ライフサイエンスコーパス: burn injury

1 educe lung injury following pancreatitis and burn injury.

2 ll as stimulating tissue repair after severe burn injury.

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

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

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

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

7 etabolic and inflammatory response following burn injury.

8 graft failure and secondary infection after burn injury.

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

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

11 oteomic survival signature following a major burn injury.

12 d thereby reduce hepatocytic apoptosis after burn injury.

13 d the gut microbiota in the acute setting of burn injury.

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

15 exist for onset of ARDS nor in patients with burn injury.

16 at occur after combined smoke inhalation and burn injury.

17 the perfused livers of fasted rats receiving burn injury.

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

19 perturbed in pediatric and adult patients by burn injury.

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

21 can offer protection against infection after burn injury.

22 the early inflammatory response to a severe burn injury.

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

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

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

26 the intestine from damage following EtOH and burn injury.

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

28 to wound infections may be protective after burn injury.

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

30 al edema and permeability following EtOH and burn injury.

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

32 treating insulin resistance following severe burn injury.

33 se in cardiomyocyte expression of C5aR after burn injury.

34 erses these pathologic changes incurred from burn injury.

35 dical conditions influence outcomes in acute burn injury.

36 omorbidities have not been examined in acute burn injury.

37 n vitro were significantly reduced following burn injury.

38 hepatic encephalopathy, and fibromyalgia and burn injury.

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

40 and subsequent systemic complications after burn injury.

41 e immune dysfunction that occurs early after burn injury.

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

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

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

45 vitamin D supplementation is necessary after burn injury.

46 nds potentially involved in the pathology of burn injury.

47 prevent T-cell dysfunction encountered after burn injury.

48 nd DC functions and improving immunity after burn injury.

49 infectious challenge is also impaired after burn injury.

50 ed skeletal muscle hypercatabolism following burn injury.

51 tudy and prevention of ARDS in patients with burn injury.

52 tus, burns to critical areas, and time since burn injury.

53 namic interstitia through its application to burn injury.

54 d subjected to a 30% total body surface area burn injury.

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

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

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

58 ajor complications that hamper recovery from burn injury.

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

60 blished clinical predictor of survival after burn injury.

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

62 ajor complications that hamper recovery from burn injury.

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

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

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

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

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

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

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

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

71 c value and delay lethal complications after burn injuries.

72 oing challenges and stigmata associated with burn injuries.

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

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

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

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

77 tion accidents, falls, violent assaults, and 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 ong the biomarkers measured in patients with burn injuries, a one-standard deviation increase in log-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 e examination of the contributing factors of burn injury and severity.

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

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

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

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

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

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

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

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

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

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

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

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

110 Thermal burn injuries are an important environmental stressor th

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

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

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

114 Patients with large burn injuries are susceptible to opportunistic infection

115 Burn injuries are under-appreciated injuries that are as

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

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

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

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

120 Advances in the management of burn injuries as well as successful public health effort

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

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

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

124 adults who survived to discharge after major burn injury between 2003 and 2013 were matched to betwee

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

126 lmonary immunosuppression often occurs after burn injury (BI).

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

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

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

132 Burn injury can be a devastating traumatic injury, with

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

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

135 Accordingly, patients with burn injury cannot be considered recovered when the woun

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

137 Burn injury carries the highest incidence of acute respi

138 Burn injury caused mobilization of human inflammatory ce

139 Burn injury causes a major systemic catabolic response t

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

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

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

143 (8 weeks of age) were randomized to sham or burn injury consisting of a dorsal scald burn injury cov

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

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

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

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

148 Burn injury destroys skin, the second largest innate imm

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

150 Burn injury disrupts the mechanical and biological barri

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

152 Response to the burn injury during the acute phase response after burn i

153 ted an increase in the relative mortality of burn injury during the study period.

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

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

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

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

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

159 Patients with major burn injury frequently require multiple blood transfusio

160 Domestic cats (n = 51) sustaining burn injuries from the Tubbs (2017) and Camp (2018) wild

161 We included all patients with an acute burn injury greater than or equal to 20% total body surf

162 adult patients (age >= 18 years) with severe burn injury (>= 20% total body surface area) to generate

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

164 However, the relative mortality of burn injury has been fixed over the 26-year study period

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

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

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

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

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

170 Contact burn injuries in rats were treated with varying treatmen

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

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

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

174 Thermal hyperalgesia induced by PMA or burn injury in KI was identical to WT.

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

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

180 The overall incidence of burn injury in the United States has decreased from 215

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

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

185 Burn injury increases the predilection to osteogenic dif

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

187 Burn injury induced robust atrophy in muscles located bo

188 Burn injury induced significant liver damage, which was

189 Burn injury induced significant splenic apoptosis and sy

190 Additionally, burn injury induced skeletal muscle regeneration, satell

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

192 Severe burn injury induces satellite cell proliferation and fus

193 Severe burn injury induces skeletal muscle regeneration and myo

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

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

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

197 Burn injury involves inflammatory mechanisms that can le

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

199 Burn injury is associated with a catabolic state persist

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

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

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

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

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

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

206 o determine if the acute phase response post burn injury is significantly different in elderly patien

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

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

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

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

211 overed when the wounds have healed; instead, burn injury leads to long-term profound alterations that

212 A severe burn injury leads to marked hypermetabolism and cataboli

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

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

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

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

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

218 previous studies have indicated that thermal burn injury of the skin keratinocyte in vitro results in

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

220 nd understand the long-term social impact of burn injuries on adult populations.

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

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

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

224 The effect of sustaining a major burn injury on long-term life expectancy is poorly under

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

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

227 s in combat for immediate use at the site of burn injury on the battlefield.

228 ticenter study of 113 patients with isolated burn injury or inhalation injury.

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

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

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

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

233 Burn injuries, particularly severe burns, are accompanie

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

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

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

237 Severe burn injury predisposes patients to burn wound infection

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 seminating pathological processes underlying burn injury's clinical challenges are orchestrated from

256 Severe burn injury seriously affects multiple aspects of glucos

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

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

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

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

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

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

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

264 Of note, burn injury-stimulated microvesicle particles do not car

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

266 pulmonary immunosuppression: extrapulmonary burn injury suppresses bacterial endotoxin-induced pulmo

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

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

269 tochondrial protective agents in alleviating burn injury symptoms.

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

271 oked by stimuli (including skin pinching and burn injury) that-in humans-produce sustained pain, with

272 Burn injury therefore exemplifies a superficial temporal

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

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

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

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

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

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

279 The present studies demonstrate that thermal burn injury to keratinocytes in vitro and human skin exp

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

284 18 hospitalized with a primary diagnosis of burn injury using ICD-9 codes.

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

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

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

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

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

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

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

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

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

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

295 derstanding the metabolic changes induced by burn injury will help to guide therapeutic intervention

296 ling was used to estimate the association of burn injury with mortality.

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

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

299 e aim of this study is to report patterns of burn injury within the United States from 1990 to 2016 w

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