ライフサイエンスコーパス: necrotic

1 es, but few of these myocytes appeared to be necrotic.

2 ular supply and >80% of the tumor tissue was necrotic.

3 Deletion of CTSB affected apoptotic but not necrotic acinar cell death.

4 Numbers of necrotic airway epithelial cells were elevated and corre

5 e of pro-interleukin-1alpha (IL-1alpha) from necrotic alveolar macrophages (AM), which activated endo

6 emonstrate a key role for pro-IL-1alpha from necrotic alveolar macrophages in LPS-mediated ALI, as a

7 ical changes occurring to the NE, during the necrotic and apoptotic cell death process, using the xCE

8 Radiological examination showed a necrotic and cystic mass arising from the operated area

9 C3HeB/FeJ mice, which develop necrotic and hypoxic tuberculosis lesions, were aerosol-

10 tics is to reinstate normal pulp function in necrotic and infected teeth that would result in reestab

11 ive' response in which meristem cells become necrotic and kill E. solidaginis hatchlings before gall

12 and within tumors, and discriminates between necrotic and living tumor areas.

13 Macrophages in necrotic and symptomatic atherosclerotic plaques in huma

14 nventional, R+5, R+10, and R+20 lesions were necrotic and transmural, whereas some R+0 lesions were n

15 average values in the whole tumor or average necrotic and viable tissues.

16 or star-shaped chlorotic lesions that become necrotic, and infested plants may be distorted.

17 f rat brain, and in human ovarian cancerous, necrotic, and normal tissues was achieved.

18 Worthy of note, eATP did not cause necrotic, apoptotic, or pyroptotic cell death, and its e

19 Significant lower viabilities and more necrotic/apoptotic cells were found when these cancer ce

20 ted significantly (p < 0.05) decreased acute necrotic/apoptotic injury and significantly (p < 0.05) i

21 of necrotic fibers (+115%) and percentage of necrotic area (+204%) at 7 d, increased number of intram

22 isotropic ratio and the percentage of muscle necrotic area was found.

23 y comparing mice with no or mild (0%-5% mean necrotic area) and severe (>5% mean necrotic area) muscl

24 -5% mean necrotic area) and severe (>5% mean necrotic area) muscle necrosis, an area under the receiv

25 o caused massive DNA deposition within liver necrotic areas, together with an intravascular DNA coati

26 tated discrimination between blood lakes and necrotic areas.

27 dose and form dense cellular clusters around necrotic areas.

28 marginal), 2 (partial), 3 (segmental), or 4 (necrotic) as previously defined.

29 athway as a key factor in the development of necrotic atherosclerotic plaques.

30 rophage TIM-4 in the engulfment of apoptotic/necrotic bodies in innate immunity-mediated disease stat

31 swelling, recurrent facial pain and exposed necrotic bone after previous extraction of tooth 47.

32 bone marrow-derived macrophages treated with necrotic bone showed increased extracellular signal-regu

33 In conclusion, necrotic bone stimulates macrophage-inflammatory respons

34 and lack of collagen fiber insertion in the necrotic bone were associated with impaired socket heali

35 receptor mechanisms involved in sensing the necrotic bone, using a piglet model of Legg-Calve-Perthe

36 t activity was responsible for resorbing the necrotic bone, which in turn stimulated the deposition o

37 d by surgical intervention with resection of necrotic bowel loops and in more than half of the cases

38 In response to ischemia, damaged/necrotic brain cells discharge factors that polarize MPh

39 o rapid, predictable, and consistently sized necrotic brain lesions, inflammatory responses, and beha

40 etry (MS), we report the lipid MS profile of necrotic breast cancer with Desorption Electrospray Ioni

41 Recruited monocytes clear necrotic cardiomyocytes and differentiate into cardiac m

42 We found that necrotic cardiomyocytes released a heat-labile proinflam

43 Indeed, necrotic cardiomyocytes released IL-1alpha, but not IL-1

44 Rifampicin even accumulates in necrotic caseum, a critical lesion site where persisting

45 low toxicity and the absence of apoptotic or necrotic cell death after 24 or 48 h of incubation.

46 ore, hematoxylin and eosin staining revealed necrotic cell death and cell loss in Pgc-1(c) livers and

47 AKI is histologically characterized by necrotic cell death and inflammation.

48 mitochondrial respiratory chain defects and necrotic cell death are mutually dependent on and obliga

49 The mechanism of neutrophil impairment was necrotic cell death as determined by morphological analy

50 In contrast, programmed necrotic cell death causes release of immunostimulatory

51 -associated caspase-8 activity and increased necrotic cell death following antigenic stimulation, imp

52 g of CAPN5, has been shown to be involved in necrotic cell death in Caenorhabditis elegans.

