ライフサイエンスコーパス: burn injury

1 d thereby reduce hepatocytic apoptosis after burn injury.

2 in a 21-year-old male after a self-inflicted burn injury.

3 at occur after combined smoke inhalation and burn injury.

4 the perfused livers of fasted rats receiving burn injury.

5 of the immune response to severe trauma and burn injury.

6 perturbed in pediatric and adult patients by burn injury.

7 tients (n = 8) were followed up to 1 y after burn injury.

8 can offer protection against infection after burn injury.

9 the early inflammatory response to a severe burn injury.

10 wound infection in a rodent model of severe burn injury.

11 IL-2 and IFN-gamma production after EtOH and burn injury.

12 ajor complications that hamper recovery from burn injury.

13 IL-2 and IFN-gamma production after EtOH and burn injury.

14 the intestine from damage following EtOH and burn injury.

15 p47(phox), and p67(phox) following EtOH and burn injury.

16 to wound infections may be protective after burn injury.

17 rophil O(2)(-) production following EtOH and burn injury.

18 al edema and permeability following EtOH and burn injury.

19 decline in pulmonary function at 1 day after burn injury.

20 treating insulin resistance following severe burn injury.

21 se in cardiomyocyte expression of C5aR after burn injury.

22 erses these pathologic changes incurred from burn injury.

23 ucial to avoid the consequences of AKI after burn injury.

24 dical conditions influence outcomes in acute burn injury.

25 omorbidities have not been examined in acute burn injury.

26 n vitro were significantly reduced following burn injury.

27 hepatic encephalopathy, and fibromyalgia and burn injury.

28 ell hyperresponsiveness late (14 days) after burn injury.

29 and subsequent systemic complications after burn injury.

30 y of lean tissue recovery following a severe burn injury.

31 e immune dysfunction that occurs early after burn injury.

32 (-/-), or CD8(-/-) mice 7 days after sham or burn injury.

33 re reduced after sepsis or after sepsis plus burn injury.

34 is or after sepsis complicated by a previous burn injury.

35 vitamin D supplementation is necessary after burn injury.

36 prevent T-cell dysfunction encountered after burn injury.

37 nd DC functions and improving immunity after burn injury.

38 infectious challenge is also impaired after burn injury.

39 ed skeletal muscle hypercatabolism following burn injury.

40 lerating action of EPO on the healing of the burn injury.

41 longed reduction in fluid requirements after burn injury.

42 l component of a high-quality survival after burn injury.

43 ould be the stimulus for the apoptosis after burn injury.

44 erved in C3H/HeJ and B6x129tnf-/- mice after burn injury.

45 We also studied a mouse model of 25% burn injury.

46 ility to infections caused by prednisone and burn injury.

47 erichia coli and 20% total body surface area burn injury.

48 increased rates of arginine degradation from burn injury.

49 ffect neutrophil deposition in tissues after burn injury.

50 tients may help children survive very severe burn injury.

51 ajor complications that hamper recovery from burn injury.

52 bjected to 30% total body surface area steam burn injury.

53 are, and worry/concern up to 48 months after burn injury.

54 educe mortality rate in a rat model of major burn injury.

55 be a new predictor of sepsis onset in severe burn injury.

56 l administered 30 minutes before a 15% scald burn injury.

57 ntial for the early diagnosis of sepsis post-burn injury.

58 levels of apoptosis in spleen in response to burn injury.

59 educe lung injury following pancreatitis and burn injury.

60 ll as stimulating tissue repair after severe burn injury.

61 s of 3-4 weeks old were exposed to a hindpaw burn injury.

62 n early indicator of sepsis in patients with burn injury.

63 s are major barriers to preventing AKI after burn injury.

64 l, i.p.), for 14 days beginning 3 days after burn injury.

65 ances PP cell IL-17 and IL-22 after EtOH and burn injury.

66 graft failure and secondary infection after burn injury.

67 IL-17 but not IL-22 after EtOH exposure and burn injury.

68 n progression, i.e., to control damage after burn injury.

69 oteomic survival signature following a major burn injury.

70 the conversion of partial- to full-thickness burn injuries.

71 ed for treating partial-thickness wounds and burn injuries.

72 terminant of wound-healing outcomes for deep burn injuries.

73 , who account for about 40% of all pediatric burn injuries.

74 tion accidents, falls, violent assaults, and burn injuries.

75 eristics and well-defined outcomes for major burn injuries.

76 ear, more than 4500 die as a result of their burn injuries.

77 c value and delay lethal complications after burn injuries.

