ライフサイエンスコーパス: necrosis

1 eath (apoptosis) or uncontrolled cell death (necrosis).

2 ausing cell death mainly by apoptosis and/or necrosis.

3 vements in serum biomarkers of apoptosis and necrosis.

4 a-mediated necroptosis, a form of programmed necrosis.

5 ted peroxisomal proliferation, steatosis and necrosis.

6 m susceptible to cystine deprivation-induced necrosis.

7 flammatory infiltrates without cardiomyocyte necrosis.

8 tinued PM10 exposure activated apoptosis and necrosis.

9 ucing hypertrophic signaling, apoptosis, and necrosis.

10 isolated allograft enterectomy due to bowel necrosis.

11 eased P. aeruginosa killing and earlier cell necrosis.

12 we propose that they are forms of programmed necrosis.

13 forms of cell death including apoptosis and necrosis.

14 provide a molecular mechanism for secondary necrosis.

15 lly manifests with morphological features of necrosis.

16 with loss of parallel collagen structure and necrosis.

17 defined by angiogenesis and pseudopalisading necrosis.

18 ne the best-characterized forms of regulated necrosis.

19 helium, leading to vascular inflammation and necrosis.

20 ytic and inflammatory phase called secondary necrosis.

21 the SHS-Tg(+) mice had pronounced epithelial necrosis, alveolar space consolidation, and lymphoid hyp

22 primary acini, CSE+EtOH induced cell death (necrosis and apoptosis), but neither agent alone had thi

23 culosis (Mtb) growth, or progress to central necrosis and cavitation, facilitating pathogen growth.

24 e depletion significantly reduced glomerular necrosis and crescent formation and abrogated monocyte,

25 role of monocytes/macrophages for glomerular necrosis and crescent formation in a renal ANCA-associat

26 K) reduces efferocytosis and promotes plaque necrosis and defective resolution.

27 Necrosis and ethylene-inducing peptide 1-like (NLP) prot

28 Because DFNA5-induced secondary necrosis and GSDMD-induced pyroptosis are dependent on c

29 Finger skin necrosis and histologic signs of severe chronic allograf

30 pectrum of pulmonary granulomas with central necrosis and hypoxia exists.

31 nder 140 mm Hg oxygen showed reduced central necrosis and increased insulin release, compared to thos

32 (Ile81; n=25) displayed reduced limb-tissue necrosis and increased limb tissue perfusion compared wi

33 on macrophages, and (b) whether the reduced necrosis and macrophage apoptosis in plaques of these mi

34 ABV infection, exhibiting only limited tumor necrosis and no change in TME cytokines or TAM phenotype

35 re both compatible with small bowel ischemia-necrosis and perforation.

36 Accumulated ACs in GCs can undergo necrosis and release self-ligands, which may influence t

37 ures of tumor heterogeneity such as adjacent necrosis and stroma in HGSC.

38 tinal inflammation associated with extensive necrosis and systemic dissemination of the bacteria.

39 However, the molecular links between necrosis and the development of atherosclerosis are not

40 aques, MerTK cleavage correlated with plaque necrosis and the presence of ischemic symptoms.

41 ies and redox status that lead to apoptosis, necrosis, and autophagy of tumour cells.

42 signals generated by aberrant proliferation, necrosis, and hypoxia.

43 ntributes to defective efferocytosis, plaque necrosis, and impaired resolution during the progression

44 se largely prevented trypsinogen activation, necrosis, and other parameters of pancreatic injury in m

45 ell disassembly and progression to secondary necrosis, and provide a molecular mechanism for secondar

46 arming resulted in increased mortality, leaf necrosis, and respiration as well as lower carbohydrate

47 It is considered to be a form of regulated necrosis, and, by lacking the "find me" and "eat me" sig

48 s of L. monocytogenes that robustly activate necrosis, apoptosis, or pyroptosis.

49 Therapeutic efficacy and tumor necrosis area were compared by using a one-way analysis

50 the diagnosis and treatment of acute retinal necrosis (ARN).

