ライフサイエンスコーパス: blast

1 ver to imatinib]; imatinib group, n=1 [1%]), blast cell crisis (nilotinib group, n=1 [1%]; imatinib g

2 Five weeks after blast exposure, 8 of the 13 blasted rats exhibited chronic tinnitus.

3 s into aggressive lethal leukemias with >30% blasts in the peripheral blood.

4 mal residual disease (MRD) response (<10(-4) blasts), including 22 CR/CRh responders, 2 patients with

5 3 (46%) had bone marrow blast clearance (<5% blasts).

6 used this single-cell approach to identify a blast-crisis-specific SC population, which was also pres

7 ecreased pTau levels in vitro, and abolished blast-induced elevation of pTau in vivo.

8 Transformation to accelerated/blast phase occurred in 5% and 7% of patients in the das

9 lower rates of transformation to accelerated/blast phase were reported compared with patients with BC

10 es lining the ventricles; all cases of acute blast exposure showed early astroglial scarring in the s

11 ronic blast exposure, three cases with acute blast exposure, five cases with chronic impact traumatic

12 These changes were detected 30 days after blast exposure, suggesting the possibility of long-lasti

13 develop heterotopic ossification (HO) after blast-related extremity injury and traumatic injuries, r

14 levels in ApoE4 mice did not increase after blast TBI.

15 Five weeks after blast exposure, 8 of the 13 blasted rats exhibited chron

16 e P1-N1 amplitude reduction persisted in all blast-exposed rats.

17 timing, frequency, and properties of BCP-ALL blasts entering the CNS compartment are unknown.

18 enhance phagocytosis of patient-derived ALL blasts by human macrophages in vitro.

19 allele is preferentially retained in HD-ALL blasts consistent with inherited genetic variation contr

20 Freshly isolated pediatric ALL blasts also expressed high levels of Bcl-2 and exhibited

21 -positive acute lymphoblastic leukemia (ALL) blasts, was approved for use in patients with relapsed o

22 decreased, suggesting that DAC enhances AML blast susceptibility to BI 836858 by upregulating NKG2DL

23 e concentrations, resulting in arrest of AML blast proliferation and a reduction in AML engraftment i

24 ates bone marrow stromal cells (BMSC) to AML blast transfer of mitochondria through AML-derived tunne

25 e, we report a novel interaction between AML blasts and BM-MSCs, which benefits AML proliferation and

26 rectional, prosurvival mechanism between AML blasts and BM-MSCs.

27 cell surface markers are shared between AML blasts and healthy hematopoietic stem and progenitor cel

28 Treatment with IFNgamma drove AML blasts toward a more differentiated state, wherein they

29 h also induced lethal mitophagy in human AML blasts with clinically relevant FLT3 mutations.

30 ic cell divisions and differentiation in AML blasts and AML stem/progenitor cells, inhibited cell gro

31 Transfer was greater in AML blasts compared with normal cord blood CD34(+) cells.

32 d a profound gene expression decrease in AML blasts for cytokine and chemokine signaling (e.g., IL15,

33 In vitro treatment of AML blasts with decitabine (DAC) or 5-azacytidine, 2 hypomet

34 re, we show that sequential treatment of AML blasts with decitabine followed by selinexor (XPO1 inhib

35 -receptor pair CD70/CD27 is expressed on AML blasts and AML stem/progenitor cells.

36 Treatment of patient AML blasts with recombinant EGFL7 in vitro leads to increase

37 her to target AML cell lines and patient AML blasts.

38 105 prevented the engraftment of primary AML blasts and inhibited leukemia progression following dise

39 ntibody using AML cell lines and primary AML blasts as targets.

40 1), rendering AML cell lines and primary AML blasts dependent on exogenous arginine and sensitized to

41 nt killing of AML cell lines and primary AML blasts in vitro and in vivo.

42 and impaired colony formation in primary AML blasts.

43 e, we demonstrate that IFNgamma promotes AML blasts to act as effector cells within the context of an

44 senchymal stromal cells (BM-MSC) protect AML blasts from spontaneous and chemotherapy-induced apoptos

45 Furthermore, CHD4 depletion renders AML blasts more sensitive both in vitro and in vivo to genot

46 We show that AML blasts alter metabolic processes in adipocytes to induce

47 We show that AML blasts constitutively express the arginine transporters

48 We further show that AML blasts secrete EGFL7 protein and that higher levels of E

49 both simultaneously up-regulated on the AML blasts, we tested whether IFNgamma treatment of the AML

50 ansfer of fatty acids from adipocytes to AML blasts.