78 FU/mL), after sepsis complicated by previous burn injury (40% total body surface area), and after ami

79 day for five days starting 45 minutes after burn injury (500 IU/kg body weight: EPO 500 or 2500 IU/k

80 oid-induced lymphocyte apoptosis early after burn injury abolishes both the late homeostatic accumula

81 In this study, we found that burn injury activated mTORC1 and hypoxia-inducible facto

82 sepsis, acute respiratory distress syndrome, burn injury, acute pancreatitis and stroke.

83 ctive review of all 1665 patients with acute burn injuries admitted from 1990 to 1994 to Massachusett

84 prospectively on all 530 patients with acute burn injuries admitted in 1995 or 1996.

85 dependent on intact organ function; however, burn injury affects the structure and function of almost

86 On the other hand, burn injury alone caused a substantial T-cell proliferat

87 E. coli infection on the effects produced by burn injury alone.

88 t patients younger than 55 years with severe burn injuries and inhalation injury to survive these dev

89 Patients with severe traumatic or burn injury and a mouse model of burn injury were studie

90 lonization sites and cause a fatal sepsis in burn injury and acute lung infection models.

91 the hospital as a result of a combination of burn injury and anoxic brain injury (n = 8) or cardiac a

92 tiple aspects of metabolic alterations after burn injury and as a novel potential molecular target to

93 were greatly attenuated 1, 6, and 12 h after burn injury and completely abolished 24 h after burn.

94 lic alterations and insulin resistance after burn injury and determine their magnitude and persistenc

95 ation of bacterial pellet, or combination of burn injury and E. faecalis infection (B+EF group).

96 Mice were treated with Flt3L after burn injury and examined for survival, wound and systemi

97 al muscle stem cells, is altered following a burn injury and likely hinders regrowth of muscle.

98 treatment may be useful for reducing risk of burn injury and questions the use of 'drug holidays'.

99 norepinephrine stimulated myelopoiesis after burn injury and sepsis, but the site of this stimulation

100 ce were also used to evaluate the effects of burn injury and simvastatin treatment on burn-induced li

101 spread of P. aeruginosa infection following burn injury and suggests that MBL deficiency in humans m

102 lymph produced during the first 2 hrs after burn injury and tested at a 5% concentration, but not sh

103 Mice were subjected to 30% full-thickness burn injury and then treated either with or without simv

104 depleted of CD4+CD25+ T cells before sham or burn injury and then were immunized to follow the develo

105 e apoptotic index in the livers of mice with burn injury and this effect could be abrogated by TNF-al

106 neutrophil function longitudinally following burn injury and to examine the relationship between neut

107 oteins accumulated in diaphragm 3 days after burn injury and were rapidly removed from the tissue dur

108 termine the prevalence of hypoglycemia after burn injury and whether hypoglycemia is associated with

109 rease the resistance of mice to a subsequent burn injury and wound infection by a dendritic cell-depe

110 nificant complication of major trauma (e.g., burn injury) and include various aspects of metabolism,

111 temic endotoxemia have been reported after a burn injury, and caspase-3 activation due to TNF-alpha a

112 ith a major risk of local excessive heating, burn injury, and fire.

113 d its associated mortality is high following burn injury, and sepsis diagnosis is complicated by the

114 Recent studies have suggested that epidermal burn injuries are associated with inflammation and immun

115 Immunodeficient patients with severe burn injuries are extremely susceptible to infection wit

116 bstitutes for healing following third-degree burn injuries are fraught with complications, often resu

117 Patients with large burn injuries are susceptible to opportunistic infection

118 st, effective anabolic strategies for severe burn injuries are: early excision and grafting of the wo

119 Hyperglycemia and insulin resistance after burn injury are associated with increased morbidity and

120 ted to the hospital after sustaining a large burn injury are at high risk for developing hospital-ass

121 sponsiveness that occur subsequent to severe burn injury are not merely the result of global or passi

122 velopment of acute kidney injury (AKI) after burn injury as an independent risk factor for increased

123 kocyte transcriptome after severe trauma and burn injury, as well as in healthy subjects receiving lo

124 l populations, primarily adult and pediatric burn injury, as well as patients undergoing elective hip

125 ent and palmitate composition decrease after burn injury because of a decrease in the rate of phospha

126 These new findings in the body's response to burn injury between children and adults support further

127 ovine model of combined smoke inhalation and burn injury, bronchospasm and acute airway obstruction c

128 limb Achilles' tendon transection and dorsal burn injury (burn/tenotomy) to induce HO.

129 erved in the thymus and spleen 3 hours after burn injury but were not seen in liver or lung.

