ライフサイエンスコーパス: coma

1 physiological end point (just prior to heat coma).

2 lurane (1.25%-1.5%) and induced hypoglycemic coma.

3 on history of prior seizures and presence of coma.

4 ors of critical illness spent in delirium or coma.

5 ney injury as a risk factor for delirium and coma.

6 peak serum creatinine and both delirium and coma.

7 the other head, blocking binding of Mif2 and COMA.

8 d had convulsions, altered consciousness, or coma.

9 bjects go from wake to sleep, anesthesia, or coma.

10 ed patients who were arousable from those in coma.

11 lotherms enter into a reversible, protective coma.

12 brain displacement and awakening from acute coma.

13 bjects (10.7%) were managed with therapeutic coma.

14 with DNA binding by the transcription factor ComA.

15 nd treatment in patients with acute onset of coma.

16 is weakened after adjusting for delirium and coma.

17 ale, and 78% had cerebrovascular etiology of coma.

18 ystem during recovery from prolonged post-CA coma.

19 lobal suppression of brain activity, such as coma.

20 E is clinically obvious disorientation, even coma.

21 Saturn, has remained undetected in cometary comas.

22 eter were: total HOA RMS: 0.41 +/- 0.30 mum, coma: 0.32 +/- 0.22 mum and spherical aberration: 0.21 +

23 odel patients had shorter length of delirium/coma (1.5 d [interquartile range, 1.0-3.0] vs 3.0 d [int

24 state/unresponsive wakefulness syndrome, six coma; 15 females; mean age 49 +/- 18 years, range 11-87;

25 dentified 3 patients with late recovery from coma (17-37 days) following CA who recovered to function

26 r delirium, 2.56; 95% CI, 1.57-4.16) (OR for coma, 3.34; 95% CI, 1.85-6.03).

27 variables of greatest predictive value were coma (31% had seizures; odds ratio [OR] = 1.8, p < 0.01)

28 Coma aberrations remained unchanged (P = 0.07) while the

29 survival and more days free of delirium and coma after adjusting for age, severity of illness, and p

30 Management of coma after cardiac arrest has improved during the past d

31 any previously reported outcome predictor of coma after cardiac arrest, including visual electroencep

32 eurologic outcomes in adults with persistent coma after resuscitated out-of-hospital cardiac arrest.

33 d with major neurological disorders, such as coma and Alzheimer's disease, as well as in normal cogni

34 ic mice with CM by performing a rapid murine coma and behavior scale experiment.

35 At a Rapid Murine Coma and Behavioral Scale (RMCBS) score of less than 15,

36 rasitic infection that usually progresses to coma and death unless treated.

37 trum, ranging from headache and dizziness to coma and death, with a mortality rate ranging from 1 to

38 te that the O2/H2O ratio is isotropic in the coma and does not change systematically with heliocentri

39 ween 18% (no clinical risk factors) and 64% (coma and history of seizures).

40 tween 9% (no clinical risk factors) and 36% (coma and history of seizures).

41 e of delirium and shorter length of delirium/coma and ICU stay.

42 This encephalopathy is characterized by coma and is thought to result from mechanical microvesse

43 r perfusion is central to the development of coma and lactic acidosis in severe falciparum malaria.

44 Outcome measures were Glasgow coma and outcome scores; CSF to serum albumin ratio, ref

45 h DNA repair (recA and ddrR) and competence (comA and pilX) genes.

46 s consistent with reported trends in the 67P coma and raises awareness of the role of energetic negat

47 disconnections are specifically observed in coma and their structural counterpart provides informati

48 ration, impaired consciousness, convulsions, coma), and malaria status were not related to referral c

49 gressed rapidly to hepatic insufficiency and coma, and died 8 days later.

50 here were changes in posterior corneal tilt, coma, and hexafoil in the PCRI group.