53 te that the C-terminal domain of CpnT causes necrotic cell death in eukaryotic cells.

54 Virulent M. tuberculosis strains induce necrotic cell death in macrophages by an obscure molecul

55 a CD44/ITGA4 containing complex and triggers necrotic cell death in multiple myeloma cell lines.

56 and neurobehavioral deficits; apoptotic and necrotic cell death in neurons were reduced by Rapamycin

57 sine triphosphate depletion, and the ensuing necrotic cell death in skin fibroblasts, and this effect

58 s oxidative burst, mitochondrial damage, and necrotic cell death in TSC-deficient cells in a highly s

59 fication and discrimination of apoptotic and necrotic cell death in vitro is challenging.

60 Programmed necrotic cell death induced by the tumor necrosis factor

61 ELLigence technology and AFM have shown that necrotic cell death induced the expansion of the cell ad

62 gical and genetic analyses revealed that the necrotic cell death is distinct from the RIP1/3 pathway-

63 mpound 1 concentration-dependently inhibited necrotic cell death pathway activation and 2.5 mM compou

64 chondrial membrane potential (DeltaPsim) and necrotic cell death pathway activation.

65 on, lactate dehydrogenase (LDH) release, and necrotic cell death that were blocked by cyclosporin A (

66 mitochondrial respiratory chain defects and necrotic cell death to the BH3-only protein Bcl-2-like 1

67 amage caused by UVA to mitochondria leads to necrotic cell death via adenosine triphosphate depletion

68 termined reduced cell proliferation, massive necrotic cell death, and fibrosis.

69 to I/R increased reactive oxygen species and necrotic cell death, both of which were mitigated by ATF

70 to I/R increased reactive oxygen species and necrotic cell death, both of which were mitigated by ATF

71 scription and affected genes associated with necrotic cell death, chromosome condensation, and mRNA p

72 eases (HD) selectively induces a new form of necrotic cell death, in which endoplasmic reticulum (ER)

73 cellular molecules associated with regulated necrotic cell death, replicating the characteristics of

74 Necroptosis, a regulated form of necrotic cell death, requires the activation of the RIP3

75 nvolves a newly described form of programmed necrotic cell death, termed necroptosis.

76 ating and suppressing two regulated forms of necrotic cell death, termed pyroptosis and necroptosis,

77 iving increased generation of superoxide and necrotic cell death, which was rescued by genetic inhibi

78 ve oxygen species production, culminating in necrotic cell death.

79 ction of reactive oxygen species and massive necrotic cell death.

80 ining uPAS cargo and leading to AIF-mediated necrotic cell death.

81 entiates MLKL phosphorylation/activation and necrotic cell death.

82 pecifically the role of Bax/Bak in regulated necrotic cell death.

83 mage in TEN through activation of programmed necrotic cell death.

84 X was accompanied by contractile failure and necrotic cell death.

85 todynamic injury, resulting in predominantly necrotic cell death.

86 fy mucosal inflammation, ii) the capacity of necrotic cell lysates from HT29 cells or human IECs to i

87 Necrotic cell lysates potently induced HIF IL-6 and IL-8

88 IL-1alpha was the key IEC-derived necrotic cell product involved in HIF cytokine productio

89 We investigated: i) whether IEC-released necrotic cell products (proinflammatory mediators) ampli

90 re composite mass consisting of tumor cells, necrotic cell, or inflammatory tissues.

91 Taken together, these results suggest that necrotic cell-derived TLR4 agonists activate intrarenal

92 eyond the simple view of 'apoptotic' versus 'necrotic' cell death.

93 ation when released from activated immune or necrotic cells and drives the pathogenesis of various in

94 s) were incubated with cellular fragments or necrotic cells and incubated with either indirect or dir

95 We hypothesized that sensing of necrotic cells by DNGR-1 plays a determinant role in the

96 cious cycle including the uptake of infected necrotic cells by other phagocytes, Mtb growth therein,

97 pheres with an outer rim of viable cells but necrotic cells centrally.