51 ffer from dental infections, leading to pulp necrosis, arrested tooth-root development and tooth loss

52 milestone in our understanding of regulated necrosis as they identify a ferroptosis-like cell death

53 s-related cell death pathways (apoptosis and necrosis) as they relate to the heart and cardiovascular

54 stine deprivation triggered rapid programmed necrosis, but not apoptosis, in the basal-type breast ca

55 We report acute retinal necrosis caused by the vaccine Oka strain following immu

56 s had significantly lower rates of avascular necrosis, cytomegalovirus, cataracts, new-onset diabetes

57 ion resulted in significantly enhanced tumor necrosis, extensive CD4 T cell accumulation, and high le

58 terestingly, the transmembrane form of tumor necrosis factor (tmTNF) is necessary to robustly activat

59 risk of lymphoma associated with anti-tumor necrosis factor (TNF) agents either alone or in combinat

60 ent P. aeruginosa had higher levels of tumor necrosis factor (TNF) and interleukin-6 (IL-6), more neu

61 previously treated with at least one tumour necrosis factor (TNF) antagonist (which had failed in 96

62 BACKGROUND & AIMS: Although tumor necrosis factor (TNF) antagonists reduce many clinical f

63 thesis that interleukin 17 (IL-17) and tumor necrosis factor (TNF) are key cytokines involved in ampl

64 ery of barrier function in response to tumor necrosis factor (TNF) compared with normal donor EC cult

65 The tumor necrosis factor (TNF) family ligand ectodysplasin A (EDA

66 ive oxygen species (ROS) and paracrine tumor necrosis factor (Tnf) from Kupffer cells caused JNK-medi

67 Tumor necrosis factor (TNF) has a critical role in diverse cel

68 BACKGROUND AND AIMS: Tumor necrosis factor (TNF) is a cytokine that promotes inflam

69 Some mice were given siRNA against tumor necrosis factor (Tnf) mRNA for 6 days; colon tissues wer

70 Dysregulation of tumor necrosis factor (TNF) receptor signaling is a key featur

71 adaptive response driven by increased tumor necrosis factor (TNF) secretion, which leads to activati

72 Analysis of tumor necrosis factor (TNF) signaling pathway which regulates

73 we show that synergistic IFN-gamma and tumor necrosis factor (TNF) stimulation promotes strong activa

74 n the absence of Eiger, the only known tumor necrosis factor (TNF) superfamily homolog in Drosophila,

75 flammatory innate cytokines, including tumor necrosis factor (TNF), IL-6, IL-12, IL-23, and IL-1beta.

76 linked immunosorbent assays quantified tumor necrosis factor (TNF), interleukin (IL)-12, and IL-10 in

77 ory cytokines interleukin 6 (IL-6) and tumor necrosis factor (TNF), leading to activation of signal t

78 , TRIF and ZBP1/DAI and inhibition of tumour necrosis factor (TNF), lipopolysaccharide or polyinosini

79 RG coactivator 1 alpha (PPARGC1A), and tumor necrosis factor (TNF), was changed in adipose tissue by

80 n and osteoclastogenesis by modulating tumor necrosis factor (TNF)-alpha and -beta.

81 and decreased interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and IL-1beta protein levels.

82 production of interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and interleukin (IL)-2, but

83 endothelial growth factor (VEGF-A) and tumor necrosis factor (TNF)-alpha levels.

84 Cytokine interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha produced by NK cells are imp

85 ic effects of P4 and the expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and

86 ted dendritic spine plasticity through tumor necrosis factor (TNF)-alpha-dependent mechanisms.

87 ntiation primary response gene-88, and tumor necrosis factor (TNF)-alpha.

88 Tumor necrosis factor (TNF)-related apoptosis-inducing ligand

89 s of inflammatory cytokines, including tumor necrosis factor (TNF).

90 that of the pro-inflammatory cytokine tumor necrosis factor (TNF).

91 in 6 receptor [sIL-6R], soluble gp130, tumor necrosis factor [TNF]), enterocyte turnover (intestinal

92 s (CD107, CD154, interleukin-2 [IL-2], tumor necrosis factor [TNF], and IFN-gamma) and memory phenoty

93 nt trough drug concentrations for anti-tumor necrosis factor agents and thiopurines to inform clinica

94 No association was found for anti-tumor necrosis factor agents.

95 logics (e.g. vedolizumab) and the anti-tumor necrosis factor agents.