51 nificantly better DCNVA; higher negative SA, coma, and Q value (P < .05), and smaller pupil size (P =

52 ndary outcomes included duration of delirium/coma; any ICU-acquired infection; ICU-acquired bloodstre

53 sted odds ratio [AOR], 0.28; CI, 0.22-0.36), coma (AOR, 0.35; CI, 0.22-0.56), delirium (AOR, 0.60; CI

54 to the inner kinetochore when both Bir1 and COMA are defective, we show that localization of Ipl1-Sl

55 rolonged (>2 weeks) post-cardiac arrest (CA) coma are expected to remain permanently disabled.

56 clinical tests for prognosis of post-anoxic coma are informative of poor outcome.

57 lic acidosis, delirium on the prior day, and coma are risk factors for delirium, that gender is not a

58 r of days alive without delirium and without coma at day 14 did not differ significantly between the

59 significant difference in total HOA, SA, and coma between the initial and follow-up visits in both th

60 We defined the subunit topology of COMA, bound with inner kinetochore proteins Nkp1 and Nkp

61 two novel mechanisms of regulating Spo0A and ComA by Rap60 and expands our general understanding of h

62 laria"), allowing differentiation between 1) coma caused by sequestration of Plasmodium falciparum-in

63 e BSCVA, Kmax, refraction, corneal cylinder, coma, central corneal thickness, and vision function wer

64 lying pathology of life-threatening malarial coma ("cerebral malaria"), allowing differentiation betw

65 /Okp1(CENP-U/Q) heterodimer, which forms the COMA complex with Ctf19/Mcm21(CENP-P/O), selectively bou

66 One of these assemblies-COMA-consists of subunits Ame1(CENP-U), Ctf19(CENP-P), M

67 Fear of brain damage, coma, convulsions, death and dehydration was high across

68 2.2 d; 95% CI, -3.2 to -1.3; p < 0.001), and coma days decreased from 14% to 9% (risk ratio, 0.5; 95%

69 ential Organ Failure Assessment, duration of coma, delirium, hypoxemia, sepsis, education level, hosp

70 e), symptom-related (mechanical ventilation, coma, delirium, pain, restraint use), and system-related

71 luding survival, mechanical ventilation use, coma, delirium, restraint-free care, ICU readmissions, a

72 Daily mental status was classified as "coma," "delirium," or an "awake without delirium" state.

73 Coma-, delirium-, and invasive mechanical ventilation-fr

74 across the cytoplasmic membrane (i.e., pilX, comA) did not exhibit increased transcription in the pre

75 f ComA in a unique manner by forming a Rap60-ComA-DNA ternary complex that inhibits transcription of

76 F EPO levels also correlated positively with coma duration (P = .05 and P = .02, respectively).

77 sma EPO levels are associated with prolonged coma duration and increased mortality in children >18 mo

78 inopathy, acute kidney injury, and prolonged coma duration, all P < .05), and an increased CSF:plasma

79 ney injury is a risk factor for delirium and coma during critical illness.

80 % CI = 1.157-1.831, p = 0.001), nontraumatic coma etiology (OR = 4.464, 95% CI = 1.011-19.608, p = 0.

81 ic hypothermia and pharmacologically induced coma for many indications associated with TBI, where acu

82 e therapy for SRSE requiring pharmacological coma for seizure control.

83 interesting case of a child, who stayed in a coma for several months following brainstem surgery, but

84 trations were associated with fewer delirium/coma-free days after adjusting for age, Charlson comorbi

85 The safety outcome was coma-free days assessed by the Richmond Agitation-Sedati

86 rs collected at delirium onset and delirium-/coma-free days assessed through Richmond Agitation-Sedat

87 uartile 4 were not associated with delirium-/coma-free days at both time points.

88 4 were negatively associated with delirium-/coma-free days by 1 week and 30 days post enrollment.

89 DERPIN-ICU program on the number of delirium-coma-free days in 28days and several secondary outcomes,

90 ding hospital survival and delirium-free and coma-free days in community hospitals.

91 Coma-free days was also similar between groups (placebo

92 s of hospital survival and delirium-free and coma-free days, after adjusting for age, severity of ill

93 alive and was assessed as delirium-free and coma-free in the first 14 days after being randomly allo

94 as comatose, and 62% were delirium-free and coma-free.

