ライフサイエンスコーパス: coma

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

2 d had convulsions, altered consciousness, or coma.

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

4 ed patients who were arousable from those in coma.

5 lotherms enter into a reversible, protective coma.

6 brain displacement and awakening from acute coma.

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

8 with DNA binding by the transcription factor ComA.

9 nd treatment in patients with acute onset of coma.

10 is weakened after adjusting for delirium and coma.

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

12 on history of prior seizures and presence of coma.

13 0.001) in subjects managed with therapeutic coma.

14 state/unresponsive wakefulness syndrome and coma.

15 lsive or nonconvulsive status epilepticus in coma.

16 for severe disability to vegetative state or coma.

17 pilepticus necessitating a medically induced coma.

18 s of costs and health gains than barbiturate coma.

19 s: decompressive craniectomy and barbiturate coma.

20 ur patients needed pharmacologically induced coma.

21 ould improve monitoring of medically-induced coma.

22 corded as having 0 days free of delirium and coma.

23 ors of critical illness spent in delirium or coma.

24 ors of critical illness spent in delirium or coma.

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

26 peak serum creatinine and both delirium and coma.

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

28 Saturn, has remained undetected in cometary comas.

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

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

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

32 d significant differences in both Horizontal Coma (3,1) (p<0.001, ICC = -0.207, LoA = -0.15+/-0.48) a

33 er also differed from Wavescan in Horizontal Coma (3,1) (P<0.001, ICC = 0.725, LoA = -0.07+/-0.25).

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

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

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

37 stablished using clinical criteria including coma, absence of brainstem reflexes and loss of central

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

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

40 Most patients had burst suppression during coma, although often short-lived (median [interquartile

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

42 ences were found in the tHOA, SA, horizontal coma and astigmatism.

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

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

45 tive impairment to tremor, ataxia, seizures, coma and death.

46 These data suggest that iatrogenic coma and delirium are not mechanistically linked.

47 esics that increase their risk of developing coma and delirium.

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

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

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

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

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

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

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

55 modulate ion balance while in a cold-induced coma and this ongoing physiological acclimation process

56 incidence of severe (hypoglycemic seizure or coma) and moderate hypoglycemia (an event requiring assi

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

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

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

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

61 Decompressive craniectomy and barbiturate coma are often used as second-tier strategies when intra

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

63 The three main mechanisms of coma are structural brain lesions, diffuse neuronal dysf

64 of days alive, without delirium, and without coma as did patients in the placebo group (median 5 days

65 Time in burst suppression during coma, as measured by processed electroencephalography, w

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

67 The group mean RMS of the coma at the initial and final visit was 0.06 (0.04) and

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

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

70 eased corneal astigmatism by 27% and corneal coma by 5%, but on average, the overall amount of HOA di

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

72 of the RapJ-PhrC, RapI, RapH-Spo0F, and RapF-ComA(C) crystal structures reveals the mechanistic basis

73 This coma can be manipulated based on controlled environmenta

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

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

76 oard the Rosetta spacecraft has measured the coma composition of comet 67P/Churyumov-Gerasimenko with

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

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

79 The combined prevalence of delirium/coma decreased from 90.8% pre protocol implementation to

80 dently predicted a higher prevalence of post-coma delirium (odds ratio, 4.16; 95% CI, 1.27-13.62; p =

81 tive-exposed patients is a predictor of post-coma delirium during critical illness.

82 hese analyses; 42 of these 69 (61%) had post-coma delirium.

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

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

85 ICU delirium prevalence and characteristics (coma/delirium-free days, first day in delirium, and deli

86 However, coma/delirium-free days, first day in delirium, and moto

87 However, the coma/delirium-free days, the first day in delirium, and

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

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

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

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

92 f the tolerant species to recover from chill coma during low temperature exposure.

93 and the prevalence/duration of delirium and coma, early mobilization, mortality, time to discharge,

94 % CI = 1.157-1.831, p = 0.001), nontraumatic coma etiology (OR = 4.464, 95% CI = 1.011-19.608, p = 0.

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

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

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

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

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

100 s-Campbell Sleep Questionnaire) and delirium/coma-free days.