96 ed interleukin-2 (IL-2) (66.4%) and/or tumor necrosis factor alpha (TNF-alpha) (63.7%).

97 cteria-specific CD4+ T cells secreting tumor necrosis factor alpha (TNF-alpha) but not interferon gam

98 ole-4-carboxamide riboside (AICAR), on tumor necrosis factor alpha (TNF-alpha) induction of complemen

99 on of interferon gamma (IFN)-gamma and tumor necrosis factor alpha (TNF-alpha) that induced tumor cel

100 nsitive biosensor for the detection of tumor necrosis factor alpha (TNF-alpha) within the randomly ch

101 interleukin 8 (IL-8), CXCL2, IL-1beta, tumor necrosis factor alpha (TNF-alpha), and IL-6.

102 elicits gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin 2 (IL

103 ers, including interleukin (IL) 1beta, tumor necrosis factor alpha (TNF-alpha), CXCL10, CCL5, IL-6, a

104 dy, we demonstrate that treatment with tumor necrosis factor alpha (TNF-alpha)-neutralizing antibodie

105 t similar to that of cells primed with tumor necrosis factor alpha (TNF-alpha).

106 varphi and inhibited the production of tumor necrosis factor alpha (TNF-alpha)/interleukin-6 (IL-6) i

107 ion during the 12 study weeks to anti-tumour necrosis factor alpha (TNFalpha) agents, immunomodulator

108 ma levels of the inflammatory cytokine tumor necrosis factor alpha (TNFalpha) are increased in age-re

109 r was constructed for the detection of tumor necrosis factor alpha (TNFalpha) by using Poly(3-thiophe

110 Similar results were obtained from tumor necrosis factor alpha (TNFalpha) detection with 3 ng/mL

111 The homotrimeric ligand tumor necrosis factor alpha (TNFalpha) is a key cytokine and i

112 re matching tested the effect of anti-tumour necrosis factor alpha (TNFalpha) therapy exposure within

113 ctivation (i.e. phosphorylation) links tumor necrosis factor alpha (TNFalpha) to pro-inflammatory gen

114 Our previous work demonstrated that tumor necrosis factor alpha (TNFalpha)-activated MSCs signific

115 eactive protein, soluble receptors for tumor necrosis factor alpha 1 and 2, the percentages of CD4+CD

116 type 1 (gamma interferon [IFN-gamma], tumor necrosis factor alpha [TNF-alpha], and interleukin-2 [IL

117 es showed increased expression of A20 (tumor necrosis factor alpha [TNF-alpha]-induced protein 3 [TNF

118 long-term efficacy and safety of anti-tumor necrosis factor alpha agents (anti-TNF) in treating cuta

119 nsitize PEL to the proapoptotic agents tumor necrosis factor alpha and etoposide and are the first to

120 to the extracellular medium, inducing tumor necrosis factor alpha and interleukin 6 expression, thus

121 finitively proven a critical role for tumour necrosis factor alpha and interleukin 6 in disease patho

122 uble interleukin-2 receptor alpha, and tumor necrosis factor alpha and lower levels of insulin-like g

123 cept (trade name, Enbrel), which is a tumour necrosis factor alpha blocker currently used to treat rh

124 rmalized lipopolysaccharide-stimulated tumor necrosis factor alpha expression in Kupffer cells from e

125 ns expressed more gamma interferon and tumor necrosis factor alpha in response to Tax peptides corres

126 ma but without PTSD had higher average tumor necrosis factor alpha receptor II levels (B = 0.05, p <

127 f inflammation (C-reactive protein and tumor necrosis factor alpha receptor II) and endothelial funct

128 arly indicated a potent suppression of tumor necrosis factor alpha release.

129 lasts and brown adipose tissues and by tumor necrosis factor alpha that reduces p63 transcriptional a

130 to modulate the biological activity of tumor necrosis factor alpha through stabilization of the disto

131 l conformational sampling of the human tumor necrosis factor alpha trimer.