95 ng selected patients with cardiac arrest and coma from publicly reported mortality statistics after p

96 2 and NGC 4889 at the centres of the Leo and Coma galaxy clusters, which together form the central re

97 ort of 250 patients admitted to the ICU with coma (Glasgow Coma Scale score </= 8) and treated with i

98 In addition, cometary comas have been found to contain a rich array of other m

99 Rap60 regulates the activity of ComA in a unique manner by forming a Rap60-ComA-DNA tern

100 idney injury is associated with delirium and coma in critically ill adults.

101 imvastatin modifies duration of delirium and coma in critically ill patients.

102 of axonal injury, have been associated with coma in severe malaria (cerebral malaria [CM]).

103 l1(INCENP/Aurora-B) core-CPC interacted with COMA in vitro through the Ctf19 C-terminus whose deletio

104 During the first 3 days of acute coma, increasing lateral brain displacement is associate

105 Here, we show that the COMA inner kinetochore sub-complex physically interacts

106 Myxedema coma is a life-threatening form of decompensated hypothy

107 Therapeutic coma is advocated in guidelines for management of refrac

108 provides class III evidence that therapeutic coma is associated with poorer outcome after status epil

109 inopathy-negative CM and the etiology of the coma is entirely non-malarial.

110 ditory discrimination over the first days of coma is predictive of awakening.

111 acilities to identify non-malarial causes of coma, it has not been possible to evaluate the contribut

112 All 3 patients with late recovery from coma lacked evidence of overwhelming cortical injury but

113 outcomes were brain dysfunction (delirium or coma), length of ICU stay, and hospital mortality.

114 leads to molecular O2, whose presence in the coma may thus be linked directly to water molecules and

115 elopmental delay, severity of illness, prior coma, mechanical ventilation, and receipt of benzodiazep

116 Recovery from coma might critically depend on the structural and funct

117 21(CENP-O) and Okp1(CENP-Q) A description of COMA molecular organization has so far been missing.

118 th the Coma Recovery Scale-Revised indicated coma (n = 2), vegetative state (n = 3), minimally consci

119 These results indicate a complex coma-nucleus relationship where seasonal variations may

120 p = 0.007) independent of disease severity (coma, number of seizures, acute kidney injury) and socio

121 r vapour is the main species observed in the coma of comet 67P/Churyumov-Gerasimenko and water is the

122 e we report in situ measurement of O2 in the coma of comet 67P/Churyumov-Gerasimenko, with local abun

123 ecraft analyzed the isotopes of xenon in the coma of comet 67P/Churyumov-Gerasimenko.

124 ndant molecular oxygen was discovered in the coma of comet 67P/Churyumov-Gerasimenko.

125 impairment, seizures, abnormal movements, or coma of unknown cause, had an autoimmune disease.

126 The composition of the neutral gas comas of most comets is dominated by H2O, CO and CO2, ty

127 e address the specific impact of therapeutic coma on status epilepticus outcome.

128 rily neurologic in nature, with two cases of coma-one resulting in death.

129 1.002-1.079, p = 0.040), higher GCS score at coma onset (OR = 1.455, 95% CI = 1.157-1.831, p = 0.001)

130 of patients had midline shift on head CT at coma onset and 43 (51%) patients awakened.

131 hy (CT) scans were analyzed independently at coma onset, after awakening, and at follow-up.

132 Severe hypoglycemia can lead to coma or death.

133 No coma or deaths occurred.

134 up to a maximum of 28 days, irrespective of coma or delirium status.

135 embolic events, the number of days free from coma or delirium, acute kidney injury according to sever

136 tion group had a median of 27 days free from coma or delirium, and those in the sedation group had a

137 tion group had a median of 26 days free from coma or delirium.

138 re to thrive and metabolic crisis leading to coma or even death.