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

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

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

104 in both PK and DSAEK groups were trefoil and coma from the anterior corneal surface (P < 0.05) and tr

105 2 and NGC 4889 at the centres of the Leo and Coma galaxy clusters, which together form the central re

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

107 osis, age (odds ratio [OR] 1.37 per decade), coma grade (OR 2.02 grade 2, 2.65 grade 3, 5.29 grade 4)

108 Because coma has many causes, physicians must develop a structur

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

110 emic medical center intensive care unit with coma, hypersalivation, hyperreflexia, and stimulus-induc

111 and was more cost-effective than barbiturate coma in 78% of cases if our willingness-to-pay threshold

112 urate real-time control of medically-induced coma in a rodent model suggesting this strategy could be

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

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

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

116 d by processed electroencephalography during coma in sedative-exposed patients is a predictor of post

117 Therapeutic coma is advocated in guidelines for management of refrac

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

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

120 The medical coma is often required for several days.

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

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

123 Higher-order aberrations and coma-like aberrations decreased significantly, but spher

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

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

126 21(CENP-O) and Okp1(CENP-Q) A description of COMA molecular organization has so far been missing.

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

128 In patients with only coma (n=15), only delirium (n=7), and neither ever (n=14

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

130 omes of Plasmodium falciparum infection, the coma of cerebral malaria (CM) is particularly deadly.

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

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

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

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

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

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

137 pilepticus needing pharmacologically induced coma; one with epilepsia partialis continua), four had s

138 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)

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

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

141 Severe hypoglycemia can lead to coma or death.

142 No coma or deaths occurred.

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

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

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

146 and monitored, 55 patients either never had coma or never emerged from coma, yielding 69 patients fo

147 logic disability, and 10.2% among those in a coma or vegetative state (P<0.001 for all comparisons).

148 Imaging should be done in post-traumatic coma or when structural brain lesions are probable or po

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

150 95% confidence interval [CI], 1.07-2.26) and coma (OR, 2.04; 95% CI, 1.25-3.34) as was stage 3 injury

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

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

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

154 .56 D, respectively; and RMS (P < .0005) and coma (P < .0005) decreased.

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

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

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

158 e observational study included all new onset coma patients admitted to the Neurosciences Critical Car

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

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

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

162 cans on admission and daily thereafter while coma persisted.

163 cal hospital because of rapid progression to coma preceded by lower back pain and recurrent falls.

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

165 We present novel ways to assess coma recovery and survival using readily available labor

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

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

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

169 Coma Recovery Scale-Revised total scores correlated with

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

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

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

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

174 es desiccation tolerance but lengthens chill coma recovery time, and injection of capa peptide analog

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

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

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

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

179 ysis of the inner kinetochore cluster (Cse4, COMA) reveals structural features not apparent in singly

180 The coma root mean square also was higher (P < .005) in the

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

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

183 Diffuse neurological signs or a Glasgow Coma Scale <9 resulted in more expeditious neuroimaging

184 The Glasgow Coma Scale (GCS) is used frequently to define the extent

185 rity Score (ISS) greater than 9, and Glasgow Coma Scale (GCS) score less than 9.

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

187 d neurological status as assessed by Glasgow Coma Scale (GCS) was identified.

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

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

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

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

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

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

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

195 Glasgow Coma Scale and Full Outline of UnResponsiveness score we

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

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

198 40 years later, the Glasgow Coma Scale has become an integral part of clinical pract

199 Since 1974, the Glasgow Coma Scale has provided a practical method for bedside a

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

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

202 lse-positive rates were higher for a Glasgow Coma Scale motor score showing extensor posturing or wor

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 re traumatic brain injury (admission Glasgow Coma Scale score </= 8, International Classification of

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

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

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

212 edian (interquartile range) modified Glasgow Coma Scale score at 72 hours (10 [8-11] vs 7 [4-9], p <

213 Secondary outcome was modified Glasgow Coma Scale score at 72 hours after enrollment, length of

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

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

216 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

217 intracranial pressure and a modified Glasgow Coma Scale score less than or equal to 8 were enrolled.