132 ocytes that proliferated and produced tumour necrosis factor alpha upon ex-vivo exposure to NAGLU ant

133 percentages of CD4+ Th1 (interleukin2, tumor necrosis factor alpha) and Th17 (interleukin 17A) cells

134 interleukin 6, interleukin 1beta, and tumor necrosis factor alpha) in circulating monocytes, pulmona

135 rophils fed CA-MRSA was independent of tumor necrosis factor alpha, active RIPK-1, and MLKL, but depe

136 IL-8, IL-10, IL-12, interferon gamma, tumor necrosis factor alpha, and granulocyte-macrophage colony

137 ranzyme K, perforin, gamma interferon, tumor necrosis factor alpha, and interleukin-2 production and

138 d the gingival expression of IL-1beta, tumor necrosis factor alpha, and RANKL was significantly reduc

139 l (ie, they produced interferon gamma, tumor necrosis factor alpha, granulocyte-macrophage colony-sti

140 anine amino transferase, expression of tumor necrosis factor alpha, Il6, interferon mRNA, and liver p

141 za A (H5N1) virus induce expression of tumor necrosis factor alpha, interleukin-6, and interleukin-8

142 infarcts were associated with elevated tumor necrosis factor alpha, macrophage inflammatory protein 1

143 Tumour necrosis factor alpha, vascular cell adhesion molecule-1

144 parallel, the proteolytic activity of tumor necrosis factor alpha-converting enzyme (TACE; ADAM17, C

145 NASH, we identified the deubiquitinase tumor necrosis factor alpha-induced protein 3 (TNFAIP3) as a k

146 mutations including Stat3, Stat5b, and tumor necrosis factor alpha-induced protein 3 have been demons

147 oportion of polyfunctional (IFN-gamma+/tumor necrosis factor alpha-positive) CD4+ and CD8+ T cells an

148 ols) exposed to cell stressors such as tumor necrosis factor and adherent-invasive Escherichia coli.

149 ed increased release of IL-10, whereas tumor necrosis factor and cathepsin L release was reduced, fur

150 induced proinflammatory cytokines like tumor necrosis factor and interleukin-1.

151 conventional therapy or therapy with a tumor necrosis factor antagonist were randomly assigned to rec

152 ted to the anti-inflammatory effect of tumor necrosis factor blockers, but a 52-week study conducted

153 APRIL is a member of the tumor necrosis factor cytokine family involved in the regulati

154 ding the long-sought-after nephrin and tumor necrosis factor genes.

155 mide, cyclophosphamide, hemoperfusion, tumor necrosis factor inhibitors, and granulocyte colony-stimu

156 0 of 106 patients (18.9%) treated with tumor necrosis factor inhibitors, but did not lead to disconti

157 was more likely with methotrexate than tumor necrosis factor inhibitors, but having 1 or more infecti

158 had previously inadequate response to tumour necrosis factor inhibitors, with a safety profile consis

159 ss of efficacy, or were intolerant to tumour necrosis factor inhibitors.

160 Monocytes that produce tumor necrosis factor interact with cerebral endothelial cells

161 precise mechanism by which binding of tumor necrosis factor ligands to the extracellular domain of t

162 on of GATA3, and mice with deletion of tumor necrosis factor receptor (TNFR) 1 and TNFR2 (TNFR double

163 The interaction of the tumor necrosis factor receptor (TNFR) CD27 with its ligand CD7

164 Activation of the tumor necrosis factor receptor 1 (TNFR1) death receptor by TNF

165 We hypothesized that tumor necrosis factor receptor 1 (TNFR1) levels are associated

166 aling and cell death pathways, notably tumor necrosis factor receptor 1 (TNFR1) signaling.

167 Tumor necrosis factor receptor 1, E-selectin, hK11, tumor necr

168 Tumor necrosis factor receptor 2 (TNFR2) is known to mediate i

169 Wild-type C57Bl/6 mice or tumor necrosis factor receptor 2 knockout mice, either fed a h

170 kade, by either monoclonal antibody or tumor necrosis factor receptor gene knockout, reduced inflamma

171 eficiency (IMD) pathway resembles the tumour necrosis factor receptor network in mammals and senses d

172 le of neuronally expressed, paralogous tumor necrosis factor receptor super family (TNFRSF) members i

173 4-1BB (CD137, tumor necrosis factor receptor superfamily 9) is an inducible

174 recursors expressed high levels of the tumor necrosis factor receptor superfamily molecule GITR, whos

