ライフサイエンスコーパス: traumatic injury

1 nts for the treatment of tissue ischemia and traumatic injury.

2 of 20.5 million yielded 7080 cases of severe traumatic injury.

3 ne cataract surgery, and 10.4% had sustained traumatic injury.

4 d with chronic health conditions following a traumatic injury.

5 severe critical illnesses such as sepsis and traumatic injury.

6 tality in patients who suffered severe blunt traumatic injury.

7 educed CSPG to enhance CNS axon growth after traumatic injury.

8 ronal turnover and neuronal replacement upon traumatic injury.

9 n outgrowth, severely limiting recovery from traumatic injury.

10 ratory abdominal laparotomy was negative for traumatic injury.

11 ariety of growth related functions following traumatic injury.

12 ndrome and delirium tremens in patients with traumatic injury.

13 tary casualties could be applied to civilian traumatic injury.

14 o develop organ dysfunction and sepsis after traumatic injury.

15 prouting'-in the human spinal cord following traumatic injury.

16 em cells into a rat spinal cord 9 days after traumatic injury.

17 ing novel, noninvasive treatment options for traumatic injury.

18 es are activated in response to sepsis after traumatic injury.

19 , secondary to meningitis, encephalitis, and traumatic injury.

20 rom rat spinal cord at early times following traumatic injury.

21 bacterial cell wall/membrane components, or traumatic injury.

22 severity of the injury in patients suffering traumatic injury.

23 t from neurodegenerative disease, stroke, or traumatic injury.

24 ons that range from acute coronary events to traumatic injury.

25 tions, influence network structure following traumatic injury.

26 uromuscular pathology that was made worse by traumatic injury.

27 candidate biomarkers for survival following traumatic injury.

28 nt changes in the use of resuscitation after traumatic injury.

29 munocompromised patients or individuals with traumatic injury.

30 counts for approximately 20% of deaths after traumatic injury.

31 spiratory illness, nor was there a preceding traumatic injury.

32 iratory distress syndrome early after severe traumatic injury.

33 t are able to regenerate any body part after traumatic injury.

34 y of neurological disorders, including acute traumatic injury.

35 tection and prognostication in patients with traumatic injury.

36 g old RBCs in patients with life-threatening traumatic injuries.

37 e ability of adult CNS axons to extend after traumatic injuries.

38 re, and understanding the pathophysiology of traumatic injuries.

39 juries and contusion or occult fracture) for traumatic injuries.

40 al course in a group of patients with severe traumatic injuries.

41 l pain, staging in cancer, and evaluation of traumatic injuries.

42 ts required mechanical ventilation following traumatic injuries.

43 sed interventions to regenerate large scale, traumatic injuries.

44 transections, spinal cord injuries and brain traumatic injuries.

45 ause of death on battlefield and in civilian traumatic injuries.

46 damage and can be reversible in ischemic and traumatic injuries.

47 gh death rates and mass casualties with many traumatic injuries.

48 ic stroke and possibly for other ischemic or traumatic injuries.

49 in various neurological disorders, including traumatic injuries.

50 ligible deaths-83 percent from unintentional traumatic injuries, 14 percent from homicide, and the re

51 [SD, 16.2]; men, 197 [61%]; had experienced traumatic injury after a fall, 223 [69%]), 258 completed

52 ta (IL-1beta) that is up-regulated following traumatic injuries also promotes BBB dysfunction and hyp

53 mmon mechanism of axonal self-destruction in traumatic injuries and degenerative diseases.

54 It is thought to be present in 10% of all traumatic injuries and in almost 40% of patients who sus

55 this study was to estimate the prevalence of traumatic injuries and injury-related deaths in low-reso

56 Both traumatic injuries and medical illnesses were treated.

57 These can be divided into two categories: traumatic injuries and overuse injuries.

58 copolymers, protects non-neuronal cells from traumatic injuries and rescues hippocampal neurons from

59 ertrophic scars (HTS), frequently seen after traumatic injuries and surgery, remain a major clinical

60 Twelve of these patients had suffered traumatic injuries and underwent a surgical procedure th

61 btained from 27 patients with major burns or traumatic injury and 18 healthy persons and were studied

62 entral nervous system axons, associated with traumatic injury and demyelinating diseases such as mult

63 ally induced coma for brain protection after traumatic injury and during status epilepticus.

