time.

202 It is unclear whether intracranial hemorrhage is a consequence of the extracorporeal interv

203 oxygenation, the occurrence of intracranial hemorrhage is associated with a high mortality.

204 rtesunate in patients with trauma and severe hemorrhage is planned.

205 Intraventricular hemorrhage (IVH) is a negative prognostic factor in intr

206 CSF accumulation following intraventricular hemorrhage (IVH), is a common disease usually treated by

207 ntrinsic vessels (4% vs 33%, P < .0001), and hemorrhage (<1% vs 3%, P = .0001).

208 sing a deep learning algorithm for detecting hemorrhage, mass effect, or hydrocephalus (HMH) at non-c

209 atment is of high clinical relevance because hemorrhage may aggravate the disease state and increase

210 Thus, subarachnoid hemorrhage may constitute an important exception to curr

211 ratio transfusion in the setting of massive hemorrhage may not be appropriate for all patients, and

212 g on intraretinal or subretinal fluid or new hemorrhages may be expanded to include PED changes.

213 In response to hemorrhage, mean arterial pressure fell in all groups, w

214 h inferior outcomes, to compare subarachnoid hemorrhage mortality with other neurological diagnoses,

215 e (0%), peripheral embolism (0%), and severe hemorrhage (n = 1, 3.7%).

216 tional retinal detachment (n = 49), vitreous hemorrhage (n = 40), full-thickness macular hole (n = 33

217 ocated intraocular lens (n = 10), submacular hemorrhage (n = 7), endophthalmitis (n = 6), and retaine

218 Noncompressible torso hemorrhage (NCTH) is a major cause of potentially surviv

219 y reduce the pancreatic edema, infiltration, hemorrhage, necrosis, the release of amylase and lipase.

220 athy of prematurity, severe intraventricular hemorrhage, necrotizing enterocolitis, and chronic lung

221 Shortly after intracerebral hemorrhage, neutrophils infiltrate the intracerebral hem

222 phenotype for the treatment of intracerebral hemorrhage.Neutrophils are important modulators of tissu

223 ing a chronic stroke but no acute infarct or hemorrhage, no evidence of transient ischemic attack or

224 in death, seizures, stroke, and intracranial hemorrhage occurring during extracorporeal membrane oxyg

225 rmine the cumulative incidence of optic disc hemorrhage (ODH) before and after development of primary

226 per 1.73 m(2) had adjusted relative risks of hemorrhage of 1.9 (95% confidence interval [95% CI], 1.5

227 single spontaneous or traumatic intracranial hemorrhage, of whom 39 (83%) had hearing loss, ataxia, o

228 firmed spontaneous or traumatic intracranial hemorrhage, of whom none had hearing loss, ataxia, or my

229 risk of ICH and poor prognosis after a major hemorrhage on anticoagulation.

230 tentorial PICH, two points; intraventricular hemorrhage, one point; PICH volume greater than 2% of to

231 Major hemorrhage or cardiac tamponade leading to reoperation o

232 concentration increase in mice subjected to hemorrhage or EPO therapy, that ERFE acts on hepatocytes

233 sit with a primary diagnosis of intracranial hemorrhage or gastrointestinal, urogenital, or other ble

234 lication was defined as any transfusion, any hemorrhage or hematoma, or the need for percutaneous or

235 d in infarcted segments with intramyocardial hemorrhage or microvascular obstruction.

236 e strategy and the degree of intramyocardial hemorrhage or microvascular obstruction.

237 x 10(-5) ; N = 3,670), but not intracerebral hemorrhage (OR [95% CI] = 0.97 [0.84-1.12]; p = 0.71; 1,

238 al imaging and lack histological evidence of hemorrhage organization or thrombosis.

239 0.01), but not size of retinal or subretinal hemorrhage (P = 0.41).

240 ar rates of major complications (symptomatic hemorrhage, P > .999; pneumothorax requiring chest tube

241 Subarachnoid hemorrhage patients admitted to ICU in Australia and New

242 ularly to vulnerable regions in subarachnoid hemorrhage patients at risk for delayed cerebral ischemi

243 Intracerebral hemorrhage patients discharged between September 2011 an

244 h other neurological diagnoses, subarachnoid hemorrhage patients had significantly greater risk-adjus

245 ence palliative care use among intracerebral hemorrhage patients in the United States.

246 scribe in-hospital mortality in subarachnoid hemorrhage patients requiring ICU admission.

247 mol/L) on clinical outcomes in intracerebral hemorrhage patients treated with continuous IV infusion

248 re for both white and minority intracerebral hemorrhage patients was lower in minority compared with

249 A total of 11,327 subarachnoid hemorrhage patients were identified in the Australian an

250 kidney injury in patients with subarachnoid hemorrhage patients.