51 ly expressed on acute myeloid leukemia (AML) blasts and is targeted by gemtuzumab ozogamicin (GO).

52 ly expressed in acute myeloid leukemia (AML) blasts compared with normal hematopoietic stem and proge

53 tion of CHD4 in acute myeloid leukemia (AML) blasts induces a global relaxation of chromatin that ren

54 were stratified according to donor, age, and blast count.

55 or samples related to coal carbonization and blast furnaces overlapped within a range of +0.1 to +10.

56 bodies in mice transplanted with chronic and blast phase CML cells resulted in therapeutic effects me

57 the absence of significant BM dysplasia and blast cells can be difficult to address in FA patients,

58 the re-establishment of EZH2 expression and blast clearance.

59 smear revealed anemia, thrombocytopenia, and blast cells, and a diagnosis of acute myeloid leukemia w

60 S1, no blasts; CNS2a to 2c, < 5 WBCs/muL and blasts with/without >/= 10 RBCs/muL or >/= 5 WBCs/muL pl

61 tanical remains are reinterpreted in part as blast deposits that resulted from several episodes of ai

62 emonstrated enhanced responses to autologous blasts in vitro, and primed CD56bright cells controlled

63 netic changes, cells become committed to a B-blast fate <12 days post-infection and are unable to de-

64 phenotypically resemble antigen-activated B-blasts.

65 In vivo similar B-blasts can differentiate to become memory B cells (MBC),

66 d a concomitant increase in peripheral blood blast cells.

67 ize, and high leukocyte and peripheral-blood blast counts.

68 Blood blasts greater than 3% (hazard ratio [HR], 1.41; 95% CI,

69 had cytopenias, and 12.0% presented >/=5% BM blast cells.

70 e in MDS-E, as patients with 10% to < 20% BM blasts from TNCs fulfill erythroleukemia criteria; howev

71 diagnosed within WHO categories with < 5% BM blasts, were reclassified into higher-risk categories an

72 yperplasia, calculating the percentage of BM blasts from NECs improves prognostic assessment of MDS.

73 In these instances, when BM blasts are >/= 20%, the disorder is classified as erythr

74 s classified as erythroleukemia, and when BM blasts are < 20%, as myelodysplastic syndrome (MDS).

75 mainly on the percentage of bone marrow (BM) blasts.

76 e chronic myelogenous leukemia (CP-CML), but blast crisis CML (BC-CML) and acute myeloid leukemias (A

77 nces in spatial cognition were observed, but blasted rats as a whole exhibited increased anxiety.

78 management of secondary events triggered by blast-induced, mild traumatic brain injury that is commo

79 ing a xenograft model, we find that CD105(+) blasts are endowed with superior leukemogenic activity c

80 hesis and N-glycan branching in mouse T cell blasts by starving the hexosamine pathway of glucose and

81 S-causative p110delta variants and in T-cell blasts derived from patients.

82 All cases of chronic blast exposure had an antemortem diagnosis of post traum

83 All five cases with chronic blast exposure showed prominent astroglial scarring that

84 brain specimens from five cases with chronic blast exposure, three cases with acute blast exposure, f

85 m male military service members with chronic blast exposures and from those who had died shortly afte

86 9)/L, platelets < 100 x 10(9)/L, circulating blasts >/= 2%, bone marrow fibrosis grade >/= 2, constit

87 ly aggressive chronic myeloid leukemia (CML)-blast phase-like disease in mice compared with less mali

88 lished in most patients with TBI from combat blast exposure and reveals high rates of visual field de

89 led active-duty US military after concussive blast injury (n = 50) in the acute to subacute stage and

90 All concussive blast injuries met the Department of Defense definition

91 Worsening of symptoms in concussive blast TBI was also observed on measures of posttraumatic

92 Thirty-six of 50 patients with concussive blast TBI (72%) had a decline in the GOS-E from the 1- t

93 nificantly worse in patients with concussive blast TBI compared with combat-deployed controls, wherea

94 Service members with concussive blast TBI experienced evolution, not resolution, of symp

95 in military service members with concussive blast TBI when comparing 1- and 5-year clinical outcomes

96 roleukemia criteria; however, by considering blasts from NECs, 72 patients were recoded as RAEB-2 and

97 day-29 minimal residual disease < 0.1%, CSF blast, regardless of cell count, was an independent adve

98 l, Ebinger et al. describe rare, non-cycling blasts in acute lymphoblastic leukemia that combine the

99 hase in a patient who subsequently developed blast crisis.