64 e pathologic lesions likely resulting from a traumatic injury and followed by secondary infection at

65 in many neurodegenerative diseases and after traumatic injury and is a self-destructive program indep

66 the nervous system begins within hours after traumatic injury and is characterized primarily by react

67 presence of tissue hypoperfusion and severe traumatic injury and is mediated by activation of the PC

68 inical research on cellular therapeutics for traumatic injury and its sequelae and discuss prospects

69 ased mortality in patients with sepsis after traumatic injury and may represent a novel marker of ris

70 versial for unconscious patients after blunt traumatic injury and negative findings on computed tomog

71 system is dysregulated in sepsis, shock, and traumatic injury and that interruption or termination of

72 as associated with increased mortality after traumatic injury and this association was primarily obse

73 se in specific subsets of neurologic injury, traumatic injury, and cardiovascular surgery.

74 ty of insults including metabolic disorders, traumatic injury, and exposure to neurotoxins such as vi

75 dical services (EMS) personnel, did not have traumatic injury, and received attempts at external defi

76 sease; cause disabling symptoms, faints, and traumatic injuries; and substantially reduce quality of

77 Pediatric patients with traumatic injuries are common at deployed U.S. military

78 missions after discharge from acute care for traumatic injury are frequent, persist beyond 30 days, a

79 intraoperatively from 10 patients with acute traumatic injuries as a result of motor vehicle collisio

80 provides baseline data on the mechanisms of traumatic injuries as well as the sociodemographic facto

81 Using traumatic injury as a model, we systematically investiga

82 to discharge for patients sustaining severe traumatic injury assessed by EMS.

83 years or younger who were admitted following traumatic injury between January 1, 2008, and December 3

84 immediate, early, and late responses to this traumatic injury by characterizing several histologic fe

85 Severe traumatic injury can lead to immune dysfunction that ren

86 acidification in inflammation, ischemia, or traumatic injury can sensitize VR1 to eicosanoids and tr

87 ing pursued for the biomedical management of traumatic injury, cancer, and degeneration.

88 d mortality in the pediatric population, and traumatic injury causes > 50% of all childhood deaths.

89 ust literature that states that the CML is a traumatic injury commonly encountered in physically abus

90 rse gliosis-dependent central nervous system traumatic injury conditions and diseases, and for orphan

91 Traumatic injuries continue to be a significant cause of

92 al interventions can now be applied to treat traumatic injury, David J Lockey calls for research to d

93 incidence and outcome associated with severe traumatic injury differs across geographic regions of No

94 Widely different traumatic injuries evoke surprisingly similar gene expre

95 Traumatic injury evokes two characteristic forms of foca

96 ransplantation strategies in a wide range of traumatic injuries for which therapeutic intervention is

97 ites (6 US and 3 Canadian) sustaining severe traumatic injury from April 1, 2006 to March 31, 2007 fo

98 In traumatic injury, haemorrhage is responsible for almost

99 Traumatic injury has a profound immunomodulatory effect

100 bolism influence the normal host response to traumatic injury has not been extensively studied.

101 Racial disparities in survival after traumatic injury have been described.

102 egulatory mechanisms for tissue repair after traumatic injury have developed under strong evolutionar

103 death caused by demyelinating, ischemic, and traumatic injuries, implying its involvement in a wide s

104 travenous injection of CR2-Crry 1 hour after traumatic injury improved functional outcome and patholo

105 n laboratory animals and naturally occurring traumatic injury in humans.