251 vations may impact outcomes in intracerebral hemorrhage patients.

252 validate a modified pediatric intracerebral hemorrhage (PICH) (mPICH) score and to compare its assoc

253 mes regarding the occurrence of intracranial hemorrhage, regardless of the antenatal management strat

254 retinal/sub-retinal pigment epithelial (RPE) hemorrhage related to neovascular AMD (odds ratio 1.55 [

255 emorrhage (ICH) care, particularly for lobar hemorrhages related to amyloid angiopathy.

256 or intracerebral hemorrhage and subarachnoid hemorrhage remained stable, with the exception of declin

257 hospital mortality, hospital length of stay, hemorrhage requiring transfusion, and permanent pacemake

258 defined as the first occurrence of vitreous hemorrhage, retinal detachment, anterior segment neovasc

259 lmitis, hypotony maculopathy, suprachoroidal hemorrhage, retinal detachment, stromal necrosis, and in

260 ion, but its risks of major and intracranial hemorrhages rival overall harms from intermediate PE.

261 sive consequences of aneurysmal subarachnoid hemorrhage (SAH).

262 athological processes including subarachnoid hemorrhage (SAH).

263 y; retinal tear; retinal detachment; retinal hemorrhages; scotomas; and an increased number of floate

264 -gauge pars plana vitrectomy for intraocular hemorrhages secondary to traumatic brain injury, and the

265 the majority of individuals with intraocular hemorrhages secondary to traumatic brain injury, irrespe

266 al outcomes after vitrectomy for intraocular hemorrhages secondary to traumatic brain injury.

267 erwent pars plana vitrectomy for intraocular hemorrhages secondary to traumatic brain injury.

268 Critically ill patients with subarachnoid hemorrhage show a strong association between hyperchlore

269 f the 6 false negatives had large subretinal hemorrhage (SRH) and sensitivity improved to 94% for bot

270 d to explore the variability in subarachnoid hemorrhage standardized mortality ratios.

271 trast, treatment of internal noncompressible hemorrhage still heavily depends on transfusion of whole

272 he Ethnic/Racial Variations of Intracerebral Hemorrhage study (n = 209).

273 ction (SOR) is more strongly associated with hemorrhage than cortical venous reflux (CVR) in patients

274 e report a higher prevalence of intracranial hemorrhage than has previously been described with high

275 y more likely to have died from intracranial hemorrhage than were all other deceased organ donors (85

276 Following hemorrhage, the total amount of infused fluid (bolus res

277 s independently associated with intracranial hemorrhage to be duration of ventilation (d) (odds ratio

278 l artery, tPA administration increased brain hemorrhage transformation, infarct volume, and edema.

279 ed symptoms, as well as risks of thrombosis, hemorrhage, transformation to myelofibrosis, and leukemi

280 ases), carcinogenesis, stroke, intracerebral hemorrhage, traumatic brain injury, ischemia-reperfusion

281 The aggregate traumatic subarachnoid hemorrhage (tSAH) component of the Stockholm CT score wa

282 ranial hemorrhage (1% vs 4%) and parenchymal hemorrhages type 1 (1% vs 3%) or type 2 (1% vs 2%) did n

283 izumab (IVB) use in patients with a vitreous hemorrhage (VH) secondary to proliferative diabetic reti

284 tive diabetic retinopathy (PDR) and vitreous hemorrhage (VH).

285 The prevalence of intracranial hemorrhage was 16.4% in extracorporeal membrane oxygenat

286 The presence of hemorrhage was directly correlated with both presence an

287 Intracranial hemorrhage was lower with higher-dose NOACs than with wa

288 In 18 patients (30%), subarachnoid hemorrhage was present.

289 IT (group A, n = 25; group B, n = 21); major hemorrhage was seen in 0 of 46 patients.

290 Intracranial hemorrhage was the most frequent type, and survival for

291 f calcification, lipid core, and intraplaque hemorrhage) was assessed by magnetic resonance imaging.

292 and PED thickness, and presence of baseline hemorrhage were all significant predictors of new MA dev

293 l features such as diffusion restriction and hemorrhage were also recorded.

294 Responses to hemorrhage were remarkably similar at 2 and 5 months pos

295 gestive heart failure and one fatal cerebral hemorrhage were reported.

296 detected on 1- or 2-year photographs; these hemorrhages were not associated with antiplatelet or ant

297 nts with high-grade spontaneous subarachnoid hemorrhage who underwent continuous surface (scalp) EEG

298 atest risk of suffering a major intracranial hemorrhage with anticoagulation.

299 ebral ischemia after aneurysmal subarachnoid hemorrhage with hemoglobin 7-13 g/dL.

300 ies of argon after experimental subarachnoid hemorrhage with mortality as the primary endpoint and fu