100 a highway construction site with documented blasting in New Hampshire.

101 hat were genomically similar to the dominant blast populations at diagnosis and were fully clonally r

102 This novel in vivo model for dormant blasts will facilitate the dissection of the niche and t

103 ML-DS blast cells ex vivo have increased sensitivity to cytara

104 nal Prognostic Scoring System by enumerating blasts from NECs in MDS-E and in the overall MDS populat

105 By enumerating blasts systematically from NECs, 22% of patients with MD

106 diagnosis of refractory anaemia with excess blasts (RAEB)-1, RAEB-2, RAEB-t, or chronic myelomonocyt

107 commendations, refractory anemia with excess blasts (RAEB)-2 diagnosis is not possible in MDS-E, as p

108 s with myelodysplastic syndromes with excess blasts after failure of azacitidine or decitabine treatm

109 In the presence of excessive blasts and other poor prognostic factors, hypomethylatin

110 differentiate patterns of injury that follow blasts in intermediate environments.

111 Following blast TBI, phospho-Tau (pTau) levels were unchanged in A

112 ells in FLK1 mesoderm that were enriched for blast colony forming potential, whereas the P/-8-kb enha

113 nic RNA binding protein that is required for blast crisis CML.

114 he groundwater samples, while the values for blast furnace sludge (-26.9 +/- 1.5 per thousand), comme

115 ples collected from the parent rock, freshly blasted waste rock (less than 10 days old), and aged was

116 g may indicate specific areas of damage from blast exposure consistent with the general principles of

117 Injury from blast exposure is becoming a more prevalent cause of dea

118 primary ocular blast exposure resulting from blast wave pressure has been reported among survivors of

119 ng neurological impairments that result from blasts are significant and lifelong.

120 Grit-blasted acid-etched titanium disks were contaminated wit

121 After 6 months, grit-blasted acid-etched (GBAE) PS implants with and without

122 anemia, thrombocytopenia, leukopenia, higher blast count, symptoms, large splenomegaly, and unfavorab

123 T1 expression not only is activated in human blast crisis CML and de novo acute myeloid leukaemia, bu

124 CD36 also marks a fraction of human blast crisis CML and acute myeloid leukemia (AML) cells

125 ability and induced apoptosis of mutant IDH1 blasts in vitro.

126 ocess leading to an accumulation of immature blasts in the blood.

127 In blast crisis chronic myeloid leukemia (BC CML), we show

128 tic syndrome, acute myeloid leukemia, and in blast crisis transformation of chronic myeloid leukemia.

129 tic target for enhancing chemosensitivity in blast cells.

130 ncogenic function through BCAA production in blast crisis CML cells.

131 Injury severity in blast induced Traumatic Brain Injury (bTBI) increases wi

132 GFL7 mRNA and EGFL7 protein are increased in blasts of patients with acute myeloid leukemia (AML) com

133 patient each: myalgia (one [2%]), increased blast cell count (one [2%]), and general physical health

134 romegakaryocytes in the absence of increased blasts.

135 rate the efficacy of rapamycin in inhibiting blast trauma-induced HO by a multipronged mechanism.

136 We found that 300-kPa blasts yielded no detectable cognitive or motor deficits

137 iferation of primary acute myeloid leukaemia blast cells (p=0.028).

138 We isolated primary acute myeloid leukaemia blast cells from heparinised blood and human peripheral

139 iferation of primary acute myeloid leukaemia blast cells.

140 G 330 targets CD33 on acute myeloid leukemia blast cells.

141 iferation and self-renewal rates of leukemia blast populations, that is, leukemia progenitor cells.

142 Leukemia blasts show a myeloid differentiation phenotype when the

143 ating active viral transcription in leukemia blasts as well as intact virions in serum.

144 -derived B-cell acute lymphoblastic leukemia blasts compared with standard TCR transfer.

145 and BCR-ABL1-negative acute myeloid leukemia blasts, which express readily detectable IKAROS.

146 irect T cells against acute myeloid leukemia blasts.