218 h severe TBI (ie, blunt head trauma, Glasgow Coma Scale score of <9, and abnormal intracranial findin

219 ed with median (interquartile range) Glasgow Coma Scale score of 15 (12-15), and median (interquartil

220 ty Score of 15 (range, 9-18), median Glasgow Coma Scale score of 15 (range, 12-15), and mean (SD) FI

221 te-to-severe, or moderate acute TBI (Glasgow Coma Scale score of 4 to 12, on a scale from 3 to 15, wi

222 rtonic Saline Trial in patients with Glasgow Coma Scale score of 8 or less (traumatic brain injury) o

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

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

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

226 .6% had subdural hematoma; admission Glasgow Coma Scale score was 3 +/- 1 (3-15) and head Abbreviated

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

228 to 70 years of age, with severe TBI (Glasgow Coma Scale score, </=8 [on a scale of 3 to 15, with lowe

229 olic blood pressure, 128 [28] mm Hg; Glasgow Coma Scale score, 14 [2]; Injury Severity Score, 6.8 [6.

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

231 eath were increasing age, decreasing Glasgow Coma Scale score, increasing ICH volume, presence of int

232 n reported in adult studies, initial Glasgow Coma Scale score, primary location of the hemorrhage, an

233 s at 6 months: six patients had poor Glasgow Coma Scale scores (< 8) that remained low and all died b

234 8-11.9 mL]; p = 0.002) increased and Glasgow Coma Scale scores improved (median, 4 [3-6] to 7 [6-9];

235 18 years with blunt head trauma and Glasgow Coma Scale scores of 14 and 15 evaluated in 25 emergency

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

237 Glasgow Coma Scale scores were assessed within 24 hours from rea

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

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

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

241 0.20-0.58; for one unit increase in Glasgow Coma Scale) were independently associated with the devel

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

243 27 patients (age, 39 yr [24-54 yr]; Glasgow Coma Scale, 7 [6-8]; 24/27 [89%] with diffuse injury).

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

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

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

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

248 the trauma resuscitation room: age, Glasgow Coma Scale, base excess, and prothrombin time.

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

250 sure, and the motor component of the Glasgow Coma Scale, comorbidities, and year of admission.

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

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

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

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

255 t differ with regard to age, gender, Glasgow Coma Scale, or diagnosis.

256 5 years, in those with a decrease in Glasgow Coma Scale, or in those with hypotension as the reason f

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

258 rtality than the verbal component of Glasgow Coma Scale.

259 as well as mortality were linked to Glasgow Coma Scale/Full Outline of UnResponsiveness score inform

260 est described by the three components of the coma scale; whereas the derived total coma score should

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 agnosis of traumatic brain injury, a Glasgow Coma Score less than or equal to 12, and abnormal head i

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

265 of the coma scale; whereas the derived total coma score should be used to characterise groups.

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

267 with severe traumatic brain injury (Glasgow Coma Score, </= 8).

268 ith moderate traumatic brain injury (Glasgow Coma Score, 9-12) was 8.5% and was 33.5% in those with s

269 ad fever at admission, and had lower Glasgow Coma scores than in those whom vasospasm did not develop

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

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

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

273 Coma, seizures, tachycardia and anaemia were all signifi

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

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

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

277 The lower-order aberrations, coma, spherical aberration (SA), and total root mean squ

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

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

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

281 lyze recovery from pharmacologically induced coma to show that neuronal activity en route to consciou

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

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

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

285 sodes (87.30%), and duration of drug-induced coma was (mean [SD]) 11.0 (17.9) days.

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

287 Time to first coma was associated with fentanyl and midazolam doses (p

288 Therapeutic coma was associated with poorer outcome in the whole coh

289 The number of days in coma was associated with the number of days of coadminis

290 Coma was identified in 32.7% of delirious compared with

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

292 Delirium and coma were evaluated daily.

293 ance for prognostication of early postanoxic coma, whereas somatosensory-evoked potentials do not add

294 igmatism, spherical aberration, trefoil, and coma with accommodation, which must arise from geometric

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

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

297 -adjusted life years relative to barbiturate coma, with an incremental cost-effectiveness ratio of $9

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

299 either never had coma or never emerged from coma, yielding 69 patients for whom we performed these a

300 both pre- and postoperatively were vertical coma (Z3(-1)), vertical trefoil (Z3(-3)), and secondary