139 n men, 31% in women) but death from diabetic coma or ketoacidosis was associated with the largest per

140 in blood urea nitrogen [95% CI 1.58, 1.86]), coma (OR 3.59 [95% CI 3.07-4.21]), seizures (OR 1.40 [95

141 h delirium (OR, 1.35; 95% CI, 1.18-1.55) and coma (OR, 1.44; 95% CI, 1.20-1.74).

142 95% confidence interval [CI], 1.07-2.26) and coma (OR, 2.04; 95% CI, 1.25-3.34) as was stage 3 injury

143 after adjusting for delirium and persistent coma (OR, 5.63 [1.55-20.45]).

144 Episodes with altered consciousness, coma, or convulsions constituted 36.6% of all episodes i

145 ulation in, for example, wakefulness, sleep, coma, or neuropsychiatric diseases.

146 lites, rings or other dust structures, a gas coma, or solar wind interactions was detected.

147 ry score, 3 [severe neurologic sequelae], 4 [coma], or 5 [death]).

148 onnection might be particularly relevant for coma outcome prediction and could inspire innovative pre

149 oved and root mean square (RMS) (P < .0005), coma (P < .0005), and secondary astigmatism (P < .005) l

150 erior corneal surface had significantly less coma (P <= 0.003) and total HOA (P <= 0.001) in DMEK com

151 ment in the spherical aberration (P = .018), coma (P = .23) and total higher order aberrations (P = .

152 -weighted images were acquired in 126 anoxic coma patients ("learning" sample) 16 +/- 8 days after ca

153 n injury and anoxo-ischemic (cardiac arrest) coma patients by using an original multimodal MRI protoc

154 Coma patients displayed significantly lower medial prefr

155 An additional sample of 18 anoxic coma patients, recruited in Toulouse, was used to test p

156 music and motor imagery was only observed in coma patients.

157 he most severe outcomes for patients include coma, permanent neurological deficits, and death.

158 cans on admission and daily thereafter while coma persisted.

159 ent models of deep pharmacologically-induced coma (PIC): isoflurane (1.25%-1.5%) and induced hypoglyc

160 ze adaptation abilities to better understand coma recovery and survival limitations.

161 mine whether repeated examinations using the Coma Recovery Scale-Revised (CRS-R) have an impact on di

162 ses based on one, two, three, four, and five Coma Recovery Scale-Revised assessments were compared wi

163 of imaging, behavioural evaluation with the Coma Recovery Scale-Revised indicated coma (n = 2), vege

164 lt) for whom the clinical diagnosis with the Coma Recovery Scale-Revised was congruent with positron

165 All patients were followed up (Coma Recovery Scale-Revised) 3 months after acute brain

166 te), (3) clinical measures of consciousness (Coma Recovery Scale-Revised), and (4) injury etiology.

167 that discriminates a binary outcome based on Coma Recovery Scale-Revised).

168 subgroup of patients, underestimated by the Coma Recovery Scale-Revised, showing residual cognition

169 ere wide ranging (eg, improvement on the JFK Coma Recovery Scale-Revised, the Unified Parkinson Disea

170 rediagnosed as minimally conscious with the Coma Recovery Scale-Revised.

171 s in the goldstandard revised version of the Coma Recovery Scale; (ii) a proportion of ~15-20% clinic

172 ssociated with the quantitative trait, chill coma recovery time, in the unrelated, sequenced inbred l

173 e response, starvation resistance, and chill coma recovery) in the unrelated, sequenced inbred lines

174 tion, cannulation methods, hemoglobin level, coma, renal impairment, and hepatic impairment were not

175 motor regression, irritability and stupor or coma resulting in major handicap or death.

176 Among them, 27 awoke from coma, resulting in a positive predictive value of awaken

177 Total, spherical and coma root mean square (RMS) postoperative ocular higher-

178 l Organ Failure Assessment criteria (Glasgow Coma Scale </= 14, respiratory rate >/= 22 breaths/min,

179 with severe traumatic brain injury (Glasgow Coma Scale </= 8; intracranial pressure monitoring).