147 rphologic similarities with patient leukemia blasts including a subset with mixed phenotype, a distin

148 ith Alox5 overexpression in MLL-AF9-leukemic blast cells; inhibition of the above signaling pathways

149 ells with MDR activity (MDR(+)) and leukemic blast cells without MDR activity (MDR(-ve)).

150 nd phenotypic heterogeneity between leukemic blast cells is a well-recognized phenomenon, there remai

151 GFL7 in vitro leads to increases in leukemic blast cell growth and levels of phosphorylated AKT.

152 ) cells were frequently observed in leukemic blast cells in both pretherapy and relapsed samples, con

153 This enabled categorization into leukemic blast cells with MDR activity (MDR(+)) and leukemic blas

154 egulator ZEB1 significantly reduced leukemic blast invasion.

155 Leukemic blasts could also be distinguished from benign white blo

156 In addition, leukemic blasts in one-fourth of JMML patients present with monos

157 ls, leukemic stem cells [LSCs], and leukemic blasts).

158 in functional MDR activity between leukemic blasts was observed, with MDR(+) cells not infrequently

159 fy heterogeneity in MDR activity in leukemic blasts.

160 in MDR activity between individual leukemic blasts are lacking.

161 rine mechanism supporting growth of leukemic blasts in patients with AML.

162 se was identified in populations of leukemic blasts that did not demonstrate this activity before tre

163 is exposed on the cell membrane of leukemic blasts.

164 te that targeting CD19 and CD123 on leukemic blasts represents an effective strategy for treating and

165 CART123, but not CART19, recognized leukemic blasts, established protracted synapses, and eradicated

166 to existing chemotherapy drugs than leukemic blasts because of a distinctive lower proliferative stat

167 n of myeloid differentiation of the leukemic blasts.

168 mples from 20 adults with AML whose leukemic blasts had MDR activity against the anthracyline daunoru

169 than pairwise similarity search methods like blast and ssearch because they build a position specific

170 he proliferation of immature myeloid lineage blasts.

171 (CML)-like disease manifesting in "lymphoid blast crisis." The biological heterogeneity of BCR-ABL1-

172 Malignant blasts from patients with acute myeloid leukemia (AML) e

173 , and defective differentiation of malignant blasts are key oncogenic drivers in acute myeloid leukem

174 exposure on the plasma membrane of malignant blasts positively correlated with the frequency of circu

175 aracterized by the accumulation of malignant blasts with impaired differentiation programs caused by

176 f the 116 patients, 53 (46%) had bone marrow blast clearance (<5% blasts).

177 n was stratified by pretreatment bone marrow blast percentage.

178 -4 toxic effects, and changes in bone-marrow blast counts from baseline.

179 d for minimal residual disease (0.01% marrow blasts) (78.4% vs. 28.1%, P<0.001); the duration of remi

180 ients with active disease (ie, >/= 5% marrow blasts by morphology) in treatment algorithms for alloge

181 pendency, white blood cell count, and marrow blasts retained independent prognostic value.

182 ercent showed >/=50% decrease in bone marrow blasts from baseline.

183 -2 or high-risk MDS or AML, with bone marrow blasts of 50% or less, and had either grade 4 thrombocyt

184 0(9) platelets per L; had 10-50% bone-marrow blasts; or were platelet transfusion dependent were rand

185 nter complete remission (CR), whereas MDR(+) blasts were frequently observed in patients who failed t

186 Mild blast traumatic brain injury (B-TBI) induced lasting cog

187 recent study of the pathophysiology of mild, blast-induced traumatic brain injury (bTBI) the exposure

188 nts, 84.2% (688 of 817) reported one or more blast-related incident and 63.0% (515 of 817) reported l

189 tive diagnosis or directed treatment of most blast-associated traumatic brain injuries, partly becaus

190 and decreased clonogenic capacity of myeloid blasts.

191 leukemia-initiating cells and CD19-negative blasts in bulk B-ALL at baseline and at relapse after CA

192 (18)O) from dissolution of unexploded NH4NO3 blasting agents in oxic groundwater; (2) delayed and red

193 F status was designated as follows: CNS1, no blasts; CNS2a to 2c, < 5 WBCs/muL and blasts with/withou

194 benefits for participants with tonal and non-blast induced tinnitus at the end of 6 (24.3% vs. 2%, p

195 rom that associated with impact-induced, non-blast traumatic brain injuries.