98 tic accumulation of macrophages, which clear necrotic cells from the liver after carbon tetrachloride

99 HIF-1alpha in orchestrating the clearance of necrotic cells from the liver and demonstrated a key rol

100 that extracellular RNA (exRNA) released from necrotic cells induces cytokine production in cardiomyoc

101 day 1 and were full of intact neutrophils or necrotic cells on day 2.

102 into account the balance between living and necrotic cells proved to be able to reproduce the experi

103 hus, in addition to bacterial dissemination, necrotic cells provide first a niche for bacterial repli

104 e of micro-organisms (sterile inflammation), necrotic cells release damage-associated molecular patte

105 Necrotic cells release danger signals, activating innate

106 During sterile inflammation, necrotic cells release pro-inflammatory molecules includ

107 In contrast, many neutrophils and necrotic cells were present at the edge of Deltasse muta

108 ids (layers of proliferating, quiescent, and necrotic cells).

109 pair (CCP1/2), tethering active IL-33 within necrotic cells, preventing its release, and forestalling

110 ous nucleic acids released from apoptotic or necrotic cells.

111 (CD8alpha(+) DCs) and is involved in sensing necrotic cells.

112 urfaces such as the extracellular matrix and necrotic cells.

113 e LL37 and double stranded-RNA released from necrotic cells.

114 damage molecules, HMGB1 or hyaluronan, or to necrotic cells; although they secreted IL-6 and IL-8 in

115 led different cancer cells with induction of necrotic cellular morphology while causing no detectable

116 F ablation was noted in 3% (95% CI: 0, 9) of necrotic CLMs with margins of at least 5 mm.

117 Postpancreatitis necrotic collections were enriched in UFAs.

118 Patients with postpancreatitis necrotic collections were obese, and 13 of 15 had biliar

119 The mature plaque (necrotic, containing dendritic cells and CD8 Tcells) cou

120 vo quantitation of calcification, lipid-rich necrotic core (LRNC), and matrix was assessed with stati

121 as characterized by halted expansion of the necrotic core and accumulation of macrophages along with

122 impaired inflammation resolution, notably a necrotic core and thinning of a protective fibrous cap t

123 , including a thinner fibrous cap, increased necrotic core area, and increased intraplaque hemorrhage

124 /-4.82 versus 8.42+/-4.57 mm(2); P=0.01) and necrotic core areas (1.59+/-0.99 versus 1.03+/-0.85 mm(2

125 rosclerotic plaques, characterized by bigger necrotic core areas and increased macrophage apoptosis.

126 erosclerotic plaques characterized by bigger necrotic core areas, enhanced VSMC apoptosis, and reduce

127 eased the relative fibrous cap and decreased necrotic core areas.

128 including fibrous cap thinning and extensive necrotic core areas.

129 lesions and controlling the expansion of the necrotic core by impairing efferocytosis.

130 macrophage content, overt cap thinning, and necrotic core expansion as the most prominent features.

131 The poor definition of necrotic core facing border of FC and the neointimal pre

132 RATIONALE: Necrotic core formation during the development of athero

133 (T188A) showed increased atherosclerosis and necrotic core formation in vivo, whereas VSMC-specific T

134 The necrotic core has long been a hallmark of the vulnerable

135 LO1-750 specifically identified necrotic core in ex vivo human coronary lesions.

136 posure of highly thrombogenic, red cell-rich necrotic core material.

137 ques, and that it does so without increasing necrotic core of plaques or causing detectable side effe

138 Furthermore, in the BVS arm, necrotic core pre-procedure was an independent determina

139 and underlying thrombus burden: presence of necrotic core prolapse was more frequent in thrombosed l

140 eated mice, determined by an 80% decrease in necrotic core size and a 50% increase in plaque collagen

141 Necrotic core size was also reduced in the model of shea

142 d monocyte responses were not modulated, but necrotic core size was greater, even when adjusting for

143 Both lesion and necrotic core size were significantly reduced in ApoE(-/

144 oronary events have larger plaque volume and necrotic core size with greater positive vessel remodeli

145 Minimum cap thickness over necrotic core was 155 +/- 90 mum.

146 y lesions that are unlikely to possess large necrotic core, rendering them safe for treatment with me

147 dvanced lesions by formation of a lipid-rich necrotic core, which may rupture and cause myocardial in

148 romotes lesion growth and establishment of a necrotic core.

149 hough the atherosclerotic plaques with large necrotic cores (independent of the degree of luminal ste

150 ed necrosis, contributes to the formation of necrotic cores in atherosclerotic plaque in animal model

151 s characterized by organized granulomas with necrotic cores that bear striking resemblance to those o

152 loid-specific deletion of CaMKII had smaller necrotic cores with concomitantly thicker collagen caps.