180 predict mortality using time-updated Glasgow Coma Scale (GCS) and plasma sodium measurements, togethe

181 ed with an ACO were age >=65, fever, Glasgow Coma Scale (GCS) score <13, and seizures (all P values <

182 Objective: To evaluate whether Glasgow Coma Scale (GCS) score or the Simplified Motor Score at

183 The median Glasgow Coma Scale (GCS) score was 13 (IQR 9-15), and the leadin

184 troke Score, 15.8 (IQR 9-25); median Glasgow Coma Scale (GCS), 9.1 (IQR 6-14,5).

185 dary outcome measures were discharge Glasgow Coma Scale (GCS), modified Rankin Scale, Glasgow Outcome

186 organ failure assessment (qSOFA) and Glasgow coma scale (GCS).

187 tion of mortality: postresuscitation Glasgow coma scale (P-GCS) (adjusted odds ratio, 0.42; 95% confi

188 14 yr, 28.5% male, median admission Glasgow Coma Scale 14 [10-15]) were analyzed.

189 dren with clinical diagnosis of TBI (Glasgow Coma Scale [GCS] 3-15) and 40 healthy subjects, evaluate

190 atients with moderate or severe TBI (Glasgow Coma Scale [GCS] score <=12).

191 nts younger than 18 years with mTBI (Glasgow Coma Scale [GCS] score, 13-15) and ICI on computed tomog

192 tively, for discriminating mild TBI (Glasgow Coma Scale [GCS] score, 13-15, n = 162) from healthy con

193 s with apparently minor head trauma (Glasgow Coma Scale [GCS] scores >/=13 who appear well on examina

194 ical information (age, sex, outcome, Glasgow Coma Scale [GCS], and HIV status) was ascertained at sel

195 nd arterial blood pressure, baseline Glasgow Coma Scale and 6 months Glasgow Outcome Scale were recor

196 disorganization was associated with Glasgow Coma Scale and Sequential Organ Failure Assessment in ad

197 f neurologic and systemic illness by Glasgow Coma Scale and Sequential Organ Failure Assessment, and

198 Median Glasgow Coma Scale at admission was 7 (range 3-14), and median G

199 eness score was more useful than the Glasgow Coma Scale for predicting mortality.

200 The Glasgow Coma Scale has value but is incomplete and cannot be ass

201 ated with encephalopathy severity by Glasgow Coma Scale in critically ill patients (rho, -0.54; p = 0

202 ostic tool of ICU mortality than the Glasgow Coma Scale in critically ill patients, most likely a res

203 ankin Scale </=3, ICH volume < 60ml, Glasgow Coma Scale of <9, and severe IVH with tamponade of the t

204 ients admitted to the ICU with coma (Glasgow Coma Scale score </= 8) and treated with invasive mechan

205 ] vs. 25.0% [23 of 92]; p = 0.0003), Glasgow Coma Scale score <=4 (22.7% [10 of 44] vs. 0% [0 of 92])

206 suspected from the initial or early Glasgow Coma Scale score (13-14/15) if not directly recorded by

207 increase in age) and lower admission Glasgow Coma Scale score (relative risk, 0.34; 95% CI, 0.20-0.58

208 of patients with mild head injuries (Glasgow Coma Scale score 13-15) and calculated accuracy using ru

209 ed patients with normal CT findings (Glasgow Coma Scale score 13-15) who consented to venepuncture wi

210 Those with Glasgow Coma Scale score above 8 (OR = 1.22; 95% CI, 1.08-1.39)

211 sociated with worse Hunt-Hess grade, Glasgow Coma Scale score and Acute Physiology and Chronic Health

212 ard, with lower age, higher baseline Glasgow Coma Scale score and higher individual rifampicin plasma

213 Younger age and lower admission Glasgow Coma Scale score are independently associated with the d

214 r associated with disagreement was a Glasgow Coma Scale score between 10 and 15 (odds ratio, 2.92 [1.