106 of 1,520,599 patients hospitalized following traumatic injury in Massachusetts or New York during the

107 CAP examinations rarely if ever reveal acute traumatic injury in patients who have experienced low-ve

108 findings suggest that, for axons undergoing traumatic injury in response to applied mechanical loads

109 Scar tissue at sites of traumatic injury in the adult central nervous system pre

110 ssion of other trophic factors in vivo after traumatic injury in the adult CNS.

111 of IL-6 in tissue repair processes following traumatic injury in the CNS.

112 The frequency of acute traumatic injury in the CT CAP examinations was also det

113 ty-two respondents (12%) reported at least 1 traumatic injury in the preceding year.

114 n a rat model of brachial plexus avulsion, a traumatic injury in which nerve roots are torn from the

115 experience a unique inflammatory response to traumatic injury in which the ability of alveolar effect

116 r for increased morbidity and mortality with traumatic injuries, in part through inhibition of bone f

117 and important regional differences in severe traumatic injury, incidence, and outcome.

118 Expectedly, traumatic injury induced dramatic changes in apparent ge

119 Traumatic injury initiates a complex inflammatory respon

120 milar manner to typical penetrating or blunt traumatic injuries, injuries caused by the blast pressur

121 ansplantation strategies for a wide range of traumatic injuries is the determination of a suitable ti

122 Because traumatic injury is a common acute condition with import

123 Traumatic injury is a major human health problem, with m

124 The development of PTSD symptoms after traumatic injury is associated with a more fragmented pa

125 Traumatic injury is generally considered to have a suppr

126 Mortality and sepsis after a traumatic injury is greater in the elderly than in young

127 t effective at reducing alcohol misuse after traumatic injury is not known.

128 Traumatic injury is the leading cause of death in childr

129 A small traumatic injury itself does not lead to recruitment of

130 These data suggest that traumatic injury may modify stem cell characteristics th

131 Following traumatic injury, mice deficient in C3 had a significant

132 Using an in vitro traumatic injury model, we examined the effects of mecha

133 is and decreased bleeding times in vivo in a traumatic injury model.

134 rated appendicitis, other perforated viscus, traumatic injuries more than 4 hours old, or intraabdomi

135 (n = 64) or chronic (n = 36) dissection, or traumatic injury (n = 39).

136 Traumatic injuries occur in > 20 million children each y

137 Recovery of neurological function after traumatic injury of the adult mammalian central nervous

138 ell transplantation to promote recovery from traumatic injury of the CNS, focusing on axonal regenera

139 otential of POSTN as a therapeutic agent for traumatic injury of the CNS.

140 nter experience of endograft repair of blunt traumatic injury of the thoracic aorta.

141 , we examined the effects of stretch-induced traumatic injury on the AMPA subtype of ionotropic gluta

142 dramatic change in the CNS environment after traumatic injury or disease is hemorrhage because of vas

143 ability to restore visual function following traumatic injury or disease-induced degeneration.

144 ul strategy to restore muscle function after traumatic injury or disease.

145 h as those that may be encountered following traumatic injury or during delayed reconstruction/regene

146 mage to the central nervous system caused by traumatic injury or neurological disorders can lead to p

147 ruption of the lymphatic system secondary to traumatic injury or obstruction.

148 the previous 30 days; (2) were admitted for traumatic injury or surgery; (3) had hypercoagulability

149 tions, which may influence outcome following traumatic injury or they have not been fully validated f

150 postoperative cardiac surgery patients, post-traumatic injury patients, and neurologic injury patient

151 The median incidence of EMS-assessed severe traumatic injury per 100,000 population across sites was

152 ry severity score, and the presence of blunt traumatic injury, pulmonary contusion, massive transfusi

153 Many patients with moderate-to-severe traumatic injuries receive care at nontrauma hospitals,

154 Information on traumatic injuries recorded between January 1, 2002, and

155 variation in incidence and outcome of severe traumatic injury remain to be analyzed.