196 Sequences obtained blasted to 9 phyla, 66 genera, and 401 human oral taxa (

197 lying debris are more common, primary ocular blast exposure resulting from blast wave pressure has be

198 Although secondary ocular blast injuries due to flying debris are more common, pri

199 asts are detected in vitro around day 1.5 of blast colony differentiation, within the cell population

200 mia (with CD22 expression on at least 70% of blast cells) were enrolled at six centres in France.

201 Magnaporthe oryzae, the causal agent of blast disease, is one of the most destructive plant path

202 c hyperactivity, the non-auditory effects of blast and potential traumatic brain injury may also exer

203 for understanding the subsequent effects of blast exposure in a sample of Florida National Guard mem

204 le deficiency, myelodysplasia with excess of blast cells, and various developmental aberrations, we i

205 (ie, non-military) cases with no history of blast exposure, including cases with and without chronic

206 s as a single disease entity irrespective of blast count.

207 In a mouse model of blast crisis chronic myeloid leukemia (CML), adipose-res

208 signaling, on HO formation in a rat model of blast-related, polytraumatic extremity injury.

209 l system in both humans and animal models of blast injury.

210 d to maintain the developmental potential of blast cells that are generated in the embryo but divide

211 re consistent with the general principles of blast biophysics, and further, could account for aspects

212 fferentiation and impairs the propagation of blast crisis CML both in vitro and in vivo.

213 OS patients had the lowest proportion of blast trauma and burns.

214 The high volume of blast injuries in SO scenario supports the idea that the

215 (3) relatively persistent concentrations of blasting-related biogenic NO3(-) derived from nitrificat

216 Identification of blasting-related NO3(-) can be complicated by other NO3(

217 tive and resistant cell lines, as well as of blasts from patients with sorafenib-resistant AML, sugge

218 ified endoglin expression on the majority of blasts from patients with acute myeloid leukemia (AML) a

219 In the latter, the percentage of blasts is considered from TNCs.

220 Retrieval of blasts from the CNS showed no evidence for chemokine rec

221 To determine the prognostic significance of blasts, and of white and red blood cells, in CSF samples

222 Most injuries were the results of gunshot or blast injury (50 and 29 patients, respectively).

223 ths, and two additional patients had partial blast clearance.

224 stitutively activated in primary AML patient blasts but not in normal mononuclear cells.

225 iR-99 inhibition induced primary AML patient blasts to undergo differentiation.

226 death in AML cell lines, primary AML patient blasts, and isolated AML patient leukemic progenitor/ste

227 at the majority of newly diagnosed patients' blasts have deficiencies in the arginine-recycling pathw

228 Ruxolitinib treatment decreased peripheral blast counts relative to pretreatment levels and compare

229 e loaded autologous phytohemagglutinin (PHA) blasts.

230 er of RBCs; CNS3a to 3c, >/= 5 WBCs/muL plus blasts with/without >/= 10 RBCs/muL or clinical signs of

231 thout >/= 10 RBCs/muL or >/= 5 WBCs/muL plus blasts, with WBCs >/= 5 times the number of RBCs; CNS3a

232 le injuries collectively known as polytrauma/blast-related injury (PT/BRI).

233 tested if down-regulation of synj1 prevented blast-induced Tau hyper-phosphorylation.

234 Primary blast wave pressure resulted in activation of Muller gli

235 jury and neuronal inflammation after primary blast exposure.

236 Pure primary blast waves were simulated in compressed gas shock-tubes

237 H2 expression in resistant cells and primary blasts from a subset of relapsed AML patients resulted f

238 bserved with atovaquone treatment of primary blasts isolated from patients with acute myelogenous leu

239 rague Dawley adult rats to unilateral 14 psi blast exposure to induce tinnitus and measured auditory

240 also show improvement over conventional Psi-blast and HMM profile based methods in sequence matching

241 significantly improved over conventional Psi-blast.

242 lt amino acid substitution matrix in the Psi-blast algorithm is replaced by our structure-based matri

243 We found that after exposure to repetitive blast-induced TBI, phosphoinositol biphosphate (PIP2) le

244 Down-regulation of synj1 rescues blast-induced phospholipid dysregulation and prevents de

245 Rice blast is a devastating disease of rice caused by the fun

246 Rice blast is a recurrent fungal disease, and resistance to f

247 Rice blast is thought to involve distinct SNARE-mediated tran

248 feeds half the world's population, and rice blast is often a destructive disease that results in sig

249 To cause rice blast disease, the fungal pathogen Magnaporthe oryzae de

250 such as Magnaporthe oryzae which causes rice blast.