153 A distinct type of plaque containing large necrotic cores with thin fibrous caps often precipitates

154 It is proposed that the presence of large necrotic cores within the neointima may be associated wi

155 ssociated with increased atherosclerosis and necrotic cores, and a decrease in plaque collagen.

156 Apoptotic cells, necrotic cores, and proinflammatory VCAM-1 (vascular cel

157 soluble Mer, improved efferocytosis, smaller necrotic cores, thicker fibrous caps, and increased rati

158 membranes, the internal elastica lamina, and necrotic cores.

159 infarctions have thin fibrous caps and large necrotic cores; however, these features alone do not rel

160 The organism was isolated from the patient's necrotic cornea, which perforated despite coverage with

161 ssues correlates directly with the extent of necrotic damage during F. tularensis infection.

162 ndrial depolarization, oxidative stress, and necrotic death also in B16 mouse melanoma cells.

163 trations and glucosyltransferase-independent necrotic death at higher concentrations.

164 ter of survival) induced rapid apoptotic and necrotic death in infected cells.

165 Defining the in vivo relevance of necrotic death is hampered because the molecules initiat

166 ization significantly diminished LPS induced necrotic death of AM and pro-IL-1alpha release.

167 P2X7R deficiency significantly reduced necrotic death of AM and release of pro-IL-1alpha into t

168 Specifically, oxidative stress increased necrotic death of inflammatory cells, thereby resulting

169 High doses of sorafenib induced necrotic death of isolated myocytes in vitro, but lower

170 melanoma growth in C57BL/6 mice by inducing necrotic death of tumor cells, without causing liver, sp

171 en species production, eventually leading to necrotic death of U251 glioma cells but not primary astr

172 es a previously unrecognized novel regulated necrotic death pathway that involves mitochondrial homeo

173 erile injuries is necessary for clearance of necrotic debris and for coordination of tissue regenerat

174 In vitro, AIM enhanced the engulfment of necrotic debris by macrophages derived from zymosan-indu

175 sue from mutant-infected mice had widespread necrotic debris, but the spleens lacked necrosis and dis

176 nclude antigens present in apoptotic bodies, necrotic debris, exosomes or even release of non-vesicul

177 The percentage of apoptotic or necrotic dendritic cells was evaluated by annexin-V and

178 ted protein DFNA5 after Asp270 to generate a necrotic DFNA5-N fragment that targets the plasma membra

179 y IL-1alpha from adjacent damaged VSMCs, and necrotic ECs could activate neighboring normal ECs and V

180 kine activity, and what controls cleavage in necrotic ECs is currently unknown.

181 However, necrotic endometrial cells did not accumulate intracellu

182 Necrotic enteritis (NE) caused by Clostridium perfringen

183 , causing autologous immune stimulation upon necrotic exposure.

184 iency as demonstrated by increased number of necrotic fibers (+115%) and percentage of necrotic area

185 srupted granuloma architecture with expanded necrotic foci and reduced tissue hypoxia, and accelerate

186 c-Fos-expressing livers display necrotic foci, immune cell infiltration, and altered hep

187 in the pseudopalisading cells that surround necrotic foci.

188 DICE), a type of cell death that resembles a necrotic form of mitotic catastrophe suggesting that CD9

189 r with exposure of P-selectin, distinguishes necrotic from apoptotic platelets and correlates with pr

190 he macrophage phagosome and later within the necrotic granuloma.

191 t & Microbe, Pagan et al. (2015) reveal that necrotic granulomas develop when macrophage supply is in

192 Second, stable necrotic granulomas with low CFU counts and limited infl

193 MCs have the ability to label differentially necrotic HeLa cells from living cells.

194 Indeed, necrotic hepatocytes were efficiently captured/engulfed

195 mic liver IRI, we employed hydrogen peroxide-necrotic hepatocytes, which readily present PS.

196 Necrotic human primary hepatocytes exposed to acetaminop

197 rosis was associated with virulence, whereas necrotic hypersensitive-like response was not.

198 Moreover, immune responses triggered by necrotic Il1a(-/-) cardiomyocytes were markedly reduced.

199 of the pulp-dentin complex, particularly in necrotic, immature permanent teeth.