215 r associated with disagreement was a Glasgow Coma Scale score between 10 and 15, suggesting that clin

216 c amnesia is superior to the initial Glasgow Coma Scale score for predicting traumatic brain injury r

217 ractures (34.2% vs 18.5%; P = .001), Glasgow Coma Scale score less than 8 (31.5% vs 10.7%; P < .001),

218 atio [OR], 3.47; 95% CI, 2.04-5.91), Glasgow Coma Scale score less than 8 (OR, 2.75; 95% CI, 1.53-4.9

219 with TBI aged 15 years or older with Glasgow Coma Scale score of 12 or less and systolic blood pressu

220 th no evidence of trunk injury and a Glasgow Coma Scale score of 15.

221 examination of the trunk, and had a Glasgow Coma Scale score of 15.

222 c brain injury and postresuscitation Glasgow Coma Scale score of 4-12 were included.

223 umatic brain injury characterized by Glasgow Coma Scale score of 4-12.

224 ss, amnesia, or disorientation and a Glasgow Coma Scale score of 9-15).

225 at least 7 days beforehand and had a Glasgow Coma Scale score of at least 8.

226 tic amnesia duration and the initial Glasgow Coma Scale score to predict performance on the Glasgow O

227 Conversely, the initial Glasgow Coma Scale score was not (area under the curve, 0.63).

228 s; 255 [74%] male participants; mean Glasgow Coma Scale score, 8).

229 ssigned to each variable considered (Glasgow Coma Scale score, age, sex, intensive care unit admissio

230 ard, with lower age, higher baseline Glasgow Coma Scale score, and higher individual rifampicin plasm

231 without differentiating between the Glasgow Coma Scale scores from 10 to 15.

232 8-11.9 mL]; p = 0.002) increased and Glasgow Coma Scale scores improved (median, 4 [3-6] to 7 [6-9];

233 entricular volume, serum sodium, and Glasgow Coma Scale scores were assessed using Spearman rank corr

234 initial systolic blood pressure; and Glasgow Coma Scale scores.

235 f predicting ICU mortality using the Glasgow Coma Scale was 0.715 (95% CI, 0.663-0.768) and using the

236 The median admission Glasgow Coma Scale was 6, the median Glasgow Outcome Scale was 3

237 0.20-0.58; for one unit increase in Glasgow Coma Scale) were independently associated with the devel

238 alidated measures of encephalopathy (Glasgow Coma Scale), multiple organ system function (Sequential

239 te or severe traumatic brain injury (Glasgow Coma Scale, 3-13).

240 27 patients (age, 39 yr [24-54 yr]; Glasgow Coma Scale, 7 [6-8]; 24/27 [89%] with diffuse injury).

241 Health Evaluation III scores, lower Glasgow Coma Scale, and admission prior to 2004 were all associa

242 Age, Glasgow Coma Scale, and hematoma volume did not modify the effec

243 After adjusting for age, initial Glasgow Coma Scale, and mean intracranial pressure, percentage o

244 white blood cell count, hemoglobin, Glasgow Coma Scale, and pulse rate), and were used in the deriva

245 Admission (day 1) variables of age, Glasgow coma scale, arterial pH and lactate, creatinine, interna

246 for age, sex, injury severity score, Glascow Coma Scale, base excess, platelet count and hemoglobin,

247 ting for brain herniation, admission Glasgow Coma Scale, duration on vasopressors and midline shift a

248 age, pupil responsiveness, admission Glasgow Coma Scale, glucose level, and hemoglobin level) and use

249 ssessed the modifying effect of age, Glasgow Coma Scale, hematoma volume, and timing of surgery with

250 Admission Glasgow Coma Scale, increasing haematoma volume and cortical inv

251 d with survival were year of injury, Glasgow Coma Scale, Injury Severity Score, age, and pupil reacti

252 ity, independently of age, admission Glasgow Coma Scale, intracranial pressure, pressure reactivity i

253 at admission, including hypotension, Glasgow Coma Scale, mechanism and intent of injury, and Injury S

254 rrhage, had a low score (3-5) on the Glasgow Coma Scale, or required immediate neurosurgery.

255 ervations on admission including the Glasgow Coma Scale, respiratory rate and blood pressure.