130 ty in combined smoke inhalation/third-degree burn injury, but does not affect the vascular permeabili

131 echanical (pressure) stimuli develop after a burn injury, but the neural mechanisms underlying these

132 tes recovery of mitochondrial function after burn injury by increasing ATP synthesis rate, improving

133 surface area (third-degree) cutaneous flame burn injury can induce severe RDS (PaO2/F(IO2) <200) wit

134 , these findings reveal that a second-degree burn injury can initiate an immediate novel zonal degran

135 Because the mouse inflammatory response to burn injury cannot account for the contribution of human

136 on of nociceptive primary sensory neurons by burn injury, capsaicin application or sustained electric

137 Burn injury caused mobilization of human inflammatory ce

138 Burn injury causes a major systemic catabolic response t

139 n mortality, controlling for demographic and burn injury characteristics.

140 and by 41% in sepsis complicated by previous burn injury compared with shams.

141 o characterize the mechanisms by which local burn injury compromises epithelial barrier function in b

142 (8 weeks of age) were randomized to sham or burn injury consisting of a dorsal scald burn injury cov

143 neutrophil migratory phenotype in rats with burn injuries correlates with improved survival in a cla

144 intestinal bacterial translocation caused by burn injury could be related to the increased infiltrati

145 or burn injury consisting of a dorsal scald burn injury covering 30% of total body surface area.

146 Burn injury damages tissue at the site of the burn and a

147 e hypothesis that Flt3L administration after burn injury decreases susceptibility to wound infections

148 ains the leading cause of death from serious burn injury despite recent advances in the care of burn

149 Burn injury destroys skin, the second largest innate imm

150 Ossicles from mice with burn injuries developed significantly more bone than sha

151 Burn injury disrupts the mechanical and biological barri

152 Although local burn injury does not alter high-energy phosphates or pH,

153 In addition, burn injury enhanced vascularization of the ossicles (P

154 Additionally, treatment with FL after a burn injury enhances neutrophil-mediated control of bact

155 Robust skeletal muscle atrophy occurs after burn injury, even in muscles located distally to the sit

156 staphylococcal enterotoxin B at 1 day after burn injury exhibited high mortality, whereas no mortali

157 These data emphasize that the burn injury experienced by these pediatric patients alte

158 Patients with major burn injury frequently require multiple blood transfusio

159 Thirteen patients were studied after severe burn injury (>60% total body surface area).

160 Compared with sham controls, animals with burn injury had a significantly higher mortality in resp

161 the effect of blood transfusion after major burn injury has had limited study.

162 Metabolic alterations after burn injury have been well described in children; howeve

163 f medical comorbidities on outcomes in acute burn injury have produced inconsistent results, chiefly

164 metabolic responses to catecholamines, after burn injury, have not been elucidated.

165 nd delayed fluid resuscitation (>2 hrs after burn injury), identified in 82% of the nonsurvivors vs.

166 ndicate that PMN-II appearing in response to burn injury impair host antibacterial resistance against

167 reatment with low doses of insulin following burn injury improved the outcome of rats in response to

168 -alarm-giveaway program in the prevention of burn injuries in an area with a high rate of such injuri

169 We collected data on burn injuries in Oklahoma City from September 1987 throu

170 Contact burn injuries in rats were treated with varying treatmen

171 Major advances in treatment of burn injuries in the last 20 years have made it possible

172 pact of age on the temporal gene response to burn injury in a large-scale clinical study.

173 re is growing evidence for increased risk of burn injury in children with Attention Deficit/Hyperacti

174 Information regarding the risk of burn injury in children with symptoms of Attention Defic

175 CD4 CD25 T regulatory (Treg) activity after burn injury in mice.

176 f myofibre area and volume following a scald burn injury in mice.

177 ptosis of muscle satellite cells following a burn injury in paediatric patients.

178 Burn injury in rats results in accumulation of neutrophi

179 also significantly reduced at 14 days after burn injury in the glutamine group (p <.01).

180 gulated significantly within 1 wk of thermal burn injury in the muscle and fat tissues of patients fr

181 rn morbidity and poorer adjustment following burn injury in these patients.