175 es to mediate signal transduction from Tumor Necrosis Factor Receptor to downstream effector molecule

176 1, angiopoietin-2, IL-6, IL-8, soluble tumor necrosis factor receptor-1, soluble vascular cell adhesi

177 We examined the role of tumor necrosis factor receptor-associated factor 2 (Traf2) in

178 The tumor necrosis factor receptor-associated factor 2 (TRAF2) is

179 mitochondria, where it interacts with tumor necrosis factor receptor-associated factor 2 (TRAF2), a

180 M2 subsets was critically dependent on tumor necrosis factor receptor-associated factor 6 (TRAF6) and

181 ifically induces the ubiquitination of tumor necrosis factor receptor-associated factor 6 (TRAF6).

182 levels of Cathepsin K, TRAP, RANK, and tumor necrosis factor receptor-associated factor 6 mRNAs, wher

183 ptors, IL-1 receptor-associated kinase/tumor necrosis factor receptor-associated factor-6, IL8/CXCR2,

184 , immune deficiency (IMD) signalling (tumour necrosis factor receptor/interleukin-1 receptor, TNFR/IL

185 in the C1QTNF5 gene, encoding C1q And Tumor Necrosis Factor Related Protein 5 (C1QTNF5) has been sho

186 ppaB ligand and increased osteoblastic tumor necrosis factor superfamily member 11 (Tnfsf11) expressi

187 BACKGROUND & AIMS: Variants in the tumor necrosis factor superfamily member 15 gene (TNFSF15, als

188 strongest in those initiated with anti-tumor necrosis factor therapy (beta = 0.79; 95% CI, 0.269-1.31

189 w that timely escalation with an anti-tumour necrosis factor therapy on the basis of clinical symptom

190 by death receptors ligands TNF-alpha (Tumor Necrosis Factor) or TRAIL (TNF-Related Apoptosis-Inducin

191 ear factor-kappaB) activation and TNF (tumor necrosis factor) production by myeloid cells.

192 ls and expression of interferon-gamma, tumor necrosis factor, and EOMES.

193 ad significantly higher levels of CRP, tumor necrosis factor, and interleukin 6 and shorter leukocyte

194 ry markers including interferon gamma, tumor necrosis factor, CXCL13, and CXCL10 with leniolisib ther

195 high levels of inflammatory cytokines: tumor necrosis factor, interleukin (IL)-6, and reactive oxygen

196 d with serum C-reactive protein (CRP), tumor necrosis factor, interleukin 1beta, 6, and 10, leukocyte

197 hophysiologic domains: "inflammation" (tumor necrosis factor, interleukin-6, and -10); "coagulation"

198 d LPS-stimulated ex vivo production of tumor necrosis factor-alpha (P = 0.04) in the WG group than in

199 ng growth factor-beta1 (TGF-beta1) and tumor necrosis factor-alpha (TNF-alpha) play key roles in prog

200 tivity, resulting in downregulation of tumor necrosis factor-alpha (TNF-alpha) production and concomi

201 ts in a significantly higher level of tumour-necrosis factor-alpha (TNF-alpha) secretion and markedly

202 Tumor necrosis factor-alpha (TNF-alpha) stimulation can increa

203 After stimulation of ECs with tumor-necrosis factor-alpha (TNF-alpha) the supernatants of EC

204 of cytokines (interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha)), were analyzed in mat

205 ), interleukin-1beta (IL-1beta), IL-6, tumor necrosis factor-alpha (TNF-alpha), and chemokine (C-X-C

206 ed in Muller cells upregulated retinal tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL

207 e (p38 MAPK) activation and release of tumor necrosis factor-alpha (TNF-alpha).

208 Here we identify that tumour necrosis factor-alpha (TNFalpha) selectively reduces BMP

209 ls, which produced elevated amounts of tumor necrosis factor-alpha (TNFalpha) that contributed to the

210 rations both cytokines synergized with tumor necrosis factor-alpha (TNFalpha) to increase recruitment

211 LPS)-induced human monocyte release of tumor necrosis factor-alpha (TNFalpha) was assessed by ELISA.

212 ression (interleukin-1beta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha], and IL-6) by quantita

213 Third, expression of tumor necrosis factor-alpha and amyloid A mRNA levels increase

214 CC chemokine ligand 20 induction by tumor necrosis factor-alpha and IL-17A was reduced in Trim32-d

215 eas CC chemokine ligand 5 induction by tumor necrosis factor-alpha and IL-4 was enhanced.