256 intracerebral haemorrhage size, age, Glasgow Coma Scale, stability intraventricular haemorrhage size,

257 sted for age, injury severity score, Glascow Coma Scale, systolic blood pressure, base excess, platel

258 ality, together with base excess and Glasgow Coma Scale.

259 rtality than the verbal component of Glasgow Coma Scale.

260 those with impaired consciousness (Blantyre Coma Score <=4), transfusion was associated with improve

261 h heart rate >/= 108) or severe TBI [Glasgow Coma Score (GCS) </= 8].

262 Twenty-four percent had a reduced Glasgow Coma Score (GCS) at presentation with a ninefold increas

263 ad fever at admission, and had lower Glasgow Coma Score scores.

264 A normal coma score was associated with an elevated interleukin 1

265 dline shifts, Injury Severity Score, Glasgow Coma Score, hypotension, hypoxia, and pupillary reaction

266 blood-brain barrier integrity, and improved coma scores, as well as higher levels of gamma interfero

267 hour ICU shifts patients spent alive without coma (Sedation Agitation Scale </= 2) or delirium (p = 0

268 the following being attributed to methanol: coma, seizures, new vision deficits, metabolic acidosis

269 ne cognition, severity of illness, delirium, coma, sepsis, mechanical ventilation, and sedatives/opia

270 As she emerged from coma, she spent weeks of hospital recovery and months of

271 ally associated with different brain states (coma, sleep, wakefulness) can coexist within the same br

272 Similarities with the detected coma species of comet Halley suggest the presence of a r

273 re adult falciparum malaria with and without coma, suggesting that falciparum-like microvascular sequ

274 ased on in situ mass-spectral studies of the coma surrounding cometary ice.

275 Coma, temporal lobe involvement, hematoma volume, and el

276 dds ratio, 4.88; CI, 1.36-17.57; p = 0.015); coma, temporal lobe involvement, intraparenchymal hemorr

277 uctuations in composition in a heterogeneous coma that has diurnal and possibly seasonal variations i

278 nitial loss of neuromuscular function (chill coma) that is caused by decreased membrane potential and

279 he anterior coma to 90 degrees and posterior coma to 90 degrees .

280 nterior coma to 90 degrees and the posterior coma to 90 degrees .

281 the minimal corneal thickness, the anterior coma to 90 degrees and posterior coma to 90 degrees .

282 the minimum corneal thickness, the anterior coma to 90 degrees and the posterior coma to 90 degrees

283 functional outcomes after prolonged post-CA coma to identify electroencephalographic (EEG) markers o

284 Corneal higher-order aberrations (SA, coma, trefoil, and corneal asphericity) for a 6 mm pupil

285 We assessed patients for delirium and coma twice daily after enrollment using the Confusion As

286 death and disorders of consciousness such as coma, vegetative state, and minimally conscious state ar

287 diagnosing disorders of consciousness (e.g., coma, vegetative-state, locked-in syndrome), these theor

288 t predictors (PSI-BLAST, HHblits, Hmmer, and Coma) via the rank aggregation approach.

289 ed median time between medication intake and coma was 5 minutes (range, 1-38 minutes); to death it wa

290 Coma was identified in 32.7% of delirious compared with

291 eral displacement during the first 3 days of coma was significantly different between functional outc

292 ate of acute brain dysfunction (delirium and coma) was 68.4% in the deep sedation group and 55.6% in

293 Mental status (normal vs. delirium vs. coma) was assessed daily with the Confusion Assessment M

294 operator, cardiac arrest upon admission, and coma were associated with a lower first-attempt success

295 normothermia (37 degrees C) in patients with coma who had been admitted to the intensive care unit (I

296 Among patients with coma who had been resuscitated from cardiac arrest with

297 ced more days alive and free of delirium and coma with both total bundle compliance (incident rate ra

298 um-infected erythrocytes in the brain and 2) coma with other underlying causes.

299 the case of a 66-year-old man who developed coma with subsequent DOC after a severe traumatic brain

300 the centromere-proximal components, Mif2 and COMA, with the principal microtubule-binding component,