182 intestinal barrier loss in a model of severe burn injury in which injury was associated with decrease

183 In the early period after a burn injury, increased apoptosis is observed primarily i

184 Innate immune dysfunction after major burn injuries increases the susceptibility to organ fail

185 Furthermore, burn injury increases density and shifts activation of t

186 Burn injury increases the predilection to osteogenic dif

187 rates of ED presentation for chemical ocular burn injuries, independent factors associated with all,

188 Burn injury induced robust atrophy in muscles located bo

189 Burn injury induced significant liver damage, which was

190 Burn injury induced significant splenic apoptosis and sy

191 Additionally, burn injury induced skeletal muscle regeneration, satell

192 model of beta-adrenergic receptors to study burn injury-induced alterations in receptors and in sign

193 stigate the molecular and cellular basis for burn injury-induced pain.

194 Severe burn injury induces satellite cell proliferation and fus

195 Severe burn injury induces skeletal muscle regeneration and myo

196 atients survive the initial 72 hours after a burn injury, infections are the most common cause of dea

197 The exact mechanism by which burn injury influences bone formation is unknown.

198 epatic structure and function after a severe burn injury; insulin also restores hepatic homeostasis a

199 Burn injury involves inflammatory mechanisms that can le

200 liver in the hypermetabolic phase after the burn injury involves transcription factors, stress and i

201 Burn injury is associated with a catabolic state persist

202 We find that such burn injury is associated with early mast cell (MC) degr

203 Immune suppression early (3 days) after burn injury is associated with glucocorticoid-mediated T

204 Burn injury is associated with insulin resistance.

205 Severe burn injury is associated with vitamin D deficiency, low

206 A major component of burn injury is caused by additional local damage from ac

207 Patient survival after severe burn injury is largely determined by burn size.

208 Burn injury is often associated with immune suppression.

209 However, major burn injury is precluded from these studies.

210 The optimal transfusion strategy in major burn injury is thus needed but remains unknown.

211 IL-10, produced in response to burn injuries, is shown to be inhibitory on Th17 cell ge

212 tical illness, including sepsis, trauma, and burn injury, is often complicated by multiple organ dysf

213 d if they dealt with pediatrics, geriatrics, burn injuries, isolated hand injuries, chronic (i.e., no

214 A severe burn injury leads to marked hypermetabolism and cataboli

215 nous beta-adrenergic receptor agonists after burn injury may be attributed to decreased affinity for

216 Survival rates from burn injury may have been maximized by current treatment

217 In vivo experiments in a porcine burn injury model showed that P12 limited burn injury pr

218 In a burn injury model, the dermal inflammatory response may

219 Using a mouse burn injury model, we demonstrate that injury significan

220 Resuscitation of large burn injuries must quickly restore and maintain cardiova

221 uary 1 through December 31, 2002, with acute burn injuries of >or=20% total body surface area.

222 The patient with severe burn injuries offers significant challenges to the anest

223 Understanding the role of burn injury on heterotopic bone formation is an importan

224 develop a mouse model to study the effect of burn injury on heterotopic bone formation.

225 ain a better understanding of the effects of burn injury on liver metabolism.

226 study compares the early and late effects of burn injury on SAg reactivity in vivo to establish how i

227 we examined the effects of EtOH exposure and burn injury on Th17 responses within intestinal lymphoid

228 paB KO mice were subjected to full-thickness burn injury or sham treatment.

229 ntial treatment for tissue loss secondary to burns, injuries, or resections.

230 Rats were given third-degree burn injury over 40% of the total body surface area, wer

231 amine-supplemented patients at 14 days after burn injury (p <.01 and.04, respectively).

232 g of skeletal muscle dysfunction suffered by burn injury patients.

233 inical studies to improve the care of severe burn injury patients.

234 Before the intervention the rate of burn injuries per 100,000 population was 4.2 times highe

235 Overall, our study supports the concept that burn injury per se can significantly suppress T-cell med

236 Severe burn injury predisposes patients to burn wound infection

237 r sepsis or sepsis complicated by a previous burn injury prevented myocardial Na and Ca accumulation,

238 We have recently reported that burn injury primes innate immune cells for a progressive

239 ntravenous administration of curcumin limits burn injury progression in a rat model.

240 ne burn injury model showed that P12 limited burn injury progression, suggesting an active role in ti

241 rovascular perfusion is a central element of burn injury progression, we hypothesized that curcumin m

242 endoplasmic reticulum stressors, and limited burn-injury progression in a rat hot comb model.