216 n of proinflammatory cytokines such as tumor necrosis factor-alpha and IL-6.

217 inflammatory effects of OxPAPC against tumor necrosis factor-alpha and lipopolysaccharide challenge w

218 Tumor necrosis factor-alpha and, to a lesser extent, IL-1beta

219 icenter study evaluated the effects of tumor necrosis factor-alpha antagonist adalimumab on vascular

220 nflammation in patients treated with a tumor necrosis factor-alpha antagonist or placebo and a modest

221 Furthermore, tumor necrosis factor-alpha decreased both mineralocorticoid r

222 release of the proinflammatory marker tumor necrosis factor-alpha in blood displayed a reduction (41

223 ticotropic hormone, interleukin-6, and tumor necrosis factor-alpha in mice exposed to chronic mild st

224 ession of the proinflammatory cytokine tumor necrosis factor-alpha in microglia, and the recruitment

225 Tumor necrosis factor-alpha induced extrinsic apoptosis in con

226 AAT-treated mice showed reduced serum tumor necrosis factor-alpha levels, decreased lymphocytic infi

227 -cell induction and inhibiting T-cell tumour-necrosis factor-alpha production through arginase-2 acti

228 ath compared with wild-type cells, and tumor necrosis factor-alpha release was completely blocked in

229 kin (IL)-1beta, IL-4, IL-6, IL-17, and tumor necrosis factor-alpha using an assay system.

230 A diabetic retinopathy (DR) biomarker, tumor necrosis factor-alpha was selected to evaluate the propo

231 re, TRX80 was found to colocalize with tumor necrosis factor-alpha, a macrophage M1 marker, in human

232 eins (inducible nitric oxide synthase, tumor necrosis factor-alpha, and interleukin 6).

233 0, monocyte chemoattractant protein-1, tumor necrosis factor-alpha, C-reactive protein, and phospholi

234 This dataset showed tumor necrosis factor-alpha, IFN-gamma, transforming growth fa

235 pancreatitis patients, including IL-6, tumor necrosis factor-alpha, IL-1beta, chemokine (C-C motif) l

236 ls of cytokines and chemokines such as tumor necrosis factor-alpha, interferon-gamma, interleukin 10

237 Serum tumor necrosis factor-alpha, interleukins, hemogram, and liver

238 that ECs treated with M1 macrophages, tumor necrosis factor-alpha, or IL-1beta decreased the express

239 ted levels of CB1R, interleukin-1beta, tumor necrosis factor-alpha, the chemokine CCL2, and interfero

240 ed to the targeted treatment with anti-tumor necrosis factor-alpha, which was highly effective in ind

241 st, the matrix metalloproteinase/TACE (tumor necrosis factor-alpha-converting enzyme) inhibitor GM600

242 ivated B cells and negative regulators tumor necrosis factor-alpha-induced protein 3 (A20) and mitoge

243 ivation and upregulation of CXCL10 and tumor necrosis factor-alpha.

244 ukocyte adhesion after treatment with tumour necrosis factor-alpha.

245 t day 1 with an associated decrease in tumor necrosis factor-beta, interferon-gamma, and monocyte che

246 Ectodysplasin (Eda), a tumor necrosis factor-like ligand, is essential for the develo

247 Similarly, orally given LPA blocked tumor necrosis factor-mediated intestinal barrier defect in mi

248 e upregulation of both interferon- and tumor necrosis factor-positive CD4(+) T cells and CD8(+) T cel

249 oxygenation index, interleukin-8, and tumor necrosis factor-R2 was superior to a model of oxygenatio

250 8, interleukin-10, interleukin-18, and tumor necrosis factor-R2 were each strongly associated with al

251 s factor receptor 1, E-selectin, hK11, tumor necrosis factor-related activation-induced cytokine, CHI

252 While tumor necrosis factor-related apoptosis inducing ligand (TRAIL

253 by up-regulation of gene expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL

254 individual cells following exposure to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL

255 and assists TRXR1-regulated arrest of tumor necrosis factor-related apoptosis-inducing ligand-induce

256 d C1QTNF2, encoding for Complement C1q tumor necrosis factor-related protein 2, a secreted adipocytok

257 Tumor necrosis factor-stimulated enhanced expression and secre

258 sted of inflammatory genes, VCAM1, and tumor necrosis factor.