251 1 and MHP1, are highly expressed during rice blast infections.

252 y understanding the role of glycerol in rice blast disease.

253 and microRNA regulation during initial rice blast infection, which would help to develop more robust

254 nicity of filamentous fungi such as the rice blast fungus (Magnaporthe oryzae) remains unclear.

255 al metabolic sources of glycerol in the rice blast fungus and how appressorium turgor is focused as p

256 The rice blast fungus Magnaporthe oryzae elaborates a specialized

257 The rice blast fungus Magnaporthe oryzae spreads in rice biotroph

258 rane trafficking in pathogenesis of the rice blast fungus Magnaporthe oryzae, we identified MoGlo3 as

259 a novel synthetic system involving the rice blast fungus Magnaporthe oryzae.

260 and ETFDH encoding gene (ETFDH) in the rice blast fungus Magnaporthe oryzae.

261 ate Rbp35/CfI25 complex and Hrp1 in the rice blast fungus, some of which are also conserved in other

262 the physiology and pathogenicity of the rice blast fungus.

263 ssorium-mediated plant infection by the rice blast fungus.

264 the most important plant pathogen, the rice blast fungusMagnaporthe oryzae(Mo), was expressed inPich

265 onses, llb shows enhanced resistance to rice blast (Magnaporthe oryzae) and bacterial blight (Xanthom

266 ion, which would help to develop more robust blast-resistant rice plants.

267 from those who had died shortly after severe blast exposures.

268 ional anisotropy and years since most severe blast exposure in a subset of the blast-exposed group, s

269 tral nervous system (CNS) cells to simulated blast resulted in propagating waves of elevated intracel

270 Furthermore, in response to simulated blast, human CNS cells have increased expressions of a r

271 t CNS cells are less responsive to simulated blast.

272 at either one or three months after a single blast event.

273 d groundwater from coal carbonization sites, blast furnace operations, and commercial cyanide applica

274 h trial and delivers increasingly loud sound blasts to the participants, successfully provoking them.

275 rafts, with marked reduction in mean splenic blast counts (P < .01) in 6 of 6 samples.

276 We aimed to test the hypothesis that blast exposure produces unique patterns of damage, diffe

277 es of visual field deficits, indicating that blast forces may significantly affect the eye and visual

278 The blast exposure cases showed a distinct and previously un

279 analysis of host species determinants in the blast fungus resulted in the cloning of avirulence genes

280 to be indicative for a cyanide source in the blast furnace.

281 ost severe blast exposure in a subset of the blast-exposed group, suggesting a specific influence of

282 y of Bruton's tyrosine-kinase (BTK) in their blast cells compared with normal haemopoietic cells, ren

283 The potential effects of brain injury due to blast exposure are of great concern as a history of mild

284 Traumatic brain injury due to blast exposure is currently the most prevalent of war in

285 progressive granulocytosis with evolution to blast crisis, similar to the course of human chronic mye

286 male and female C57BL/6 mice were exposed to blast wave pressure of 300 kPa (43.5 psi) per day for 3

287 evaluate brain injury following exposure to blast is also highlighted.

288 TKI-refractory CML, or after progression to blast crisis (BC), are lacking.

289 that confers non-race-specific resistance to blast.

290 e, they had a high rate of transformation to blast phase.

291 ms and tinnitus were directly dependent upon blast exposure, with both acting as bridge symptoms to o

292 MDR(-ve) blasts were observed to be enriched in samples taken fro

293 Wheat blast first emerged in Brazil in the mid-1980s and has r

294 spotting diseases, and, more recently, wheat blast (in South America and Bangladesh) have become dise

295 at cultivation in Brazil, suggest that wheat blast emerged due to widespread deployment of rwt3 wheat

296 opathological studies have addressed whether blast exposure produces unique lesions in the human brai

297 Taken together, our data suggest that while blast-induced tinnitus may play a role in auditory and l

298 Traumatic Brain Injury (bTBI) increases with blast overpressure (BOP) and impulse in dose-dependent m

299 vational study of US military personnel with blast-related concussive traumatic brain injury (n = 38)

300 ith mild TBI, but they were synergistic with blast exposure in influencing PTSD arousal symptoms.