200 zobia and their symbiotic plant cells become necrotic immediately after rhizobia are released from in

201 exerts cardioprotective effects by reducing necrotic injury and edema formation via adenosine-depend

202 al neuron cultures and reduced infarct size, necrotic injury, and cerebral edema formation after midd

203 perfusion failure, and reduced apoptotic and necrotic injury.

204 ite (tibia vs jaw) nor pathology (healthy vs necrotic jaw bone tissue) affected the averaged spectral

205 to the release of noncoding RNA (ncRNA) from necrotic keratinocytes that activates Toll-like receptor

206 ted the percentage of CHX-damaged cells from necrotic/late to early apoptotic events, and modulated m

207 rapid weight loss, bacteremia, and abdominal necrotic lesion formation.

208 ed approaches are an important complement to necrotic lesion-based approaches and should be used in c

209 sis and treatment can prevent progression of necrotic lesions and bone collapse.

210 eins, and manganite [Mn(III)] accumulated in necrotic lesions apparently through low Mn sequestration

211 es of seedlings showed significantly smaller necrotic lesions compared with nonprimed plants, coincid

212 pregulate p50 transcription and induce local necrotic lesions in an A. tumefaciens infiltration assay

213 red delivery of antifungals to hyphae within necrotic lesions is thought to contribute to therapeutic

214 ct plants, but they can colonize and develop necrotic lesions on wounded leaves and stems.

215 D mice verified that they do not exhibit the necrotic lesions that are usually associated with SCD.

216 seedlings silenced for Sl2/3-MMP expression, necrotic lesions were observed at the base of the hypoco

217 drug-tolerant persister population only when necrotic lesions were present.

218 chelerythrine-driven caspase activation and necrotic-like cell death.

219 f caspases prevented chelerythrine-triggered necrotic-like cell death.

220 aspases can drive cells to undergo a form of necrotic-like regulated cell death.

221 -mediated cytotoxicity was compatible with a necrotic-like type of cell death.

222 ed from damaged hepatocytes accumulates into necrotic liver and the impact of its recognition by the

223 onse to necrotic liver injury and found that necrotic liver cells induced eosinophil recruitment.

224 Necrotic liver induced eosinophil IL-1beta and IL-18 sec

225 n vivo model to study the immune response to necrotic liver injury and found that necrotic liver cell

226 These mutant mice presented with severely necrotic liver parenchyma and significantly larger hypox

227 paucibacillary model in mice, which develops necrotic lung granulomas after infection with Mycobacter

228 that have alleviated cell death, less severe necrotic lung lesions, more efficient Mtb growth control

229 significant levels of active IL-1alpha in EC necrotic lysates without alteration in protein levels.

230 Type 3 seeds were composed of more than 90% necrotic material admixed with few macrophages and viabl

231 Oxidized necrotic material loses its stimulatory capacity for MSC

232 e and dilated bile ducts filled with caseous necrotic material were seen intra-operatively.

233 "Cloud" seeds are mostly composed of necrotic material, explaining their lack of therapeutic

234 at 3-bromopyruvate promotes cell death via a necrotic mechanism that does not involve reactive oxygen

235 eral miliary lesions in the lungs along with necrotic mediastinal lymphadenopathy.

236 iR-218) is decreased significantly in highly necrotic mesenchymal GBM, and orthotopic tumor studies r

237 ival and tumor angiogenesis, particularly in necrotic mesenchymal tumors.

238 Here, we show that pro-necrotic murine CMV M45 mutant virus drives virus-induce

239 We observed that regenerating and necrotic muscle fibers in muscle biopsy samples from DMD

240 thy (NAM) is characterized pathologically by necrotic muscle fibers with absent or minimal inflammati

241 ion in dermatomyositis, lupus nephritis, and necrotic muscle fibres in Duchenne dystrophy.

242 T1 cutoff values for oedematous versus necrotic myocardium were identified as 1251 ms and 1400

243 from survival analysis); low risk/completely necrotic (n = 7; zero relapses), intermediate risk (n =

244 ther positive, viable tumor (V) or negative, necrotic (N).

245 lso shows that cellular RNA decreases during necrotic, necroptotic, and apoptotic cell death caused b

246 sented with higher percentages of healthy or necrotic neutrophils but lower percentages of apoptotic

247 Few intact and necrotic neutrophils were detected at MGAS315 infection

248 ntages of early apoptotic and late apoptotic/necrotic neutrophils were similar.

249 defense, little is known about Mtb-infected necrotic neutrophils.