243 The initial infusion of HSD 1 hr after the burn injury promptly restored cardiac index, promoted di

244 c cell enhancement by Flt3L treatments after burn injury protects against opportunistic infections th

245 thod to quantify urinary 3MH was tested in a burn injury rat model and on urine specimens from pediat

246 Burn-injury rats received the IMPACT diet supplemented w

247 1 with alkaline phosphatase, indicating that burn injury-related hyperphosphorylation of IRS-1 is sim

248 al abnormalities, we propose a mechanism for burn injury-related intestinal barrier dysfunction that

249 high-risk setting for operating room fires; burn injuries represent 20% of monitored anesthesia care

250 Skeletal muscle regrowth following a burn injury requires satellite cell activity, underscori

251 erate-dose IL-12 therapy in a mouse model of burn injury restored resistance to a later infectious ch

252 The majority of severe and fatal burn injuries result from residential fires.

253 L-2 and IFN-gamma production after EtOH plus burn injury resulted from a decrease in IL-12.

254 l of five therapy sessions after the initial burn injury, resulted in a 57.9% reduction of the scar a

255 Our results demonstrate that burn injury results in a localized intramyocellular lipi

256 Concurrently, burn injury results in an immunocompromised state, and s

257 ed that acute ethanol (EtOH) exposure before burn injury results in intestinal T cell suppression and

258 Severe burn injury seriously affects multiple aspects of glucos

259 Thus, pain after burn injury should be aggressively treated using pharmac

260 of blood products in the treatment of major burn injury should be reserved for patients with a demon

261 improve the quality of life of survivors of burn injury should ultimately have very favorable impact

262 Mice treated with MPLA after burn injury showed improved survival and less local and

263 When combined with EtOH intoxication, burn injury significantly decreased IL-17 and IL-22, as

264 ter injury, we found that EtOH combined with burn injury significantly increased neutrophil O(2)(-) p

265 d the hypothesis that Flt3L treatments after burn injury stimulate the production of functional effec

266 r levels of education, exposure to grotesque burn injuries, stressful life events following exposure,

267 An initial burn injury suppressed T-cell proliferation at a level t

268 ol/ethanol (EtOH) intoxication combined with burn injury suppresses T cell IL-2 and IFN-gamma product

269 r intravenous fluids in patients with trauma/burn injuries, surgery, cancer, pancreatic disease, infl

270 tochondrial protective agents in alleviating burn injury symptoms.

271 d dampened inflammatory response early after burn injury that changes to an augmented response at lat

272 SI, mortality, or organ dysfunction in major burn injury, these outcomes were no worse than the liber

273 Three hours after burn injury, tissue samples were obtained from the thymu

274 a combined smoke inhalation and third-degree burn injury to 40% of total body surface area.

275 f 31,338 adults who were admitted with acute burn injury to 70 burn centers from the American Burn As

276 entify 95579 patients admitted with an acute burn injury to 80 tertiary American Burn Association bur

277 ome of survivors and nonsurvivors of massive burn injury to determine the proteomic survival signatur

278 microbiome and antimicrobial peptides after burn injury to identify potential mechanisms leading to

279 ish a new mouse model of focal second-degree burn injury to investigate the molecular and cellular ba

280 cal application of human MC chymase restores burn injury to scalded mMCP-4-deficient mice but not to

281 propose that, in sensory neurons damaged by burn injury to the hindpaw, Na(v)1.7 currents contribute

282 Deficit/Hyperactivity Disorder on pediatric burn injury, to identify specific considerations and tre

283 ial resuscitation of large body surface area burn injury using a colloid (hetastarch), and can be fur

284 y could be selectively assessed after severe burn injury using humanized mice.

285 18 hospitalized with a primary diagnosis of burn injury using ICD-9 codes.

286 ty years ago, survival from the most serious burn injuries was not possible even in the most advanced

287 Next, burn injury was accompanied by evidence of histologic lu

288 purpose, a deep partial thickness cutaneous burn injury was applied on the back of mice, followed by

289 Genomic and protein analysis revealed that burn injury was associated with alterations in the signa

290 A mouse model of burn injury was used to confirm the human findings and t

291 o assess further the role of mitochondria in burn injury, we performed in vivo (31)P NMR spectroscopy

292 Using a mouse model of burn injury, we show CD8+ T cell hyperresponsiveness lat

293 ite cells during muscle recovery following a burn injury, we utilized a genetically modified mouse mo

294 In Experiment 2, young rats with burn injury were administered with morphine (10mg/kg, s.

295 raumatic or burn injury and a mouse model of burn injury were studied early after injury to determine

296 rmin had a strong antilipolytic effect after burn injury when compared with insulin and was associate

297 s obtained from 60 patients within 14 hrs of burn injury who underwent bronchoscopy for suspected smo

298 n ameliorate the muscle catabolism of severe burn injury with normal feedings.

299 ought to determine the influence of thermal (burn) injury with sepsis and norepinephrine on the clono

300 We hypothesized that burn injury would enhance early vascularization and subs