259 diac restricted overexpression of TNF (tumor necrosis factor; Myh6-sTNF).

260 ge of how cells die by regulated pathways of necrosis has increased tremendously.

261 Diverse pathways of regulated necrosis have been reported to contribute to AKI, but th

262 round segregates with protection from tissue necrosis in a shorter congenic fragment of Lsq-1 (C.B6-L

263 ction positively correlated with the area of necrosis in lesions and duration of the lesions.

264 e describe a virus that causes severe thymic necrosis in neonatal mice, characterized by a loss of CD

265 nt groups due to direct induction of thermal necrosis in the tumor core and efficient drug delivery t

266 hat induces cancer cell apoptosis and avoids necrosis in vivo and exploring its molecular mechanism o

267 ANX-A1-deficiency increased cardiac necrosis, inflammation, hypertrophy and fibrosis followi

268 Sensitive detection of cell necrosis is crucial for the determination of cell viabil

269 A key cause of plaque necrosis is defective clearance of apoptotic cells, or e

270 Recent data demonstrate that secondary necrosis is not an accidental epiphenomenon of apoptosis

271 Necroptosis, a programmed form of necrosis, is executed by the mixed lineage kinase domain

272 an occur by apoptosis or a regulated form of necrosis known as necroptosis.

273 lobar distribution, multiple lesions, absent necrosis, microvascular invasion, and tumors beyond the

274 emical, or genetic similarities with classic necrosis, necroptosis, parthanatos, or other forms of no

275 h, such as cells undergoing apoptosis versus necrosis/necroptosis.

276 cytosis of ICs toward the programmed form of necrosis, NETosis.

277 To study the impact of hypoxic necrosis on the efficacy of antimycobacterials and drug

278 such mechanism in vertebrates is programmed necrosis, or "necroptosis", driven by receptor-interacti

279 proteins or genes), which cause cell death, necrosis, or other phenotypes of phloem elements or comp

280 the canonical categories such as apoptosis, necrosis, paraptosis, and autophagy, suggesting that a n

281 gets the plasma membrane to induce secondary necrosis/pyroptosis.

282 Whereas apoptosis and mitochondria-mediated necrosis signaling is well established, the regulatory m

283 d for the prognostic stage, size, grade, and necrosis (SSIGN) score as well as within low-, intermedi

284 molecular machinery that controls secondary necrosis stands out as a promising target for the develo

285 vascular thrombi often exhibited endothelial necrosis surrounded by hemorrhagic effusions and pulmona

286 Necroptosis is a form of programmed necrosis that is regulated by receptor-interacting prote

287 pancreatic edema, infiltration, hemorrhage, necrosis, the release of amylase and lipase.

288 t failure comprised rejection, acute tubular necrosis, urinary tract infection/pyelonephritis, viral

289 Cucumber necrosis virus (CNV) is a member of the genus Tombusviru

290 ect zoospore transmission.IMPORTANCECucumber necrosis virus (CNV), a member of the genus Tombusvirus,

291 he fish rhabdovirus infectious hematopoietic necrosis virus (IHNV) as a model to study aquatic envelo

292 th our model virus, infectious hematopoietic necrosis virus (IHNV), infectivity was significantly inh

293 Satellite tobacco necrosis virus (STNV) is one of the smallest viruses kno

294 Necrosis was observed in these three cell types, and vir

295 Neutrophil necrosis was required for Mtb growth after uptake of inf

296 unknown estrogen receptor status, and comedo necrosis were more likely to have received an RT boost.

297 ected haematoma and an area of proximal skin necrosis were surgically treated.

298 Tumors were assessed for necrosis with hematoxylin-eosin staining.

299 calcium electroporation effectively induced necrosis, with a range of sensitivities observed (36%-88

300 ized that proinflammatory cell death such as necrosis would be proimmunogenic while apoptosis would b