156 casualties with severe burns and associated traumatic injuries requires a coordinated interaction of

157 HO) after blast-related extremity injury and traumatic injuries, respectively.

158 Mechanistically, we found that traumatic injury resulted in increased uncorrelated netw

159 US of the clenched fist in two patients with traumatic injury revealed dislocated but grossly intact

160 atients with tissue hypoperfusion and severe traumatic injury showed a strong activation of the PC wh

161 e CNS at both cognate antigen-containing and traumatic injury sites after intracerebral antigen deliv

162 ion of activated antigen-specific T-cells at traumatic injury sites, in addition to antigen-containin

163 the CNS, including autoimmune inflammation, traumatic injury, stroke, and neurodegenerative diseases

164 We prospectively recorded 92 traumatic injuries sustained by 73 mineclearers working

165 48-hr and 30-day survival for patients with traumatic injuries that require massive transfusion.

166 eposition in the mouse spinal cord following traumatic injury, the role of complement in the developm

167 and their concomitant heightened exposure to traumatic injury, the trauma burden among this patient p

168 taneously or after provoking events, such as traumatic injuries to the pelvis, upper and lower exterm

169 Traumatic injuries to the teeth are among the most serio

170 mple, and effective adjunct to the repair of traumatic injuries to the thoracic aorta.

171 emiology of pediatric patients admitted with traumatic injuries to U.S. combat support hospitals and

172 nrolled 1138 patients recently admitted with traumatic injury to 1 of 4 major trauma hospitals across

173 Traumatic injury to CNS fiber tracts is accompanied by f

174 Traumatic injury to mixed neuronal/glial cultures induce

175 Traumatic injury to one bird's retina was also successfu

176 mical and molecular changes that occur after traumatic injury to reproduce the pathological events as

177 fy the contribution of antigen deposition or traumatic injury to the accumulation of T-cells in the b

178 This review focuses on traumatic injury to the brain and spinal cord, and highl

179 Traumatic injury to the brain is a problem as old as hum

180 Traumatic injury to the brain often manifests itself sym

181 Emerging data indicate that traumatic injury to the brain or spinal cord activates B

182 Traumatic injury to the brain or spinal cord is one of t

183 ically relevant to most patients living with traumatic injury to the brain or spinal cord, very littl

184 as very recently been seen after ischemic or traumatic injury to the central nervous system (CNS), su

185 unction and cell loss following ischemic and traumatic injury to the central nervous system (CNS).

186 Traumatic injury to the central nervous system results i

187 a wide range of pathophysiologies including traumatic injury to the central nervous system, neurodeg

188 a for this study were found to have an acute traumatic injury to the chest, abdomen, or pelvis.

189 Traumatic injury to the CNS results in chronic partial d

190 el species of Lophotrichus in a patient with traumatic injury to the cornea from a dog paw.

191 ndophthalmitis (in 1.3 percent of patients), traumatic injury to the lens (in 0.7 percent), and retin

192 Traumatic injury to the mammalian spinal cord activates

193 , we first demonstrate that a mouse model of traumatic injury to the pediatric brain reproduces many

194 The primary traumatic injury to the spinal cord triggers a cascade o

195 rapeutic potential in the treatment of acute traumatic injury to the spinal cord.

196 We show that traumatic injury to the ventral midline of the embryonic

197 evel decision that affects how patients with traumatic injury (trauma patients) interact with locoreg

198 In this study, a traumatic injury was administered to a mouse model and h

199 The moderate and mild traumatic injury was inflicted by focal laser lesion and

200 g mouse optic nerve crush as a model for CNS traumatic injury, we performed a detailed analysis of AI

201 leukocyte subpopulations, and the effect of traumatic injury, were also explored.

202 providers to patients with life-threatening traumatic injuries with hemorrhage.

203 ine clearance in obtunded adults after blunt traumatic injury with negative results from a well-inter

204 tically different outcomes after suffering a traumatic injury (www.gluegrant.org).