250 Necrotic nuclei showed a round shape and presence of nuc

251 (mdDCs) and murine DCs and did not have any necrotic or apoptotic effects even at high densities.

252 tosis, without altering recognition of live, necrotic, or Ig-opsonized cells.

253 hole tumor (P = 0.0009, P = 0.02) as well as necrotic (P = 0.008, P = 0.02) and viable (P = 0.003, P

254 (18)F-FDG in the whole tumor (P = 0.001) and necrotic (P = 0.02) and viable (P = 0.0001) tissues.

255 The cysts and twisted necrotic part of the greater omentum were excised at sur

256 ifference in longest diameter (P = .001) and necrotic part of the tumor (P = .014) between low-risk t

257 hich it prevents the activation of intrinsic necrotic pathway in response to oxidative stress.

258 airway epithelial cells via the apoptotic or necrotic pathway; involvement of the pyroptosis pathway

259 red to be caused by deposition of AIM at the necrotic peritoneum in AIM (+/+) mice.

260 When released from activated or necrotic phagocytes, extracellular MRP8/MRP14 promote in

261 ogenous ROS in the form of H2O2 reversed the necrotic phenotype and restored CD95 expression on infec

262 urred 72 hours after treatment; eosinophilic necrotic plugs formed within sebaceous glands, and the n

263 On necropsy, a large number of necrotic polymorphonuclear leukocytes (PMNs) were observ

264 f interest (ROIs) corresponding to enhancing necrotic portions of tumor and peritumoral edema were dr

265 r heterogeneity, and spatial distribution of necrotic/proliferating cells.

266 nfection, a population of macrophages became necrotic, providing a niche for M. tuberculosis replicat

267 c implants and adjacent teeth with vital and necrotic pulps.

268 Strong correlations were found for the necrotic (r = 0.88) and viable fractions (r = 0.87) betw

269 Prolonged necrotic regenerative cycles coupled with oncogenic STAT

270 Furthermore, we successfully detected necrotic regions within these tumor spheroids based on i

271 , in terms of location, size and presence of necrotic regions, to determine the ideal infusion site a

272 They are also enriched in perivascular and necrotic regions.

273 osteocalcin in the osteoblasts localized in necrotic regions.

274 nto Arabidopsis accession Columbia induced a necrotic response, whereas accession Brno (Br-0) showed

275 pro), which serves to abrogate RIP3-mediated necrotic signaling and induce a nonnecrotic form of cell

276 Necrotic signaling requires RIP3 binding to one of three

277 -HAC, wheat ears accumulated up to 40% fewer necrotic spikelets.

278 OX lines developed brown necrotic spots on the leaves that did not appear on null

279 hannels also participate as causal actors in necrotic swelling and apoptotic volume decrease.

280 very common clinical sign - hardening of the necrotic testicle.

281 ges plays a major role in the development of necrotic, thin-capped plaques.

282 is 100%, but reduced to 80% if targeting of necrotic tissue from previous transurethral resections o

283 Defective clearance of necrotic tissue interferes with amelioration of tissue i

284 low activity on SPECT and the percentage of necrotic tissue on immunohistochemistry.

285 w muscle synthesis, the human heart replaces necrotic tissue with deposition of a noncontractile scar

286 otomy and resection of this area showed only necrotic tissue with no viable melanoma cells.

287 Surgery included debridement of necrotic tissue, carpal tunnel decompression, and extern

288 ic cells specialize in cross-presentation of necrotic tissue-derived epitopes to directly activate cy

289 IAIP and HMW-HA colocalized with histones in necrotic tissues and areas that displayed neutrophil ext

290 n (the time points at which cells migrate to necrotic tissues).

291 ssociated with well-perfused, hypoxic and/or necrotic tumor compartments.

292 The amount of necrotic tumor tissue on contrast material-enhanced arte

293 detected in seconds with single MS scans of necrotic tumor tissue smears, which further accelerates

294 crosis, may permit rapid characterization of necrotic tumors from tissue slices.

295 th PC but considered them as opportunists in necrotic tumour.

296 from bluish-red infiltrations to mutilating necrotic ulcerations.

297 duces vessel inflammation after release from necrotic vascular smooth muscle cells (VSMCs).

298 enograft, (2) classification of these areas (necrotic/viable) to compare similar types of tissues, (3

299 ation of anti-MG1 HNPs can enlarge a tumor's necrotic zone with photothermal ablation.

300 immunologic response at the perimeter of the necrotic zone.